Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

CLINICAL TEXTBOOK OF ADDICTIVE DISORDERS

Clinical Textbookof Addictive DisordersTHIRD EDITIONEdited byRICHARD J. FRANCESSHELDON I. MILLERAVRAM H. MACKTHE GUILFORD PRESSNew York London

© 2005 The Guilford PressA Division of Guilford Publications, Inc.72 Spring Street, New York, NY 10012www.guilford.comAll rights reservedNo part of this book may be reproduced, translated, stored in a retrieval system, ortransmitted, in any form or by any means, electronic, mechanical, photocopying,microfilming, recording, or otherwise, without written permission from the Publisher.Printed in the United States of AmericaThis book is printed on acid-free paper.Last digit is print number: 9 8 7 6 5 4 3 2 1Library of Congress Cataloging-in-Publication DataClinical textbook of addictive disorders / edited by Richard J. Frances, Sheldon I.Miller, Avram H. Mack.—3rd ed.p. cm.Includes bibliographical references and index.ISBN 1-59385-174-X (hardcover)1. Substance abuse. 2. Alcoholism. I. Frances, Richard J. II. Miller, Sheldon I.III. Mack, Avram H.RC564.C55 2005616.86—dc222004026092

About the EditorsRichard J. Frances, MD, is Clinical Professor in the Department of Psychiatryat New York University School of Medicine and Director of Public and ProfessionalEducation at Silver Hill Hospital in New Canaan, Connecticut. He isalso in private practice in New York City. Dr. Frances was former President andMedical Director at Silver Hill Hospital; was founding president of the AmericanAcademy of Addiction Psychiatry; and helped found and chaired theCouncil of Addiction Psychiatry for the American Psychiatric Association. Heis the author of several hundred articles and several books, and is on numerouseditorial boards of journals. Dr. Frances frequently lectures on addiction psychiatryand has appeared numerous times as a guest on Court TV.Sheldon I. Miller, MD, is the Lizzie Gilman Professor of Psychiatry and formerChairman of the Department of Psychiatry and Behavioral Sciences at NorthwesternUniversity. During his career, he has served on many boards and committeesof many national and local organizations. Dr. Miller has authored orcoauthored over 60 scientific articles, chapters, and books. He is Editor-in-Chief of the American Journal on Addictions and was a founder of the AmericanAcademy of Addiction Psychiatry. Dr. Miller is on the Board of Directors of theAccreditation Council for Graduate Medical Education and the AmericanBoard of Emergency Medicine. He also currently serves as Vice Chair of theAmerican Psychiatric Association’s Council on Medical Education and LifelongLearning.Avram H. Mack, MD, is Assistant Professor of Psychiatry at the Institute ofPsychiatry of the Medical University of South Carolina in Charleston. He is agraduate of the University of Michigan–Ann Arbor and of Cornell Universityv

viAbout the EditorsMedical College. Dr. Mack has extensive experience in organized medicine andpsychiatry. His other areas of interest in psychiatry have included development,the psychiatric presentation of medical disorders, and the history of psychiatricclassification. As a child and forensic psychiatrist, he has treated or evaluatedindividuals with addictions in many different settings, including general inpatient,outpatient, correctional, juvenile justice, and community. Dr. Mack haslectured to medical groups, bar associations, patient groups, and other mentalhealth professionals as well.

ContributorsMichelle C. Acosta, PhD, Department of Psychiatry, St. Luke’s–Roosevelt HospitalCenter, New York, New YorkD. Andrew Baron, PhD, Department of Psychiatry and Behavioral Medicine,Temple University, Philadelphia, PennsylvaniaDavid A. Baron, DO, MSEd, Department of Psychiatry and Behavioral Medicine,Temple University, Philadelphia, PennsylvaniaSteven H. Baron, PhD, Department of Social Sciences, Montgomery CountyCommunity College, Blue Bell, PennsylvaniaJudith S. Beck, PhD, Beck Institute for Cognitive Therapy, Bala Cynwyd,PennsylvaniaSheila B. Blume, MD, Department of Psychiatry, State University of New York atStony Brook School of Medicine, Stony Brook, New YorkOscar G. Bukstein, MD, MPH, Department of Psychiatry, Western PsychiatricInstitute and Clinic, Pittsburgh, PennsylvaniaAlisa B. Busch, MD, Department of Psychiatry, Harvard Medical School,Cambridge, Massachusetts; Alcohol and Drug Abuse Treatment Program, McLeanHospital, Belmont, MassachusettsKathleen M. Carroll, PhD, Department of Psychiatry, Yale University School ofMedicine, New Haven, Connecticut; Department of Psychiatry, VA ConnecticutHealthcare System, West Haven, ConnecticutRicardo Castañeda, MD, Department of Psychiatry, New York University School ofMedicine, New York, New YorkStephen L. Dilts, Jr., MD, MBA, Department of Psychiatry, Penn State College ofMedicine, University Park, Pennsylvania; Department of Behavioral Health,WellSpan Health, York, Pennsylvaniavii

viiiContributorsStephen L. Dilts, MD, PhD, Department of Psychiatry, University of ColoradoHealth Sciences Center, Denver, ColoradoLance M. Dodes, MD, Department of Psychiatry, Harvard Medical School,Cambridge, MassachusettsCaroline M. DuPont, MD, DuPont Clinical Research, Rockville, Maryland;Department of Psychiatry, Johns Hopkins University, Baltimore, MarylandRobert L. DuPont, MD, Institute for Behavior and Health, Rockville, Maryland;Department of Psychiatry, Georgetown University, Washington, DCRichard J. Frances, MD, Silver Hill Hospital, New Canaan, Connecticut;Department of Psychiatry, New York University School of Medicine, New York,New York; private practice, New York, New YorkHugo Franco, MD, Dual Diagnosis Unit, New York University Hospital, New York,New York; private practice, Eatontown, New JerseyJohn Franklin, MD, Department of Psychiatry and Behavioral Sciences, FeinbergSchool of Medicine, Northwestern University, Chicago, IllinoisMarc Galanter, MD, Department of Psychiatry, New York University School ofMedicine, New York, New YorkTony P. George, MD, Department of Psychiatry, Yale University School ofMedicine, New Haven, ConnecticutJon E. Grant, JD, MD, Department of Psychiatry and Human Behavior, BrownUniversity, Providence, Rhode IslandDeborah L. Haller, PhD, Department of Psychiatry, St. Luke’s–Roosevelt HospitalCenter, New York, New YorkFrancis Hayden, MD, Department of Psychiatry, New York University School ofMedicine, New York, New YorkAnthony W. Heath, PhD, United Behavioral Health, Schaumburg, IllinoisJames M. Hill, PhD, Department of Psychiatry, University of Medicine andDentistry of New Jersey, Newark, New JerseyNorman Hymowitz, MD, Department of Psychiatry, University of Medicine andDentistry of New Jersey, Newark, New JerseyJeffrey P. Kahn, MD, Department of Psychiatry, Weill Medical College of CornellUniversity, New York, New YorkYifrah Kaminer, MD, Department of Psychiatry, University of Connecticut HealthCenter, Farmington, ConnecticutCheryl Ann Kennedy, MD, Department of Psychiatry, University of Medicine andDentistry of New Jersey, Newark, New Jersey

ContributorsixEdward J. Khantzian, MD, Department of Psychiatry, Harvard Medical School,Cambridge, MassachusettsKenneth L. Kirsh, PhD, Symptom Management and Palliative Care Program,Markey Cancer Center, University of Kentucky, Lexington, KentuckyHerbert D. Kleber, MD, Department of Psychiatry, College of Physicians andSurgeons, Columbia University, New York, New YorkThomas R. Kosten, MD, Department of Psychiatry, Yale University School ofMedicine, New Haven, Connecticut; Department of Psychiatry, VA ConnecticutHealthcare System, West Haven, ConnecticutPetros Levounis, MD, The Addiction Institute of New York, St. Luke’s–RooseveltHospital Center, and Department of Psychiatry, College of Physicians and Surgeons,Columbia University, New York, NYBruce S. Liese, PhD, Department of Family Medicine, University of Kansas MedicalCenter, Kansas City, KansasMarsha M. Linehan, PhD, Department of Psychology, University of Washington,Seattle, WashingtonDavid Lussier, MD, Division of Geriatric Medicine, Montreal General Hospital,McGill University, Montreal, Quebec, CanadaThomas R. Lynch, PhD, Department of Psychiatry and Behavioral Sciences, DukeUniversity Medical Center, and Department of Psychology, Duke University,Durham, North CarolinaAvram H. Mack, MD, Institute of Psychiatry, Medical University of SouthCarolina, Charleston, South CarolinaMarylinn Markarian, MD, FEGS Continuing Day Program, Brooklyn, New YorkElinore F. McCance-Katz, MD, Department of Psychiatry, Virginia CommonwealthUniversity, Richmond, VirginiaDavid McDowell, MD, Department of Psychiatry, Columbia University, New York,New YorkSheldon I. Miller, MD, Department of Psychiatry and Behavioral Sciences, FeinbergSchool of Medicine, Northwestern University, Chicago, IllinoisEdgar P. Nace, MD, Department of Psychiatry, University of Texas SouthwesternMedical School, Dallas, TexasLisa M. Najavits, PhD, Department of Psychiatry, Harvard Medical School,Cambridge, Massachusetts; Trauma Research Program, McLean Hospital, Belmont,MassachusettsSteven D. Passik, PhD, Symptom Management and Palliative Care Program,Markey Cancer Center, University of Kentucky, Lexington, Kentucky

xContributorsRussell K. Portenoy, MD, Department of Pain Medicine and Palliative Care, BethIsrael Medical Center, New York, New YorkMarc N. Potenza, MD, Department of Psychiatry, Yale University, New Haven,ConnecticutM. Zachary Rosenthal, PhD, Department of Psychiatry and Behavioral Sciences,Duke University Medical Center, Durham, North CarolinaRichard N. Rosenthal, MD, Department of Psychiatry, St. Luke’s–RooseveltHospital Center, and Department of Psychiatry, College of Physicians and Surgeons,Columbia University, New York, New YorkSteven J. Schleifer, MD, Department of Psychiatry, University of Medicine andDentistry of New Jersey, Newark, New JerseySidney H. Schnoll, MD, Purdue Pharma LP, Stamford, ConnecticutM. Duncan Stanton, PhD, School of Professional Psychology, Spalding University,Louisville, Kentucky; The Morton Center, Louisville, KentuckyRalph E. Tarter, PhD, School of Pharmacy, University of Pittsburgh, Pittsburgh,PennsylvaniaRoger D. Weiss, MD, Department of Psychiatry, Harvard Medical School,Cambridge, Massachusetts; Alcohol and Drug Abuse Treatment Program, McLeanHospital, Belmont, MassachusettsJoseph Westermeyer, MD, Department of Psychiatry, Minneapolis VA Hospital,University of Minnesota, Minneapolis, MinnesotaMonica L. Zilberman, MD, PhD, Institute of Psychiatry, University of São Paulo,São Paulo, BrazilSheldon Zimberg, MD, Department of Psychiatry, College of Physicians andSurgeons, Columbia University, New York, New York

PrefaceThis third edition of the Clinical Textbook of Addictive Disorders appears 20years after the founding of the American Academy of Addiction Psychiatry(AAAP). During this period, major progress has occurred in both general psychiatryand addiction psychiatry. There has been movement ranging fromdescription of the phenomenology of psychiatric disorders, including substanceuse disorders (SUDs), to the beginnings of understanding neurobiologicalmechanisms, pathophysiology, genetic and family influences, and etiology.Addiction treatment research, including that for comorbid conditions, hasadvanced and the development of evidence-based guidelines for addictiontreatment has been launched. While treatment methods are still very much tiedto the craft and art of psychotherapy (including self-help and spirituality), disseminationof research findings and evidence-based treatment approaches willadd to the quality of care of patients.Unfortunately, our advances in the understanding of addiction psychiatryare not necessarily associated with reductions in the incidence of substance use.The magnitude of use seems to be subject to fads and fluctuations in perceptionsof risk of use. Over the past 30 years there have been important variationsin the use of substances by age, gender, ethnic, and racial groups. The mostrecent estimate on the cost of substance use is for 1998, with the cost of drugabuse directly estimated at $143.4 billion (Office of National Drug Control Policy,2001) and the costs of alcohol abuse projected to be $185 billion(Harwood, 2000). This figure (estimated in 1992) reflects the estimated 8.3%of the population ages 12 or older who were current illicit drug users in 2002and perhaps also includes the 2.6% of the population ages 12 or older who werecurrent users of psychotherapeutic drugs taken nonmedically in 2002. The rateof current drug use among adolescents in 2002 was 11.6%, but that rate was surpassedby young adults (ages 18–25 years) at 20.2%. As for alcohol, an estimated120 million Americans ages 12 or older reported being current drinkersxi

xiiPrefaceof alcohol in the 2002 survey (51%). In terms of diagnosis, an estimated 22 millionAmericans in 2002 were classified with substance dependence or abuse(9.4% of the total population ages 12 or older). Of these, 3.2 million were classifiedwith dependence on or abuse of both alcohol and illicit drugs, 3.9 millionwere dependent on or abused illicit drugs but not alcohol, and 14.9 millionwere dependent on or abused alcohol but not illicit drugs (Office of AppliedStudies, 2003). As for children, according to the Monitoring the Future study,Ecstasy use among 12th graders finally began to lessen after increases since 1998and use of illicit substances other than marijuana continued to decline amongboth 10th and 12th graders. Yet inhalant use increased and cocaine useremained steady among eighth graders (Johnston, O’Malley, Bachman, &Schulenberg, 2004). These numbers suggest that treatment and preventionefforts need to be tailored to particular diagnoses and to members of particulargroups, as the magnitude of substance use remains large.In order to address this great and costly social and medical problem, thistextbook, written previously by the founders and many of the leaders of AAAP,again includes many of the prestigious, internationally renowned clinicians,educators, and researchers from the original pool of talent, with extensive revisionand updating of their work. We have also added new chapters on theneuroscientific basis of addiction, gambling and other “behavioral” addictions,occupational issues and addiction, and dialectical behavior therapy of addictedborderline patients. Many excellent authors were added, and a third editor,Avram H. Mack, provides a fresh perspective. This new volume presents historicalbackground, scientific basis, diagnostic tools, substance-specific information,and a full range of treatment approaches, including individual,group, self-help, family, cognitive-behavioral, psychodynamic, psychopharmacological,and integrated treatment for comorbid conditions. Competency intailoring addiction treatment to specific concerns that relate to culture, ethnicity,spirituality, gender, age, legal and occupational problems, and medical andpsychiatric comorbidity are all vital clinical skills covered throughout the book.Integrating the right combination of treatments for the addicted patient is atthis point as much art as science.Greater attention has been given to integrating treatment for co-occurringpsychiatric disorders; medical conditions such as HIV/AIDS, hepatitis, andtuberculosis; and the psychosocial problems that complicate addictive illness.Clinicians need skills to tailor addiction treatment to women, different socioculturalgroups, age-specific groups, the medically ill, and those with legal problems.Some of the newer treatment approaches are being formatted as manualsand advocate pure application of their methods. What is the reader of a volumelike this to do with the disparate kinds of practices authors describe, when westill are at the infancy of scientifically based differential therapeutics? Whilecontroversy surrounds this area, we recommend integration and blending ofmany of these tools with the personality and style of the informed clinician and

Prefacexiiiwith respect for the particular and salient needs of each case. Slavish adherenceto one method or school of thought, hammering every nail with the same hammer,is not what most experienced, skillful therapists do. Addiction treatment,especially psychotherapy and psychopharmacology, is still very much an art.However, even the experienced clinician must stay abreast of treatment outcomeresearch, evidence-based approaches, and technical and pharmacologicaladvances in the field. Knowledge of how to address comorbid problems is vital,and integration of treatment is the best approach. Patients will seek therapistswith wisdom, compassion, modesty, honesty, knowledge, skill, and good judgment,and will want their therapists to be available, practical, affordable, andactive. Increasingly, patients and their families come to treatment well armedwith scientific knowledge and with high expectations that their health careexpenditure is a value proposition, and they reasonably expect to see positiveresults from their efforts.Addiction is a disease of denial, stigma, and hopelessness, and patientswith severe mental illness and addictions more often than not suffer their darkestdays without the compassionate, evidence-based care advocated in this volume,which can provide a path to a more productive and happier life that is frequentlythe product of recovery. Addiction is a disease of the brain and of thespirit. Helping patients and their families progress to acceptance of their illness,acceptance of a need for help, and making healthier choices to take actionrestores hope and is half the battle. Maintaining progress, developing a treatmentalliance that leads to continued engagement in help, rebuilding of selfesteemand self-care, and development of coping skills that help prevent relapseare essential ingredients of successful treatment programs.The mutual help that patients provide each other in self-help programs,groups, organized rehabilitation programs, network and family treatment, andthrough organized religion and in their daily encounters with others is a forcethat needs to be tapped by the skillful therapist. Some individuals with addictivedisorders are particularly gifted at helping others or providing models ofhope by communicating how they moved past their darkest days, accepted theirillness, reached out for help, developed coping skills, and restored balance intheir lives.Exciting research is under way studying the familial patterns of genetictransmission, localization and sequencing of multiple genes and alleles foraddiction and interaction with other illnesses, and how gene expression occurs.Effects on membrane chemistry, receptor sites, neurotransmission, neuroplasticity,apoptosis, and regeneration of nerve and glial cells, and localization ofbrain effects through imaging, are other areas of basic science that can lead tobetter targeted future treatments. Development of new agents that can provideneurotropic healing of damage caused by alcohol and other drugs and possiblyother psychiatric illnesses such as manic–depression or schizophrenia is a distinctpossibility.

xivPrefaceResearch (1) on health systems; (2) on effects of public health, advertising,and educational campaigns on decisions to use drugs, on prevention, and onearly diagnosis; and (3) on cost effectiveness of treatment is also important.Integrating treatment for psychiatric and addictive disorders needs to be ahigher priority, and barriers within systems of funding, treatment agencies, andtraining programs for staff need to be removed. Substance abuse clinicians mustlearn about other mental illnesses, and no one who works with mentally ill personsshould be without addiction treatment training.Two of us (R. J. F. and S. I. M.) were the founders of AAAP and havespent our careers in fostering training, education, and addiction psychiatry rotationsfor medical students, psychiatrists, addiction psychiatry fellows, other primarycare physicians, nurses, social workers, psychologists, addiction counselors,and rehabilitation therapists. In addition to students and clinicians in thesefields, this book will be of great interest to teachers, to those who work in thecriminal justice system, and to others interested in learning more about addictiontreatment. Practitioners, from beginners to the more experienced, willenhance their skills by reading this well-referenced textbook. At this point,psychiatry is the only medical specialty with a board-certified subspecialty inaddictions. At present, approximately 2,000 board-certified addiction psychiatristsare able to provide consultation, education, and research, to spearhead themuch larger number of clinicians engaged in treating the nation’s number onepublic health problem.A small but growing percentage of those with alcohol or other substanceproblems are properly screened, diagnosed, and treated, and lapses and relapsesare a regular experience. The denial exhibited by addicted individuals—oftenpresent in their families and enabling workplaces—mirrored by society’s lack ofadequate funding for prevention and treatment, the absence of universal healthcare, and the criminal justice system’s neglect of addiction and mental illnesstreatment are reasons most people do not get the help they need. The countertransferenceand attitudinal problems of staff can be an important barrier totreatment, and these can be reduced significantly when the clinician has a goodknowledge of addictions and effective treatment tools at hand. While many cliniciansmay fear or dread working with addicts, those armed with the properskills, attitude, and knowledge have wonderful opportunities to benefit theirpatients. We hope readers enjoy this volume and find the tools in it as useful aswe do in helping addicted patients. Few people suffer more than addicts, fewpatients will gain more from the efforts they put into treatment, and we find nopopulation more interesting, challenging, and rewarding to treat.We wish to thank the many contributors to this volume; they have workedhard to provide comprehensive reviews in a timely manner so that readersreceive the most up-to-date perspectives. Most importantly, we want to espe-

Prefacexvcially thank our respective wives, Marsha Frances, Sarah Miller, and HallieLightdale, MD, for their tireless support and care as we worked with pride onthis project.RICHARD J. FRANCES, MDSHELDON I. MILLER, MDAVRAM H. MACK, MDREFERENCESHarwood, H. (2000). Updating estimates of the economic costs of alcohol abuse in the UnitedStates: Estimates, updated methods and data. Available at www.drugabuse.gov/Infofax/costs.htmlJohnston, L. D., O’Malley, P. M., Bachman J. G., & Schulenberg J. E. (2004). Monitoringthe future: National results on adolescent drug use. Bethesda, MD: U.S. Departmentof Health and Human Services.Office of Applied Studies. (2003). Overview of findings from the 2002 National Survey onDrug Use and Health (NHSDA Series H-21, DHHS Publication No. SMA 03–3774). Rockville, MD: Author.Office of National Drug Control Policy. (2001). The economic costs of drug abuse in theUnited States, 1992–1998 (Publication No. NCJ-190636). Washington, DC: ExecutiveOffice of the President.

ContentsPART I. FOUNDATIONS OF ADDICTION1. The Neurobiology of Substance Dependence:Implications for TreatmentTHOMAS R. KOSTEN, TONY P. GEORGE, and HERBERT D. KLEBER2. Historical and Social Context of Psychoactive SubstanceUse DisordersJOSEPH WESTERMEYER316PART II. ASSESSMENT OF ADDICTION3. Psychological Evaluation of Substance Use Disorderin Adolescents and AdultsRALPH E. TARTER374. Laboratory Testing for Substances of Abuse 63DAVID A. BARON, D. ANDREW BARON, and STEVEN H. BARONPART III. SUBSTANCES OF ABUSE5. Alcohol 75EDGAR P. NACE6. Tobacco 105NORMAN HYMOWITZxvii

xviiiContents7. Opioids 138STEPHEN L. DILTS, JR., and STEPHEN L. DILTS8. Marijuana, Hallucinogens, and Club Drugs 157DAVID MCDOWELL9. Cocaine and Stimulants 184MICHELLE C. ACOSTA, DEBORAH L. HALLER, and SIDNEY H. SCHNOLL10. Sedatives/Hypnotics and Benzodiazepines 219ROBERT L. DUPONT and CAROLINE M. DUPONTPART IV. SPECIAL POPULATIONS11. Polysubstance Use, Abuse, and Dependence 245RICHARD N. ROSENTHAL and PETROS LEVOUNIS12. Co-Occurring Substance Use Disordersand Other Psychiatric DisordersALISA B. BUSCH, ROGER D. WEISS, and LISA M. NAJAVITS27113. Pathological Gambling and Other “Behavioral” Addictions 303JON E. GRANT and MARC N. POTENZA14. Substance Abuse in Minority Populations 321JOHN FRANKLIN and MARYLINN MARKARIAN15. Addictions in the Workplace 340AVRAM H. MACK, JEFFREY P. KAHN, and RICHARD J. FRANCES16. Addiction and the Law 354AVRAM H. MACK, RICHARD J. FRANCES, and SHELDON I. MILLER17. Pain and Addiction 367RUSSELL K. PORTENOY, DAVID LUSSIER, KENNETH L. KIRSH,and STEVEN D. PASSIK18. Alcoholism and Substance Abuse in Older Adults 396SHELDON ZIMBERG19. HIV/AIDS and Substance Use Disorders 411CHERYL ANN KENNEDY, JAMES M. HILL, and STEVEN J. SCHLEIFER20. Addictive Disorders in Women 437SHEILA B. BLUME and MONICA L. ZILBERMAN

ContentsxixPART V. TREATMENTS FOR ADDICTIONS21. Individual Psychodynamic Psychotherapy 457LANCE M. DODES and EDWARD J. KHANTZIAN22. Cognitive Therapy 474JUDITH S. BECK, BRUCE S. LIESE, and LISA M. NAJAVITS23. Group Therapy, Self-Help Groups, and Network Therapy 502MARC GALANTER, FRANCIS HAYDEN, RICARDO CASTAÑEDA,and HUGO FRANCO24. Family-Based Treatment: Stages and Outcomes 528M. DUNCAN STANTON and ANTHONY W. HEATH25. Treating Adolescent Substance Abuse 559YIFRAH KAMINER and OSCAR G. BUKSTEIN26. Psychopharmacological Treatments 588ELINORE F. MCCANCE-KATZ and THOMAS R. KOSTEN27. Dialectical Behavior Therapy for Individuals with BorderlinePersonality Disorder and Substance Use DisordersM. ZACHARY ROSENTHAL, THOMAS R. LYNCH,and MARSHA M. LINEHAN28. Matching and Differential Therapies:Providing Substance Abusers with Appropriate TreatmentKATHLEEN M. CARROLL615637Index 665

PART IFOUNDATIONS OF ADDICTION

CHAPTER 1The Neurobiologyof Substance DependenceImplications for TreatmentTHOMAS R. KOSTENTONY P. GEORGEHERBERT D. KLEBERTolerance, dependence, and addiction are all manifestations of brain changesresulting from chronic substance abuse and involve different brain pathwaysthan those subserving acute drug reinforcement. Acute drug reinforcementappears to share a final common dopaminergic pathway from the ventraltegmental area of the brain to the nucleus accumbens. These acute processesare relatively unimportant for pharmacotherapy of dependence and addiction;instead, the neurobiology of changes associated with chronic use forms the basisfor rational pharmacotherapy. This translation of neurobiology into effectivetreatments has been most successful for opioids, with more limited success foralcohol, nicotine, and stimulant dependence. Opioid treatments such as methadone,levo-alpha-acetyl methadol (LAAM), buprenorphine, and naltrexoneact on the same brain structures and processes as addictive opioids, but withprotective or normalizing effects. This concept of normalization is critical foreffective treatments and is illustrated in this chapter, with opioids as the primaryexample. As we understand the molecular biology of dependence morefully, normalization appears to be a process very similar to learning andmay involve similar changes in gene activation and neuronal long-termpotentiation (LTP) and long-term depression (LTD) that appear to underlielearned behaviors and emotional states.3

4 I. FOUNDATIONS OF ADDICTIONWhile the individual patient, rather than his or her disease, is the appropriatefocus of treatment for substance abuse, an understanding of the neurobiologyof dependence and addiction can clarify the rationales for treatment methodsand goals. Patients who are informed about the brain origins of addictionalso can benefit from understanding that their addiction has a biological basisand does not mean that they are “bad” people.Brain abnormalities resulting from chronic use of nicotine, stimulants,opioids, alcohol, hallucinogens, inhalants, cannabis, and many other abusedsubstances are underlying causes of dependence (the need to keep taking drugsto avoid a withdrawal syndrome) and addiction (intense drug craving and compulsiveuse). Most of the abnormalities associated with dependence resolveafter detoxification, within days or weeks after the substance use stops. Theabnormalities that produce addiction, however, are more wide-ranging, complex,and long-lasting. They may involve an interaction of environmentaleffects—for example, stress, the social context of initial opiate use, and psychologicalconditioning—and a genetic predisposition in the form of brain pathwaysthat were abnormal even before the first dose of opioid was taken. Suchabnormalities can produce craving that leads to relapse months or years afterthe individual is no longer opioid-dependent.In this chapter we describe how drugs affect brain processes to produce drugliking, tolerance, dependence, and addiction. Although these processes arehighly complex, like everything that happens in the brain, we try to explain themin terms that can be understood by patients. We also discuss the treatment implicationsof these concepts. Pharmacological therapy directly offsets or reversessome of the brain changes associated with dependence and addiction, greatlyenhancing the effectiveness of behavioral therapies. Although researchers do notyet have a comprehensive understanding about how these medications work, it isclear that they often renormalize brain abnormalities that have been induced bychronic, high-dose abuse of various substances.ORIGINS OF DRUG LIKINGMany factors, both individual and environmental, influence whether a particularperson who experiments with drugs will continue taking them long enoughto become dependent or addicted. For individuals who do continue, the drug’sability to provide intense feelings of pleasure is a critical reason.When abused drugs travel through the bloodstream to the brain, theyattach to specialized proteins on the surface of neurons that may be receptors,transporters, or even structural elements of the neurons. For example, opiatessuch as heroin bind to mu opioid receptors, which are on the surfaces of opiatesensitiveneurons, and have their effects by inhibiting the cyclic adenosinemonophosphate (cyclic AMP) second messenger system. Inhibition occurs

1. The Neurobiology of Substance Dependence 5through a guanine nucleotide-binding (G)-protein-mediated coupling leadingto a series of changes in phosphorylation for a wide range of intraneuronal proteins(Nestler, 2002). The linkage of heroin with the receptors imitates thelinkage of endogenous opioids such as beta-endorphin with these same receptorsand triggers the same biochemical brain processes that reward people withfeelings of pleasure when they engage in activities that promote basic life functions,such as eating and sex. Opioids such as oxycodone or methadone are prescribedtherapeutically to relieve pain, but when these exogenous opioids activatethe reward processes in the absence of significant pain, they can motivaterepeated use of the drug simply for pleasure.One of the brain circuits activated by opioids and most, if not all, abuseddrugs is the mesolimbic (midbrain) reward system. This system generates signalsin a part of the brain called the ventral tegmental area (VTA) that result in therelease of the chemical dopamine (DA) in another part of the brain, thenucleus accumbens (N-Ac) (Figure 1.1). This release of DA into the N-Accauses feelings of pleasure. Other areas of the brain create a lasting record ormemory that associates these good feelings with the circumstances and environmentin which they occur. These memories, called “conditioned associations,”often lead to the craving for drugs when the abuser reencounters thosepersons, places, or things, and they drive abusers to seek out more drugs in spiteof many obstacles.Other abused drugs activate this same brain pathway, but via differentmechanisms and by stimulating or inhibiting different neurons in this pathway.FIGURE 1.1. Mesolimbic dopamine (“reward”) pathways. PFC, prefrontal cortex; N-Ac,nucleus accumbens; VTA, ventral tegmental area.

6 I. FOUNDATIONS OF ADDICTIONFor example, opioids and cannabinoids can inhibit activity in N-Ac directly,whereas stimulants such as cocaine and amphetamine act indirectly by bindingto various DA transporters and either inhibiting the reuptake of DA into theVTA neurons (cocaine) or actively pumping DA out of the VTA (amphetamine)at its synapse with the N-Ac neurons (Kosten, 2002; Stahl, 1998).Since stimulation of the DA D 2receptor inhibits the cyclic AMP system, thisincrease in DA in the synapse leads to relative inhibition of the N-Ac neuron.The mechanism is more complex than this, however, since the D 1receptor hasthe opposite effect on the cyclic AMP system (e.g., it increases the amount ofcyclic AMP) and both D 1and D 2receptors are present on the N-Ac neurons.The presumption is that the D 2receptor effects predominate perhaps simply dueto more D 2receptors, or due to a higher affinity of the D 2than the D 1receptorsfor DA. Other substances may be even more indirect in their stimulation. Forexample, nicotine and benzodiazepines stimulate ion channels for calcium/sodium and chloride, respectively (Stahl, 2002). The calcium/sodium channelis a nicotinic receptor that normally binds acetylcholine, while the chloridechannel is associated with a gamma-aminobutyric acid (GABA) receptor. Thestimulation of these ion channels can lead to depolarization of the VTA neuronand release of DA into the synapse between the VTA and N-Ac. The entry ofcalcium into the VTA neuron can also directly facilitate the merging of thesynaptic vesicles in the VTA with the cell membrane, leading to release of DAfrom these vesicles (Kosten, 2002). For some substances, we do not yet have aclear idea of their biochemical mechanisms of reinforcement. For example,alcohol may act through the mu opioid receptor like heroin, or the GABAreceptor like benzodiazepines. Inhalants have direct toxic effects on the structuralproteins of neuronal membranes and may act directly to increase neurotransmissionthrough the VTA to the N-Ac by damaging these structural proteinsin neuronal membranes and allowing calcium entry into the VTA,thereby releasing DA vesicles into the synapse connecting the VTA with theN-Ac.Particularly in the early stages of abuse, the drug’s stimulation of thebrain’s reward system is a primary reason that some people take drugs repeatedly.However, the compulsion to use drugs builds over time to extend beyond asimple drive for pleasure. This increased compulsion is related to tolerance anddependence.DRUG TOLERANCE, DEPENDENCE, AND WITHDRAWALFrom a clinical standpoint, withdrawal can be one of the most powerful factorsdriving dependence and addictive behaviors. This seems particularly true foropioids, alcohol, benzodiazepines, nicotine, and to a lesser extent stimulantssuch as cocaine. For hallucinogens, cannabinoids, or inhalants, withdrawal

1. The Neurobiology of Substance Dependence 7symptoms seem of more limited importance. Treatment of the patient’s withdrawalsymptoms is based on understanding how withdrawal is related to thebrain’s adjustment to these drugs after chronic repeated high doses.Repeated exposure to escalating dosages of most drugs alters the brain, sothat it functions more or less normally when the drugs are present and abnormallywhen they are not. Two clinically important results of this alteration aredrug tolerance (the need to take higher and higher dosages of drugs to achievethe same effect) and drug dependence (susceptibility to withdrawal symptoms).Withdrawal symptoms occur only in patients who have developed tolerance.Tolerance occurs because the brain cells that have receptors or transporterson them gradually become less responsive to the stimulation by the exogenoussubstances. For example, more opioid is needed to inhibit the cyclic AMPsystem in the N-Ac neurons, as well as to stimulate the VTA brain cells of themesolimbic reward system to release the same amount of DA in the N-Ac.Therefore, more opioid is needed to produce pleasure comparable to that providedin previous drug-taking episodes. The mechanism for this reduction inresponse is related to the cyclic AMP coupling for opioids, but direct reductionsin the number of receptors or increases in the number of transporters can occur.For example, it appears that after chronic cocaine inhibition of the DA transporter,the number of DA receptors decreases, while the number of transportersmay increase to compensate for this chronic overstimulation of the N-Ac DAreceptors and chronic inhibition of the transporter (Kosten, 2002). Thesechanges associated with tolerance might be considered an attempt by the brainto attain relative homeostasis in the face of the disruption induced by theseabused drugs. Tolerance to alcohol may be due to a more complex series of neurobiologicalchanges at the neuronal and molecular levels, and involve GABA,opioid, DA, and other neurochemical systems, including the excitatory aminoacid neurotransmitters such as glutamate and its multiplicity of receptorsubtypes (Fadda & Rossetti, 1998). Tolerance to cannabinoids probably has asimilar mechanism to opioids, since the cannabinoid CB 1receptor is also a G-protein-coupled, cyclic AMP type receptor (Kosten, 2000; Stahl, 1998). Toleranceto hallucinogens such as lysergic acid (LSD) probably involves changes inthe serotonergic 5HT 2receptors, which involve the phosphoinositol phosphate(PIP) second messenger system, but this system’s relationship to chronic LSDuse has not been as extensively studied as the cyclic AMP system for the opioidsand cannabinoids (Kosten, 2000).Opioids provide an outstanding example to illustrate how the neurobiologicalchanges associated with tolerance are related to dependence and withdrawalsymptoms. Opioid dependence and some of the most distressing opioidwithdrawal symptoms stem from changes in the locus coeruleus (LC), anotherimportant brain system at the base of the brain (Figure 1.2). Neurons in the LCproduce noradrenaline (NA) and widely distribute it to other parts of the brainincluding the cerebral cortex, brainstem, and various subcortical regions, where

8FIGURE 1.2. Neuronal coupling of receptor to G protein and adenyl cyclase (converting enzyme) at baseline (Panel A), changes during acute opiateeffects (Panel B), changes after chronic opiate use (Panel C), and changes during acute opiate withdrawal (Panel D). After “resetting” of opiate receptorswith naltrexone, the number of receptors appears to increase to match the increased converting enzyme activity (see text).

1. The Neurobiology of Substance Dependence 9it stimulates wakefulness, breathing, blood pressure, and general alertness,among other functions. When opioid molecules link to mu receptors on braincells in the LC, they suppress the neurons’ release of NA, resulting in drowsiness,slowed respiration, and low blood pressure—familiar effects of opioidintoxication. With repeated exposure to opioids, however, LC neurons adjustby increasing their level of activity. Now, when opioids are present, their suppressiveimpact is offset by this heightened activity, with the result that roughlynormal amounts of NA are released and the patient feels more or less normal.When opioids are not present to suppress the LC brain cells’ enhanced activity,however, the neurons release excessive amounts of NA, triggering jitters, anxiety,muscle cramps, and diarrhea. Figure 1.2 illustrates this development of opiatetolerance and withdrawal.Other brain areas in addition to the LC also contribute to the productionof opiate withdrawal symptoms, including the mesolimbic reward system. Forexample, opioid tolerance that reduces the VTA’s release of DA into the N-Acmay prevent the patient from obtaining pleasure from normally rewardingactivities such as eating. These changes in the VTA and the DA reward systems,though not fully understood, form an important brain system underlyingcraving and compulsive drug use.TRANSITION TO ADDICTIONAs we have seen, the pleasure derived from various drugs’ activation of thebrain’s natural reward system promotes continued drug use during the initialstages of opioid addiction. Subsequently, repeated exposure to these drugsinduces the brain mechanism of dependence, which leads to daily drug use toavert the unpleasant symptoms of drug withdrawal for many substances,although for some drugs, withdrawal symptoms are minimal and may contributeminimally to dependence features and relapse after discontinuation. Furtherprolonged use of drugs that produce dependence lead to more long-lastingchanges in the brain that may underlie the compulsive drug-seeking behaviorand related adverse consequences that are the hallmarks of addiction. Recentresearch has generated several models to explain how habitual drug use produceschanges in the brain that may lead to drug addiction. In reality, the processof addiction probably involves components from each of these models, aswell as other features.The “Changed Set Point” ModelThe “changed set point” model of drug addiction has several variants based onthe altered neurobiology of the DA neurons in the VTA and of the NA neuronsof the LC during the early phases of withdrawal and abstinence. The basic

10 I. FOUNDATIONS OF ADDICTIONidea is that drug abuse alters a biological or physiological setting or baseline.One variant, by Koob and LeMoal (2001), is based on the idea that neurons ofthe mesolimbic reward pathways are naturally “set” to release enough DA inthe N-Ac to produce a normal level of pleasure. Koob and LeMoal suggest thatabused drugs cause addiction by initiating a vicious cycle of changing this setpoint, such that the release of DA is reduced when normally pleasurableactivities occur and these abused drugs are not present. Similarly, a change inset point occurs in the LC, but in the opposite direction, such that NA releaseis increased during withdrawal, as described earlier, thus accounting for boththe positive (drug liking) and negative (drug withdrawal) aspects of drug addiction.A specific way that the DA neurons can become dysfunctional relates toan alteration in their baseline (“resting”) levels of electrical activity and DArelease (Grace, 2000). In this second variant of the changed set point model,this resting level is the result of two factors that influence the amount of restingDA release in the N-Ac: cortical excitatory (glutamate) neurons that drive theVTA DA neurons to release DA, and autoreceptors (“brakes”) that shut downfurther release when DA concentrations become excessive. Activation of varioustypes of receptors by abused substances, such as mu opiate receptors by heroin,initially bypasses these brakes and leads to a large release of DA in the N-Ac. However, with repeated drug use, the brain responds to these successivelarge DA releases by increasing the number and strength of the brakes on theVTA DA neurons. Eventually, these enhanced “braking” autoreceptors inhibitthe neurons’ resting DA release. When this happens, the dependent addict willtake even more of the abused drug, such as heroin, to offset the reduction ofnormal resting DA release. When he or she stops the drug use, a state of DAdeprivation will result, manifesting in dysphoria (pain, agitation, and malaise)and other withdrawal symptoms, which can lead to a cycle of relapse to druguse.A third variation on the set point change emphasizes the sensitivity toenvironmental cues that leads to drug wanting or craving rather than just reinforcementand withdrawal (Breiter et al., 1997; Robinson & Berridge, 2000).During periods when the drug is not available to addicts, their brains canremember the drug, and desire or craving for the drug can be a major factorleading to drug use relapse. This craving may represent increased activity of thecortical excitatory (glutamate) neurotransmitters, which drive the restingactivity of the DA-containing VTA neurons, as mentioned, and also drive theLC NA neurons. As the glutamate activity increases, DA will be released fromthe VTA, leading to drug wanting or craving, and NA will be released from theLC, leading to increased withdrawal symptoms, particularly with opiates such asheroin. This theory suggests that these cortical excitatory brain pathways areoveractive in addiction, and reducing their activity would be therapeutic. Basicscientists and clinicians are currently researching compounds called “excitatory

1. The Neurobiology of Substance Dependence 11amino acid antagonists” to see whether this potential treatment strategy reallycan work.Thus, several mechanisms in the LC and VTA–N-Ac brain pathways maybe operating during addiction and relapse. The excitatory cortical pathwaysmay produce little response in the VTA during the resting state, leading toreductions in DA. However, when the addict is exposed to cues that producecraving, the glutamate pathways may get sufficiently active to raise DA andstimulate desire for a greater high. This same increase in glutamate activity willraise NA release from the LC to produce a dysphoric state predisposing torelapse and continued addiction.The Cognitive Deficits ModelThe cognitive deficits model of drug addiction proposes that individuals whodevelop addictive disorders have abnormalities in an area of the brain calledthe prefrontal cortex (PFC). The PFC is important for regulation of judgment,planning, and other executive functions. To help us overcome some of ourimpulses for immediate gratification in favor of more important or ultimatelymore rewarding long-term goals, the PFC sends inhibitory signals to the VTADA neurons of the mesolimbic reward system.The cognitive deficits model proposes that PFC signaling to the mesolimbicreward system is compromised in individuals with addictive disorders; asa result, they have reduced ability to use judgment to restrain their impulses andare predisposed to compulsive drug-taking behaviors. Consistent with thismodel, stimulant drugs such as methamphetamine appear to damage the specificbrain circuit—the frontostriatal loop—that carries inhibitory signals fromthe PFC to the mesolimbic reward system. In addition, a recent study usingmagnetic resonance spectroscopy showed that chronic alcohol abusers haveabnormally low levels of GABA, the neurochemical that the PFC uses to signalthe reward system to release less DA (Behar et al., 1999). As well, the cognitivedeficits model of drug addiction could explain the clinical observation thatheroin addiction is more severe in individuals with antisocial personalitydisorder—a condition that is independently associated with PFC deficits(Raine, Lencz, Bihrle, LaCasse, & Colletti, 2000).In contrast to stimulants and perhaps alcohol, heroin apparently damagesthe PFC but not the frontostriatal loop. Therefore, individuals who becomeheroin addicts may have some PFC damage that is independent of their opioidabuse, either inherited genetically or caused by some other factor or event intheir lives. This preexisting PFC damage, which predisposes individuals toimpulsivity and lack of control, may be important for most individuals whobecome addicted to drugs, and the additional PFC damage from chronicrepeated drug abuse, particularly abuse of stimulants, increases the severity ofthese problems (Kosten, 1998).

12 I. FOUNDATIONS OF ADDICTIONTHE IMPORTANT ROLE OF STRESSThat drug abuse patients are more vulnerable to stress than the general populationis a clinical truism. Numerous preclinical studies have documented thatphysical stressors (e.g., foot shock or restraint stress) and psychological stressorscan cause animals to reinstate drug use (e.g., Shaham, Erb, & Stewart, 2000).Furthermore, stressors can trigger drug craving in addicted humans (Sinha,Catapano, & O’Malley, 1999). One potential explanation for these observationsis that abused drugs, including opiates and stimulants, raise levels ofcortisol, a hormone that plays a primary role in stress responses; cortisol, inturn, raises the level of activity in the mesolimbic reward system (Kreek &Koob, 1998). By these mechanisms, stress may contribute to the abuser’s desireto take drugs in the first place, as well as to his or her subsequent compulsion tokeep taking them.PHARMACOLOGICAL INTERVENTIONSAND TREATMENT IMPLICATIONSIn summary, the various biological models of drug addiction are complementaryand broadly applicable to chemical addictions. We next illustrate how longtermpharmacotherapies for opioid dependence, such as methadone, naltrexone,and buprenorphine, can counteract or reverse the abnormalitiesunderlying dependence and addiction. These agents are particularly informative,because they are an agonist, antagonist, and partial agonist, respectively.We do not review short-term treatments for relieving withdrawal symptomsand increasing abstinence but refer readers elsewhere for detailed neurobiologicalexplanations for various abstinence initiation approaches (see Kosten &O’Connor, 2003).Methadone, a long-acting opioid medication with effects that last for days,causes dependence, but because of its sustained stimulation of the mu receptors,it alleviates craving and compulsive drug use. In addition, methadone therapytends to normalize many aspects of the hormonal disruptions found in addictedindividuals (Kling et al., 2000; Kreek, 2000; Schluger, Borg, Ho, & Kreek,2001). For example, it moderates the exaggerated cortisol stress response (discussedearlier) that increases the danger of relapse in stressful situations.Naltrexone is used to help patients avoid relapse after they have beendetoxified from opioid dependence. Its main therapeutic action is to occupy muopioid receptors in the brain with a 100-fold higher affinity than agonists suchas methadone or heroin, so that addictive opioids cannot link up with themand stimulate the brain’s reward system. Naltrexone does not activate the G-protein-coupled cyclic AMP system and does not increase or decrease levels ofcyclic AMP inside the neuron, and it does not promote these brain processes

1. The Neurobiology of Substance Dependence 13that produce feelings of pleasure (Kosten & Kleber, 1984). An individual whois adequately dosed with naltrexone does not obtain any pleasure from addictiveopioids and is less motivated to use them. An interesting neurobiologicaleffect of naltrexone is that it appears to increase the number of available muopiate receptors, which may help to renormalize the imbalance between thereceptors and G-protein coupling to cyclic AMP (Kosten, 1990). Naltrexone isalso sometimes used to detoxify patients rapidly from opioid dependence. Inthis situation, while naltrexone keeps the addictive opioid molecules away fromthe mu receptors, clonidine may help to suppress the opioid-induced excessiveNA output that is a primary cause of withdrawal (Kosten, 1990). Clonidine iscapable of this withdrawal relief because alpha-adrenergic autoreceptors are colocalizedwith mu opiate receptors on the neurons of the LC, and both receptortypes inhibit cyclic AMP synthesis through similar inhibitory G proteins.Buprenorphine’s action on the mu opioid receptors elicits two differenttherapeutic responses within the brain cells, depending on the dose. At lowdoses, buprenorphine has effects like methadone, but at high doses, it behaveslike naltrexone, blocking the receptors so strongly that it can precipitate withdrawalin highly dependent patients (i.e., those maintained on more than 40mg methadone daily). Several clinical trials have shown that buprenorphine isas effective as methadone, when used in sufficient doses (Kosten, Schottenfeld,Ziedonis, & Falcioni, 1993; Oliveto, Feingold, Schottenfeld, Jatlow, & Kosten,1999; Schottenfeld, Pakes, Oliveto, Ziedonis, & Kosten, 1997). Buprenorphinehas a safety advantage over methadone, since high doses precipitate withdrawalrather than the suppression of consciousness and respiration seen in overdosesof methadone and heroin. Thus, buprenorphine has less overdose potentialthan methadone, since it blocks other opioids and even itself as the dosageincreases. Finally, buprenorphine can be given three times per week, simplifyingobserved ingestion during the early weeks of treatment.SUMMARYDependence and addiction are most appropriately understood as chronic medicaldisorders, with frequent recurrences to be expected. The neurobiology ofthese disorders is becoming well understood, but much remains unknown aboutthe genomic mechanisms that predispose to addictions and that are activated,perhaps irreversibly, by long-term drug use. The mesolimbic reward systemappears to be central to the development of the direct clinical consequences ofchronic abuse, including tolerance, dependence, and addiction. Other brainareas and neurochemicals, including cortisol, also are relevant to dependenceand relapse. Pharmacological interventions for addiction are highly effective foropiates, and we have illustrated three different approaches using an agonist, anantagonist, or a partial agonist. However, given the complex biological, psycho-

14 I. FOUNDATIONS OF ADDICTIONlogical, and social aspects of these diseases, they must be accompanied byappropriate psychosocial treatments. Clinician awareness of the neurobiologicalbasis of drug dependence, and information sharing with patients, can provideinsight into patient behaviors and problems, and clarify the rationale fortreatment methods and goals.ACKNOWLEDGMENTThis work was supported by Grant Nos. P50-DA-12762, K05-DA-00454, K12-DA-00167, R01-DA-13672, and R01-DA-14039 from the National Institute on DrugAbuse.REFERENCESBehar, K. L., Rothman, D. L., Petersen, K. F., Hooten, M., Delaney, R., Petroff, O. A.,et al. (1999). Preliminary evidence of low cortical GABA levels in localized 1H-MR spectra of alcohol-dependent and hepatic encephalopathy patients. Am J Psychiatry,156, 952–954.Breiter, H. C., Gollub, R. L., Weisskoff, R. M., Kennedy, D. N., Makris, N., Berke, J. D.,et al. (1997). Acute effects of cocaine on human brain activity and emotion. Neuron,19, 591–611.Fadda, F., & Rossetti, Z. L. (1998). Chronic ethanol consumption: From neuroadaptationto neurodegeneration. Prog Neurobiol, 56, 385–431.Grace, A. A. (2000). The tonic/phasic model of dopamine system regulation and itsimplications for understanding alcohol and stimulant craving. Addiction, 95(Suppl2), S119–S128.Kling, M. A., Carson, R. E., Borg, L., Zametkin, A., Matochik, J. A., Schluger, J., et al.(2000). Opioid receptor imaging with PET and [ 18 F]cyclofoxy in long-term,methadone-treated former heroin addicts. J Pharmacol Exp Ther, 295, 1070–1076.Koob, G. F., & LeMoal, M. (2001). Drug addiction, dysregulation of reward, andallostasis. Neuropsychopharmacology, 24, 97–129.Kosten, T. R. (1990). Neurobiology of abused drugs: Opioids and stimulants. J NervMent Dis, 178, 217–227.Kosten, T. R. (1998). Pharmacotherapy of cerebral ischemia in cocaine dependence.Drug Alcohol Depend, 49, 133–144.Kosten, T. R. (2000). Drugs of abuse (Chapter 32 revision). In G. B. Katzung (Ed.),Basic and clinical pharmacology (8th ed., pp. 532–547). Stamford, CT: Appleton &Lange.Kosten, T. R. (2002). Pathophysiology and treatment of cocaine dependence. In K. L.Davis, D. Charney, J. T. Coyle, & C. Nemeroff (Eds.), Neuropsychopharmacology:The fifth generation of progress (pp. 1461–1473). Baltimore: Lippincott/Williams &Wilkins.Kosten, T. R., & Kleber, H. D. (1984). Strategies to improve compliance with narcoticantagonists. Am J Drug Alcohol Abuse, 10, 249–266.

1. The Neurobiology of Substance Dependence 15Kosten, T. R., & O’Connor, P. G. (2003). Current concepts—management of drugwithdrawal. N Engl J Med, 348, 1786–1795.Kosten, T. R., Schottenfeld, R. S., Ziedonis, D., & Falcioni, J. (1993). Buprenorphineversus methadone maintenance for opioid dependence. J Nerv Ment Dis, 181, 358–364.Kreek, M. J. (2000). Methadone-related opioid agonist pharmacotherapy for heroinaddiction: History, recent molecular and neurochemical research and the future inmainstream medicine. Ann NY Acad Sci, 909, 186–216.Kreek, M. J., & Koob, G. F. (1998). Drug dependence: Stress and dysregulation of brainreward pathways. Drug Alcohol Depend, 51(1–2), 23–47.Nestler, E. J. (2002). From neurobiology to treatment: Progress against addiction. NatNeurosci, 5(Suppl), 1076–1079.Oliveto, A. H., Feingold, A., Schottenfeld, R., Jatlow, P., & Kosten, T. R. (1999).Desipramine in opioid-dependent cocaine abusers maintained on buprenorphinevs methadone. Arch Gen Psychiatry, 56, 812–820.Raine, A., Lencz, T., Bihrle, S., LaCasse, L., & Colletti, P. (2000). Reduced prefrontalgray matter volume and reduced autonomic activity in antisocial personality disorder.Arch Gen Psychiatry, 57(2), 119–127.Robinson, T. E., & Berridge, K. C. (2000). The psychology and neurobiology of addiction:An incentive-sensitization view. Addiction, 95(Suppl 2), S91–S117.Schluger, J. H., Borg, L., Ho, A., & Kreek, M. J. (2001). Altered HPA axis responsivityto metyrapone testing in methadone maintained former heroin addicts with ongoingcocaine addiction. Neuropsychopharmacology, 24(5), 568–575.Schottenfeld, R. S., Pakes, J. R., Oliveto, A., Ziedonis, D., & Kosten, T. R. (1997).Buprenorphine versus methadone maintenance treatment for concurrent opioiddependence and cocaine abuse. Arch Gen Psychiatry, 54(8), 713–720.Shaham, Y., Erb, S., & Stewart, J. (2000). Stress-induced relapse to heroin and cocaineseeking in rats: A review. Brain Res Brain Res Rev, 33, 13–33.Sinha, R., Catapano, D., & O’Malley, S. (1999). Stress-induced craving and stressresponse in cocaine dependent individuals. Psychopharmacology, 142, 343–351.Stahl, S. M. (1998). Getting stoned without inhaling: Anandamide is the brain’s naturalmarijuana. J Clin Psychiatry, 59, 566–567.Stahl, S. M. (2002). Selective actions on sleep or anxiety by exploiting GABA-A/benzodiazepine receptor subtypes. J Clin Psychiatry, 63, 179–180.

CHAPTER 2Historical and Social Contextof Psychoactive SubstanceUse DisordersJOSEPH WESTERMEYERHistorical and social factors are key to the understanding of addictive disorders.These factors affect the rates of addictive disorders in the community, the typesof substances abused, the characteristics of abusive users, the course of these disorders,and the efficacy of treatment. Knowledge of these background featureshelps in understanding the genesis of these disorders, their treatment outcome,and preventive approaches.Psychoactive substances subserve several human functions that can enhanceboth individual and social existence. On the individual level, desirableends include the following: relief of adverse mental and emotional states (e.g.,anticipatory anxiety before battle and social phobia at a party), relief of physicalsymptoms (e.g., pain and diarrhea), stimulation to function despite fatigue orboredom, and “time-out” from day-to-day existence through altered states ofconsciousness. Socially, alcohol and drugs are used in numerous rituals and ceremonies,from alcohol in Jewish Passover rites and the Roman Catholic Mass,to peyote in the Native American Church and the serving of opium at certainHindu marriages. To a certain extent, the history of human civilization parallelsthe development of psychoactive substances (Westermeyer, 1999).Paradoxically, these substances that bless and benefit our existence canalso torment and decivilize us. Individuals, societies, and cultures began learningthis disturbing truth millennia ago. We continue to rediscover this harshreality today and will do so in the future, as though each new generation must16

2. Historical and Social Context 17learn afresh for itself. As our societies become more complex, so too do our psychoactivesubstances, our means of consuming them, and the problems associatedwith them. Preventive and treatment efforts, also age-old and wrought atgreat cost, are our forebears’ gifts to us for dealing with psychoactive substanceuse gone astray (Anawalt & Berdan, 1992).PrehistoryHISTORY AND ORIGINSMethods for the study of psychoactive substance use disorders through time andspace include the archaeological record, anthropological studies of preliteratesocieties, and the historical record. Archaeological data document the importanceof alcohol commerce in late prehistorical and early historical times, bothin the Mediterranean (where wine vessels have been discovered in numerousshipwrecks) and in China (where wine vessels have been found in burial sites).Poppy seed caches have been recorded in a prehistoric site in northern Turkey.Incised poppy capsules have been noted in the prehistoric headdresses ofCretan goddesses or priestesses, indicating an early awareness of opium harvestmethods. Availability of carbohydrate in excess of dietary needs, fostered byneolithic farming technology and animal husbandry, permitted sporadic casesof alcohol abuse (Westermeyer, 1999).Anthropological studies of preliterate societies have shown the almost universaluse of psychoactive substances. Tribal and peasant societies of North andSouth America focused on the development of stimulant drugs (e.g., coca leaf,tobacco leaf, and coffee bean) and numerous hallucinogenic drugs (e.g., peyote).They used hallucinogens for ritual purposes and stimulant drugs for secularpurposes, such as hard labor or long hunts. New World peoples discovereddiverse modes of administration, such as chewing, nasal insufflation or “snuffing,”pulmonary inhalation or “smoking,” and rectal clysis (DuToit, 1977).African and Middle Eastern ethnic groups produced a smaller number of stimulants,such as qat, and hallucinogens, such as cannabis (Kennedy, Teague, &Fairbanks, 1980). Groups across Africa and the Eurasian land mass obtainedalcohol from numerous sources, such as honey, grains, tubers, fruits, and mammalianmilk. Certain drugs were also used across vast distances, such as opiumacross Asia and the stimulant betel nut from South Asia to Oceania. OldWorld peoples primarily consumed drugs by ingestion prior to Columbus’stravel to the New World.Early HistoryHistorical records of alcohol, opium, and other psychoactive substances appearwith the earliest Egyptian and Chinese writings. Opium was described as an

18 I. FOUNDATIONS OF ADDICTIONingested medication in these first documents, especially for medicinal purposes.Mayan, Aztec, and Incan statues and glyphs indicated drug use for ritual reasons(Furst, 1972). Medieval accounts recorded traditional alcohol and drug use.Travelers of that era often viewed use patterns in other areas as unusual, aberrant,or problematic; examples include reports of Scandinavian “beserker”drinkers by the English and reports by Crusaders of Islamic military units or“assassins” intoxicated on cannabis. Along with animal sacrifice and the servingof meat, the provision of alcohol, betel, opium, tobacco, or other psychoactivesubstances came to have cultural, ritual, or religious symbolism, includinghospitality toward guests (Smith, 1965). Affiliation with specific ethnic groups,social classes, sects, and castes was associated with consumption of specific psychoactivesubstances. For example, one group in India consumed alcohol butnot cannabis, whereas an adjacent group consumed cannabis but not alcohol(Carstairs, 1954). Altered patterns of psychoactive use have signaled other,more fundamental cultural changes (Caetano, 1987). Religious identity couldbe tied to alcohol or drug consumption. For example, wine has been a traditionalaspect of Jewish, Catholic, and certain other Christian rituals and ceremonies,whereas some Islamic, Hindu, Buddhist, and fundamentalist Christiansects prohibit alcohol drinking. In addition to distinguishing people from oneanother, substance use may serve to maintain cooperation and communicationacross ethnic groups and social classes, from Africa (Wolcott, 1974) to Bolivia(Heath, 1971).Cultural and Social ChangeIn recent centuries, political, commercial, and technical advances have influencedthe types, supply, cost, and availability of psychoactive substances, alongwith modes of administration (Westermeyer, 1987). International commerce,built on cheaper and more efficient transportation, and increasing income havefostered drug production and distribution. Increasing disposable income hasresulted in greater recreational intoxication (Caetano, Suzman, Rosen, &Voorhees-Rosen, 1983). Development of parenteral injection for medical purposeswas readily adapted to recreational drug self-administration in the mid-1800s, within several years of its invention. Purification and modification ofplant compounds (e.g., cocaine from the coca leaf, morphine and heroin fromopium, and hashish oil from the cannabis plant) produced substances that wereboth more potent and more easily smuggled and sold illicitly. Laboratory synthesishas produced drugs that closely mimic naturally occurring substances(e.g., the stimulant amphetamines, the sedative barbiturates and benzodiazepines,the opioid fentanyl, and the hallucinogen lysergic acid) that are morepotent and often cheaper than purified plant compounds.Historical and cultural factors may theoretically affect the pharmacokineticsand pharmacodynamics of psychoactive substance, just as the pharma-

2. Historical and Social Context 19cology of these substances may affect their historical and traditional use. A casein point is the flushing reaction observed among a greater-than-expected numberof Asians and Native Americans (but neither universal in these peoples,nor limited to them). Absence of alcohol use among the northern Asian peopleswho subsequently peopled much of East Asia and the Americas is a likelyexplanation, but the exact reason is unknown. The flushing reaction associatedwith alcohol (Johnson & Nagoshi, 1990) has been offered as a reason for twoopposite phenomena:1. The low rates of alcoholism among Asian peoples, who presumably findthe reaction aversive and hence drink little—although rates are increasingacross much of Asia (Ohmori, Koyama, et al., 1986).2. The high rates of alcoholism among certain Native American groups,who presumably must “drink through” their flushing reaction to experienceother alcohol effects.Flushing may be more or less desirable, depending upon how the culture valuesthis biological effect. Among many East and Southeast Asian peoples influencedby Buddhist precepts, flushing is viewed as the emergence of cupidity orrage, with implied loss of emotional control. Modal differences in alcoholmetabolism have also been observed among ethnic groups, and these differencessupport arguments in favor of biological causation. However, the intraethnicdifferences in alcohol metabolism greatly exceed the interethnic differences(Fenna, Mix, Schaeffer, & Gilbert, 1971). Despite some minimalpharmacokinetic differences among people of different races, the observed differencesappear to be more due to pharmacodynamics; that is, the influence ofpeople vis-à-vis the drug (i.e., their traditions, taboos, expectations, and patternsof use) appears to exert greater influence than the drug vis-à-vis the people(e.g., rates of absorption and catabolism and flushing reactions). Pharmacodynamicfactors related to culture and pharmacokinetic factors related tobiological inheritance and environmental influences probably both play rolesin the individual’s experience with psychoactive substances.As psychoactive substance use developed into substance abuse in manyadvanced civilizations, social and cultural means evolved to control usage. Onemethod was law and law enforcement. Aztecs utilized this method in pre-Columbian times to limit the frequency and amount of drinking (Anawalt &Berdan, 1992). Later, in the post-Columbian period, England countered its “ginplague” with a tax on imported alcohol-containing beverages (Thurn, 1978),and its later “opium epidemic” with prescribing laws (Kramer, 1979). Anothermethod has been religious stricture. Perhaps the first organized religion to prescribeabstinence from alcohol was Hinduism. Early Buddhist leaders counseledabstinence from alcohol as a means of quitting earthly bondage to achieve contentmentin this life and eternal nirvana after death. Islam became the third

20 I. FOUNDATIONS OF ADDICTIONgreat religion to adopt abstinence from alcohol, reportedly when a town wassacked as a result of a drunken nighttime guard. The gin plague in Englandspawned several abstinence-oriented Christian sects, despite the earlier statusof wine as a Christian sacramental substance (Johnson & Westermeyer, 2000).The Church of Jesus Christ of Latter-Day Saints (the group popularly known asthe Mormons) forbids any use of psychoactive substances, including caffeineand nicotine.In addition to religion as a preventive measure, religion has also served as atherapy for psychoactive substance abuse. Native Americans and Latin Americans,plagued with high rates of alcoholism, have joined fundamentalist Christiansects as a means of garnering social support while resisting peer pressures todrink (Mariz, 1991). Many Native Americans have joined the Native AmericanChurch, in which peyote is a sacramental substance but alcohol is proscribed(Albaugh & Anderson, 1974).Patterns of Psychoactive Substance UseTraditional patterns of psychoactive substance use in most societies were episodic,coming at times of personal celebrations (e.g., birth and marriage), rituals(e.g., arrivals, departures, and changes in status), and seasonal celebrations(e.g., harvest and New Year). Exceptions to this pattern were daily or at leastoccasional use of alcohol as a foodstuff and use of various stimulants (e.g., betelareca,tea and coffee, and coca leaf) in association with long, hard labor (e.g.,paddy rice or taro farming and silver mining). Daily beer or wine drinking waslimited to Europe, especially the para-Mediterranean wine countries and centralgrain-beer countries. Such daily or “titer” use is not without its problems,even when socially sanctioned. Hepatic cirrhosis and other organ damage (e.g.,to brain, bone marrow, neuromuscular system, and pancreas) may result fromlong-term, daily use of more than 2–4 ounces of alcohol, depending on bodyweight (Baldwin, 1977). Daily use of stimulants, especially if heavy or addictive,can lead to biomedical or psychosocial problems, such as oral cancers inthe case of betel-areca chewing (Ahluwalia & Ponnampalam, 1968) or psychobehavioralchanges in the case of coca leaf chewing (Negrete, 1978).Socially sanctioned, episodic psychoactive substance use may involveheavy use, with marked intoxication or drunkenness (Bunzel, 1940). In a lowtechnologyenvironment, this pattern may cause few problems, althoughpsychotomimetic drugs such as cannabis can cause toxic psychosis (Chopra &Smith, 1974). In a high-technology environment, with modern methods oftransportation and industrial machinery, intoxication even at mild traditionallevels may be life threatening (Stull, 1972). Binge-type alcohol problemsinclude delirium tremens, fights, sexually transmitted disease, and falls.Among other consequence of technology and advanced civilization arewidespread substance abuse epidemics, or long-lasting endemics. In the pre-

2. Historical and Social Context 21Columbian era, sporadic cases of acute and chronic substance abuse problemshad been known for at least a millennium, and probably longer. However, relativelysudden, massive substance abuse increases appeared early in the post-Columbian era. One of these was the English gin epidemic or gin plague(Thurn, 1978), which began in the late 1600s and continued for severaldecades. Transatlantic intercontinental trade and the beginnings of the IndustrialRevolution were the immediate causes. At about the same time, opiumepidemics broke out in several Asian countries. The origins of these epidemicswere somewhat different. The post-Columbian spread of tobacco smoking toAsia introduced the inhabitants to inhalation as a new mode of drug administration.This new route of administration applied to an old drug, opium, produceda combination more addictive than the old opium-eating tradition. Governmentalpressures against tobacco smoking (which was viewed as wastefuland associated with seditious elements) probably accelerated the popularity ofopium smoking. Subsequently, European colonialism and international tradecontributed to the import of Indian opium to several East Asian countries.Opium epidemics also occurred somewhat later in Europe and North America(Kramer, 1979). Although East Asian countries have largely controlled theiropium problems, opiate endemics continue in Southeast and South Asia, theMiddle East, parts of Europe, and North America.HISTORICAL MODELS OF SUBSTANCE USEAlthough ceremonial alcohol use is widely appreciated, the ceremonial use ofdrugs is not so well known. Peyote buttons are a sacramental substance in theNative American Church (Bergman, 1971). Hallucinogen use for religious purposesstill occurs among many South American ethnic groups (DuToit, 1977).Supernatural sanctions, both prescribing use within certain bounds and proscribinguse outside these bounds, inveigh against abuse of these substances bydevotees. Thus, ceremonial or religious use tends to be relatively safe. Examplesof abuse do occur, however, such as the occasional Catholic priest who becomesalcoholic, beginning with abuse of sacramental wine.Secular but social use of alcohol and drugs occurs in numerous quasi-ritualcontexts. Drinking may occur at annual events, such as New Year or harvestceremonies (e.g., Thanksgiving in the United States). Weddings, births, funerals,and other family rituals are occasions for alcohol or drug use in many cultures.Marking of friendships, business arrangements, or intergroup competitionscan virtually require substance use in some groups. For example, thedutsen in German-speaking Central Europe is a brief ritual in which friends orassociates agree to address each other by the informal du (“thou”) rather thanby the formal Sie (“you”). Participants, holding an alcoholic beverage in theirright hands, link their right arms, toast each other, and drink with arms linked.

22 I. FOUNDATIONS OF ADDICTIONThe use of betel-areca, pulque or cactus beer, coca leaf, and other intoxicantshas accompanied group work tasks, such as harvests or community corvée obligations(e.g., maintaining roads, bridges, and irrigation ditches). Although substanceuse may be heavy at ceremonial events, even involving intoxication, thesocial control of the group over dosage and the brief duration of use augursagainst chronic abuse (although problems related to acute abuse may occur).Problems can develop if the group’s central rationale for existence rests on substanceuse (e.g., habitués of opium dens, taverns, and cocktail lounges). In theselatter instances, group norms for alcohol or drug use may foster substance abuserather than prevent it (Dumont, 1967).Medicinal reasons for substance use have prevailed in one place or anotherwith virtually all psychoactive substances, including alcohol, opium, cannabis,tobacco, the stimulants, and the hallucinogens (Hill, 1990). Insofar as substancesare prescribed or administered solely by healers or physicians, abuse israre or absent. For example, the prescribing of oral opium by Chinese physiciansover many centuries had few or no adverse social consequences. On theother hand, self-prescribing for medicinal purposes carries risks. For example,certain Northern Europeans, Southeast Asians, and others use alcohol forinsomnia, colds, pain, and other maladies—a practice that can and does lead tochronic alcohol abuse. Self-prescribing of opium by poppy farmers similarlyantedates opium addiction in a majority of cases (Westermeyer, 1982). Thus,professional control over medicinal use has been relatively benign, whereasindividual control over medicinal use of psychoactive compounds has oftenbeen problematic.Dietary use of substances falls into two general categories: (1) the use ofalcohol as a source of calories and (2) the use of cannabis and other herbalintoxicants to enhance taste. Fermentation of grains, tubers, and fruits intoalcohol has been a convenient way of storing calories that would otherwisedeteriorate. Unique tastes and eating experiences associated with beveragealcohol (e.g., various wines) have further fostered their use, especially at ritual,ceremonial, or social meals. Cannabis has also been used from the Middle Eastto the Malay Archipelago as a means of enhancing soups, teas, pastries, andother sweets. Opium and other substances have been served at South Asian ceremonies(e.g., weddings) as a postprandial “dessert.”Recreational use can presumably occur in either social or individual settings.Much substance use today occurs in recreational or “party” settings that havesome psychosocial rationales (e.g., social “time-out” and meeting friends) butminimal or no ritual or ceremonial aspects. So-called recreational substance usein these social contexts may in fact be quasi-medicinal (i.e., to reduce symptomsassociated with social phobia, low self-esteem, boredom, or chronic dysphoria).Even solitary psychoactive substance use can be recreational (i.e., to enhance anenjoyable event) or medicinal (i.e., to relieve loneliness, insomnia, or pain).

2. Historical and Social Context 23Other purposes exist but are not as widespread as those described earlier. Inthe 19th century, young European women took belladonna before social eventsin order to give themselves a ruddy, blushing complexion. A particular substanceor pattern of use can represent a social or ethnic identity (Carstairs,1954). Children may inhale household or industrial solvents as a means ofmimicking adult intoxication (Kaufman, 1973). Intoxication may simply serveas a means for continuing social behaviors, such as fights or homicide, thatexisted previously without intoxication (Levy & Kunitz, 1969). Particular patternsof alcohol–drug production or use may represent rebellion by disenfranchisedgroups (Connell, 1961; Lurie, 1970).HISTORY OF SUBSTANCE ABUSE TREATMENTHistorical and literary accounts have long documented individual attempts todraw back from the abyss of alcohol and drug abuse. At various times autobiographical,biographical, journalistic, and anecdotal, these descriptions listcenturies-old recovery methods still employed today in lay and professional settings.Modalities include gradual decrease in dosage; symptomatic use of nonaddictingmedications; isolation from the substance; relocation away from fellowusers; religious conversion; group support; asylum in a supportive and nondemandingenvironment; and treatment with a variety of shamanistic, spiritual,dietary, herbal, and medicinal methods (Westermeyer, 1998).Beginning with Galenic medicine, a key strategy has been to identify certainsyndromes as having their etiology in alcohol and drug abuse. Once theetiology is determined, the specific treatment (i.e., cessation of substanceabuse) can be prescribed. Examples of such substance-associated disordersinclude delirium tremens (i.e., alcohol and sedative withdrawal), withdrawalseizures, morphinism (i.e., opioid withdrawal), cannabis-induced acute psychosis,stimulant psychosis, and various fetal effects, such as fetal alcohol syndrome.Thus, description of pathophysiological and psychopathological processes,together with diagnostic labeling, has been a crucial historical step inthe development of modern assessment and treatment for substance use disorders(Rodin, 1981).Modern treatment approaches have their origins in methods developed byBenjamin Rush, a physician from the Revolutionary War era, who is often creditedas the father of American psychiatry. Rush developed a categorization ofdrinkers and alcoholics. He further prescribed treatment that consisted of aperiod of “asylum” from responsibilities and from access to alcohol, to takeplace in a family-like setting, in a milieu of respect, consideration, and socialsupport. As Rush’s concepts were extrapolated to the growing American society,large state-supported institutions were developed—although some smaller,

24 I. FOUNDATIONS OF ADDICTIONprivate asylums or sanitoria for alcoholics have persisted up to the current time(Johnson & Westermeyer, 2000).Medical treatments can interact constructively with cultural factors. Forexample, taking disulfiram can serve as an excuse for Native American alcoholicsto resist peer pressures to drink (Savard, 1968). Ethnic similarity betweenpatients and staff appears to be more critical to the treatment process than inother medical or psychiatric conditions (Shore & Von Fumetti, 1972). Strongethnic affiliation may be associated with more optimal treatment outcomes,although ethnic affiliation may change as a result of treatment (Westermeyer &Lang, 1975).On a federal level, treatment for drug abuse (largely opiate dependence)began with the Harrison Act of 1914, which outlawed nonmedical use of opiatedrugs. For a time, heroin maintenance was prescribed and dispensed in severalclinics around the country. Although research studies were not conducted, casereports from these clinics indicated that many patients were able to resume stablelives while receiving maintenance doses of heroin. These clinics werephased out, largely because of political opposition. Two long-term, prison-likehospitals for opiate addicts were established (one in Kentucky and the other inTexas). Research in these institutions contributed greatly to our understandingof opiate addiction (and alcoholism, which was also studied), but the demonstratedinefficacy of prison treatment led to their demise as treatment facilities.These legal and medical approaches, beginning in 1914, were effective inreducing opiate dependence in the societal mainstream. However, certainoccupational, geographical, and ethnic groups continued to use drugs that weremade illicit by the Harrison Act. These included seamen, musicians, certainminority groups, and inhabitants of coastal–border areas involved in smuggling(e.g., San Antonio, Texas; Louisiana seaports; San Francisco, California; andNew York City).Following World War II, medical and social leaders were more aware ofwidespread mental disabilities in the country because of the high rate of psychiatricdisorders among inductees and veterans. This led to the establishment ofthe National Institute of Mental Health (NIMH), which had divisions of alcoholismand drug abuse. By the 1970s, it became apparent that substance use disorderswere widely prevalent. Numerous indices of alcohol abuse and alcoholismhad been increasing since World War II, including hepatic cirrhosis andviolence-related mortality. Endemic abuse of cocaine and opiates exploded intoan epidemic in the late 1960s, followed by the appearance of stimulant and hallucinogenabuse. It was evident that the NIMH was not adequately addressingeither the alcohol epidemic or the drug epidemic. This led to the formation ofthe National Institute on Alcohol Abuse and Alcoholism (NIAAA) and theNational Institute on Drug Abuse (NIDA), both of which have equal statuswith the NIMH under the Alcohol, Drug Abuse, and Mental Health Administration(ADAMHA). Located within the Department of Health and Human

2. Historical and Social Context 25Services, ADAMHA has fostered the development of substance abuse research,training, clinical services, and prevention. Governmental support for theseefforts has come largely from elected officials who have personally experiencedpsychoactive substance use disorders, either in themselves or in their families.For example, most of the last several American presidents have had a spouse,parent, sibling, offspring, or personal experience with a substance abuse disorder.SOCIAL AND SELF-HELP MOVEMENTSAbstinence-oriented social movements first appeared among organized religions(Johnson & Westermeyer, 2000). Certain South Asian sects, arising fromearly Persian religions and Hinduism, abstained from alcohol over two millenniaago. Buddhist clergy were forbidden to drink alcoholic beverages, and piousBuddhist laity were urged to refrain from drinking, or at least to drink moderately.Early on, Moslems were urged not to drink; tradition has it that Mohammedhimself established abstinence for his followers. Abstinence-orientedChristian sects evolved in England and then in Central Europe at about thetime of the gin epidemic.Religiomania has long served as a cure for dipsomania and narcotomania.Opium addicts in Asia have gone to Buddhist monasteries in the hope thatworship, meditation, or clerical asceticism would cure them, which it sometimesdid (Westermeyer, 1982). Many Latin Americans and Native Americanswith high rates of alcoholism have abandoned Catholicism and Anglicanism infavor of abstinence-prescribing fundamentalist Christian sects and the NativeAmerican Church (Albaugh & Anderson, 1974; Hippler, 1973). Childrenraised in these sects are taught the importance of lifelong abstinence from alcoholand other drugs of abuse. Despite this childhood socialization, those leavingthese sects as adults can develop substance use disorders. Thus, the effects ofvarious religions in preventing substance abuse disorders appear to persist onlyas long as one is actively affiliated with the group.Abstinent societies not tied to specific religions began to appear in the18th and 19th centuries. Examples include the Anti-Opium Society in Chinaand the Women’s Christian Temperance Union in the United States. Thesegroups engaged in political action, public education, social pressure againstaddiction or alcoholism, and support for abstinence. These led eventually toprohibition movements that sought legal strictures against the production, sale,and/or consumption of psychoactive substances outside religious or medicalcontexts. In Asia, these movements began against tobacco (which was viewedin the 1600s and 1700s as a slothful habit associated with political sedition) andthen later changed to oppose primarily opium. In Northern Europe and theUnited States, prohibition laws first involved opiates and cannabis but later

26 I. FOUNDATIONS OF ADDICTIONexpanded to include alcohol. As Moslem peoples emerged from colonialregimes, their nations passed anti-alcohol legislation that ranged from mildstrictures for Moslems alone, to harsh measures against all inhabitants of thecountry.Numerous self-help groups in the United States were founded during theDepression era. Many more were begun after World War II. These groupsinvolved individuals who banded together to meet their common financial,social, or personal needs (Lieberman & Borman, 1976). Movements of the eradiffered in several important aspects from earlier abstinence-oriented groups asfollows:• Individuals could remain in their homes, families, and jobs rather thanjoining a separate sect or going off to an asylum or special group.• Considerable structure was involved, with specific meetings and phased“step” recovery activities.• The concept of a recovery process over time was introduced, as distinctfrom a sudden cure or conversion; this had biological, psychological,social, and spiritual dimensions.• Organization was kept predominantly atomistic (i.e., autonomous smallgroups) rather than hierarchical.• Membership required self-identity as an alcoholic or addict (i.e., supportiveor concerned persons were excluded).Like earlier movements, these self-help groups emphasized the importance ofabstinence from psychoactive substance abuse (although tobacco and coffee arenotably present at some Alcoholics Anonymous [AA] meetings today), relianceon a superior spiritual force (the “Higher Power”), and social affiliation or “fellowship”for mutual support. AA, perhaps the best known of these groupstoday, was first established in the United States. It has spread to many otherparts of the world over the last 50 years and has served as a model for similargroups whose identity centers on other drugs and even other problems (i.e.,Narcotics Anonymous, Cocaine Anonymous, Overeaters Anonymous, GamblersAnonymous, and Emotions Anonymous [formerly Neurotics Anonymous]).Groups for those personally affected by alcoholism have also appeared,such as Alateen for the teenage offspring of alcoholic parents and Al-Anon forthe spouses, parents, and other concerned associates of alcoholic persons.Over the last several years, the Adult Children of Alcoholics and Addicts(ACOAA) movement has also evolved to meet the needs of those distressed ormaladaptive adults raised by alcoholic parents. Mothers Against Drunk Drivers(MADD) was originally formed to meet the support needs of parents whosechildren were killed by drunken auto drivers. MADD has since expanded itsactivities as a “watchdog” group that follows the records of legislators andjudges in regard to alcohol-related legal offenses. The social and cultural com-

2. Historical and Social Context 27position of the self-help group appears to be an important factor in attractingclients and effecting therapeutic outcomes (Jilek-Aal, 1978).FACTORS AFFECTING ALCOHOL–DRUG EPIDEMICSNumerous factors contributed to the development of substance abuse “epidemics”or “plagues.” One of the first of these, the gin epidemic (which involvedother alcohol-containing beverages besides gin) in late 17th- and 18th-centuryEngland, was fostered by the following factors:• English merchant ships returning empty from trips to its colonies loadedon gin, rum, and other alcohol-containing beverages as ballast beforereturning to England.• Rum was derived from sugar cane grown with slave labor, and gin wasfrom grains grown with indentured labor. With no import tax, calories ofthese alcohol-containing beverages were literally cheaper than caloriesof bread in London.• The beginnings of the Industrial Revolution gave rise to repressive socialconditions and a loss of traditional rural values, fostering widespreaddrunkenness with inexpensive beverage alcohol.• Although traditions and social controls existed for the drinking of meadand ale, these traditions and controls did not extend to gin and rumdrinking, with the result that daily excessive drinking appeared.During this period, numerous sequelae of alcoholism were first recognized,including the description of the fetal alcohol syndrome (Rodin, 1981). Thegin epidemic raged for several decades, perhaps as long as a century. It eventuallyreceded under such pressures as an import tax on imported alcoholcontainingbeverages, anti-alcohol propaganda in the literature and art of theday, and evolution of abstinence-oriented Protestant sects for the workingclasses.The opium epidemic in many countries of East and Southeast Asia beganabout the same time as the European alcohol epidemic. Several factors, somesimilar to the European situation but others different, contributed to the opiumepidemic:• Tobacco smoking was introduced to Asia from the New World; itbecame a popular pastime in smoking houses that were frequented by the artisans,artists, adventurists, and literati of the day.• As European and New World concepts and artifacts flooded into Asia,tobacco-smoking houses were viewed as places of cultural change and evenpolitical sedition; they were gradually outlawed.

28 I. FOUNDATIONS OF ADDICTION• Opium eating, primarily a medicinal activity that had never been a significantsocial problem, was combined with this new technology (i.e., drug consumptionby volatilization and inhalation); recreational opium smoking subsequentlybecame widespread.• Political corruption, government inefficiency, and absence of statecraftskills to deal with widespread drug abuse, abetted by the political and economicimperialism of Western colonial powers, led to centuries of widespread opiumaddiction among various Asian nations. Some countries have reversed theproblem in this century (e.g., Japan, Korea, China, and Manchuria); othershave not (e.g., Thailand, Laos, Burma, Pakistan, Afghanistan, Iran, and India).TRENDS IN PROBLEMS ACROSS TIME AND SPACEThe appearance of new drugs (or reappearance of old ones in new forms)exposed social groups to agents against which they had no sociocultural protectionor “immunity”; that is, the community or nation had no tradition forproblem-free, or at least controlled, use of the substance. Users themselves maynot have perceived the actual risks associated with the new psychoactive substance.This situation also occurred when the group was familiar with the substancebut in a different form. For example, traditions may exist for wine butnot beer or distilled alcohol; pipe smoking may be subject to customs that donot extend to cigarette smoking.Symbolic aspects of certain drugs or modes of drug administration may displacethe issue from psychoactive substance use per se to associated issues ofethnic identity, cultural change, political upheaval, class struggle, or intergenerationalconflict (Robbins, 1973). Examples include the following:• Cannabis and hallucinogen use as antiauthority symbols in the late1960s and 1970s.• Alcohol abuse among indigenous peoples (Thompson, 1992).• Illicit raising of poppy as a cash crop and opium smuggling by ethnicminorities in Asia (Westermeyer, 1982).As drug use has spread in the last few centuries, drug production and commercehave become important economic resources in many areas. Early examples inthe 1800s were the British trading companies in large areas of India, whichdepended for their wealth on opium sales to China. Numerous backward areasin the world today maintain their participation in national and world marketsthrough their participation in illicit drug production and sales: Afghanistan,Burma, Laos, Mexico, Pakistan, and Thailand in opium and heroin; the Caribbeannations and Mexico in cannabis production and cocaine commerce; andseveral South and Central American countries in cocaine production and com-

2. Historical and Social Context 29merce. During the 1980s, several states in the United States counted cannabisas a major, albeit illicit, cash crop: North Carolina, Tennessee, Kentucky, Kansas,Nebraska, New Mexico, California, and Hawaii (Culhane, 1989).Government instability, corruption, or inefficiency can cause or resultfrom drug production, export, and/or smuggling today. Unstable countries inSouth Asia, the Middle East, Africa, and Latin America have become producers,transshippers, or importers of illicit drugs. Societal breakdown has led tosubstance abuse in some Moslem countries, contributing to a backlash ofIslamic fundamentalism. Likewise, in the United States and Latin America,widespread alcoholism predates the shift to Christian fundamentalism.Industrialization and technological advances have fostered a redefinitionof substance abuse (Stull, 1972). An intoxicated or “hungover” (withdrawing)oxcart driver can effect limited damage, other than to cart, ox, and self. Thealcohol- or drug-affected driver of a modern high-speed bus, the captain of aferry boat, or the pilot of a jet transport can kill scores of people and destroyequipment and material worth millions of dollars. Handicraft artisans under theinfluence of drugs or alcohol can do little damage, whereas workers in a factorycan harm themselves or others, as well as destroying expensive machinery andbringing production to a halt.Since World War II, and especially since the 1960s, adolescent-onset substanceabuse has escalated from rare sporadic cases to a high prevalence inmany communities (Cameron, 1968). Several factors appear to have fostered it:widespread parental substance abuse, societal neglect of adolescents, poverty,rapid social changes, family breakdown, and political upheaval. Whatever thecause, the consequences are remarkably similar: undermining of normal adolescentpsychosocial development, poor socialization of children to assume adultroles, lack of job skills, emotional immaturity, increased rates of adolescent psychiatricmorbidity, and increased adolescent mortality from suicide, accidents,and homicide.TRENDS IN TREATMENT AND PREVENTIONFrom the time of Benjamin Rush, two central treatment methods were established,based on the psychiatric treatment methods of the late 1700s: (1) “asylum”in a supportive environment away from drink and companion drinkersand (2) “moral treatment,” consisting of a civil, respectful consideration for therecovering person (Johnson & Westermeyer, 2000). Both methods persist todayand remain as two standard treatment strategies. They were not and are notinevitably successful. Consequently, other methods have been tried.One of these methods was the substitution of one drug for another. Forexample, laudanum (combined alcohol and opiates) was once prescribed foralcoholism. Morphine, and later heroin, was recommended for opium addiction

30 I. FOUNDATIONS OF ADDICTIONduring the mid-1800s. This approach is not extinct, as exemplified by the frequentrecommendation in the 1970s that alcoholics substitute cannabis smokingfor alcohol. Currently, methadone is used for chronic opiate addicts whohave failed attempts at drug-free treatment. Despite aversive selection factors,methadone maintenance patients tend to do well as long as they comply withtreatment.Detoxification became prevalent in the mid-1900s. Public detoxificationfacilities, established first in Eastern Europe, spread throughout the world. Formany patients, this resource offers an entree into recovery. For others, “revolvingdoor” detoxification may actually produce lifelong institutionalization onthe installment plan (Gallant et al., 1973). The problem of the treatmentresistantpublic inebriate exists today in all parts of the United States.The so-called Minnesota Model of treatment developed from severalsources: a state hospital program (at Wilmar) and a later private program (atHazelden), supplemented by the first day program for alcoholism (at theMinneapolis Veterans Administration Hospital). The characteristics of this“model” have varied over time as treatment has evolved and changed, and definitionsstill differ from one person to the next. However, characteristics oftenascribed to the model include the following:1. A period of residential or inpatient care, ranging from a few weeks toseveral months.2. A focus on the psychoactive substance use disorder, with little or noconsideration of associated psychiatric conditions or individual psychosocialfactors.3. Heavy emphasis on AA self-help concepts, resources, and precepts,such as the “12 steps” of recovery.4. Referral to AA or another self-help group on discharge from residentialor inpatient care, with minimal or no ongoing professional treatment.5. Minimal or no family therapy or counseling (although family orientationto AA principles and Al-Anon may take place).6. Negative attitudes toward ongoing psychotherapies and pharmacotherapiesfor substance use disorder or associated psychiatric disorder.At the time of its evolution in the 1950s and 1960s, this model served to bridgethe formerly separate hospital programs and self-help groups—a laudableachievement. However, if it is applied rigidly in light of current knowledge,some patients (who might otherwise be helped) will fail in or drop out of treatment.Nowadays, many treatment programs employ aspects of the old “MinnesotaModel,” integrating them flexibly with newer methods in a more individualizedand patient-centered manner.The workplace has been a locus of prevention, early recognition, referralfor treatment, and rehabilitation. Following World War II, Hudolin and

2. Historical and Social Context 31coworkers in Yugoslavia established factory- and farm–commune-based recoverygroups, with ties to treatment facilities. Over the last two decades, alcoholismcounselors have worked in similar “employee assistance programs” in theUnited States.More sophisticated methods of pharmacotherapy have appeared recently,although these remain few in comparison with other areas of medicine. Safedetoxification is possible through increased basic and clinical appreciation ofwithdrawal syndromes. Disulfiram, naltrexone, buprenorphine, and methadonemay be selectively prescribed as maintenance drugs in the early difficult monthsand years of recovery. Other medications are currently being investigated foruse in special circumstances.Recognition of comorbid conditions accompanying substance abuse hasled to concurrent treatment for affective disorders, anxiety disorders, eating disorders,and pathological gambling. For certain chronic conditions (e.g., mildmental retardation, borderline intelligence, organic brain syndrome, or chronicschizophrenia), substance abuse treatment, rehabilitation, and self-help proceduresneed to be modified. Intensive outpatient programs, conducted during theday, evening, or weekend, assist certain patients to recover when other measuresfail. These intensive outpatient programs are modeled after similar psychiatricprograms. Much of the treatment time is spent in groups of various sizes,although individual and family sessions may occur as well. Staffing is typicallymultidisciplinary, with counselors, nurses, occupational and recreational therapists,psychologists, psychiatrists, and social workers. Monitoring of recovery inseveral contexts and by several sources (e.g., at work, by licensing agencies orunions, in the family, and with medical resources) appears to enhance outcome(Westermeyer, 1989).Preventive techniques first applied to the gin epidemic are still usefultoday: control over hours and location of sales, taxes or duties to increase cost,changing of public attitudes via the mass media, education, and abstinenceorientedreligion (Smart, 1982). The prolonged Asian opium epidemic demonstratedthat laws alone are ineffective unless accompanied by socially integratedtreatment; recovery programs; compulsory abstinence in identified cases; policepressure against drug production, commerce, and consumption; and follow-upmonitoring. Experience with anti-alcohol prohibition laws in Europe andNorth America demonstrated the futility of outlawing substance use that wassupported by many citizens. Adverse results from the Prohibition era in theUnited States included increased criminality associated with bootlegging alcohol,lack of quality control (e.g., methanol and lead contaminants), and developmentof unhealthy drinking patterns (e.g., surreptitious, rapid, without food,and in a deviant setting). Public interest groups such as MADD may aid inreducing certain alcohol- and drug-related problems. The United States hasexpended several 10’s of billions of dollars since 1970 to reduce the supply ofand demand for drugs. But mortality from hepatic cirrhosis, alcohol-related

32 I. FOUNDATIONS OF ADDICTIONaccidents, and suicide continue at an unprecedented level, especially amongyoung American males. Work still remaining includes our learning from history(our own as well as that of others) to honing that aspect of statecraft aimed ateliminating our endemic substance abuse.REFERENCESAhluwalia, H. S., & Ponnampalam, J. T. (1968). The socioeconomic aspects of betelnutchewing. J Trop Med Hyg, 71, 48–50.Albaugh, B., & Anderson, P. (1974). Peyote in the treatment of alcoholism amongAmerican Indians. Am J Psychiatry, 131, 1247–1256.Anawalt, P. R., & Berdan, F. F. (1992). The Codex Mendoza. Sci Am, 266, 70–79.Baldwin, A. D. (1977). Anstie’s alcohol limit: Francis Edmund Anstie 1833–1874. Am JPublic Health, 67, 679–681.Bergman, R. L. (1971). Navaho peyote use: Its apparent safety. Am J Psychiatry, 128,695–699.Bunzel, R. (1940). The role of alcoholism in two Central American cultures. Psychiatry,3, 361–387.Caetano, R. (1987). Acculturation and drinking patterns among U.S. Hispanics. Br JAddict, 82, 789–799.Caetano, R., Suzman, R. M., Rosen, D. H., & Voorhees-Rosen, D. J. (1983). The ShetlandIslands: Longitudinal changes in alcohol consumption in a changing environment.Br J Addict, 78, 21–36.Cameron, D. C. (1968). Youth and drugs: A world view. JAMA, 206, 1267–1271.Carstairs, G. M. (1954). Daru and bhang: Cultural factors in the choice of intoxicant. QJ Stud Alcohol, 15, 220–237.Chopra, G. S., & Smith, J. W. (1974). Psychotic reactions following cannabis use inEast Indians. Arch Gen Psychiatry, 30, 24–27.Connell, K. H. (1961). Illicit distillation: An Irish peasant industry. Hist Stud Ireland, 3,58–91.Culhane, C. (1989). Pot harvest gains across country. USJ, 13, 14.Dumont, M. (1967). Tavern culture: The sustenance of homeless men. Am J Orthopsychiatry,37, 938–945.DuToit, B. M. (1977). Drugs, rituals and altered states of consciousness. Rotterdam, Netherlands:Balkema.Fenna, D. L., Mix, O., Schaeffer, J., & Gilbert, A. L. (1971). Ethanol metabolism invarious racial groups. Can Med Assoc J, 105, 472–475.Furst, P. T. (1972). Flesh of the gods: The ritual use of hallucinogens. New York: Praeger.Gallant, D. M., Bishop, M. P., Mouledoux, A., Faulkner, M. A., Brisolara, A., &Swanson, W. A. (1973). The revolving door alcoholic. Arch Gen Psychiatry, 28,633–635.Heath, D. (1971). Peasants, revolution, and drinking: Interethnic drinking patterns intwo Bolivian communities. Hum Organ, 30, 179–186.Hill, T. W. (1990). Peyotism and the control of heavy drinking: The NebraskaWinnebago in the early 1900s. Hum Organ, 49, 255–265.

34 I. FOUNDATIONS OF ADDICTIONThompson, J. W. (1992). Alcohol policy considerations for Indian people. Am IndianAlsk Native Ment Health Res, 4, 112–119.Thurn, R. J. (1978). The gin plague. Minn Med, 61, 241–243.Westermeyer, J. (1982). Poppies, pipes and people: Opium and its use in Laos. Berkeley:University of California Press.Westermeyer, J. (1987). Cultural patterns of drug and alcohol use: An analysis of hostand agent in the cultural environment. UN Bull Narc, 39, 11–27.Westermeyer, J. (1989). Monitoring recovery from substance abuse: Rationales, methodsand challenges. Adv Alcohol Subst Abuse, 8, 93–106.Westermeyer, J. (1998). Historical–social context of psychoactive substance disorders.In R. J. Frances & S. I. Miller (Eds.), Clinical textbook of addictive disorders (2nd ed.,pp. 14–32). New York: Guilford Press.Westermeyer, J. (1999). The role of cultural and social factors in the cause of addictivedisorders. Psychiatr Clin North Am, 22, 253–273.Westermeyer, J., & Lang, G. (1975). Ethnic differences in use of alcoholism facilities.Int J Addict, 10, 513–520.Wolcott, H. F. (1974). African Beer Garden of Bulawayo: Integrated drinking in a segregatedsociety. New Brunswick, NJ: Rutgers Center of Alcoholism Studies.

PART IIASSESSMENT OF ADDICTION

CHAPTER 3Psychological Evaluationof Substance Use Disorderin Adolescents and AdultsRALPH E. TARTERPsychological evaluation is directed at characterizing cognitive, emotional, andbehavioral processes. The evaluation of substance use disorders thus focuses onmultiple domains of psychological functioning. The instruments selectivelyreviewed in this chapter satisfy the following criteria: (1) the psychometricproperties have been empirically established, (2) the measures have practicalutility, and, (3) they are applicable to diverse populations.It has been previously argued that the assessment of substance abuse shoulduse comparable measures in clinical and research settings (Rounsaville, 1993).The ultimate usefulness of psychological measurement is to delineate theunique factors within the individual that predispose to substance use onset, sustainhabitual consumption, and impede psychosocial adjustment. Moreover, acomprehensive evaluation should directly guide the selection of prevention andtreatment strategies that are most likely to be successful. In the managed careenvironment, where there is an emphasis on cost containment and empiricaldocumentation, it is invaluable to obtain as much information as possible thatcould expedite effective treatment.Psychological evaluation must also accommodate contemporary understandingof the disorder. Hence, evaluation must encompass an approach thataligns with an appreciation of the multifactorial etiology of substance use disorder.A multivariate assessment protocol is therefore necessary to characterizethe individual fully. Finally, it needs to be recognized that manifold psychologi-37

38 II. ASSESSMENT OF ADDICTIONcal disturbances presage, are concomitant to, and emerge as consequences ofchronic substance use. A comprehensive psychological evaluation must thereforeencompass the natural history of the disorder.This chapter is divided into three sections. First, I discuss the scope andrequirements of a psychological assessment. Next, the methods for conducting apsychological assessment are described. A presentation of a decision-tree formatthat links the results of psychometric evaluation to specific modes of treatmentconcludes the chapter.SCOPE AND ATTRIBUTES OF COMPREHENSIVE ASSESSMENTThree broad categories of processes require psychological evaluation in cases ofknown or suspected substance abuse: cognition, emotion, and behavior. A disturbancein one domain may or may not involve a disturbance in another. Forinstance, among individuals with a substance use disorder, some are disturbedemotionally, whereas others primarily have a cognitive disorder. Hence, withina given diagnostic category, there is substantial heterogeneity in the populationwith respect to the profile of psychological disturbance. A major task is thereforeto ascertain what processes are disturbed, the severity of disturbance, andthe relationships among the various components of psychological functioning.Importantly, the pattern of psychological disturbance is related to the typeof facility in which the individual is obtaining treatment. For example, patientswith alcohol use disorder in a gastroenterology service typically manifest lesssevere emotional disorder and present with better social adjustment than individualstreated in psychiatric facilities (Ewusi-Mensah, Saunders, & Williams,1984). In contrast, patients with chronic liver disease are more likely to sufferacute and chronic hepatic encephalopathy compared to persons admitted topsychiatric facilities. Clinicians must therefore be cognizant of the generalcharacteristics of the population from which their clients are drawn in order todesign the most informative examination.PSYCHOMETRIC STANDARDSThe information acquired from the psychological assessment must satisfy twobasic requirements: validity and reliability.ValidityEmployed for either research or clinical purposes, a psychological test musthave empirically documented validity. This ensures that the test results are factual;that is, the score is an accurate description of the individual. Validity has

3. Psychological Evaluation 39several facets. Construct validity means that the psychological processes claimedto be measured are, in fact, what are being assessed. For instance, it is essentialto be confident that a poor score on a neuropsychological test of memory capacityis due to a central nervous system (CNS) disorder and is not spurious.Hence, utility of a particular instrument depends on its capacity to evaluateaccurately the process intended to be measured.In addition, psychological measures should have predictive validity; that is,the processes evaluated by the test should yield scores that predict the individual’sbehavior. For example, low scores on tests of educational aptitudeshould portend academic underachievement. High scores on tests of anxietyshould predict avoidant social behavior. These predictions should be orientedto meaningful and specific domains of functioning, such as the person’spotential to respond to a particular type of treatment or hold a certain type ofjob. Predictive validity is therefore an essential aspect of a comprehensiveassessment, because it yields information that guides selection of the particulartype of rehabilitation program that in turn impacts on long-term prognosis.Finally, it should be noted that psychological testing is warranted onlywhen the obtained data have incremental validity; that is, the test should yieldinformation beyond what can be acquired from informal interviewing or casualobservation. It is pointless to measure depression if the patient readily providesa self-report of symptoms. Psychometric procedures are most prudently utilizedin situations where the objectivity of measurement yields information that iseither too complex or too subtle to be obtained from observation or ordinaryinteraction with the client. Because it is both expensive and labor-intensive,clinicians should not request a psychological evaluation to merely confirm aclinical impression.ReliabilityOf the various types of reliability, two need to be considered here: test–retestand interrater reliability. Test–retest reliability refers to the temporal stability ofthe score. The clinical meaningfulness of test results is contingent upon itsrepeatability. Thus, any changes observed in the individual over time shouldreflect a true change in the person’s status and not be due to random fluctuationsof unknowable origin. A psychological test that has established test–retestreliability can be thus used repeatedly to monitor changes in status that occurduring the course of treatment and aftercare.The second type of reliability is interrater reliability. A test score obtainedby one clinician should ideally be the same as the test administered by another,equally skilled clinician. In this fashion, confidence can be placed in theresults. In effect, the results should not reflect the idiosyncratic interactionbetween the clinician and the client.

40 II. ASSESSMENT OF ADDICTIONPSYCHOLOGICAL PROCESSES INTEGRALTO SUBSTANCE ABUSECognitive processes encompass both cognitive style and cognitive capacity.Both aspects are relevant to understanding substance abuse. Cognitive stylerefers to the general strategy an individual uses to process information. Forexample, substantial evidence indicates that substance abusers are more inclinedthan the general population to analyze perceptual stimuli in a global,inarticulate manner (Sugerman & Schneider, 1976). This stable trait is referredto as perceptual field dependence. Significantly, field-dependence cognitive styleappears to be related to treatment prognosis (Karp, Kissin, & Hustmeyer,1970).Another facet of cognitive style commonly found among substance abusersis stimulus augmentation—the propensity to magnify sensory input (Buchsbaum& Ludwig, 1980). Stimulus augmentation is overtly featured by impulsivity,behavioral disinhibition and sensation, or novelty seeking. Interestingly, thiscognitive style correlates with low platelet monoamine oxidase (MAO) activity(Schooler, Zahn, Murphy, & Buchsbaum, 1978). Low platelet MAO activity isparticularly associated with alcoholism in cases in which there is a comorbidantisocial disorder (Von Knorring, Bohman, Von Knorring, & Oreland, 1985).Understanding the person’s cognitive style may thus assist in treatmentplanning and in formulating a differential diagnosis. Unfortunately, the techniquesfor assessing this aspect of cognition have not been inculcated into generalpsychometric assessment practice, although it is possible to make inferencesabout perceptual field dependence by using a simple test measuringflexibility of perceptual closure (Jacobson, Pisani, & Berenbaum, 1970) andstimulus augmenting by measuring sensation-seeking behavior (Zuckerman,Bone, Neary, Mangelsdorff, & Brastman, 1972).Another important aspect of cognition pertains to attributional style. Ineffect, individuals at high risk for substance abuse and currently active users areinclined mistakenly to harbor beliefs about the putative benefits of alcohol andother drugs (Finn, Sharkansky, Brandt, & Turcotte, 2000; Vernon, Lee, Harris,& Jang, 1996). Because these types of cognitions portend how an individualwill behave, it is important also to assess attributional style.Cognitive capacities are commonly impaired in people with alcohol usedisorders as a result of CNS injury either directly caused by alcohol neurotoxicityor indirectly mediated by organ–system damage (e.g., hepatic encephalopathy,obstructive pulmonary disease, hypertension). Multiple factors typicallycompromise CNS functioning. Besides the direct effects of drugs oralcohol on the brain, these factors include trauma (e.g., head injuries from accidentsand fights), poor nutrition, and exposure to toxic substances in the environment.The psychological evaluation must therefore not only be aimed atdetecting and describing the pattern of CNS disturbances by means of validated

3. Psychological Evaluation 41neuropsychological tests but should also attempt to determine from other psychometricinstruments (as well as from biomedical or laboratory tests) the possibleetiological basis for the manifest disturbances.Approximately 75% of individuals with alcohol dependence demonstratesome form of CNS disturbance, as measured by neuropsychological tests (Tarter& Edwards, 1985). Emerging findings also suggest that other forms of substanceabuse are frequently associated with deficits on neuropsychological tests. Generallyspeaking, chronic alcohol abuse can cause both cognitive and physicaldamage to the brain that is typically expressed as visuomotor deficits, while verbalability remains essentially intact. Impairments have also been frequentlyobserved on tasks measuring abstract thinking and memory capacity, as well ason tests measuring visuospatial processes (Tarter & Ryan, 1983). These deficitsappear to be most pronounced in individuals who are in less than optimalhealth, or who have experienced the cumulative effects of multiple CNS insults(Grant, Adams, & Reed, 1979). With respect to biomedical factors, a low-gradechronic hepatic encephalopathy may contribute substantially to the cognitivedeficits found in cirrhotic alcoholics. This neuropsychiatric disturbance has acomplex etiology. For example, the encephalopathy, revealed as poor performanceon cognitive tests, is caused to large degree by the liver’s failure tocatabolize circulating neurotoxins (Tarter, Edwards, & Van Thiel, 1986). Furthermore,it should be noted that a hepatic encephalopathy may have a varietyof other etiological determinants (Tarter et al., 1986). In effect, the manifestcognitive deficits have a multifactorial etiology.Neuropsychological deficits associated with alcoholism are well documented.Indeed, two syndromes of cognitive disorder have been described. Adementia has been observed that is distinguishable according to both neuroanatomicaland cognitive manifestations from the more florid amnestic orKorsakoff’s syndrome (Wilkinson & Carlen, 1980). A number of other neurologicalconditions have also been described, although their neuropsychologicalmanifestations have not yet been studied.Less is known regarding neuropsychological sequelae following other typesof substance abuse. Evidence has been presented indicating that the chronic useof phencyclidine (PCP), inhalants, benzodiazepines, heroin, cocaine, andamphetamines may be associated with neuropsychological impairments in someindividuals (Parsons & Farr, 1981). One major methodological problem in thisarea of study is that it is not possible to ascertain the specific effects of a certaindrug on CNS functioning, because polydrug abuse is the typical pattern of consumption.Also, the frequency and quantity of drug use are extremely variable;hence, determining a dose–effect relationship is difficult, if not impossible.These qualifications notwithstanding, the available evidence indicates that, asa group, substance abusers perform deficiently on certain neuropsychologicaltests indexing CNS integrity. As is the case among individuals with alcoholdependence, poor neuropsychological test performance has a multifactorial eti-

42 II. ASSESSMENT OF ADDICTIONology. For instance, poor performance may be reflective of multiple minor braininjuries, poor overall health, and premorbid neurodevelopmental disorder.Neuropsychological tests are very sensitive indicators of cerebral integrity(Lezak, Howieson, & Loring, 2004). In the early stages of a demential disease,these psychometric procedures complement neuroradiological procedures,where gross morphological injury may not be detectable upon visual inspection.Neuropsychological tests are especially informative for rehabilitation purposes,because the data describe functional cerebral integrity and, as such, characterizethe person according to the cognitive processes (e.g., attention, memory, language,learning, and concentration) that are generally understood to be importantfor educational, vocational, and social adjustment. Indeed, it is the relationshipbetween neurological status and these latter processes, rather than thetest scores per se, that underscores the importance of the neuropsychologicalassessment.Documenting cognitive capacity and efficiency via neuropsychologicalassessment is important for several reasons. During the drug withdrawal phaseat the onset of rehabilitation, cognitive capacity may be too impaired for theperson to achieve meaningful gains from didactic therapy or counseling. Assessmentof the subjective effects of intoxication or withdrawal status from varioussubstances of abuse has been developed by the Addiction Research Center(Haertzen, 1974). Handelsman and colleagues (1987) have also developedassessment instruments to evaluate severity of withdrawal.A brief cognitive screening used on repeated occasions is an efficientmethod to determine the client’s readiness for rehabilitation. Individuals withsubstantial cognitive limitations may not be able to solve daily problems,develop strategic plans to organize their lives, acquire insight into their problems,or benefit from vocational rehabilitation. A neuropsychological assessmentcan thus assist in formulation of a treatment plan and aftercare program.For instance, most persons respond to didactic psychotherapy, whereas thosewhose thinking is concrete benefit most from structured interventions that dorequire problem solving (Kissin, Platz, & Su, 1970). Furthermore, it is importantto note that everyday activities such as driving a car, using power machinery,or performing tasks in which there are safety risks may be impaired becauseof CNS damage consequent to chronic heavy substance use. Neuropsychologicaltesting, particularly in the area of psychomotor capacities, may thereforeassist in the determination of injury risk to self and others.Neuropsychological assessment has also been increasingly utilized as partof forensic evaluation. In criminal cases, objective quantitative assessment ofcognitive capacities contributes to a better understanding the underlying causesof behavior disturbance. In this regard, expertise of the neuropsychologist whounderstands brain–behavior relationships that may be disrupted following alcoholor substance use can inform about the mechanisms underlying cognitivedisturbances such as blackouts and anterograde amnesia.

3. Psychological Evaluation 43In summary, systematic delineation of cognitive strengths and weaknesses,particularly as they relate to the onset and pattern of substance use behavior, isimportant for several reasons. For example, an attentional disorder or learningdisability often precedes the onset of substance abuse (Tarter, Alterman, &Edwards, 1985). This has treatment implications, because it may be possible toprevent or treat the substance use behavior in some individuals by amelioratingthe problem that initially motivated drug use. In addition, the assessment ofcognitive deficits is important for understanding the person’s everyday abilities,such as remembering appointments, following directions, and learning newinformation and skills. Demonstrating the presence of a cognitive deficit alsoinforms about implementing a treatment plan that encompasses a cognitiverehabilitation component. For example, cognitive retraining by teaching theperson compensatory strategies when there is an irreversible deficit, or by reestablishinga capacity that was not permanently impaired, affords the opportunityto maximize social and vocational adjustment within the framework ofcomprehensive rehabilitation.EmotionThe intensity of emotional experience and appropriate expression of emotionare strongly associated with the quality of psychological adjustment. Conflictsover anger and guilt, and the display of intense emotional reactions commonlyaccompany substance use. These disruptive emotions may either presage substanceuse or emerge following drug use onset. Not uncommonly, consumptionof psychoactive substances is motivated by a need to ameliorate negative affectivestates such as anger, depression, and fear. The inability to express emotionseffectively in the social context, particularly negative feelings, is also frequentlyassociated with drug abuse.Emotional disturbance is often encompassed within psychopathology.From the psychometric perspective, clinically significant psychopathology ispresent when severity exceeds two standard deviations from the populationmean. In effect, the severity score ranks in excess of the 95th percentile in thepopulation on a trait (e.g., anxiety). Whether the magnitude of severity of psychopathologicaldisturbance points to the need for treatment can only be determinedby integrating the findings obtained from a diagnostic psychiatric interviewand psychometric assessments. For example, anxiety or depression mayfoster substance abuse in an individual even if the severity is subthreshold fordiagnosis. Notably, subthreshold negative affective states predispose to drugseeking (Khantzian, 1985). As pointed out by Dodes (1990), psychoactivedrugs modulate affect in part by ameliorating negative feelings concomitant tohelplessness and powerlessness.It is important to be cognizant of the possibility that a psychiatric disordermay remit following effective treatment of substance abuse. It is not uncommon

44 II. ASSESSMENT OF ADDICTIONfor psychopathological symptoms to dissipate in conjunction with abstinencefrom alcohol and drugs following the initial period of detoxification and withdrawal.Furthermore, it is essential to recognize that emotional distress can bothprecipitate and sustain a psychopathological disorder. Characterizing the client’semotional status therefore enables the clinician to determine the relationof psychopathology to substance abuse either as a predisposing condition, a correlateof the disorder, or a consequence of the disorder.In contrast to diagnostic psychiatric assessment, psychological tests measuretraits. The evaluation is thus concerned with quantifying the person onparticular dimensions, whereas the psychiatric evaluation categorizes the personaccording to presence or absence of a disorder. Hence, commonly used psychiatricinterviews such as the Schedule for Affective Disorders and Schizophrenia,Diagnostic Interview Schedule, and Structured Clinical Interview forDSM-III-R are concerned primarily with dichotomous classification. Whethera categorical or dimensional approach is utilized, the most frequently observedpsychopathological disturbances comorbid to alcohol or drug abuse are anxietyand depression. However, virtually every Axis I and Axis II disturbance hasbeen observed concomitant to substance use disorder (Dackis, Gold, Pottash, &Sweeney, 1985; Daley, Moss, & Campbell, 1987; Helzer & Pryzbeck, 1988;Peace & Mellsop, 1987; Weissman, 1988).BehaviorThe third component of a comprehensive psychological assessment pertains todetermining the degree to which the individual’s behavioral characteristics arerelated to substance abuse. Behavioral adjustment can be characterized in bothmicroenvironment (e.g., family and friends) and macroenvironment (e.g.,work, community, and school). Importantly, behavioral disposition, such asantisocial personality disorder, mitigates optimal functioning in a variety ofsocial contexts. The point to be emphasized is that behavioral adjustment is theproduct of the interaction between the individual and the particular context. Abehavioral characteristic (e.g., aggressiveness) can be adaptive in one contextand maladaptive in another context.Many behavioral characteristics have been shown to augment the risk forsubstance abuse, as well as to covary with substance abuse severity. The mostcommonly reported features include impulsivity, aggressivity, thrill seeking,poor goal persistence, hyperactivity, and social nonconformity (Spear, 2000;Tarter et al., 1999).Cognition, emotion, and behavior comprise the major domains of psychologicalfunctioning. Notably, the facets of these three processes pertaining toself-regulation are indicators of a unidimensional trait termed neurobehavioraldisinhibition (Tarter et al., 2003). The score on this trait is highly predictive of

3. Psychological Evaluation 45substance use disorder between childhood and young adulthood (Tarter et al.,2003). These findings indicate that a core disorder of psychological selfregulationunderlies the risk for substance abuse (Tarter, Kirisci, Habeych,Reynolds, & Vanyukov, 2004). It should be emphasized, however, that there issubstantial population heterogeneity with respect to the expression of thesethree domains of psychological functioning. At the individual level, therefore,a disturbance may be confined to only one area of functioning, may pervade allpsychological domains, or (theoretically, at least) may not be present to a significantdegree in any of the three areas.METHODS OF PSYCHOLOGICAL ASSESSMENTThe overarching purpose of a psychological evaluation is to identify and quantifyseverity of problems integral to substance abuse that are amenable tomodification. Based on evaluation results, interventions can thus be directed atchanging the individual, the environment, or the quality of person–environmentinteraction to assist the client in terminating substance consumptionfrom the person’s behavioral repertoire.In addition to promoting an intervention strategy, psychological assessmentoffers the opportunity to monitor quantitatively changes occurring duringthe course of treatment. The use of brief standardized self-report checklists orrating scales, for example, facilitates objective and quantitative documentationof therapeutic progress. One multivariate instrument designed for this purposeis the revised Drug Use Screening Inventory (Tarter, 1990). The obtainedinformation not only provides ongoing feedback to the clinician but also servesthe purpose of goal setting for the client. Furthermore, demonstrating to the clientvia objective and quantitative indices that he or she is benefiting fromtreatment serves the important purpose of sustaining motivation for continuedinvestment in the rehabilitation. The following discussion reviews the mostcommonly used instruments for drug and alcohol assessment.Alcohol and Drug UseConsumption of alcohol and other drugs is closely linked to developmental processes.Not surprisingly, therefore, it unfolds in a more or less regular order.Typically, consumption begins with licit compounds (alcohol, tobacco) andprogresses, if at all, to the use of illicit drugs. Although much has been writtenabout the gateway hypothesis, in which drug use staging is presumably influencedby prior history of drug use (Kandel, 1975), the evidence to support thisspeculation is at best equivocal (Morral, McCaffrey, & Paddock, 2002). Rather,the progression across stages of substance use is most parsimoniously explained

46 II. ASSESSMENT OF ADDICTIONby severity of the predisposing liability (Vanyukov et al., 2003). In effect, thefactors contributing to the risk for one type of drug abuse largely apply to allother abusable drugs.The onset of use of each type of substance needs to be documented todescribe fully the natural history of consumption. As each type of substanceemerges in the person’s history, it is essential to ascertain whether it hasreached problematic severity to warrant a diagnosis of abuse or dependence. Inaddition, the occurrence of remission and number of lifetime episodes should bedescribed. Moreover, polydrug use should be investigated because of the substantiallethal risk posed by the combined use of psychoactive drugs. For example,conjointly using alcohol and benzodiazepines is especially dangerousbecause of the risk of respiratory arrest.To date, no single assessment measure evaluates all aspects of consumptionbehavior and its psychological manifestations. Certain instruments measurequantity and frequency, others measure severity, and yet others measure patternsof current and lifetime abuse. Several rating scales quantifying severity ofalcohol problems in adults are, however, routinely used. The Michigan AlcoholismScreening Test (MAST; Selzer, 1971) is best known for this purpose.The MAST is easy to administer, because it consists of only 25 true–false statements.Paralleling the MAST, the Drug Abuse Screening Test (DAST; Skinner,1982) is a self-report measure that is brief (20 items) and easy to score.Alcohol problems can also be evaluated within a multivariate perspectiveemploying the Alcohol Use Inventory (AUI; Wanberg & Horn, 1985). Thisinstrument captures primarily the motivational aspects of alcohol use. TheAUI, consisting of 228 items in a self-report format, can be administered toindividuals or groups. A limiting characteristic of the AUI is that the questionsare not phrased to inform about a specific time frame.A frequently used instrument to assess problem severity is the AddictionSeverity Index (McLellan, Luborsky, Woody, & O’Brien, 1980). This interviewwas designed to assist treatment planning. A homologous version has also beendeveloped for adolescents. Referred to as the Teem Addiction Severity Index(T-ASI; Kaminer, Bukstein, & Tarter 1991), this semistructured interviewinforms about problem severity in multiple spheres of health and psychosocialfunctioning.A subscale of the Minnesota Multiphasic Personality Inventory (MMPI)—the MacAndrew Alcoholism Scale (MAC)—consists of 49 items that differentiatepersons with psychiatric disorders from those with substance use disorders.Another important feature of the MAC is that it assists in the assessment ofparticular characteristics associated with addiction, such as impulsivity, poorjudgment, and sensation-seeking behavior. Also, when analyzed within thecontext of the MMPI validity scales, the MAC can identify persons who mightbe minimizing their substance abuse by endorsing socially desirable responses. It

3. Psychological Evaluation 47is important to note that individuals with substance abuse disorders who arecourt-ordered to receive a drug and alcohol evaluation are often motivated tohide or minimize their substance abuse (Shaffer, 1992).Psychometric tests designed specifically for adolescent drug users have alsobeen validated. The Personal Experience Inventory (PEI; Henly & Winters,1988) and the Chemical Dependency Assessment Survey (Oetting, Beauvais,Edwards, & Waters, 1984) are two examples. The PEI, suitable for a clinicalpopulation, assesses multiple psychosocial domains that may be adverselyaffected by substance abuse.The Drug Use Screening Inventory (DUSI; Tarter, 1990) is the mostrecently developed self-report that is in widespread use. This inventory hashomologous forms for adolescents and adults. It profiles frequency of substanceuse behavior in conjunction with severity of disturbance in 10 spheres of functioningthat are integral to both the etiology and sequelae of substance abuse.Each scale quantifies problem severity from 0 to 100%. The measurementdomains are (1) substance use consequences, (2) psychiatric disorder, (3)health status, (4) behavior disorder, (5) school performance, (6) work adjustment,(7) social competence, (8) peer relationships, (9) family adjustment, and(10) leisure and recreation. The revised DUSI-R also contains a Lie scale as avalidity check. The reliability and validity of the DUSI-R, as well as cutoffscores for diagnosis, are documented (Kirisci, Hsu, & Tarter, 1994; Tarter &Kirisci, 1997). Importantly, the overall problem density score in early adolescenceis predictive of substance use disorder by young adulthood (Tarter &Kirisci, 2001).It is readily apparent that psychological inventories that measure the multifacetedtopology of alcohol and drug use have not been developed. The previouslydescribed procedures only clarify current use patterns and problem severity.Other information that can most easily be gathered in the course of aninterview is also important to obtain. Questioning should therefore be directedat determining the following: (1) patterns of substance use (e.g., episodic vs.continuous), (2) context of substance use (solitary vs. social consumption), (3)availability of drugs and opportunity to access drugs in the social environment,(4) perceived importance of drugs, (5) expected and experienced effects ofdrugs on mood and behavior, and (6) family history of drug and alcohol abuse.Health StatusThere is no standardized instrument to assess health status in individuals withsubstance use disorders. This lack of instrumentation in a critical area of healthcare is the result of current health policy, which has shifted emphasis fromhealth status to health care delivery and quality of life. Some general healthsurveys that are not specific to substance abuse but can be applied to this popu-

48 II. ASSESSMENT OF ADDICTIONlation are the Nottingham Health Profile (Hunt, McEwen, & McKenna,1985), the Duke–University of North Carolina Health Profile (Parkerson et al.,1981), and the General Health Survey (Stewart, Hays, & Ware, 1988).Psychiatric DisturbanceSubstance abuse can occur conjointly with virtually any Axis I or Axis II psychiatricdisorder. This has important treatment implications, the most obviousof which is that for some individuals, alcohol or drug consumption may constitutean attempt at self-medication. Hence, treatment of the primary disordermay in some circumstances be sufficient to ameliorate the substance use disorder.Alternatively, prolonged drug abuse may precipitate a psychiatric disturbance,either directly by inducing neurochemical changes or indirectly throughstress or maladjustment concomitant to a substance abusing lifestyle. A majortask is therefore to delineate the type and severity of psychiatric morbidity thatmay be present and to determine whether it preceded or developed after thesubstance use disorder.Structured diagnostic interviews have been increasingly utilized in theobjective formulation of substance use disorder diagnoses, as well as other psychiatricdiagnoses. Several instruments, all with good psychometric properties,are currently available. The Structured Clinical Interview for DSM-III-R(SCID; Spitzer, Williams, & Gibbon, 1987) is presently the most frequentlyused instrument. Other structured interviews are the Diagnostic InterviewSchedule (DIS; Robins, Helzer, Croughan, & Ratcliff, 1981) and the Schedulefor Affective Disorders and Schizophrenia (SADS; Spitzer, Endicott, & Robins,1975). There are some important differences among the SCID, DIS, andSADS. In contrast to the SCID and SADS, which are semistructured interviewsrequiring a high level of clinical skill to administer and interpret, the DISis fully structured, so that it can be administered by paraprofessionals.Three diagnostic interviews are available for adolescents. These includethe Diagnostic Interview Schedule—Revised for Children (Costello, Edelbrock,& Costello, 1984), the Kiddie Schedule for Affective Disorders and Schizophrenia(Orvaschel, Puig-Antich, Chambers, Tabrizi, & Johnson, 1982), andthe Diagnostic Interview for Children and Adolescents (Wellner, Reich,Herianic, Jung, & Amado, 1987). Each of these interviews also has a versionthat can be administered to a parent, so as to ensure accuracy of the evaluation.By employing a structured psychiatric interview, it is possible to relate substanceuse involvement with psychiatric status. Myriad configurations of comorbidityare possible. The pattern of comorbidity has important ramificationsfor treatment. For example, if an affective disorder preceded the substance usedisorder and is still present at the time of the assessment, it would suggest theneed to treat this disorder as the primary condition.

3. Psychological Evaluation 49Self-report questionnaires can also yield important information by quantifyingthe presence and severity of psychiatric disorder that is not severe enough towarrant a diagnosis but may nonetheless be a contributor to, or a consequence of,substance abuse. Thus, self-rating scales may provide a more valid picture of theseverity of psychopathology than that afforded by only an interview. For example,the MMPI (Hathaway & McKinley, 1951) contains three validity scales thatmeasure the person’s test-taking attitude; hence, truthfulness and a response biastoward either over- or underreporting symptoms are documented. A disadvantageis that the MMPI profile does not yield a diagnosis. However, the configuration ofscores in the 10 basic scales, in conjunction with the many specialized scales,makes it possible to identify personality disorders, family problems, health disturbances,and social maladjustment comprehensively.Other self-report rating scales can be employed when either time or expertiseis not available to conduct a structured interview or obtain an MMPI profile.The most commonly used test in this regard is the Symptom Checklist90—Revised (Derogatis, 1983). This self-rating scale is brief and easy to score.Severity of psychopathology is quantified across nine dimensions of psychopathology.The importance of evaluating psychopathology in the substance use disorderscannot be overemphasized. Treatment of the underlying psychiatric disordermay itself, in many cases, be sufficient to ameliorate a substance use disorder.For this reason, it is essential to document the type, onset, and presentationof psychopathology as it relates to alcohol or drug use behavior. In addition,documentation of psychiatric illness in other family members, using instrumentssuch as the Family History Chart (Mann, Sobell, Sobell, & Pavan, 1985)and the Family Informant Schedule and Criteria (Manuzza, Fryer, Endicott, &Klein, 1985), can assist in obtaining a clear picture of the primary psychiatricdisorder.PersonalityCertain personality characteristics are commonly associated with the etiologyand maintenance of alcohol and drug abuse. The extent to which the particularfeature presages the onset of substance use or is shaped by the long-term consequenceof consumption needs to be ascertained on a case-by-case basis. Traitssuch as low self-esteem, impulsivity, aggressiveness, and behavioral undercontrolare highly prevalent in the drug-abusing population.No single instrument currently assesses all dimensions of personality thatmay be relevant to understanding drug use behavior. The MMPI, described previously,is very useful for profiling psychopathology and facilitating the formulationand testing of hypotheses about specific personality characteristics. However,other inventories are also informative for elucidating the role of particulartraits on the risk for and maintenance of drug abuse. Notably, the Multidimen-

50 II. ASSESSMENT OF ADDICTIONsional Personality Questionnaire (MPQ) quantifies traits that have frequentlybeen found to be characteristic of alcoholics and drug abusers. Significantly, thetraits comprising the MPQ scales have a strong heritable basis (Tellegen, 1982,1985; Tellegen et al., 1988). Numerous other personality questionnaires havebeen developed; however, none measures traits that are so integrally linked tosubstance abuse as the MPQ.Self-esteem disturbances are also present in substance-using individuals.Low self-esteem can occur in a number of areas of daily living and may be secondaryto psychopathology. The Self-Esteem Inventory (Epstein, 1976) is amultidimensional scale with good breadth of coverage and superior psychometricproperties. It taps aspects of psychological well-being that are not ordinarilycovered by personality tests.CognitionA neuropsychological evaluation is important for a variety of reasons. It providesinformation regarding the person’s amenability to treatment. For example,individuals who have a mental deficiency, have suffered neurologicalinjury, or have dementia as the result of alcoholism or habitual drug use areunlikely to profit from insight-oriented treatment. In addition, in the earlystages of substance withdrawal, cognitive assessment can determine whethermental confusion is present, in which case the benefit of participation in individualor group therapy is likely to be minimal. Importantly, emotional andbehavioral changes associated with neurological impairment may impede rehabilitation.Hence, clarifying cognitive impairment due to CNS injury and dysfunctionhas important ramifications for treatment planning and aftercare,including long-term rehabilitation.Tarter and Edwards (1987) proposed a three-stage assessment procedurefor documenting neuropsychological functioning. At the outset, neuropsychologicalscreening provides the opportunity to determine whether there is evidenceof a CNS disturbance. If a neurocognitive impairment is not observed,the evaluation is terminated, thereby saving substantial time and cost. The secondstage of evaluation involves delineation of cognitive abilities and limitations.In standardized batteries, complemented when necessary by specializedtests, cognitive capacity is quantified across multiple domains. Typically, thisincludes speech and language, attention, psychomotor efficiency, learning andmemory, and abstract reasoning. The results at this stage can inform aboutlesion localization and lateralization. Several standardized neuropsychologicalbatteries are currently in wide use. The Halstead–Reitan Battery (Reitan,1955), Luria–Nebraska Neuropsychological Test Battery (Golden, 1981), andthe Pittsburgh Initial Neuropsychological Test System (Goldstein, Tarter,Shelly, & Hegedus, 1983) are examples of multidomain assessment batteries.Based on the profile of results describing cognitive strengths and weaknesses, a

3. Psychological Evaluation 51decision is made regarding the need for focused comprehensive testing. This isthe third and last stage of assessment. In-depth information is obtained regardinga particular cognitive domain. The results inform about “real-life” prospectsof success. Moreover, the results inform about potential risks to the person. Forexample, it is important to describe psychomotor impairments fully if the clientworks with power machinery. Visuoperceptual disturbances must be comprehensivelydocumented if the person drives a car. Similarly, if the clinician identifiesa learning or memory deficit, it has direct ramifications for educationaland vocational rehabilitation. The reader is referred to Nixon (1999) for a discussionof instrument selection for neuropsychological evaluation.In interpreting the results of a neuropsychological evaluation, it is importantto be cognizant of the multifactorial etiology of any identified impairment.Not only do alcohol and other drugs act directly on the brain but their habitualconsumption may also induce organ–system injury, which in turn disruptsintegrity of the brain. For example, cirrhosis, independent of alcoholism, causeshepatic encephalopathy, Thus, neuropsychological deficits commonly found inalcoholics may be, in large part, the result of advanced liver disease (Tarter,Van Thiel, & Moss, 1988). This fact is not inconsequential, because treatmentof low-grade hepatic encephalopathy caused by alcoholic liver disease hasbeen tentatively shown to improve cognitive capacities (McClain, Potter,Krombout, & Zieve, 1984). Thus, medically significant problems that potentiallydisrupt brain functioning should be recorded and incorporated into thetreatment plan.Family AdjustmentFamily organization and quality of interaction among its members impact onthe risk for and maintenance of substance abuse. Indeed, the transmission ofalcoholism across generations is to some degree influenced by attitudes and ritualsof the family pertaining to consumption (Steinglass, Bennett, Wolin, &Reiss, 1987). Inasmuch as the family is the primary influence shaping the valuesand behavioral patterns of children, parenting style and family environmentexercise a profound influence on the child’s development until at least adolescence,when psychoactive substance use may first become problematic.From the standpoint of psychological evaluation, a number of issues mustbe addressed. First, it is essential to characterize the contribution of psychiatricdisorder, including substance abuse, in the family. The greater the family densityof substance use disorder and pervasiveness of psychiatric disorder in familymembers of the client undergoing evaluation, the more severe the psychologicalproblems. Among young substance-abusing clients, it is especially importantto record the presence and history of physical and sexual abuse as an etiologicalfactor on any manifest psychological disturbances. Second, the causal relationshipbetween family dysfunction and drug use behavior needs to be ascertained.

52 II. ASSESSMENT OF ADDICTIONHow substance abuse precipitated the family problems or, conversely, how familyproblems triggered substance abuse needs to be investigated in the course ofthe evaluation. Third, the reinforcement contingencies, if any, exercised by thefamily on the member with the substance abuse problem need to be analyzed. Itthus needs to be determined whether substance abuse is ignored, punished, orpositively reinforced. Fourth, the roles and status of each family member mustbe understood to the extent that individual maladjustment, conflict, and instabilitycontribute to overall family dysfunction that in turn propels one memberto consume alcohol or other psychoactive drugs.Five self-report instruments are commonly used to quantify family functioning.The Family Environment Scale (FES; Moos, 1974; Moos & Moos,1981) was the first instrument developed to evaluate family system functioning.The FES evaluates three major dimensions: (1) Relationships, (2) PersonalGrowth, and (3) Systems Maintenance. Each major dimension consists of severalscales. The Relationship dimension encompasses scales that measure familyconflict, cohesion, and expressiveness. The Personal Growth dimension includesscales that evaluate the family’s emphasis on independence and achievement,as well as intellectual, religious, and recreational pursuits. The SystemsMaintenance dimension contains scales that measure the family’s success atorganization and control. The Self-Report Family Inventory (SFI) is based onthe theoretical orientation of the Beavers Systems Model of Family Functioning(Beavers & Hampson, 1990). It measures health/competence, level andtype of conflict, communication patterns, cohesiveness, leadership, and emotionalexpression.Epstein, Baldwin, and Bishop (1983) developed the Family AssessmentDevice (FAD) to evaluate current level of family functioning. The FAD can beadministered to children as young as 12 years of age. In addition to providing ageneral functioning score, the FAD provides useful information pertaining toaffective involvement, behavior control, family roles, problem solving, communicationpatterns, and affective responsiveness.The Family Assessment Measure (FAM) focuses on the individual perceptionsof each family member (Skinner, Steinhauer, & Santa Barbara, 1983;Steinhauer, Santa Barbara, & Skinner, 1984). The family system characteristicsassessed by the FAM include affective involvement, control, role performance,task accomplishment, communication patterns, affective expression, and valuesand norms.The Family Adaptability and Cohesion Evaluation Scales (FACES),developed by Olson, Russell, and Sprenkle (1980, 1983) and Olson and colleagues(1989) for both research and clinical applications, is another frequentlyused measure of family functioning. It takes only 10–15 minutes to administerand is appropriate for children (ages 10–12). It assesses three dimensions offamily functioning: cohesion (degree of emotional bonding), adaptability (familypower/roles/rules), and communication (dyadic patterns/styles).

3. Psychological Evaluation 53Social AdjustmentSocial adjustment is defined as the individual’s success at fulfilling age-appropriateroles according to expectations (Barrabee, Barrabee, & Finesinger, 1955). Themeasurement domains encompass social support, social roles, social skills, peeraffiliations, school and vocational adjustment, and recreation and leisure activities.Social Functioning/Social SupportAs previously discussed, the Addiction Severity Index (McLellan et al., 1980)profiles the individual’s problems, including social support, along with psychological,legal, family, and vocational status. The Substance Abuse ProblemChecklist (SAPC; Carroll, 1983) assesses social functioning in relation to treatmentplanning. An especially useful feature of the SAPC is its capacity todetermine the client’s readiness to initiate substance abuse treatment. TheSAPC evaluates health status, personality, social relationships, vocational status,use of leisure time, religious orientation, and legal status. The Social RelationshipScale (SRS; McFarlane, Neale, Norman, Roy, & Steiner, 1981) is oneof only a few instruments developed with the specific intention to measuresocial support. It assesses three facets of social support: (1) total number of individualswho make up the social support network, (2) type of relationships, and(3) quality of relationships. These facets of social adjustment are integral toprognosis following treatment for substance use disorders (see McLellan, 1986;Woody et al., 1983).Peer AffiliationsA social network in which drug use is commonplace increases the likelihoodthat the individual will adopt this behavior. Ameliorating a substance abuseproblem may thus require abandoning long-standing peer affiliations. Whetherthe quality of peer relationships is embedded in an antisocial behavior dispositionneeds to be evaluated. Antisociality impedes work, school, and familyadjustment. One self-report measure, the revised Drug Use Screening Inventory(Tarter, 1990), described earlier, quantifies deviancy in both the individual andfriendships.Because the social environment is a major source of reinforcement, it isessential to identify the reward contingencies, role models, and contextual factorsassociated with alcohol or drug use. It should be recognized that the individualnot only responds to the particular social environment but also seeks out an environmentthat has reinforcing value. Hence, during the course of the psychologicalassessment, an attempt should be made to learn why the substance abusing clientseeks out social interactions that have maladaptive consequences.

54 II. ASSESSMENT OF ADDICTIONSocial SkillsSocial skills deficits are common among substance abusers (Van Hasselt,Hersen, & Milliones, 1978). Deficiencies in assertiveness skills, refusal skills,and compliment-giving skills have all been documented. Poor ability to manageconflict in interpersonal situations may also be linked to a propensity for substanceabuse. Moreover, the exacerbation of poor social skills by stress or anxietypotentiates the risk for substance use as a coping strategy. Consequently,describing the person’s coping style also needs to be an integral component ofthe social skills assessment.There are currently no standardized instruments for evaluating social skills.Various self-rating scales, although lacking in normative scores, have beenemployed for identifying the presence and severity of deficits and for targetingbehaviorally focused interventions. The same limitations exist with respect tocoping style; however, two measures that have been found to be informative arethe Ways of Coping Scale (Folkman & Lazarus, 1980) and the ConstructiveThinking Inventory (Epstein, 1987).In conjunction with a social skills evaluation, it is important to documentthe individual’s capacity to exercise the competencies required for everyday living.As society becomes more technologically complex, it is valuable to learnwhether the individual is capable of performing the everyday tasks that arerequired for successful adjustment. For example, it is important to determinewhether the individual can manage a bank account, use bankcard machines,access the Internet, obtain services information, utilize public transportation,and attend to personal needs with respect to food and clothing. Deficiencies inany of these areas exacerbate stress that in turn promotes the risk for substanceuse.School AdjustmentThe school is the primary social environment during adolescence. It is importantto document school adjustment and academic performance of adolescentsubstance abusers. Drug accessibility and the adolescent’s peer affiliation networkare especially influential determinants of drug use initiation. Conductproblems and social deviance are also commonly associated with both poorschool adjustment and substance abuse. The teacher version of the ChildBehavior Checklist (CBCL; Achenbach & Edelbrock, 1983) affords the opportunityto identify and quantify severity of behavioral problems in the schoolenvironment. Also, comparing the findings to the parallel parent versionenables the clinician to ascertain whether adjustment problems are confined tothe school or are also present in the home.Assessing the teacher’s perceptions of a child’s behavior in the classroom isa highly desired component of a comprehensive evaluation. The Disruptive

3. Psychological Evaluation 55Behavior Rating Scale (Pelham & Murphy, 1987), based on DSM-III-R criteria(American Psychiatric Association, 1987), quantifies severity of conduct, andattention-deficit/hyperactivity and oppositional defiant disturbance. Anotherbrief symptom rating scale that can be completed by the teacher is the IowaConners Teachers Rating Scale (Loney & Milich, 1982).One important aspect of school adjustment pertains to the extent to whichthe child participates in athletics and other extracurricular activities. Theseactivities indicate how well the person is socially integrated and accepted bypeers. In addition, it is essential to evaluate academic achievement and learningaptitude in the basic skill areas. For example, learning disability compoundedby low self-esteem may be a major factor propelling a youngster towarddrug use, as well as other non-normative behaviors. Standardized learning andachievement tests can readily document whether a learning deficit is present.Vocational AdjustmentStress in the workplace fosters substance use as a coping strategy. Inability tomeet work performance standards, conflicts with other employees or supervisors,an inconsistent work schedule, and low job satisfaction exemplify thecommon proximal causes of substance use. The impact of unemployment andunderemployment as a source of stress also needs to be evaluated. In addition,extensive travel and associated social obligations may frequently place the individualin situations where alcohol consumption is expected. Over the longterm, social drinking may lead to problems controlling intake.Besides evaluating the job demands and workplace environment, it isessential to evaluate the client’s behavioral disposition. For example, premorbidpersonality disorders contribute to job failure, which in turn predisposes theindividual to substance abuse. Furthermore, it is important to evaluate substanceabuse in the context of specific circumstances of the job. Access toaddictive substances places the person at heightened risk simply by virtue offacile availability. Not surprisingly, bartenders have a high rate of alcoholabuse. The vocational evaluation must therefore identify the specific jobrelatedcharacteristics that predispose the individual to substance abuse.Recreation/Leisure ActivitiesSubstance use is commonly circumscribed to recreational activities. Furthermore,an individual who does not have socially satisfying leisure activities mayuse alcohol or drugs to cope with the stress of boredom. This may be particularlyproblematic among members of the elderly population who have notdeveloped a rewarding goal directed lifestyle following retirement. A somewhatsimilar problem may confront adolescents who have substantial unstructuredtime. Presently, there are no standardized procedures to evaluate recreation and

56 II. ASSESSMENT OF ADDICTIONleisure activities. As noted above, however, the DUSI-R (Tarter, 1990) screensfor severity of problems related to leisure and recreation.LINKING ASSESSMENT AND TREATMENT:THE DECISION-TREE PROCEDUREA three-stage evaluation procedure provides a systematic framework for connectingassessment and treatment. The first stage involves brief screening usingthe DUSI-R (Tarter, 1990). At this stage, the areas of disturbance that point tothe need for comprehensive evaluation are identified. In the second stage, adiagnostic evaluation is performed in the identified problem areas. This informationin turn is applied to a focused, in-depth evaluation to formulate a multidisciplinarytreatment plan.Using a decision-tree multistage evaluation procedure has several advantages:• The areas of disturbance can be quickly identified at minimal cost.• Labor-intensive, comprehensive diagnostic evaluation is guided by theresults obtained in initial screening.• The client’s rehabilitation needs are clearly delineated, based on aggregatefindings from the initial screening and the comprehensive diagnosticevaluation.• Once the required treatment interventions are specified, a coordinatedintervention program can be developed. In this fashion, evaluation andtreatment are integrally linked in an ongoing reciprocal and interactivemanner.Matching assessment results with treatment is rapidly becoming standardclinical practice. For example, Annis and Graham (1995) link treatment planning,including relapse prevention counseling, to particular client profiles onthe Inventory of Drinking Situations (IDS; Annis, 1982). The IDS categorizesheavy alcohol abusers into four types: (1) the negative profile—individualswhose alcohol abuse is a consequence of negative emotions (e.g., boredom,anxiety, and depression); (2) the positive profile—individuals who drinkheavily due to social pressure, wanting to have a good time, or wanting to relax;(3) low-testing personal control—individuals whose abuse of alcohol is undifferentiated,possibly due to lack of motivation to change and lack of awarenessof the antecedents of abuse; and (4) low physical discomfort—individuals whoalso presents with an undifferentiated profile characterized by limited use ofalcohol. Substance abuse treatment is thus individualized according to the fourIDS client profiles. For example, in the case of the negative and positiveprofilers, the focus of intervention is on teaching alternate ways of coping with

3. Psychological Evaluation 57social pressures and interpersonal conflicts, teaching alternate forms of relaxation,providing assertiveness training, and resolving interpersonal stress. Thepoint to be made is that psychological assessment is not an intellectual exercise.Rather, the information should be applied to improving treatment outcome.Toward that goal, psychological evaluation is pertinent to determining the client’sreadiness for treatment, designing the most appropriate treatment, monitoringchange during the course of treatment, documentation of individual outcome,and determining effectiveness of the treatment program.REFERENCESAchenbach, T., & Edelbrock, C. (1983). Manual for the Child Behavior Checklist andRevised Child Behavior Profile. Burlington: University of Vermont, Department ofPsychiatry.American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders(3rd ed., rev.). Washington, DC: Author.Annis, H. M. (1982). Inventory of Drinking Situations (IDS-100). Toronto: AddictionResearch Foundation of Ontario.Annis, H. M., & Graham, J. M. (1995). Profile types on the Inventory of Drinking Situations:Implications for relapse prevention counseling. Psychol Addict Behav, 9,176–182.Barrabee, R., Barrabee, E. L., & Finesinger, J. E. (1955). A normative social adjustmentscale. Am J Psychiatry, 112, 252–259.Beavers, W. R., & Hampson, R. B. (1990). Successful families: Assessment and intervention.New York: Norton.Buchsbaum, M., & Ludwig, A. (1980). Effects of sensory input and alcohol administrationon visual evoked potentials in normal subjects and alcoholics. In H. Begleiter(Ed.), Biological effects of alcohol. New York: Plenum Press.Carroll, J. F. (1983). Substance Abuse Problem Checklist manual. Eagleville, PA: EaglevilleHospital.Costello, J., Edelbrock, C., & Costello, A. (1984). The reliability of the NIMH DiagnosticInterview Schedule for Children: A comparison between pediatric and psychiatric referrals.Pittsburgh, PA: Western Psychiatric Institute and Clinic.Dackis, C. A., Gold, M. S., Pottash, A. L. C., & Sweeney, D. R. (1985). Evaluatingdepression in alcoholics. Psychiatry Res, 17, 105–109.Daley, D., Moss, H. B., & Campbell, F. (1987). Dual disorders: Counseling clients withchemical dependency and mental illness. Center City, MN: Hazelden.Derogatis, L. R. (1983). SCL-90-R: Administration, scoring and procedures manual II(rev.). Towson, MD: Clinical Psychometric Research.Dodes, L. M. (1990). Addiction, helplessness, and narcissistic rage. Psychoanal Q, 59,398–419.Epstein, N. B., Baldwin, L., & Bishop, D. (1983). The McMaster Family AssessmentDevice. J Marital Fam Ther, 9, 213–228.Epstein, S. (1976). Anxiety, arousal and the self-concept. In I. G. Sarason & C. D.Spielberger (Eds.), Stress and anxiety. Washington, DC: Hemisphere.

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CHAPTER 4Laboratory Testingfor Substances of AbuseDAVID A. BAROND. ANDREW BARONSTEVEN H. BARONFor the professional working in clinical settings and in consultative roles(including sports, criminal/forensic, and occupational settings), there willalways be a need for corroborative sources of information. Testing of human tissuesusually provides invaluable, albeit not definitive, information in workingwith substance-using individuals. This information may assist in diagnostic orin therapeutic decisions, which are especially important in this population,because drugs are illegal and drug-abusing individuals often present in denial oftheir problem. Furthermore, this is particularly relevant when comorbid psychiatricsymptoms are present. Drug testing can also aid in determining whetherpresenting symptoms are primarily psychiatric or substance-induced. Drug testingmay be utilized as part of an initial treatment contract between the patientand treating clinician. Coercion often helps to improve treatment outcomes.This is especially so in methadone maintenance programs, where testing is typicallymandatory. There is evidence to suggest that testing deters use. For example,prior to testing in 1981, 48% of military personnel used drugs, but this ratedeclined to 5% after 3 years of testing, and this appears to have occurred amongathletes as well.A number of questions must be contemplated before settling on a finaldecision:63

64 II. ASSESSMENT OF ADDICTION1. For what drugs ought we to test?2. What biological sample should be tested: urine, blood, sweat, saliva,hair, and so forth?3. How fast do we want to see the results?4. How much of our resources should be spent on testing?This chapter reviews testing methodologies and the fundamental aspects ofplanning effective testing procedures in both clinical and consultative settings.TESTING METHODOLOGIESA multitude of methods are available to aid in the detection of drug use inhumans. The most common drug testing technologies are listed in Table 4.1.The most popular initial test screen is an enzyme immunoassay (EIA) analysisof a urine sample. If this is positive, a confirmatory gas chromatography–massspectroscopy (GC-MS) test is performed on the split sample. Given the greatersensitivity of GC-MS over EIA, the cutoff levels are reduced. The most commonlyused analytic technique for a “comprehensive drug screen,” thin-layerchromatography (TLC), is the least expensive test available. TLC utilizes thedifferences in polarity and chemical interaction with developing solvents toproduce different visualizations on a thin-layer coating. The visualizations arehighlighted using ultraviolet (UV) or fluorescent lighting, or by color reactionscreated after being sprayed with chemical dyes. Identical molecules cluster inthe same area, yielding specific color reactions. Unfortunately, TLC is somewhatinsensitive to detection of controlled substances.Of all the available tests, how does a clinician decide on which test toadminister? If there is no clinical indication to test for a specific compound,a “comprehensive drug screen” may be performed. There are settings andinstances when it is important to contact the laboratory to ensure that there is ameans to test for the substance, or to prompt the laboratory to test for the sub-TABLE 4.1. Most Common Drug Testing Technologies• Thin-layer chromatography• Radio immunoassay, enzyme immunoassay, fluorescentpolarization immunoassay, enzyme-linked immunosorbent assay• Gas chromatography• Gas chromatography–mass spetroscopy• Liquid chromatography

4. Laboratory Testing 65stance. It is common for general hospital laboratories to screen only for a limitednumber of substances. For example, many do not screen for gammahydroxybutyricacid (GHB) (although methods for testing for GHB continue toundergo refinement; Chappell, Meyn, & Ngim, 2004). A drug screen doneusing TLC will only detect high levels of the following compounds: amphetamine,barbiturates, cocaine, codeine, dextromethorphan, diphenylhydantoin,morphine, phenylpropanolamine, methadone, propoxyphene, or quinine(a heroin diluent). TLC does not detect the following compounds: 3, 4-methlyenedioxyamphetamine (MDA), 3, 4-methylenedioxymethamphetamine(MDMA), fentanyl, D-lysergic acid diethylamide (LSD), marijuana, mescaline,and phencyclidine (PCP).Although urine analysis is the most widely used and best overall body fluidto screen for drug use, other body fluids can be measured as well. Hair testing isgrowing in popularity but is not as sensitive to marijuana use as urine. Despitecommercial success, the scientific foundation for using hair analysis is limited.Its primary utility might be as a tool in the diagnosis and treatment of drugabuse disorders, particularly cocaine dependence. Salivary measurements offerthe advantage of ease of collection but only detect recent drug use, limitingtheir utility. A number of drugs, including cocaine, morphine, amphetamine,and ethanol, have been detected in sweat. Unfortunately, there is a wideintersubject variability of drug concentration in sweat. This results in a significantdisadvantage when sweat is compared with other body fluids. To add tothe problem, sweat collection takes several days to several weeks and requiresthe use of a sweat patch (Cone, 1996).For some substances, other tests can be helpful in determining qualitativeor quantitative aspects of use. For example, likely alcohol use may be detectedby liver enzymes or by the new test for carbohydrate-deficient transferrin(CDT), and some investigators are studying whether certain combinations ofthese tests have varying specificities or sensitivities (see Chapter 5 on alcohol,this volume). And, certain blood or urine tests are vital in determining thepresence of dangerous effects of substances, such as muscle breakdown leadingto rhabdomyolysis and a high creatine kinase among users of cocaine and PCP.For the consultant who works in the “field,” requiring on-the-spot testing,a number of kits can be used. Most of these are the “on-site” screeningimmunoassays. “On-site” testing has a variety of features that make it bettersuited for companies than its counterpart, TLC. “On-site” testing can produceresults in as little as 10 minutes, with significant accuracy. Thus, “on-site”screening is the preferred method outside of the hospital. Despite the popularityof “on-site” kits and the fact that these kits have demonstrated a greater than97% agreement with GC/MS tests, it must be stressed that these kits provideonly preliminary results. For best results, it is recommended that a more thoroughanalysis on the sample be performed.

66 II. ASSESSMENT OF ADDICTIONINTERPRETATIONIn an ideal world, testing biological samples should lead to definitive answers.However, test results sometimes lead to more questions than answers. Adeptinterpretation of results will lead to improved clinical care or to more surety inconsultative cases. Interpretation depends on awareness of which test was usedand its meaning to the situation.In most settings, the primary purpose of drug testing is to identify individualswho are using illegal or illicit drugs. Falsely accusing someone of using drugsis highly problematic and undermines the testing program. Similarly, not beingable to identify active drug users because of false-negative results renders a programof limited value. It does not deter use or identify users. This is so both forthe emergency room physician wondering if the agitated patient used PCP, andfor the consultant to the local college track team. For these situations, highlysensitive qualitative screening tests should be employed, even if this leads tosome false-positive results. On the other hand, definitive tests should have thehighest level of specificity: They should exclude as many true negatives as possible.For nonusers who are subjected to drug testing, issues related to falsepositiveresults are of great concern. Questions addressing which foods, prescribedmedications, dietary supplements, or potentially secondhand marijuanasmoke could result in a positive test are common, and some laboratories haveresponded by raising the level required in order to render a positive test result.With the proliferation of private laboratories and commercially manufacturedkits, there has grown to be some interlaboratory variation in standardsand thresholds for results. The industry even has its own trade organization, theDrug and Alcohol Testing Industry Association (DATIA). The major concernin drug testing occurs with the reporting of laboratory results. Unlike NationalInstitute on Drug Abuse (NIDA)–certified testing of the Standard Drug Panel(see Table 4.2), clinical drug testing for drugs of abuse currently has no standardtechnical criteria, no standard screening cutoffs for positive tests, no confirmationcutoffs, no chain-of-custody requirements, no blind proficiency submissionrequirements, and no certification programs. As a result, a sample testing posi-TABLE 4.2. “NIDA 5” or the DOT StandardDrug Panel 1990DrugCutoffs (ng/ml)Cocaine 300/150Cannabinoids 50/15PCP 25/25Opiates 2,000/2,000Amphetamines 1,000/500

4. Laboratory Testing 67tive in laboratory A may be reported as negative by laboratory B, based on differentcutoff levels. This is not a new development (Hansen, Caudill, & Boone,1985). Unfortunately, little progress has been made in correcting it over thepast 17 years. The issue is not the type of test administered, or poor-quality laboratories,but rather the nonstandardized threshold for reporting a test as positive.Evasion of True Positive ResultsFor obvious reasons, drug users are highly motivated to “produce” a clean sample.In response to this need, a black market has emerged to provide products with thesole purpose of creating a false-negative test result. These products include pretestedand certified drug-free urine substitution kits, and a variety of adulterants.These include the “Whizzinator” (an artificial penis used to deliver a known drugfreeurine under direct observation conditions) and passingpisstest.com, whichprovides a nontechnical description of how blood and urine drug tests work.Those who interpret test results should be aware that addicts can be highlycreative in their efforts to thwart detection and monitoring. As an example,adulterants are substances placed in a sample to alter the results of a drug test.They accomplish this by physically altering the characteristics of the sample, suchas temperature, pH, and specific gravity, which disrupts the mechanisms of theassay. Adulterants range from inexpensive household products, such as soap, salt,bleach, lemon juice, or vinegar, to expensive additives specifically marketed toproduce a negative test. One Internet product selling for over $100 comes with a300% money-back guarantee. As a result of adulterant use, drug testers must nowemploy techniques to screen for these additives. If the sample does not fall withinestablished physiological parameters at the time of collection, it is voided on thespot, and another sample must be produced, which is then sent to the laboratoryfor analysis. One “do-it-yourself” kit, available on the Internet, includes a concealedIV bag with tubing (to be strapped to the lower abdomen or upper thigh)and two heating elements with temperature strips, all in an attempt to mask theuse of adulterants. One study demonstrated the ability of one adulterant to createfalse negative tests (Cody & Valtier, 2001).MECHANICS OF DRUG TESTING PROGRAMSChain of Custody and the Medical Review OfficerA critical component of all drug testing protocols (sports and workplace) ischain of custody, which refers to the policy whereby the collected sample (usuallyurine) never leaves the direct observation of a member of the drug testingteam until it arrives at the laboratory. Once collected, the processed sampleremains under the direct observation of the testing team until it is hand-

68 II. ASSESSMENT OF ADDICTIONdelivered to the shipping company, which also maintains direct observationuntil the sample is hand-delivered to the certified laboratory. The goal is toeliminate any potential tampering with the specimen. The MRO (medicalreview officer) is responsible for reviewing the chain of custody form to ensureno potential tampering. If chain of custody cannot be verified, the test result isconsidered invalid. The overarching goal and philosophy of the Drug-FreeWorkplace (DFW) program is to deter, not merely detect, drug use in the workplace.The role of the MRO physician is to advocate for the employee–athletedonor and ensure the ongoing integrity of the testing program.Testing Programs for AthletesUnlike drug use in the general workplace, drugs have been used for thousandsof years to enhance athletic performance, increase work endurance, recreate,and to self-medicate pain and psychopathology. Doping, the term used todescribe the use of drugs to increase athletic performance, has been documentedback to the ancient Greeks. Throughout history, the use of drugs togain an advantage over one’s competitors has been considered morally wrongand worthy of severe sanctions. Fair competition was, in theory, the keystone ofcompetitive sports. In fact, the Creed of the Olympics states that the mostimportant factors are taking part and giving one’s best effort, not winning.Fighting well and honorably took precedence over conquering the opponent,thus separating sport from war (where all was fair). Cheaters disgraced not onlythemselves and their families but also the sport itself. Dopers in ancient timeswere stripped of their winnings and often ended up as slaves, attempting to payback their debt to the sporting world. These drastic measures, including usingvictory awards from cheaters to build statues to honor the gods ringing theOlympic Stadium, were intended to deter drug use and other forms of cheating(e.g., casting spells on competitors) by producing a constant reminder to everyathlete who entered the arena of the potential perils of attempting to gain anunfair advantage. Unfortunately, the spoils of victory and the cost of defeat,combined with an overwhelming drive to win at any cost, have kept doping amajor issue in sports at every age and level of competition.Despite the long history of drug abuse in sports and in the workplace, laboratorytesting to detect drug use is a modern phenomenon. Only since 1967 hasthe International Olympic Committee Medical Commission banned certaindrugs and tested for their use. Full-scale drug testing for doping by athletesbegan in the 1972 Munich Games. Since 1967, the number of banned substanceshas grown every year, and the sophistication of laboratory analysis andtesting protocols has advanced.Sports doping control is not federally regulated in the United States, as it isin Australia, but typically is closely monitored by the specific sports governingbodies. For example, the National Collegiate Athletic Association (NCAA)closely monitors the testing of collegiate athletes while the U.S. Anti-Doping

4. Laboratory Testing 69Agency (USADA) monitors and conducts all Olympic-related events in theUnited States. In sports testing, as in DFW programs, there are two types oftesting: in-competition and out-of-competition programs. No advanced notice(NAN) out-of-competition testing is the preferred method of USADA and isreported by athletes themselves to be the best deterrent of drug use. As its nameimplies, this form of testing consists of approaching an athlete at any time, withoutprior notice, and obtaining a urine sample. Olympic caliber athletes mustconsent to participate in the program, which includes providing a personal log oftheir whereabouts at all times. Failure to comply leads to sanctions by the individualsport governing body (track and field, swimming, etc.).Testing Programs in Occupational SettingsThere are two types of workplace testing: regulated and nonregulated. Regulatedtesting refers to programs conducted under the Federal Testing Guidelinesand includes industries working with the Department of Transportation(DOT), Federal employees, and companies with Federal contracts over $25,000per year. Nonregulated programs are typically private sector employers who arenot federally required to have a DFW program but voluntarily choose to drugtestemployees. These programs are not required to have an MRO and are notfederally regulated.Drug testing in the workplace has seen dramatic growth since 1988. FormerPresident Ronald Reagan proclaimed the need for a drug-free workplace inAmerica during his years in office. This initiative resulted in the Drug-FreeWorkplace (DFW) Act signed into law in November 1988. This legislation(HR-5210-124 Section 5152) laid the groundwork for the existing regulations(49-CFR-40) for virtually all of the drug-testing policies and protocols currentlyenforced in the workplace today. Interestingly, the DFW legislation was a significantextension of the preexisting “catastrophe-driven” testing, in whichtesting was only done after a catastrophic event, such as a serious work-relatedaccident. This new policy offered a proactive deterrent philosophy.Each DFW program is mandated to include five elements: (1) a formalwritten policy, (2) an Employee Assistance Program, (3) formal training forsupervisors, (4) formal employee education, and (5) a drug-testing protocol.Five participants are involved with every DFW drug test: (1) the employer, (2)the donor/employee, (3) the specimen collection site, (4) the laboratory analyzingthe sample, and (5) the MRO. The employer is responsible for informingthe employee in writing of the Drug-Testing Policy, including all policiesand procedures of the test, circumstances warranting testing in addition topreemployment testing, and consequences of a positive test. Employees mustsign a form acknowledging that they are aware of the program and the existenceof an Employee Assistance Program, and participate in a DFW educational presentation.They must also sign an informed consent document, agreeing to betested under the circumstances described in the policy handbook. The collec-

70 II. ASSESSMENT OF ADDICTIONtion site must also conform to specifications described in the policy handbook.The laboratory used must be certified by the Department of Health and HumanServices (DHHS). There are over 80 certified laboratories throughout theUnited States. An up-to-date list is published regularly in the Federal Register.The laboratory is responsible for verifying appropriate chain of custody of thesample (Universal Chain of Custody forms became effective in January, 1995)and conducting a valid and reliable analysis of the specimen. The laboratorymust report any breach in protocol it discovers, including any suspicion of tamperingwith the sample.The MRO plays a unique and important role in the drug-testing process.Positive tests are reported to the MRO, who then evaluates the facts in the test.For example, if a worker was taking a prescribed stimulant for a medical conditionwith appropriate preauthorized permission, the MRO can reverse a positivetest. The MRO is an “independent agent” in the testing process and is responsiblefor investigating all positive tests before reporting to the employer.The five substances routinely tested for include marijuana, cocaine, amphetamines,opiates, and PCP. Other drugs, such as alcohol, may be added tothe panel if suspected by the employer from objective evidence (i.e., slurredspeech, alcohol on the breath). Keeping with the “Rule of Fives,” there are fivesituations in which drug testing is conducted: (1) preemployment, (2) random,(3) postaccident, (4) probable cause, and (5) return to work/follow-up. Theemployer may request testing for additional substances in the case of postaccident,reasonable suspicion, and return-to-work situations. In order toundergo this additional testing, the employee must be notified via an officialEmployee Drug Policy document. Recognizing the high prevalence of alcoholabuse, ethanol testing was mandated in a 1994 amendment. There are separateregulations for alcohol testing, including not requiring MRO participation.The program is designed always to give the employee the benefit of thedoubt, and the benefit of the MRO’s advocacy. In workplace testing, the safetyof the public, as well as the individual, is at stake. Impaired judgment andhand–eye coordination resulting from intoxication have potentially devastatingconsequences for professional drivers, pilots, and operators of heavy equipment.Virtually every job performance, with the possible exception of rock stars,will be adversely affected by drug use at the workplace. The highest rates of currentand past-year drug use were reported in construction workers, food preparationworkers, waiters, and waitresses. Excessive alcohol consumption wasobserved in these groups, as well as auto mechanics, vehicle repairmen, lighttruck drivers, and laborers (Hoffman, Brittingham, & Larison, 1996). NIDA(1989) has estimated that if every employee/worker between the ages of 18 and40 years old were drug tested randomly on any given day, between 14 and 25%would test positive. The cost to society is staggering, not to mention the impacton the user’s life. Schwab and Syne (1997) estimates workplace drug use costsbetween $60 and 100 billion a year in lost and diminished productivity.

4. Laboratory Testing 71CONCLUSIONDespite the legitimate concern with false-positive and false-negative testresults, the weakest link in the “chain” of drug testing is chain-of-custody violations.Regardless of the sophistication of laboratory technology, human error incompleting the requisite paperwork at the drug-testing site remains the singlemost important inconsistent aspect of the testing process. Given the variety ofavailable methods to cheat, it is likely that drug testing will not catch all drugusers.As is the case in all aspects of clinical medicine, an accurate diagnosis ofsubstance abuse is based on a comprehensive clinical workup; drug testing isonly one, albeit important, component of the process. Workplace drug testinghopefully will not only deter drug use by employees while on the job (eliminatingcostly accidents and errors) but may also assist in initially identifying individualswith drug use disorders. In the world of sports, drug testing is intendedto create a level playing field for all competitors and promote the health of athletesby deterring the use of potentially harmful agents. The role of educatingthe public, particularly those at highest risk for drug use, cannot be overstatedand needs to be the keystone of any drug-free program.REFERENCESChappell, J. S., Meyn, A. W., & Ngim, K. K. (2004). The extraction and infraredindentification of gamma-hydroxybutyric acid (GHB) from aqueous solutions. JForensic Sci, 49(1), 52–59.Cody, J., & Valtier, S. (2001). Effects of stealth adulterant on immunoassay testing fordrugs of abuse. J Anal Toxicol, 25, 466–470.Cone, E. J. (1996). Mechanisms of drug incorporation into hair. Ther Drug Monit, 18,438–443.Hansen, H. J., Caudill, S. P., & Boone, D. J. (1985). Crisis in drug testing: Results ofCDC blind study. JAMA, 253, 2382–2387.Hoffman, J. P., Brittingham, A., & Larison, C. (1996). Drug use among U.S. workers:Prevalence and trends by occupation and industry categories (DHHS Publication No.[SMA] 96–3089). Rockville, MD: SAMHSA Office of Applied Studies.National Institute on Drug Abuse. (1989). Drug abuse curriculum for employee assistanceprogram professionals (DHHS Publication No. ADM 89-1587, pp. i–vi, 98). Washington,DC: U.S. Government Printing Office.Schwab, M., & Syne, S. L. (1997). On paradigms, community participation, and thefuture of public health. Am J Public Health, 87, 2049–2052.

PART IIISUBSTANCES OF ABUSE

CHAPTER 5AlcoholEDGAR P. NACEAlcohol dependence continues to be one of the most costly health care problemsin American society. The estimated social cost of alcoholism includestreatment costs, productivity costs associated with alcohol-related morbidityand mortality, and costs associated with alcohol-related crime and trafficcrashes. The yearly dollar costs for alcoholism is projected to be more than$185 billion (Harwood, 2000). Violence is commonly associated with alcoholuse, with an estimated 26% of offenders using alcohol at the time of their crime(Greenfield & Henneberg, 2001).Epidemiology helps us understand the percentage of United States adultswho experience either alcohol abuse or alcohol dependence. The NationalComorbidity Study (Kessler et al., 1997) found that 2.5% of those interviewedcould be classified as having abused alcohol during the past 12 months (see sectionon diagnosis for definitions of abuse and dependence). The same studydetermined that 7.2% could be diagnosed as alcohol-dependent during the previous12 months. The Epidemiologic Catchment Area study (Regier et al.,1990) determined that 3.5% of Americans met criteria for alcohol abuse atsome point in their lives, and an additional 7.9% met criteria for alcoholdependence at some point in their lifetime.The age at which drinking is initiated has become earlier over the pastdecades. The earlier the age of onset, the greater the risk for dependence, aswell as antisocial behavior.Current dietary guidelines for Americans recommend that men consumeno more than two drinks per day and women, no more than one drink per day75

76 III. SUBSTANCES OF ABUSE(Dufour, 2001). Consumption of more than five drinks per day is consistentlyassociated with acute and chronic adverse consequences (Midanik, Tam,Greenfield, & Caetano, 1996) Cross-sectional surveys of drinking behavior inthe United States have determined that at least 65% of Americans are currentdrinkers and average 88 drinking days per year. The average number of heavydrinking days per year is 13 (Greenfield, 2000).DIAGNOSISAlcohol use may lead to two alcohol-use disorders (abuse or dependence) and11 alcohol-induced disorders (see section on clinical features). The fourth textrevised edition of the Diagnostic and Statistical Manual of Mental Disorders(DSM-IV-TR; American Psychiatric Association, 2000) requires that three ormore criteria for dependence occur at any time within a 12-month period. Thenecessity for occurrence of three or more criteria within a 12-month time frameis more diagnostically rigorous than the criteria of the DSM-III-R. In contrastto DSM-III-R, DSM-IV-TR lists only seven criteria under dependence; a formercriterion—“substance often taken to relieve or avoid withdrawal symptoms”—hasbeen subsumed under the withdrawal criteria; and the criteria onfailure to fulfill major role obligations at work, school, or home have beenshifted to the abuse criteria.Alcohol abuse criteria have been expanded from two criteria in DSM-III-Rto four criteria in DSM-IV-TR. Alcohol abuse requires at least one of the criteriato have occurred within a 12-month period.Proper diagnosis requires adherence to these criteria. The distinctionsbetween alcohol abuse and alcohol dependence (alcoholism) are clinically useful.For example, if only criteria for abuse are met, it can be assumed that thepatient is not alcohol-dependent (and is, therefore, not an “alcoholic”). Suchan individual is more likely to benefit from controlled drinking strategies and tobe able to return to nonpathological use of alcohol than is the person whoreaches criteria for dependence, where abstinence would be the preferred treatmentgoal. Higher rates of remission can be expected for clients with alcoholabuse compared to clients with alcohol dependence, even in the presence of asevere mental disorder.The symptoms associated with alcohol abuse and alcohol dependence arefar-ranging and involve biological, psychological, and social domains. The presentingsymptoms vary from patient to patient, and such heterogeneity shouldbe appreciated by the clinician making a diagnosis.In assessing a patient for alcoholism, the clinician should consider problemsrelated to the drinker, the family, and the community. Problems for thedrinker may include declining job performance, joblessness, divorce, arrests(especially for driving while intoxicated and public intoxication), accidents,

5. Alcohol 77withdrawal symptoms, broken relationships, and associated medical and psychiatricillnesses. Assessment of family functioning may reveal marital discord,spousal abuse, child abuse, financial problems, depression or anxiety syndromes,child neglect, child developmental problems, school dropout, and delinquency.At the community level, manifestations may include violence, accidents, propertydamage, economic costs of welfare or health services, and decreased workproductivity.A diagnosis does not have to be rushed. Interviews with collateral sourcesare often necessary. Some patients will fall into a “gray zone,” which means thatit is unclear whether an alcohol use disorder is present. In such circumstances,obtaining further information and following the patient over time should clarifythe diagnosis.ScreeningSeveral instruments and interviewing techniques enable the clinician to screenfor an alcohol use disorder. Interview techniques include the CAGE (Ewing,1984) and the TWEAK (Russell et al., 1991). CAGE is a mnemonic device:(Cut down: “Has anyone ever recommended that you cut back or stop drinking?”Annoyed: “Have you ever felt annoyed or angry if someone comments onyour drinking?” Guilt: “Have there been times when you’ve felt guilty about orregretted things that occurred because of drinking?” Eye-Opener: “Have youever used alcohol to help you get started in the morning, to steady yournerves?”). Positive answers to three of these four questions strongly suggestalcoholism. “TWEAK,” a similar mnemonic device is more useful than theCAGE in interviews with women. T assesses tolerance: “How many drinks canyou hold or how many drinks does it take to get high? (If it takes more than twodrinks to get “high” or six drinks to feel drunk, tolerance can be assumed to bepresent). W: “Have close friends or relatives worried about your drinking?” Eye-Opener: “Do you sometimes take a drink in the morning to wake up?” Amnesia:“Has a friend or family member ever told you things you said or did while youwere drinking that you could not remember?” K (cut): “Do you sometimes feelthe need to cut down on your drinking?” Positive answers to three or morepoints suggest alcoholism.Laboratory tests are useful for detecting heavy drinking. Serum gammaglutamyltransferase(GGT) has been established as a sensitive test of early liverdysfunction. GGT has a sensitivity of 50% and a specificity of 80% (Bean &Daniel, 1996), meaning that 50% of patients with drinking problems will bemissed by the GGT. However, 80% of people with an elevated GGT do havean alcohol problem (therefore, 20% of people with elevated GGTs are normaldrinkers).Another useful screening test is increased erythrocyte mean corpuscularvolume (MCV), which was elevated in 26% of the patients in a Mayo Clinic

78 III. SUBSTANCES OF ABUSEstudy. In both male and female alcoholics, the combinations of elevated GGTand MCV identified 90% of alcoholic patients (Skinner, 1981). Other teststhat may be elevated are triglycerides, serum alkaline phosphates, serum bilirubin,and uric acid.A relatively new test with clinical utility is carbohydrate-deficient transferrin(CDT). Consuming more than 60 grams (5 drinks) of alcohol per day willincrease CDT. Normal CDT levels can be expected to return after 2–4 weeks ofabstinence (Allen & Anthnelli, 2003).COMORBIDITYThe Epidemiologic Catchment Area (ECA) study that involved 20,000adults in the general public determined that 7.3% had an alcohol use disorderwithin the 12 months prior to the interview (Regier et al., 1993). TheNational Comorbidity Survey (NCS) involved a sample of over 8,000 individuals,ages 15–54 years, in the noninstitutionalized civilian population ofthe United States. The 1-year prevalence rates for any alcohol use disorder(i.e., either abuse or dependence) was 9.9%. Alcohol abuse was found in2.5% of the population within the previous 12 months, and alcohol dependencein 7.2% of the sample within the past 12 months (Kessler et al., 1994).More recently, these statistics have been revised to address the issue of clinicalsignificance (Narrow, Rae, Robins, & Regier, 2002). Clinical significancewas assessed by determining whether a physician or other professional wastold about the symptoms, whether medicine was taken more than once forthe symptoms, or whether the symptoms interfered a lot with one’s life oractivities. When these aspects of clinical significance were factored in, theprevalence rates for any alcohol use disorder went from 9.9% of the sample to6.5% in the sample in the NCS and from 7.3% of the sample to 7.2% of thesample in the ECA study.For each psychiatric disorder assessed in these epidemiological studies, theprevalence rates of psychiatric disorders were higher among people diagnosedwith alcohol dependence or alcohol abuse. Furthermore, those with alcoholdependence were more likely to have a psychiatric disorder than those diagnosedwith alcohol abuse.In the NCS study, the median age for onset of a comorbid psychiatric disorderpreceded the median age of onset for all addictive disorders by about 10years. The majority of individuals who had both a psychiatric disorder and anaddictive disorder reported that they had experienced the symptoms of the psychiatricdisorder before the addictive disorder started. One exception to thisorder of onset was that nearly 72% of alcohol-abusing males reported that theiralcohol abuse preceded the onset of a mood disorder (Petrakis, Gonzales,Rosenheck, & Krystal, 2002).

5. Alcohol 79Drug Abuse–DependenceA common comorbidity associated with alcohol use disorders is co-occurringdrug use disorders. In 2001, the National Household Survey on Drug Abusefound that among teenagers who binge drink, two-thirds were also abusingdrugs. In contrast, one in 20 teenagers who did not drink abused drugs. Drawingupon the ECA and NCS data, it has been determined that one in five individualswith an alcohol use disorder will also have a drug use disorder. A breakdownof the NCS data indicates that those with either alcohol abuse or alcoholdependence in 40% of cases have either drug abuse or drug dependence.The more serious the drug use disorder, the more likely it is that alcoholabuse–dependence will be found. For example, the ECA data indicate that if nodrug problem exists, the rate of alcohol abuse–dependence is 11% (compared to13% for the total population). When tetrahydrocannabinol abuse–dependenceis present, the prevalence of alcohol abuse–dependence rises to 36%. The ratesof alcohol abuse–dependence rise even further with amphetamines (62%),opioids (67%), barbiturates (71%), and cocaine (84%) (Helzer & Pryzbeck,1988).An additional drug use comorbidity associated with drinking is that oftobacco dependence. Smoking rates among alcoholics are estimated to be ashigh as 90%, with approximately 70% of alcoholics smoking heavily, that is, atleast one pack of cigarettes per day. Smokers who are dependent on nicotinehave an approximately three times greater risk of becoming alcohol-dependentthan nonsmokers (National Institute on Alcohol Abuse and Alcoholism,1998). It is well known that the smoking rate in the general population hasgradually declined over past decades, but the smoking rates among those withalcohol dependence have remained persistently high (Hays et al., 1999).Mood DisordersWhen corrected for clinical significance (Narrow et al., 2002) 1-year majordepression prevalence rates are approximately 5%. Women are twice as likely asmen to experience major depression. Major depression will be found nearly fourtimes more commonly in individuals with alcohol dependence compared to thenon-alcohol-dependent population. Those with a diagnosis of alcohol abuse(rather than alcohol dependence) have only a slight increased risk of majordepression compared to the general population. There is a strong sex differencein order of onset. For example, in males, alcoholism precedes depression in 78%of cases, whereas for women, the reverse is true (i.e., depression precedes alcoholdependence in about 66% of cases) (Helzer & Pryzbeck, 1988).Bipolar disorder and alcohol use disorders have a strong association.Bipolar I patients have alcohol dependence in approximately 31% of cases,and another 15% meet criteria for alcohol abuse. Patients with bipolar II ill-

80 III. SUBSTANCES OF ABUSEness have a rate of alcohol dependence at approximately 21% and an alcoholabuse pattern of 18%. Non-substance-abusing patients with bipolar illnesshave a more favorable course of treatment than do those who are using alcoholor other drugs. For example, the patients with comorbid substance useand bipolar disorders have more frequent hospitalizations for mood symptoms,earlier onset of bipolar disorder, more rapid cycling, and a greater prevalenceof mixed mania. It is more common for bipolar disorder to precede alcoholism,although the reverse situation is certainly found. In either case, it is criticalthat the alcohol use disorder and the mood disorder be treated in a synchronousfashion, because failure to address one is likely to aggravate theoccurrence of the other.Anxiety DisordersCompared to depressive disorder, it is usually easier to determine whether ornot an anxiety disorder is independent of alcohol use. For example, posttraumaticstress disorder (PTSD) does require a specific traumatic event. Panicattacks are typically clearly recalled by individuals and are therefore easier toseparate from possible anxiety symptoms that have resulted from alcohol use,intoxication, or withdrawal. There is a strong comorbidity between alcohol usedisorders and anxiety disorders; nearly 37% of individuals with alcohol dependencehave met criteria for an anxiety disorder during the previous year. Generalizedanxiety disorder accounts for 11.6%, panic disorder for 3.9%, and PTSDfor 7.7%. Another way to appreciate these comorbidities is that the alcoholdependentperson is 4.6 times more likely to have generalized anxiety disorder,2.2 times more likely to have PTSD, and 1.7 times more likely to have panicdisorder than the non-alcoholic-dependent individual. The prevalence of socialanxiety disorder has been found to range from 2 to 13%, with the latter figuredetermined through the NCS. Typically, social anxiety disorder (social phobia)is present before the development of an alcohol use disorder, because individualswith social phobia are typically shy or behaviorally inhibited as small children.Conservative estimates of co-occurring social anxiety disorder and alcoholuse disorders indicate that 15% of people receiving alcoholism treatmenthave both disorders, and 20% of patients seeking treatment for social anxietydisorder also have a comorbid alcohol use disorder (Randall, Thomas, &Thevos, 2001). Generally, anxiety disorders develop prior to an alcohol use disorder,and alcohol is typically seen to achieve, at least briefly, tension reduction.SchizophreniaOther than nicotine, alcohol is the most commonly abused drug in patientswith schizophrenia. Schizophrenia occurs in about 1% of the population, butECA data revealed that 33.7% of people with schizophreniform disorder (same

5. Alcohol 81symptoms as schizophrenia but lasting less than 6 months) or schizophreniahave a diagnosis of alcohol abuse or alcohol dependence at some time in theirlives. The high rate of alcohol use disorders in patients with schizophrenia maybe related to biological factors, such as self-medication to alleviate symptoms ofschizophrenia, or side effects of antipsychotic medications; underlying abnormalitiesof dopamine regulation may provide a common basis for the high rateof co-occurrence; or patients with schizophrenia may be particularly vulnerableto the negative effects of substance use due to the impaired thinking andimpaired social judgment that are part of the schizophrenic syndrome, thusincreasing their vulnerability for a substance use disorder. It is critical that thetreatment for schizophrenia and alcohol use disorders be integrated. Thisinvolves multidisciplinary treatment teams that provide outreach and comprehensiveservices. Osher and Kofoed (1989) describe four stages that are effectivewith patients with comorbid schizophrenia and alcohol use disorders: (1)developing a trusting relationship; (2) motivating the patient to manage bothillnesses and pursue recovery goals; (3) providing active treatment that includesdevelopment of skills and supports needed for illness management and recovery;and (4) developing relapse prevention strategies to avoid and minimize theeffects of relapse.Eating DisordersOver the past decades, numerous studies among patients in treatment haveindicated the co-occurrence of eating disorders and substance use disorders.However, these studies are often methodologically limited, and have provided awide range of estimates of eating disorders in patients with substance use disorders,from 2 to 41%. More recently, improved methodological approaches havedetermined that (1) substance use disorders do not have a significantly greaterco-occurrence with eating disorders compared to other psychiatric controls, and(2) although eating disorders are frequently diagnosed among inpatients withsubstance use disorders, they are also frequently diagnosed in other psychiatricinpatients. At this time, there is no strong relationship between eating disordersand substance use disorders, and studies that report strong associations typicallyinvolve patients who have additional psychiatric disorders that frequentlyco-occur with eating disorders and substance use disorders (Dansky, Brewerton,& Kilpatrick, 2000).Personality DisordersThe assumption that alcoholism and personality traits are linked in some fashionhas a long history. Earlier editions of the DSM (DSM-I and DSM-II) classifiedalcoholism along with personality disorders. By 1980, with publication ofDSM-III, substance use disorders (including alcoholism) were understood asentities independent of the personality disorders.

82 III. SUBSTANCES OF ABUSEGenerally, antisocial personality disorder (APD) is the most prevalent personalitydisorder associated with alcoholism when samples from public treatmentcenters are studied, and borderline personality disorder (BPD) is the mostcommon disorder in studies from private treatment facilities. In a private psychiatrichospital sample, 57% of substance-abusing patients met DSM-III-R criteriafor a personality disorder; with BPD being the most commonly occurringpersonality disorder (Nace, Davis, & Gaspari, 1991).Personality disorder occurs more commonly in alcoholics than in the generalpopulation. A prospective long-term study of a nonclinical sample (Drake& Vaillant, 1985) determined that by age 47, 23% of males met criteria for apersonality disorder. However, the alcoholic males in the sample met criteriafor a personality disorder in 37% of cases. In a review of over 2,400 psychiatricpatients (Koenigsberg, Kaplan, Gilmore, & Cooper, 1985), 36% were found tohave a personality disorder. The alcoholics in this clinical sample, however,had a personality disorder in 48% of cases. ECA study data document APD in15% of alcoholic men and 4% of alcoholic women. These prevalences exceedthe rate of APD in the total population four times for men and 12 times forwomen (Helzer & Pryzbeck, 1988).Cloninger (1987) has empirically determined type I, or milieu-limitedalcoholism, that affects both men and women typically after age 25. Type II, ormale-limited alcoholism, occurs predominately in males, develops before age25, and is associated with severe medical and social consequences. In an extensivereview, Howard, Kivlahan, and Walker (1997) determined that noveltyseekingtraits predict early-onset criminality, alcoholism, and other forms ofsubstance abuse. Furthermore, children of alcoholic parents tend to be higherin novelty seeking and lower in reward dependence than children of nonalcoholicparents. The traits of reward dependence and harm avoidance aremore typical of the type I milieu-limited alcoholic and high novelty seeking,with low scores on reward dependence and harm avoidance being found morecommonly in the aggressive early-onset type II male form of alcoholism.ETHNICITY AND ALCOHOLISMEthnic minorities made up 29% of the U.S. population in 2000. Cultural attitudesexert a powerful influence on drinking behaviors and response to treatment.It has been shown that although cultural approval may increase theaccessibility of alcohol, ritualistic use of the drug by the culture may help toinhibit abuse or dependence (Westermeyer, 1986). The lower rates of drinkingproblems among Italian Americans, Italians, and Jews have been explained bythe traditional use of wine in these groups; integration of drinking into familylife; and, in the Jewish drinkers, the religious significance attached to alcohol.However, even ethnic groups with ritualistic use patterns do not consistently

5. Alcohol 83show low incidences of alcoholism or alcoholic complications. For example, theFrench have relatively high rates of alcoholism and cirrhosis.Native AmericansMany Native American tribal groups have high rates of alcohol-related problems(Westermeyer, 1986). However, attitudes toward drinking vary considerablyfrom tribe to tribe. Westermeyer noted increasing rates of alcoholism and medicalcomplications secondary to alcohol as Native American tribes have moved fromtheir rural tribal areas to cities. Those living on reservations drink less frequentlybut are more likely to binge drink and to consume more alcohol per drinking occasion(May & Gossage, 2001). A recent study that contradicted the “firewatermyth” theory that Native Americans are more sensitive to the effects of alcohol(Garcia-Andrade, Wall, & Ehlers, 1997) found that the Mission Indian men weregenerally less sensitive to alcohol effects, a physiological characteristic shown tobe associated with a greater risk for alcoholism in white populations.Alcohol-related motor vehicle fatalities are highest in the Native Americanpopulation, with a 68.1% rate compared to 44.2% for whites (NationalHighway Traffic Safety Administration, 1999). Cirrhosis is the sixth leadingcause of death in Native Americans (Stinson, Grant, & Dufour, 2001).African AmericansA 1996 report by the Group for the Advancement of Psychiatry (GAP) onalcohol abuse among African Americans found little difference in the lifetimeprevalence of alcoholism between African Americans and whites. The alcoholismprevalence for African Americans is low in the young adult group and thenincreases, in contrast to the alcoholism prevalence for whites, which starts atmoderately high levels in the young group and then decreases. Deaths fromalcohol-induced causes are about 2.5 times higher in the black population thanin the white population. Cirrhosis death rates for African American males are45.3% compared to 34.7% for whites (Caeteno & Clark, 1998b). Motor vehiclefatalities are essentially equal between blacks (45.2) and whites (44.2%)(National Highway Traffic Safety Administration, 1999).Asian AmericansAsians have the lowest rates of cirrhosis (11.5 per 100,000 males) and the lowestpercentage of motor vehicle fatalities (28.2%). A variant of aldehydedehydrogenase-2 is found in Asians (e.g., in 48% of college students of Chineseancestry and 35% of those of Korean background) (Luczak et al., 2001). Thisgenetic variant changes the way alcohol is metabolized and leads to the aversivesymptoms of headache, nausea, dizziness, and facial flushing.

84 III. SUBSTANCES OF ABUSEHispanic AmericansHispanic American men drink more than Hispanic American women regardlessof age. Mexican American men drink more and abstain less than eitherPuerto Rican or Cuban American men. Hispanic American men and womendrink more as their income increases (Group for Advancement of Psychiatry,1996). Surveys in 1984 and 1995 revealed that alcohol-related problemsincreased in Hispanic males but remained stable in women of all ethnicities,and stable in black males and white males (Caetano & Clark, 1998b). MexicanAmericans have a motor vehicle alcohol-related mortality rate of 54.6%, whilethat of Cuban Americans is 36.6% (National Highway Traffic Safety Administration,1999). Cirrhosis rates for Hispanic males are 61.8 per 100,000, which ishigher than that found in black or white males. The notion that machismo isrelated to drinking in Mexican American males is dispelled by statistics showingequal machismo influences in white and non-Hispanic minorities (Caetano& Clark, 1998a).PHARMACOLOGY OF ALCOHOLAlcohol refers to compounds with a hydroxyl group, that is, an oxygen andhydrogen (-OH) bonded to a carbon atom. Beverage alcohol consists of ethanol,which occurs naturally as a fermentation product of sugars and grains. Theethyl alcohol molecule is hydrophilic and affects all cells of the body.Alcohol is absorbed from the stomach and the proximal part of the smallbowel. Ninety-five percent of alcohol is metabolized in the liver by alcoholdehydrogenase (ADH), which converts alcohol to the toxic substanceacetaldehyde. The stomach contains at least three isoenzymes of alcoholdehydrogenase. Women have less gastric ADH and may therefore metabolizealcohol less efficiently. If gastric emptying is slowed, as with ingestion of food orwith drugs having anticholinergic properties, more metabolism of alcohol bygastric ADH occurs, resulting in a lower blood alcohol concentration (Wedel,Pieters, Pikaar, & Ockhuizen, 1991). Alternatively, aspirin and cimetidineinhibit gastric ADH and may lead to an increased blood alcohol concentration.The principal route of metabolism of alcohol is through the ADH pathway,which eliminates approximately one drink (13 g of alcohol) per hour. Themajor product is the toxic substance acetaldehyde. Acetaldehyde is further brokendown to acetic acid via the enzyme aldehyde dehydrogenase (ALDH), andsubsequently goes through the citric acid cycle to become carbon dioxide andwater. Both ADH and ALDH possess several distinct isoenzymes that mayreflect a genetic predisposition to alcoholism. Another pathway for oxidation,the microsomal ethanol-oxidizing system (MEOS), is induced by chronic ingestionof alcohol. An increase in the activity of the MEOS pathway can increase

5. Alcohol 85the rate of elimination by 50–70%. The MEOS may be responsible for theincreased metabolic tolerance seen in chronic alcoholics for other hypnotic/sedative drugs, as well as for alcohol.One action of ethanol is the disruption of the phospholipid molecularchain in the nerve cell membrane. The result is an increased “fluidity” of themembrane. This disturbance in the structure of the membrane affects the functionalprotein system (enzymes, receptors, and ionophores), which is attachedto the membrane. For example, adenylate cyclase and monoamine oxidaseactivity are lower in alcoholics than in controls. Adenylate cyclase is importantin the formation of cyclic adenosine monophosphate (cAMP), which in turninfluences metabolism within the cytoplasm. Of particular interest is the findingthat adenylate cyclase remains inhibited in alcoholics 12–48 months followingabstinence (Tabakoff et al., 1988).More important than the disruption of the cell membrane is the effect ofalcohol on the gamma-aminobutyric acid (GABA) system and glutamate systemof the brain. The brain has three types of GABA receptors: A, B, and C.GABA A receptors are the targets for alcohol, benzodiazepines, barbituates,and neurosteroids. Stimulation of the GABA receptor by the binding of thesecompounds causes an ion channel to open temporarily and emit chloride ionsinto the cell. Alcohol enhances the influx of chloride ion, and the result is sedativeand anxiolytic effects. Chronic use of alcohol down-regulates the GABAsystem, and the neuron eventually becomes dependent on alcohol to enableGABA to function. If alcohol is withdrawn, the opening of the chloride ionchannel fails, because GABA is no longer capable of performing the task secondaryto the cell, having adapted to the role of alcohol. Thus, the cellbecomes hyperexcitable, leading to irritability, insomnia, hypertension, tachycardia,and possibly hallucinations and seizures.The second major neurotransmitter system involving alcohol is the glutamatesystem, and in particular the glutamate receptor N-methyl-D aspartate(NMDA). Ethanol is a potent inhibitor of the NMDA receptor and most likelyblocks NMDA-stimulated calcium uptake. The NMDA receptor is involved inmemory formation, neuronal excitability, and seizures. Alcohol’s acute actionson this receptor leads to sedative, amnestic, and anxiolytic effects. However,when alcohol is withdrawn, the NMDA receptor becomes abnormally excited,and seizure activity and hypoxic damage may result.Low doses of alcohol activate the norepinephrine system via the reticularactivating system in the brainstem. This action stimulates behavior and arousal,and as the concentration of alcohol in the brain increases, the dopamine pathwaysin the mesolimbic system assume importance as a reward center. This system,which involves the ventral tegmental area and projections to the nucleusaccumbens, is the same system activated by opiates and stimulants.It has also been demonstrated that individuals with family histories thatare positive for alcoholism show increased beta-endorphin release and in-

86 III. SUBSTANCES OF ABUSEcreased euphoria after drinking alcohol. Similarly, serotonin function mightpredispose to alcoholism, as evidenced by the fact that some alcoholics havebeen found to have reduced serotonergic function and, although inconsistent,some serotonin medications have attenuated drinking behavior (Dackis &O’Brien, 2002; Pettinati, 2001)CLINICAL FEATURESDSM-IV (American Psychiatric Association, 1994) lists, in addition to the syndromesof alcohol abuse and alcohol dependence, 11 alcohol-induced disorders.Alcohol idiosyncratic intoxication (“pathological intoxication”) was deleted inDSM-IV.Alcohol IntoxicationAlcohol intoxication is the most common alcohol-induced disorder. It is areversible syndrome characterized by slurred speech, impaired judgment, disinhibition,mood lability, motor incoordination, cognitive impairment, andimpaired social or occupational functioning. These effects vary according tosetting, mental set, dose, and tolerance of the individual, and are a result of adirect stimulant effect of alcohol on norepinephrine and dopamine systems,combined with inhibition of the stimulating effect of the glutamate-mediatedNMDA receptor and facilitation of the inhibiting function of the GABA system.A blood alcohol level of 30 mg% will produce a euphoric effect in mostindividuals who are not tolerant. At 50 mg%, the central nervous system(CNS) depressant effects of alcohol become prominent, with associated motorcoordination problems and some cognitive deficits. In most states, the legallevel of intoxication is 80 mg%. At levels greater than 250 mg%, significantconfusion and a decreased state of consciousness may occur. Alcoholic comamay occur at this level, and at greater than 400 mg%, death may result. Becauseof tolerance, some heavy drinkers may not show these effects even at highblood levels.Alcohol WithdrawalWith prolonged exposure to ethanol, the brain adapts by down-regulating (i.e.,reducing) the inhibitory GABA A receptors—especially the alpha 1 subunit ofGABA A. Ethanol also inhibits the excitatory NMDA glutamate receptors,and the brain adapts by increasing or up-regulating NMDA receptors. Therefore,when alcohol use is discontinued there is a relative decrease in inhibiting(GABA) mechanisms and a relative increase in excitatory (NMDA) mecha-

5. Alcohol 87nisms. The symptoms of alcohol withdrawal then emerge and commonlyinclude tremor, sweating, anxiety or agitation, elevated blood pressure, increasedpulse, increased respiration, headaches, nausea, vomiting, and light andsound sensitivity. If the withdrawal is more severe, grand mal seizures (usuallyonly one) may occur 24–48 hours after the last drink.Alcohol withdrawal may be accompanied by perceptual disturbances and iscoded accordingly if the perceptual disturbance occurs with intact reality testing(i.e., the person knows that the perceptions are caused by alcohol). Theperceptual disturbances may be auditory, visual, or tactile hallucinations or illusions.They are transitory and usually develop within 48 hours of cessation ofdrinking. “Alcohol hallucinosis” is a clinical term commonly applied to theseperceptual disturbances.DeliriumAn alcohol-induced delirium may occur during intoxication (alcohol intoxicationdelirium) or during withdrawal (delirium tremens, or DTs).Alcohol intoxication delirium (unlike delirium from stimulants or hallucinogens,which may emerge in hours) requires days of heavy use of alcohol tooccur. Evidence for a delirium would include a disturbance in consciousnessmanifested by inability to shift, sustain, or focus one’s attention; reduced awarenessof the environment; and cognitive impairment, such as disorientation,memory deficits, and language disturbance (e.g., mumbling). The symptomswould fluctuate during the course of a day and would be linked by history andphysical or laboratory data to the use of alcohol (American Psychiatric Association,1994).DTs are most likely to develop if the patient has had an alcohol withdrawalseizure or a concomitant medical disorder, such as an infection, hepaticinsufficiency, pancreatitis, subdural hematoma, or a bone fracture. Onset is usually2–3 days after cessation of alcohol use and usually lasts 3–7 days, but can beprolonged. DTs must be considered a medical emergency (Goforth, Primeau, &Fernandez, 2003) and are characterized by visual, auditory, and/or tactile hallucinations,gross tremor, tachycardia, sweating, and, possibly, fever, as well as thedisturbances of consciousness described earlier.Alcohol-Induced Persisting Amnestic DisorderAlcohol-induced persisting amnestic disorder constitutes a continuum involvingWernicke’s acute encephalopathy, the amnestic disorder per se (commonlyknown as Korsakoff’s psychosis), and cerebellar degeneration. Alcohol-inducedpersisting amnestic disorder typically follows an acute episode of Wernicke’sencephalopathy. The latter consists of ataxia, sixth cranial nerve (abducens)paralysis, nystagmus, and confusion. Wernicke’s often clears with vigorous thia-

88 III. SUBSTANCES OF ABUSEmine treatment, but 50–65% of patients show persistent signs of amnesia. Ifuntreated, the mortality rate is about 15%.The amnesia is characterized by anterograde amnesia (inability to formnew memories due to failure of information acquisition), retrograde amnesia(loss of previously formed memories), and cognitive deficits, such as loss of concentrationand distractibility.The etiology is based on nutritional factors, specifically, the thiamin deficiencypresent with chronic alcohol use, either through intestinal malabsorptionor poor dietary intake associated with alcohol. Other factors, such as familialtransketolase deficiency may be important in the pathogenesis of thissyndrome in a subgroup of individuals.The disorder in memory that persists is correlated with microhemorrhagesin the dorsomedial nucleus of the thalamus, in the mammillary bodies, and inthe periventricular gray matter.In contrast to other dementias, intellectual function is typically preserved.In a review of Wernicke–Korsakoff syndrome, McEvoy (1982) points out that20% of patients show complete recovery over a period of months to years, 60%show some improvement, and 20% show minimal improvement. Previouslybelieved to be a distinct clinical entity, alcoholic cerebellar degeneration maybe indistinguishable clinically and pathophysiologically from the cerebellar dysfunctionseen with Wernicke–Korsakoff syndrome.Alcoholic amnestic disorder should not be confused with “blackouts,”which are periods of retrograde amnesia during periods of intoxication. Blackouts,caused by high blood alcohol levels, may occur in nonalcoholics, as well asat any time in the course of alcoholism.Alcohol-Induced Persisting DementiaThis disorder develops in approximately 9% of alcoholics (Evert & Oscar-Berman, 1995) and consists of memory impairment combined with aphasia,apraxia, agnosia, and impairment in executive functions, such as planning,organizing, sequencing, and abstracting. These deficits are not part of a deliriumand persist beyond intoxication and withdrawal. The dementia is caused by thedirect effects of alcohol, as well as by vitamin deficiencies.Models of cognitive impairment in alcoholics include “premature aging,”which means that alcohol accelerates the aging process, and/or that vulnerabilityto alcohol-induced brain damage is magnified in people over the age of 50;the “right-hemisphere model,” which is derived from the evidence that nonverbalskills (reading maps, block design tests, etc.) are more profoundly impairedin alcoholics than left-hemisphere tasks (language functions); and the “diffusebrain dysfunction” model, which proposes that chronic alcoholism leads towidespread brain damage (Ellis & Oscar-Berman, 1989).Personality changes, irritability, and mild memory deficits in an abstinent

5. Alcohol 89individual with a history of alcoholism are early clues suggestive of alcoholinducedpersisting dementia.Alcohol-Induced Anxiety, Affective, or Psychotic DisorderIf symptoms of an anxiety disorder, affective disorder (depressive, manic, ormixed), or psychotic disorder (hallucinations or delusions) develop during orwithin 1 month of intoxication or withdrawal, an alcohol-induced anxiety,affective, or psychotic disorder may be diagnosed. If the patient has insight thathallucinations are alcohol-induced, an alcohol-induced psychotic disorder isnot diagnosed. The anxiety and affective symptoms must exceed the usual presentationof such symptoms as they commonly occur during intoxication orwithdrawal (DSM-IV).These disorders must be distinguished from comorbid psychiatric disorders(see section on comorbidity). A careful history eliciting the onset and thecourse of symptoms during abstinence or reexposure to alcohol will help distinguishalcohol-induced syndromes from psychiatric comorbidity.Alcohol-Induced Sleep DisorderAlcohol consumed at bedtime may decrease the time required to fall asleep buttypically disrupts the second half of the sleep cycle, resulting in subsequent daytimefatigue and sleepiness. Even a moderate dose of alcohol consumed within6 hours prior to bedtime can increase wakefulness during the second half ofsleep (Vitiello, 1997). Alcohol use prior to bedtime will also aggravate obstructivesleep apnea, and heavy drinkers or those with alcoholism are at increasedrisk for sleep apnea. Patients with severe obstructive sleep apnea are at a fivefoldincreased risk for fatigue-related traffic crashes if they consume two or moredrinks per day compared to obstructive sleep apnea patients who consume littleor no alcohol (Bassetti & Aldrich, 1996).In alcoholics, heavy drinking eventually leads to increased time requiredto fall asleep, frequent awakenings, and a decrease in subjective quality of sleep.Slow-wave sleep is interrupted, and during periods of withdrawal there is pronouncedinsomnia and increased rapid eye movement (REM) sleep. Followingwithdrawal from alcohol, sleep patterns may be abnormal, even following yearsof abstinence.Alcohol-Induced Sexual DysfunctionSexual dysfunction refers to impairment in sexual desire, arousal, or orgasm, orpresence of pain associated with intercourse as a result of alcohol use. Alcoholinducedsexual dysfunction differs from a primary sexual disorder in thatimprovement would be expected with abstinence from alcohol.

90 III. SUBSTANCES OF ABUSEAlcohol consumption has been found to have a negative relationship tophysiological arousal in women. Although women state that they felt morearoused, the physical responses tend to be depressed when alcohol is consumed.Inhibition of ovulation, decrease in gonadal mass, and infertility may followchronic heavy alcohol use.In males, erectile dysfunction may occur transiently with alcohol use, especiallyat blood alcohol levels above 50 mg/100 ml. Decreased libido, erectiledysfunction, and gonadal atrophy are reported in chronic alcoholics (Adler,1992).Chronic male alcoholics, even without liver dysfunction, commonly demonstrateprimary hypogonadism, as evidenced by decreased sperm count andmotility, and altered sperm morphology. Increases in luteinizing hormone and adecrease in the free androgen index were reported in noncirrhotic males andrelated to lifetime quantity of ethanol intake (Villalta et al., 1977).However, a controlled study of abstinent alcohol males selected forabsence of physical illness and use of medications found that sexual dysfunction,level of lutenizing hormone, and level of bioavailable testosterone did notdiffer between the controls and the alcoholics (Schiave, Stimmel, Mandeli, &White, 1995).Normal sexual functioning in abstinent alcoholic men can be expected inthe absence of sexually impairing medications (e.g., disulfiram), liver disease, orgonadal failure.MEDICAL COMPLICATIONS OF ALCOHOLISMGastrointestinal Tract and PancreasSecondary to vitamin deficiencies, alcoholics suffer from inflammation of thetongue (glossitis), inflammation of the mouth (stomatitis), caries, and periodontitis.A low-protein diet, associated with alcoholism, can lead to a zinc deficiency,which impairs the sense of taste and further curbs the appetite of thealcoholic. Parotid gland enlargement may be noted.Alcohol causes decreased peristalsis and decreased esophageal sphinctertone, which leads to reflux esophagitis with pain and stricture formation (Bor etal., 1998). The Mallory–Weiss syndrome refers to a tear at the esophageal–gastric junction caused by intense vomiting. Another source of bleeding fromthe esophagus is esophageal varices secondary to the portal hypertension of cirrhosis.Alcohol decreases gastric emptying and increases gastric secretion. As aresult, the mucosal barrier of the gastrium is disrupted, allowing hydrogen ionsto seep into the mucosa, which release histamine and may cause bleeding.Acute gastritis is characterized by vomiting (with or without hematemesis),anorexia, and epigastric pain. It remains unclear whether chronic alcohol abuseincreases the risk of ulcer disease.

5. Alcohol 91The small intestine shows histological changes and contractual patternchanges even with adequate nutrition. Acute alcohol consumption impairsabsorption of folate, vitamin B 12, thiamine, and vitamin A, as well as someamino acids and lipids. Intestinal enzyme activity is altered as well (Hauge,Nilsson, Persson, & Hultberg, 1998).Alcohol consumption and gallstones are the two most common causes ofacute pancreatitis. Alcohol in moderate amounts does not increase the risk foracute pancreatitis, but consumption of 35 or more drinks per week increases theodds ratio to 4.1 (Blomgren et al., 2002). Acute pancreatitis presents as a dull,steady epigastric pain that may radiate to the back. Bending or sitting may partiallyrelieve the pain, confirming its retroperitoneal origin. Pain may be precipitatedor aggravated by meals and relieved by vomiting. A serum amylase of 1.5to 2.0 times the upper limit of normal has a sensitivity of 95% and a specificityof 98% for acute pancreatitis. Ethanol-induced acute pancreatitis is the result ofthe toxic effect of ethanol on pancreatic acinar cells, leading to inflammationand release of proteolytic enzymes. Chronic pancreatitis is caused most commonlyby alcoholism. The common presenting symptoms are abdominal pain,weight loss, nausea, vomiting, jaundice, and diarrhea. Surgical procedures areavailable for treatment of chronic pancreatitis, with favorable long-term results(Sohn et al., 2000).LiverThree histological distinct lesions occur in the evaluation of alcohol-inducedliver disease. The most common, occurring in 90% of heavy drinkers, is fattyliver (hepatic steatosis); 10–35% of heavy drinkers acquire alcoholic hepatitis,and 10–20% acquire alcohol cirrhosis (fibrosis, nodules, loss of normal structure).Alcohol leads to liver damage by several mechanisms: the production ofacetaldehyde, free radicals, and cytokines as alcohol is metabolized; the passageof bacterial endotoxins through the intestinal wall is enhanced by the presenceof alcohol; and alcohol-induced cell death and inflammation, which lead toscarring (Lieber, 1998).Hepatic steatosis is a common, reversible condition that may progress tocirrhosis in about 7% of cases (Gish, 1996). Signs and symptoms of alcoholicsteatosis include nausea, vomiting, hepatomegaly, right-upper-quadrant pain,and tenderness. Ascites and jaundice are uncommon. Laboratory data mayreveal mild elevation of transaminases, alkaline phosphatase, or bilirubin.Clinically, fatty liver may mimic or coexist with alcoholic hepatitis. Symptomsof alcoholic fatty liver, as well as alcoholic hepatitis, should resolve with abstinence.Alcoholic hepatitis frequently coexists with fatty liver and cirrhosis.Symptoms include anorexia, nausea, vomiting, fever, chills, and abdominalpain. Hepatomegaly and right-upper-quadrant tenderness are common.

92 III. SUBSTANCES OF ABUSETransaminase levels rarely exceed 500 international units (IU), with a typicalratio of aspartate aminotransferase to alanine aminotransferase of 2:1 to 5:1.Liver biopsy can be helpful in distinguishing fatty liver from hepatitis and fromcirrhosis. Ascites, encephalopathy, high bilirubin levels, and prolongation ofthe prothrombin time are poor prognostic indicators that portend an increasedmortality. Treatment consists of abstinence and nutritional support. Treatmentwith steroids, propylthiouracil, and colchicines has yielded mixed results. Thereis a relative-risk increase of 14–20 for individuals who drink more than fivedrinks per day, although wine drinkers are at a lower risk than beer or liquordrinkers (Becker, Gronbaek, Johansen, & Sorensen, 2002). Women have ahigher incidence of alcoholic hepatitis and cirrhosis than men, although themechanisms underlying these gender differences is not known. Alcoholiccirrhosis develops as a result of prolonged hepatocyte damage, leading tocentrilobular inflammation and fibrosis. The latter pathology causes portalhypertension and the development of varices. Esophageal varices may bleedspontaneously, or bleeding may be precipitated by respiratory tract infections,nonsteroidal anti-inflammatory drugs, and alcohol. Cirrhosis also leads toascites, clotting deficiencies, secondary malnutrition, and hepatic encephalopathy(Sutton & Shields, 1995).NutritionAlcoholics are especially susceptible to deficiencies of thiamine, folate, Bvitamins, and ascorbic acid. Alcohol intake leads to negative nitrogen balance,increased protein turnover, and inhibition of lipolysis (Bunout, 1999).Deficiencies in folate, vitamin B 6, and vitamin B 12play a role in elevated levelsof homocysteine, which in turn promotes atherosclerosis and thrombosisformation (Cravo & Camilo, 2000). Ethanol can suppress appetite through itseffect on the CNS. Gastric, hepatic, and pancreatic disease my furtherdecrease enteral intake and contribute to maldigestion or malabsorption.Signs of malnutrition include thinning of the hair, ecchymosis, glossitis,abdominal distention, peripheral edema, hypocalcemic tetany, and neuropathy.Nutritional management consists of abstinence and institution of a wellbalanceddiet and multivitamins, plus thiamine and vitamin B supplementswhen indicated.Cardiovascular SystemIt is well established that alcoholic heart muscle disease is a complication oflong-term alcoholism and not malnutrition or other possible causes of dilatedcardiomyopathy. In a dose-dependent fashion, left ventricular systolic functiondeclines, implicating alcohol in at least 30% of all dilated cardiomyopathies(Lee & Regan, 2002). The contractility of heart muscle is decreased through

5. Alcohol 93alcohol’s effect of increased calcium flow into muscle cells, decreased proteinsynthesis (possibly secondary to increased acetaldehyde), and mitochondrialdisruption (e.g., depressed adenosine triphosphate (ATP) level, leakage ofenzymes, and accumulation of glycogen) (Davidson, 1989).Alcoholic cardiomyopathy should not be confused with heart disease occasionallyresulting from congeners, as occurred in the 1960s when cobalt wasadded to beer to stabilize the foam. The symptoms are similar to other forms ofcongestive heart failure, and begin with shortness of breath and fatigue. Abstinenceis necessary for recovery: A 54% morality rate from this disease isreported in those who continue to drink compared to 9% who abstain (Regan,1990).Transient hypertension is noted in nearly 50% of alcoholics undergoingdetoxification and is related to quantity of drinking and severity of other withdrawalsymptoms. Epidemiological studies have demonstrated that alcohol elevatesblood pressure independently of age, body weight, or cigarette smoking(Klatsky, Friedman, & Armstrong, 1986). A 10-year follow-up study foundeven moderate intake of alcohol (60 grams/day) is associated with increased risk ofischemic and hemorrhagic stroke. Mechanisms involved include alcoholinducedhypertension, coagulation disorders, atrial fibrillation, and reduction incerebral blood flow (Reynolds, Lewis, Nolen, Kinney, & Sathya, 2003). Alcoholhas been shown directly to cause vasoconstriction of cerebral blood vessels,and this effect can be reversed or prevented by calcium-channel blocking drugsand by magnesium (Altura & Altura, 1989).Thus far, the effects of alcohol on the cardiovascular system are distinctlynegative—cardiomyopathy, hypertension, and strokes. Yet beneficial effect hasbeen observed, in that people who drink low to moderate amounts of alcoholare at lower risk for coronary artery disease. Light drinkers (two drinks per day)have a 20% reduction in risk for coronary artery disease (Klatsky, Friedman, &Armstrong, 1986). The protective effect of alcohol seems to follow a U-shapedcurve, with nondrinkers and heavy drinkers showing greater risk for coronaryartery disease (Criqui, 1990).The mechanism by which alcohol provides some protective effect againstcoronary artery disease is in the elevation of high-density lipoproteins, decreasedplatelet aggregation, and fibrinolytic activity (Zakari, 1997).Nervous SystemEthanol damages the CNS and peripheral nervous system by altering both neurotransmitterlevels and cell membrane fluidity and function. Among the neu-

94 III. SUBSTANCES OF ABUSErological effects, alcoholic dementia and Wernicke–Korsakoff syndrome werediscussed earlier. Hepatic encephalopathy occurs in the setting of severe liverfailure as a result of either severe alcoholic hepatitis or cirrhosis. Early manifestationsof encephalopathy include inappropriate behavior, agitation, depression,apathy, and sleep disturbance. Confusion, disorientation, and depressedmental status develop in the advanced stages of encephalopathy. Physicalexamination may demonstrate asterixis, tremor, rigidity, hyperreflexia, andfetor hepaticus. Treatment requires the elimination of the offending condition,dietary protein restriction, and removal of nitrogenous waste from the gutwith osmotic laxatives and antibiotics (lactulose and neomycin, respectively)(Adams & Victor, 1989).The most frequent neurological consequence of chronic alcohol intake is atoxic polyneuropathy, which results from inadequate nutrition, mainly deficiencyof thiamine and other B vitamins. Additionally, there is a relationshipto total lifetime dose of ethanol. Signs and symptoms are (1) distal sensory disturbances,with pain, paresthesia, and numbness in a glove-and-stockings pattern;(2) weakness and atrophy of distal muscles, pronounced in the lowerlimbs; (3) loss of tendon jerks; and (4) dysfunction of autonomic fibers. As aresult, therapy consists of alcohol abstinence, high-calorie nutrition, parenteralthiamine, and other vitamins. For paresthesia and pain, carbamazepine, salicylates,and amitrytiline are effective. The prognosis of alcoholic polyneuropathyis favorable with alcohol abstinence. In chronic alcoholic patients, peripheralnerves frequently are injured by compression during alcohol intoxication.Peroneal nerve lesions result from compression in the region of the neck of thefibula during a prolonged lying position, and the radial nerve is injured duringsitting with the upper arm placed on the backrest of a bench. Usually, pressurepalsies resolve spontaneously (Schuchardt, 2000).HematologyAnemia can result from hemorrhage, hemolysis, or bone marrow hypoplasia.Megaloblastic anemia, usually a result of folate deficiency, has been observed in20–40% of seriously ill, hospitalized alcoholic patients and in up to 4% ofambulatory alcoholics. Alcohol inhibits absorption of folate. There is not astrong correlation between megaloblastic anemia and the presence of liver disease.Alcohol also has a direct toxic effect on the bone marrow, which results ina transient sideroblastic anemia. Reticulocytosis commonly occurs as part ofrecovery from alcohol toxicity (Lee, 1999). Transient thrombocytopenia isfound after consumption of large quantities of alcohol, especially in bingedrinkers (Hardin, 2001).Leukopenia is less common, resulting from the same mechanisms of toxicand nutritional factors already mentioned. Hypersplenism, an irreversible complication,may also contribute to leukopenia, thrombocytopenia, and anemia.

5. Alcohol 95Bone marrow recovery with resolution of leukopenia usually occurs after 1–2weeks of abstinence.Alcohol also affects both thrombotic and coagulation functions. In particular,the cascade of clotting proteins is impeded as a result of diminished productionof the vitamin K–dependent clotting factors (prothrombin, VII, IX,and X). Fibrinolysis, and occasionally disseminated intravascular coagulationmay also occur. Transient thrombocytopenia is found after consumption oflarge quantities of alcohol, especially in binge drinkers (Hardin, 2001).Endocrine SystemAlcohol interferes with gonadal function even in the absence of cirrhosis byinhibiting normal testicular, pituitary, and hypothalamic function. Testicularatrophy, low testosterone levels, decreased beard growth, diminished spermcount, and a loss of libido result. However, testicular atrophy does not occur inall male alcoholics but is associated with alcohol dehydrogenase polymorphismin the testes, as reflected by the genetic variant of an increased frequency of theADH21 allele (Yanauchi et al., 2001).Thyroid dysfunction is common in alcoholics. Consistent findings indicatereduced thyroxine, and total and free triodothyronine concentrations in earlyabstinence. A blunted thyroid stimulation test is found in one-third of alcoholicsduring detoxification and into the early weeks of abstinence. A direct toxiceffect of alcohol on the thyroid is likely, which in turn induces a compensatoryactivation of the hypothalamic–pituitary (HP) axis (Hermann, Heinz, &Mann, 2002).Alcohol intoxication activates the HP axis and results in elevated glucocorticoidlevels. Elevated levels of these stress hormones may contribute toalcohol’s pleasurable effects. With chronic alcohol consumption, however, tolerancemay develop to alcohol’s HP axis–activating effects. Chronic alcoholconsumption, as well as chronic glucocorticoid exposure, can result in prematureaging (Spencer & Hutchison, 1999).Musculoskeletal SystemAcute alcoholic myopathy (rhabdomyolysis) may cause painful, tender swellingof one or more large muscle groups. Diagnosis depends on a high index of clinicalsuspicion, elevation of serum creatine phosphokinase, and myoglobinuria.Chronic alcoholic myopathy may accompany alcoholic polyneuropathy, presentingas painless, progressive muscle weakness and wasting.The development of osteoporosis in middle-age men is uncommon exceptin male alcoholics, where decreased bone mass has been documented (Turner,2000). In women, improvement in bone mass has been shown with moderatealcohol use, especially in postmenopausal women (Laitinen et al., 1993).

96 III. SUBSTANCES OF ABUSEImmune SystemAlcoholics often have impaired immune response, placing them at risk for frequentand severe infections. Alcohol increases hepatitis C virus (HCV) replicationand inhibits the anti-HCV effect of interferon-alpha therapy. Alcohol’seffect is most pronounced during the early phase of the immune response andinterferes with the antigen-presenting cells (not directly on T-cells). Theresult is a decreased response from immunoglobulins (Latif, Peterson, &Waltenbaugh, 2002). People who abuse alcohol are more likely to participatein behaviors that put them at risk to develop human immunodeficiency virus(HIV), and alcohol use disorders are associated with an increased incidence ofHIV, as well as opportunistic infections.SkinSkin disorders can serve as early markers of alcohol misuse. Florid facies andflushing are common. Psoriasis in men has been associated with alcohol abuse,and the treatment responsiveness of psoriasis is significantly reduced when dailyalcohol use exceeds 80 g per day (Gupta, Schork, Gupta, & Ellis, 1993). Otherearly skin markers of excessive alcohol use include discoid eczema (coinshaped,scaly lesions, usually on the lower legs), rosacea, and skin infectionssuch as tinea pedis, pityriasis, and onychomycosis (Higgins & du Vivier, 1992).Immunosuppression secondary to alcohol intake is the likely mechanismfor the increased incidence of skin infections. Squamous cell carcinoma of theoral cavity is increased with heavy alcohol consumption (Smith & Fenske,2000). Late stages of alcoholism may reveal cigarette burns, bruises, acne, andcutaneous stigmata of liver disease, such as spider nevi and palmer erythema.CancerAlcohol increases the risk for developing some types of cancer in a dosedependentfashion. Alcohol is most strongly associated with increased risk forcancer of the oral cavity and pharynx (relative risk [RR] = 5.7), esophagus (RR= 4.2), and larynx (RR = 3.2). Statistically significant increases in risk also arefound for cancers of the stomach, colon, rectum, liver, female breast, and ovaries(Bagnardi, Blangiardo, La Vecchia, & Corras, 2001).Alcohol has not been demonstrated to be a carcinogen per se, but is likelyto act as a co-carcinogen, or cancer-promoting effect, when known cancerinducingagents are present. For example, smoking heavily and drinking heavilysynergistically increase the risk factors for some cancers, as does the combinationof high alcohol consumption and low consumption of fruits and vegetables.The synergism between tobacco use and alcohol is highest for cancers ofthe oral cavity, pharynx, larynx, and esophagus.

5. Alcohol 97Female breast cancer shows a dose-dependent increased risk with alcoholconsumption (e.g., RR = 1.3 with use of two drinks per day) but anincreased RR of 2.7 if alcohol consumption averages over eight drinks per day(Bagnardi et al., 2001). The mechanism of alcohol’s interaction with breastcancer is most likely related to increased estrogen levels associated withdrinking. The increased risk of breast cancer with alcohol use may be limitedto women with a family history of breast cancer (Vachon, Cerhan, Vierkant,& Sellers, 2001).Fetal EffectsFetal alcohol syndrome (FAS) is the leading known preventable cause of mentalretardation. FAS is defined by maternal drinking during pregnancy, growthretardation, a pattern of facial abnormalities, and brain damage characterizedby intellectual difficulties or behavioral problems (Stratton, Howe, & Battaglia,1996). The fetus is most vulnerable to alcohol during the first trimester. Facialabnormalities are characterized by a thin upper lip, absence of a philtrum,midfacial hypoplasia, and short palpetral fissures. Behavioral and intellectualproblems include difficulty in shifting attention, slower reaction time, poorermemory, language problems, and deficits in executive functions such as planningand organization (Olson, Feldman, Streissguth, Sampson, & Bookstein,1998).No safe limit of alcohol use has been determined, but infants born towomen who drink more than 150 grams of alcohol per day during pregnancyhave a 33% chance of having FAS (Greenfield, Weiss, & Mirin, 1997). About3.1 per 1,000 first-grade students may show evidence of FAS in the UnitedStates (Clarren, Randels, Sanderson, & Fineman, 2001).TREATMENT PRIORITIESEstablishing a trusting therapeutic relationship is integral to treating the alcoholicpatient. A psychiatrist is in a strong position to develop a nonjudgmental,empathic relationship with alcoholic patients but, in addition, must be preparedto challenge denial and confront pathological behavior or regression. Thephysician’s awareness of the continuing incentive to drink, mediated bychronic stimulation of dopamine-rich pathways in the mesocortical system, willassist him or her in tolerating relapses and encouraging the patient to learnfrom relapses rather than either the patient or the clinician succumbing to asense of defeat. Alcoholism leads to impaired impulse control and an impairedpriority system; that is, the salience or importance of alcohol has become dominantfor the alcoholic patient, and the reversal of this priority is a slow, steady,day-by-day process.

98 III. SUBSTANCES OF ABUSEDemoralization is always a potential factor, but it can be effectively counteredby the doctor–patient relationship, combined with utilization of a supportsystem such as Alcoholics Anonymous. The development of negative countertransferenceon the part of the physician needs to be guarded against to theextent possible. Work with a sufficient number of alcoholic patients will demonstratethe heterogeniety of those who develop alcoholism and lead to thephysician’s ability to assist in recovery and witness the restoration of health, thereestablishment of effective work patterns, and the gratification of renewedrelationships.Detecting relapse is a treatment priority. The patient may report relapse, butoften this is not the case. Family members, employers, or other collateralsources may provide information that suggests relapse. Observations made bythe physician may indicate relapse. Biomarkers may be very useful in detectingrelapse—for example, an increase of 30% or more in GGT above a previouslyobtained value is likely to reflect relapse (Anton, Lieber, & CDTect StudyGroup, 2002). CDT may rise before other signs of relapse are apparent. Thereare few sources of false-positive results. An elevation can be expected if alcoholis consumed for 2 weeks at a level of five drinks (60 grams) per day (Schmidt etal., 1997). Early detection of relapse offers the potential to prevent a return toharmful or dependent drinking, as well as an opportunity to identify “triggers”that render an individual susceptible to relapse.Comorbidity with other psychiatric disorders is common in alcoholicpatients. This potential multiplicity of clinical problems raises questions aboutwhat condition is treated first, which setting, and what modalities. Severalguidelines can be offered.1. The issues of acuity and safety must receive priority (Nace, 1995). Apatient who presents as acutely suicidal would necessarily be placed in an inpatientsetting capable of offering close or constant observation. An acutely delusionalpatient would require the intensity of an inpatient psychiatric unit aswell. Addressing recovery issues would await psychotic stabilization.2. Alcohol-related and co-occurring disorders should be treated in parallelor synchronously. For example, a suicidal patient requiring the protection of alocked psychiatric unit may also require detoxification, simultaneous withefforts to protect him or her from self-harm.3. Sufficient time free of alcohol may clarify the issue of comorbidity.Alcohol-related anxiety and affective or psychotic disorders are expected toresolve in about 4 weeks, although clinical judgment is more appropriate thanfixed time intervals in determining whether symptoms are alcohol-related orpart of a comorbid condition. If symptoms abate as alcohol is withdrawn, thelikelihood of a co-occurring disorder diminishes. If symptoms persist, or if newsymptoms emerge in the absence of alcohol, a co-occurring disorder is likely.

5. Alcohol 99tion and management. Panic attacks occurring in association with alcohol mayrequire relief with alprazolam or other suitable drugs. Addressing acute symptomspharmacologically does not imply that an additional dependence will beestablished, or that alcohol dependence will be prolonged.5. Each disorder requires treatment. Severely depressed patients cannot beexpected to respond to 12-step programs or rehabilitation efforts if they are notsimultaneously receiving appropriate pharmacology and psychotherapy. Norwill a bipolar patient be likely to achieve stabilization if his or her alcoholism oralcohol abuse is not arrested. See Chapter 26, “Psychopharmacological Treatments,”for the mechanism and utility of the agents used in alcohol use disorders,including disulfiram, naltrexone, and acamprosate, all recently approvedfor use in the United States.CONCLUSIONAlcoholism is a disease that manifests itself through social, medical, legal, andfamily consequences. Alcohol dependence and alcohol abuse are amenable toreliable diagnostic criteria. Subjectively, the alcoholic struggles with prolongedcravings for the substance, fear of functioning without alcohol, and doubtsabout his or her ability to abstain, and hence to recover. Concomitant with theambivalent struggle to change, the alcoholic endures remorse, regret, guilt, andshame.The physician, if not cognizant of the protean manifestations of this disease,or if blinded to the suffering of the patient by the alcoholic’s often outrageousbehavior, may miss or decline to take the opportunity for a life-changingclinical encounter. On the other hand, the physician prepared for the diagnosisand treatment of addictive disorders will find clinical experiences that contradictthe pessimism often instilled during training years.The psychiatrist’s role in the treatment of alcoholism is especially pertinentgiven the significant issue of comorbidity and the biopsychosocial orientationof modern psychiatry. With an understanding of the overlapping relationshipsbetween substance use disorders and other psychiatric disorders, and anability to establish treatment priorities, the psychiatrist is in a unique positionto provide medical leadership to treat effectively this complex biopsychosocialdisorder.REFERENCESAdler, R. A. (1992). Clinically important effect of alcohol on endocrine function. J ClinEndocrinol Metab, 74, 957–960.

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CHAPTER 6TobaccoNORMAN HYMOWITZHISTORY AND OVERVIEW OF THE PROBLEMEarly BeginningsThe use of tobacco (Nicotine tobaccum) has been traced to early American civilizations,where it played a prominent role in religious rites and ceremonies.Among the ancient Maya, tobacco smoke was used as “solar incense” to bringrain during the dry season. Shooting stars were believed to be burning butts castoff by the rain god. The Aztecs employed tobacco (Nicotine rustica) as a powerthat was used in ceremonial rites as well as chewed as a euphoric agent withlime (Schultes, 1978).In 1492, Columbus and his crew observed natives lighting rolls of driedleaves, which they called tobacos (cigars), and “swallowing” the smoke (Schultes,1978). Twenty years later, Juan Ponce de Leon brought tobacco back to Portugal,where it soon was grown on Portuguese soil. Sir Walter Raleigh introducedsmoking to England in 1565, and the English, too, successfully grew tobacco(Vogt, 1982). The growth of world trade led to the spread of tobacco to everycorner of the globe.The popular “weed” was not without its detractors. James I of England publisheda counterblaste to tobacco in 1604, and he arranged a public debate on theeffects of tobacco in 1605. Pope Urban III condemned tobacco use in 1642,threatening excommunication of offenders. In Russia, a decree in 1634 punishedtobacco users by nose slitting, castration, flogging, and banishment.These harsh measures were abolished by Peter the Great, who took to smokinga pipe in an effort to open a window to the West. It is believed that the smok-105

106 III. SUBSTANCES OF ABUSEing of cigarettes first occurred in Mexico, where chopped tobacco was wrappedin corn husks (Van Lancker, 1977).The 19th CenturyThe most popular forms of tobacco used in the United States in the past werechewing tobacco and dipping snuff, as evidenced by spittoons in homes andpublic places. In the late 1800s, cigarette smoking grew in popularity. JamesBuchanan Duke brought Polish and Russian Jews to the United States to manufacturecigarettes in 1867, and he used advertising to enlighten Americansabout the pleasures of smoking. Cigarettes were first mass-produced in Durham,North Carolina, in 1884. Washington Duke used a newly invented cigarettemachine to produce some 120,000 cigarettes per day, thus ushering in the era ofcheap, abundant tobacco products for smoking, and setting the stage for 20thcenturyepidemics of lung cancer, emphysema, and coronary heart disease(Vogt, 1982).The “Cigarette Century”In 1900, the total consumption of cigarettes in the United States was 2.5 billion(U.S. Department of Health and Human Services, 1989b). Major advancesin agriculture, manufacturing, and marketing, the Great Depression, two worldwars, and changing cultural norms led to a marked increase in consumption.Total consumption increased from 2.5 billion in 1900 to 631.5 billion in 1980(U.S. Department of Health and Human Services, 1989b). Cigarette consumptionpeaked in 1981 (640 billion) but declined in 1987 to an estimated 574 billion,the equivalent of more than 6 trillion doses of nicotine (Jones, 1987). Anestimated 430 billion cigarettes were consumed in 2000 (U.S. Department ofAgriculture, 2001).Early Warning SignsThe decline in per capita cigarette consumption during the latter part of the20th century was due in large part to growing concerns about the adversehealth consequences of cigarette smoking and the growth of the anti-smokingmovement. Early case reports and case studies called attention to the likely roleof smoking and chewing tobacco as a cause of cancer (Samet, 2001). Key initialobservations were made in epidemiological studies carried out to examinechanging patterns of disease in the 20th century, particularly the dramatic risein lung cancer, coronary heart disease, and chronic obstructive lung disease(Samet, 2001). Dr. Luther Terry, who served as Surgeon General of the U.S.Public Health Service from 1961 to 1965, noted that the landmark 1964 Sur-

6. Tobacco 107geon General’s Advisory Committee Report, Smoking and Health, was the culminationof growing scientific concern over a period of more than 25 years(Terry, 1983). The report also recognized the “habitual” nature of tobacco usebut stopped short of recognizing tobacco use as an addiction.The Leading Preventable Cause of DeathAccording to the Centers for Disease Control and Prevention (2002), tobaccocauses approximately 440,000 deaths in the United States each year, making itthe leading preventable cause of death. Cigarette smoking accounts for about30% of all cancer deaths (87% of lung cancers) and is a major cause of heartdisease, cerebrovascular disease, chronic bronchitis, and emphysema (AmericanCancer Society [ACS], 2003). Tobacco use costs the U.S. economy nearly$150 billion in health costs and lost productivity each year (American LungAssociation [ALA], 2003). Smoking-related diseases cost the Medicare system$20.5 billion and Medicaid, the federal insurance program for the poor, $17 billionin 1997 (American Lung Association, 2003).Nicotine AddictionIt was not until 1988 that the addictive nature of cigarette smoking was formallyrecognized. Major conclusions from the 1988 Surgeon General’s report(U.S. Department of Health and Human Services, 1988) were as follows: (1)Cigarettes and other forms of tobacco are addicting; (2) nicotine is the drug intobacco that causes addiction; and (3) the pharmacological and behavioral processesthat determine tobacco addiction are similar to those that determineaddiction to drugs such as heroin and cocaine.The Anti-Smoking MovementKey events that contributed to the decline in the per capita consumption ofcigarettes in the United States were the banning of cigarette advertisements onthe air waves, increases in the excise tax on cigarettes, and evidence that secondhandsmoke harms nonsmokers. Mounting evidence of the dangers of environmentaltobacco smoke (ETS; Environmental Protection Agency [EPA],1992) served as a stimulus to advocate for smoke-free environments, and to supportpolicies and legislation to protect young people and adults from secondhandsmoke.The EPA report officially categorized ETS as a known human carcinogen,placing ETS in the Class A (most dangerous) category reserved for only a fewtoxic substances, including radon, benzene, and asbestos (Carlson, 1997). Thereport also identified ETS as a cause of serious respiratory illness in children,

108 III. SUBSTANCES OF ABUSEincluding bronchitis, asthmatic episodes, new cases of asthma, and suddeninfant death syndrome (SIDS). Nonsmokers exposed to ETS at work were 39%more likely to get lung cancer than nonexposed, nonsmoking workers (Carlson,1997).A Worldwide ProblemWhile tobacco consumption declined in the United States, global tobacco consumptionincreased, particularly in developing countries. According to theWorld Health Organization (WHO; 1999), cigarette smoking in developingcountries increased at a rate of about 3.4% per year. Worldwide tobacco-relateddeaths are expected to increase from about 4 million per year in 1999 to about10 million per year by the 2030s, with 70% of those deaths occurring in developingnations. This is a higher death toll than is expected from malaria, maternaland major childhood conditions, and tuberculosis combined (AmericanCancer Society, 2003).Big TobaccoIn response to mounting health concerns and declining demand, Big Tobaccospared little expense to fend off criticism and to assuage public concern. Cigaretteadvertising expenditures in the United States were estimated at more than$2 billion for 1985—twice the annual expenditures of the National CancerInstitute (American Cancer Society, 1986). In 1999, the five largest cigarettemanufacturers in the United States spent $8.24 billion on advertising and promotionalexpenditures (Federal Trade Commission, 2001), with additionalexpenditures for promoting and marketing cigarettes abroad.Safe CigarettesBig Tobacco used its vast resources to keep alive debates about whether cigarettesmoking is harmful or addictive, and whether secondhand smoke poses a dangerto nonsmokers. Tobacco companies also responded to mounting health concernsby designing and marketing safer cigarettes. They introduced cigarette filters,menthol flavoring, light and ultralight brands, and, most recently, high technologycigarettes, such as Omni, Advance, Eclipse, Accord, Quest, and, soon tobe released, the Phillip Morris product, SCOR. Innovations in manufacturingand design were heralded by expensive marketing campaigns, fostering theimpression that new and improved cigarettes offered satisfaction, flavor, andpeace of mind (Burns & Benowitz, 2001). Today, more than 80% of the cigarettessold in the United States are of the low-tar and low-nicotine variety(Myers, 2002), and most smokers believe light and ultralight cigarettes are lessharmful than regular cigarettes (Giovino et al., 1996).

6. Tobacco 109Smokers are wrong about the safety of low-tar and low-nicotine cigarettes(Burns & Benowitz, 2001), and the new high-technology cigarettes similarlyare likely to fall far short of the mark (Slade, Connolly, & Lymperis, 2002). A20-year study by the American Cancer Society showed that smokers whosmoked light and ultralight cigarettes experienced the same rates of lung cancerand heart disease as smokers who smoked regular cigarettes (Burns & Benowitz,2001). This was due in part to compensatory smoking patterns by smokers seekingto regulate nicotine intake, the elastic nature of newly designed cigarettesthat facilitate compensation, differences in machine-measured and biologicallymeasured yields of tar and nicotine, and deceptive marketing and labeling practices(Kozlowski, O’Connor, & Sweeney, 2001).The tactic of heralding new cigarette designs by sophisticated marketingcampaigns proved equally effective with youthful smokers. R. J. Reynolds carriedout a highly successful campaign in the 1980s and 1990s to promote theCamel brand among young people. The combination of a less harsh cigarette,sweetened to appeal to youthful tastes, and the Smooth Moves Joe Camel advertisingcampaign led to demonstrated share growth, moving progressively from2.5% of the market in 1987, to 4.0% in 1988, to 4.4% in 1989, and to 6.1% in1990 (Wayne & Connolly, 2002). Ultimately, Camel became one of the threeleading brands, along with Marlboro and Newport, which today account formore than 80% of adolescent smoking.The Challenge AheadBy the end of the 20th century, the stage was set for a life or death strugglebetween Big Tobacco and the public health community over the fate of the nextgeneration of smokers. Both parties are aware that most adults begin smoking asyouth, and if people do not start smoking by their late teens, they are unlikelyto smoke as adults (Lynch & Bonnie, 1994). Big Tobacco must recruit anothergeneration of young people to stay in business, and the public health communitymust thwart its efforts.While smoking rates in the United States have declined since the mid-1960s, much work remains. The United States failed to meet the Healthy People2000 goals for tobacco prevention and control, and smoking initiation ratesamong middle and high school students increased dramatically in the 1990s(Bonnie, 2001). In 1996, more than 1.8 million people became daily smokers inthe United States, two-thirds of them (1.2 million) under age 18 (Bonnie,2001). Rates of cigarette smoking and use of other forms of tobacco alsoincreased among college students (18–21 years old), the youngest legal targetfor tobacco advertising dollars (Rigotti, Lee, & Wechsler, 2000). According toa recent survey, 46% of college students reported using tobacco products in thepast year, and more than 25% of them started smoking for the first time whilein college (Wechsler, Kelley, Seibring, Kuo, & Rigotti, 2001).

110 III. SUBSTANCES OF ABUSEDEFINITIONSHenningfield (1986) compared tobacco dependence to other forms of drugdependence and concluded that there are more similarities than differences. Henoted that (1) tobacco dependence, like other forms of drug dependence, is acomplex process, involving interactions between drug and nondrug factors; (2)tobacco dependence is an orderly and lawful process governed by the same factorsthat control other forms of drug self-administration; (3) tobacco use, likeother forms of drug use, is sensitive to dose manipulation; (4) development oftolerance (diminished response to repeated doses of a drug or the requirementfor increasing the dose to have the same effect) and physiological dependence(termination of nicotine followed by a syndrome of withdrawal phenomena)when nicotine is repeatedly administered is similar to the development of toleranceand dependence of other drugs of abuse; and (5) tobacco, like many othersubstances of abuse, produces effects often considered a utility or benefit to theuser (e.g., relief of anxiety or stress, avoidance of weight gain, alteration inmood).Although the similarities between tobacco or nicotine dependence andother forms of drug dependence are noteworthy, there are features of tobaccouse that make it unique. In contrast to many other drugs of abuse, tobacco productsare legal and readily available. When used as intended, tobacco productslead to disease and death. Unlike alcohol, a legal drug that can be consumedsocially and in moderation without ill effects, all levels of tobacco use are harmful(U.S. Department of Health and Human Services, 1988).Large sums of money are spent each year to advertise and market tobaccoproducts, particularly cigarettes. This adds an important dimension to tobaccodependence not present to the same degree with other substances, with the possibleexception of alcohol. Few children in our society grow up free of BigTobacco’s reach, which provides unique opportunities for the tobacco companiesto teach them about the virtues of tobacco, the manner in which it shouldbe used, and the role it should play in their daily lives. So pervasive is the positiveimagery associated with cigarette smoking that it is almost impossible todistinguish between the reinforcing qualities of cigarettes that derive from pastconditioning and learning and those that derive solely from nicotine.DIAGNOSISAccording to the fourth edition of the Diagnostic and Statistical Manual of MentalDisorders (DSM-IV; American Psychiatric Association, 1994), nicotinedependence is considered to be a substance-related disorder. The key features ofsubstance dependence are a cluster of cognitive, behavioral, and physiologicalsymptoms indicating that the individual continues use of the substance despite

6. Tobacco 111significant substance-related problems. There is a pattern of repeated selfadministrationthat usually results in tolerance, withdrawal, and compulsivedrug-taking behavior (American Psychiatric Association, 2000).The diagnosis of nicotine dependence in DSM-IV is fairly straightforward.Information needed to make the diagnosis can be obtained through interviewand questionnaire, and can readily be collected along with other medical historydata. Two National Institutes of Health publications (U.S. Department ofHealth and Human Services, 1986, 1989a), a report prepared by the AmericanPsychiatric Association (1996), and a recently published clinical practiceguideline (Fiore et al., 2000) are available to help physicians inquire aboutsmoking, assess their patients’ needs, and encourage patients to quit smoking.Most of the criteria for psychoactive substance dependence are characteristicof cigarette smoking and other forms of tobacco use. Cigarette smokers oftensmoke more than they intend to, have difficulty quitting or simply cuttingdown, spend a great deal of time procuring cigarettes and smoking them, persistin smoking despite known risk and/or current illness, and readily develop tolerance,enabling them to smoke a larger number of cigarettes per day than theydid when they first started smoking. The fact that most smokers who quit smokingin the past did so on their own, without formal treatment, seems to besomewhat at odds with the popular notion of addiction. However, it is importantto note that most former heroin users also gave up heroin without formaltreatment (Johnson, 1977).When smokers, adolescents as well as adults, stop smoking, they may experiencenicotine withdrawal as defined by DSM-IV-TR (American PsychiatricAssociation, 2000). About 50% of adults who attempt to stop smoking willmeet DSM-IV criteria for nicotine dependence (American Psychiatric Association,1996), and young smokers show signs of addiction within several monthsof taking up the habit (DiFranza et al., 2002). Diagnostic criteria for nicotinewithdrawal are presented in DSM-IV-TR. Associated features include craving,a desire for sweets, and impaired performance on tasks requiring vigilance(American Psychiatric Association, 2000). Depression and difficulty sleepingare not uncommon. Associated laboratory findings include a slowing on electroencephalograph,decreases in catecholamine and cortisol levels, rapid eyemovement (REM) changes, impairment on neuropsychological testing, anddecreased metabolic rate (American Psychiatric Association, 2000). Nicotinewithdrawal also may be associated with a dry or productive cough, decreasedheart rate, increased appetite or weight gain, and a dampened orthostaticresponse (American Psychiatric Association, 2000).When smokers quit smoking, there is a fairly high probability that theywill return to smoking (relapse). Smokers often quit many times before theysucceed in remaining abstinent. Relapse is most likely to occur soon after quitting.Studies of quit-smoking programs show that most smokers relapse withinabout 3 months (Hunt & Bespalec, 1974). Although ex-smokers are less likely

112 III. SUBSTANCES OF ABUSEto relapse after they have been abstinent for 3 months, the potential for relapseremains present for many years (Ockene, Hymowitz, Lagus, & Shaten, 1991).CLINICAL FEATURESUnder normal circumstances, cigarette smoking and other forms of tobacco usedo not cause obvious states of intoxication, nor does their chronic use lead toorganic brain damage, although acute effects of nicotine may affect vigilanceand memory (U.S. Department of Health and Human Services, 1988). Overdosetypically is not a problem, and acute effects of nicotine on health havereceived less attention than chronic effects in the medical literature.A number of poisonings and deaths from ingestion of nicotine, primarilyinvolving nicotine-containing pesticides, have been reported, and acute intoxicationhas been observed in children after swallowing tobacco materials (U.S.Department of Health and Human Services, 1988). The lethal oral dose of nicotinein adults has been estimated at 40–60 mg (U.S. Department of Healthand Human Services, 1988). Nicotine intoxication produces nausea, vomiting,abdominal pain, diarrhea, headaches, sweating, and pallor. More severe intoxicationresults in dizziness, weakness, and confusion, progressing to convulsions,hypotension, and coma. Death is usually due to paralysis of respiratory musclesand/or central respiratory control (U.S. Department of Health and Human Services,1988).As noted previously, the chronic effects of cigarette smoking take a massivetoll. The role of cigarette smoking in the pathogenesis of coronary heartdisease, lung and other cancers, and chronic obstructive lung disease, as well asmany other forms of illness, has been dramatically documented in a series ofreports by U.S. surgeons general dating back to 1964 (U.S. Public Health Service,1964). Cigarette smoking has been cited as the chief avoidable cause ofdeath and morbidity in our society, and the number one public health problemof our time (U.S. Department of Health and Human Services, 1989b).The problems of cigarette smoking and tobacco-related diseases are notlimited to the United States. Worldwide, approximately 1.1 billion people ages15 and older smoke; 300 million live in developed countries, and 800 million indeveloping countries. About one-third of the world’s adults smoke. Four millionpeople die yearly from tobacco-related disease, one death every 8 seconds.If current trends continue, the toll will rise to 10 million by 2030, one deathevery 3 seconds (World Health Organization, 1999).The acute effects of nicotine also are important, having been implicated insudden heart attack death and stroke (Black, 1990). Cigarette smoking andother forms of tobacco use are contraindicated in patients with heart disease,hypertension, diabetes, chronic obstructive lung disease, and diseases of the gastrointestinaltract, for fear that nicotine and other components of tobacco will

6. Tobacco 113exacerbate existing illness as well as contribute to progressive pathogenesis,according to the U.S. Department of Health, Education, and Welfare (DHEW;1979). Direct effects of nicotine on heart rate, cerebral blood flow, blood pressure,platelet aggregation, and fibrinogen are just a few of the mechanisms bywhich nicotine and cigarette smoking exert acute influences on health andwell-being (Black, 1990).Evidence of the harmful effects of cigarette smoking also may be observedin smokers in whom frank disease has not yet developed. Shortness of breath,cough, excessive phlegm, and nasal catarrh are common symptoms that readilysubside when smokers stop smoking (U.S. Department of Health, Education,and Welfare, 1979). Smokers often report a dulling of the senses of taste andsmell, and smokers, as well as their family members, generally experience morecolds and illness than nonsmokers (U.S. Department of Health, Education, andWelfare, 1979). Tobacco smoke and products may interact with other drugsthat patients are taking (Pharmacists’ “Helping Smokers Quit” Program, 1986).Drugs that show the most significant interactions with tobacco smoke includeoral contraceptives, theophylline, propranolol, and other antianginal drugs.Drugs with moderately significant clinical interactions with smoking includepropoxyphene, pentazocine, phenylbutazone, phenothiazine, tricyclic antidepressants,benzodiazepines, amobarbital, heparin, furosemide, and vitamins(Pharmacists’ “Helping Smokers Quit” Program, 1986).Bansil, Hymowitz, and Keller (1989) showed that outpatients with schizophreniawho smoked cigarettes required significantly more neuroleptic medicationto control psychiatric symptoms than comparable nonsmokers, despite thefact that the patients were identical with respect to initial severity of illness.Multivariate analyses showed that the difference between the groups was notdue to age, weight, sex, alcohol consumption, or tea–coffee intake. In view ofthe side-effects profile of many drugs used in psychiatry, and the fact that theprevalence of tardive dyskinesia may be higher in mentally ill patients whosmoke than in patients who do not smoke (Yassa, Lal, Korpassy, & Ally, 1987),it is important to achieve clinical effectiveness with as low a dose as possible.Cigarette smoking compromises this important goal.Cigarette smoking, other forms of tobacco use, and ETS adversely affectthe health and vitality of the young (American Academy of Pediatrics, 2001).Smoking by pregnant women may lead to low birthweight, preterm delivery,birth defects, and death of the fetus, and exposure to ETS following birthincreases the risk of SIDS, respiratory distress, ear infections, and asthma(American Academy of Pediatrics, 2001). The initiation of cigarette smokingpredisposes youth to a lifetime of addiction and tobacco-related disease (Samet,2001).The evidence clearly indicates that smokers benefit in many ways whenthey stop smoking (U.S. Department of Health and Human Services, 1990).Carbon monoxide is eliminated from their systems within 24 hours, and within

114 III. SUBSTANCES OF ABUSEa few months, ex-smokers report a lessening of pulmonary symptoms, such asshortness of breath, cough, phlegm, and nasal catarrh. Their senses of taste andsmell return, peripheral vascular circulation improves, and ex-smokers mayexperience an improvement in small-airway disease and a slowing in the rate ofdecline of pulmonary function. Most important, risk of serious disease and prematuredeath declines markedly over the course of several years followingsmoking cessation, and in people already disabled by frank disease, prospects forrecovery improve greatly (U.S. Department of Health, Education, and Welfare,1979).COURSECigarette smoking starts at an early age, usually in response to peer pressureand/or curiosity (Lynch & Bonnie, 1994). The younger the age of initiation,the greater the risk of habitual smoking (Burt, Dinh, Peterson, & Sarason,2000). Social and environmental factors, personal characteristics, expectationsof personal effects of smoking, and biological factors influence the initiation ofsmoking (U.S. Department of Health and Human Services, 2001). A sizableproportion (one-third or more) of children as young as 9 years old have engagedin experimental “puffing,” and there is a steady rise with age in the proportionof children who report smoking (Oei & Fea, 1987). Among American childrenage 13 years and older, only about one-third of those surveyed had not at leastpuffed a cigarette (Chassin et al., 1981).The rate of progression from experimentation to established smoking isabout 32% (Choi, Ahluwalia, Harris, & Okuyemi, 2002). Receptivity totobacco advertisements and promotions (Sargent et al., 2000), the belief that “Ican quit smoking whenever I want” (Choi et al., 2002), and a propensity to risktaking and rebelliousness (Burt et al., 2000) are among a host of variables thatdistinguish between youth who progress to established smoking and those whodo not. Other risk factors for youth progressing to regular smoking include relativelylow grades in school, low behavioral self-control, high susceptibility topeer influence, and the belief that they would not be in trouble if their parentsknew they were smoking (Jackson, Henricksen, Dickinson, Messer, & Robertson,1998).By age 14 or 15, cigarette smoking is an established pattern, and littleexperimentation takes place thereafter (Aitken, 1980). Approximately 60% ofhigh school smokers report that they tried to stop smoking in the past year(Centers for Disease Control and Prevention, 2001). Unfortunately, they sufferfailure and relapse rates that exceed those of adults (Ershler, Leventhal, Fleming,& Glynn, 1989). Most adolescent smokers will smoke well into adulthoodbefore they are able to quit (Pierce & Gilpin, 1996).

6. Tobacco 115Substance use, in general, increases between adolescence and young adulthood,then declines in the mid-20s. Individuals may discontinue substance usein adulthood, because the responsibilities and demands of marital, occupational,and parental roles are incompatible with substance use (Yamaguchi &Kandel, 1985). Chassin, Presson, Rose, and Sherman (1996) reported that agerelatedtrends for cigarette smoking paralleled those for other drugs in showinga significant increase between adolescence and young adulthood. However,unlike other forms of drug use, there was no significant decline in cigarettesmoking in the late 20s. The persistence of cigarette smoking into the late 20s(and beyond) may be due to three factors: (1) Nicotine dependence may contributeto low cessation rates; (2) the negative health impact of cigarette smokingmay not be encountered until later ages; and (3) because smoking is a legalbehavior whose pharmacological effects are not incompatible with the day-todaydemands of adult roles, role socialization pressure for cessation may be lessintense (Chassin et al., 1996).Although psychosocial factors play a major role in smoking onset and progressionto established smoking in adolescence, addiction to nicotine also is ofparamount importance. Recent studies (DiFranza et al., 2002) suggest that childrenshow signs of nicotine dependence within a matter of months of exposure,far quicker than heretofore imagined. Like adults, young people have difficultystopping smoking (Burt & Peterson, 1998; Green, 1980). The reasons for thisdifficulty—social pressure, urges, and withdrawal symptoms—implicate behavioralfactors and dependence on tobacco (Biglan & Lichtenstein, 1984).Hansen (1983) studied abstinence and relapse in high-school-age smokers (16–18 years old) who smoked an average of 15–20 cigarettes per day. Most studentswho quit smoking relapsed within 3 months. Variables that predicted relapsewere the number of cigarettes smoked per day and the regularity of a teenager’ssmoking pattern—findings indicative of tobacco dependence.The early initiation of smoking is of considerable concern to the publichealth community. The pathogenesis of diseases such as chronic obstructivelung disease and atherosclerotic heart disease begins early in life, and durationof exposure to tobacco contributes to the likelihood of suffering adverse consequencesas an adult (U.S. Department of Health, Education, and Welfare,1979). However, it is not necessary to wait until adulthood to see signs ofimpaired health. Seely, Zuskin, and Bouhuys (1971) reported that cough,phlegm, and shortness of breath were more common among high school studentswho smoked than among nonsmokers, with no significant differencesbetween sexes. Pulmonary function testing showed that maximum ventilation(V max) at both 50% and 25% vital capacity (midmaximal flow rates, respectively)were significantly below expected levels in boys who smoked more than15 cigarettes per day and in girls who smoked more than 10 cigarettes per day(Seely et al., 1971). The authors concluded that regular smoking for 1–5 years

116 III. SUBSTANCES OF ABUSEis sufficient to cause demonstrable decreases in lung function (see also U.S.Department of Health and Human Services, 1994a).After high school, there is a gradual transition to regular adult smokinglevels, and the relative influence of dependence on nicotine increases (Sachs,1986). For most, smoking rates will hover around one pack per day and remainquite stable for most of their adult lives. Others will progress to higher smokingrates, again revealing marked day-to-day stability in nicotine ingestion.Tobacco dependence shows many features of a chronic disease (Fiore et al.,2000). Although a minority of tobacco users achieves permanent abstinence inan initial quit attempt, the majority persists in tobacco use for many years andtypically cycle through multiple periods of relapse and remission. More than70% of the 50 million smokers in the United States in 2000 had made at leastone prior quit attempt, and approximately 46% try to quit each year (Fiore etal., 2000). About 2% per year succeed (U.S. Department of Health and HumanServices, 1989b), with most making a number of attempts before succeeding.Nearly half of all living adults who ever smoked have quit (U.S. Departmentof Health and Human Services, 1989b), and most did so “on their own”(Schachter, 1982).DIFFERENTIAL DIAGNOSISThe diagnosis of nicotine dependence is relatively straightforward, particularlyin adults. Most adults admit that they smoke cigarettes, and they typicallysmoke on a daily basis. For adolescents and teens, smoking may not occur on adaily basis. The physician should ask them if they ever smoked and how frequentlythey smoke. If they do not smoke, or smoke only on occasion, the physicianshould inquire about expectations for smoking in the future. Older teens,of course, are more likely to report that they smoke on a daily basis, althoughthe number of cigarettes smoked per day may be fewer than those smoked byadults.The clinician often wishes to determine the severity of tobacco dependence,because such information provides insight into how difficult it will be forthe smoker to quit and what kind of quitting strategy will be most effective.Fagerstrom (1978) developed a brief nicotine dependence questionnaire.Among the most discriminating questions are the following: “How soon afteryou wake up do you smoke your first cigarette?”, “How many cigarettes a day doyou smoke?”, and “Have you stopped smoking or tried to stop smoking in thepast?” (Kozlowski et al., 1989).Heavy smokers, those who smoke soon after waking, and those who havenever quit smoking in the past are least likely to quit smoking on their own orwith assistance (cf. Hymowitz et al., 1997). They are the smokers who are mostlikely to benefit from nicotine replacement therapy (NRT) and other pharma-

6. Tobacco 117cological aids (Fagerstrom, 1988). Smokers with psychiatric illness such asschizophrenia, alcoholism, and depression also have an extremely difficult timequitting smoking (Glassman, 1993; American Psychiatric Association, 1996),and for smokers who succeed in quitting, negative affect and stress play a majorrole in smoking relapse (Shiffman, 1986).Youth Smoking RatesETHNICITYFindings from the Year 2000 National Youth Tobacco Survey indicate that currenttobacco use ranges from 15.1% among middle school students (17.6%,male; 12.7%, female) to 34.5% among high school students (39.1% male;29.8%, female; Centers for Disease Control and Prevention, 2001). Cigarettesmoking is the most prevalent form of tobacco use, followed by cigar smokingand smokeless tobacco use.Approximately one-half of current cigarette smokers in middle school andhigh school reported that they smoked Marlboro cigarettes. Black students weremost likely to smoke Newport (Centers for Disease Control and Prevention,2001). White (14.3%), black (17.5%), and Hispanic (16.0%) middle schoolstudents were significantly more likely than Asian (7.5%) middle school studentsto use any tobacco products. Among current users, cigarettes were themost prevalent form of tobacco used (11.0% of students). White (10.8%), black(11.2%), and Hispanic (11.4%) middle school students were significantly morelikely than Asian (5.3%) middle school students to smoke cigarettes. There waslittle difference in rates of cigarette smoking for male (11.7%) and female(10.2%) students (Centers for Disease Control and Prevention, 2001).Nationally, 34.5% of high school students were current users of anytobacco product. White students (38.0%) were significantly more likely thanblack (26.5%), Hispanic (28.4%), or Asian (22.9%) students to use tobaccoproducts (Centers for Disease Control and Prevention, 2001). Cigarettes werethe most prevalent form of tobacco (28.0%), with white students (31.8%) significantlymore likely than blacks (16.8%), Hispanics (22.6%), or Asians(20.6%) to smoke cigarettes. Male (28.8%) and female (27.3%) high schoolstudents smoked about the same number of cigarettes per day (Centers for DiseaseControl and Prevention, 2001).Adult Smoking RatesIn 2000, an estimated 46.5 million adults (23.3%) were current smokers (Centersfor Disease Control and Prevention, 2002). The prevalence of smoking washigher among men (25.7%) than among women (21.0%). Among racial/ethnicgroups, Asians (14.4%) and Hispanics (18.6%) had the lowest prevalence of

118 III. SUBSTANCES OF ABUSEadult cigarette use. Native Americans/Alaska Natives had the highest prevalence(36.0%). The smoking rates for whites and blacks were 24.1% and 23.2%,respectively, and the rates of smoking among adult men and women were similar(white: 25.9% and 22.4%, respectively; black: 26.1% and 20.9%, respectively).For Hispanics and Asians, adult men smoked at considerably higherrates than adult women (24.0%, Hispanic men; 13.3%, Hispanic women;21.0%, Asian men; 7.6%, Asian women). For Native Americans/AlaskaNatives, the opposite relationship held (29.1%, men; 42.5%, women; Centersfor Disease Control and Prevention, 2002).Adults who had earned a General Educational Development (GED)diploma had the highest prevalence of smoking (47.2%). Persons with master’s,professional, and doctoral degrees had the lowest prevalence (8.4%). The prevalenceof current smoking was higher among adults living below the povertylevel (31.7%) than those at or above the poverty level (22.9%) (CDC, 2002).In 2000, an estimated 44.3 million adults (22.2%) were former smokers,representing 24 million men and 19.7 million women (Centers for DiseaseControl and Prevention, 2002). Among smokers, 70.0% reported that theywanted to quit smoking completely; an estimated 15.7 million (41.0%) hadstopped smoking for one or more days during the preceding months becausethey were trying to quit; and 4.7% of smokers who had smoked every day orsome days during the preceding year quit and maintained abstinence for 3–12months in 2000. The percentage of ever smokers who had quit varied sharplyby demographic group. By race/ethnicity, the percentage of persons who hadever smoked and had quit was highest for whites (51.0%) and lowest for non-Hispanic blacks (37.3%; Centers for Disease Control and Prevention, 2002).Although blacks have not quit smoking at the same rate as the generalpopulation (cf. Fiore, Novotny, Pierce, et al., 1990), data from large smokingintervention studies (e.g., Multiple Risk Factor Intervention Trial [MRFIT];Hymowitz, Sexton, Ockene, & Grandits, 1991; Community Intervention Trialfor Smoking Cessation [COMMIT]; Hymowitz et al., 1995) revealed comparablequit rates for blacks and whites. Variables that emerged as significant predictorsof smoking cessation in these studies were older age, higher income, lessfrequent alcohol intake, lower levels of daily cigarette consumption, longertime to first cigarette in the morning, initiation of smoking after age 20, morethan one previous quit attempt, a strong desire to stop smoking, absence ofother smokers in the household, and male gender.PHARMACOLOGYNicotine is a tertiary amine composed of a pyridine and a pyrolidine ring(DHHS, 1988). Absorption of nicotine across biological membranes dependson pH. Modern cigarettes produce smoke that is suitably flavored and suffi-

6. Tobacco 119ciently nonirritating to be inhaled deeply into lung alveoli (Jones, 1987).When tobacco smoke reaches the small airways and alveoli of the lung, the nicotineis readily absorbed. The rapid absorption of nicotine from cigarette smokein the lung occurs because of the huge surface area of the alveoli and small airways,and because of the dissolution of nicotine at physiological pH, whichfacilitates transfer across cell membranes. Concentrations of nicotine in bloodrise quickly during cigarette smoking and peak at its completion (U.S. Departmentof Health and Human Services, 1988).Chewing tobacco, snuff, and nicotine polacrilex gum have an alkaline pHas a result of tobacco selection and/or buffering with additives by the manufacturer.The alkaline pH facilitates absorption of nicotine through mucous membranes.The rate of nicotine absorption from smokeless tobacco depends on theproduct and the route of administration. With fine-ground nasal snuff, bloodlevels of nicotine rise almost as fast as after cigarette smoking. The rate of nicotineabsorption with the use of oral snuff, chewing tobacco, and nicotinepolacrilex gum is more gradual (U.S. Department of Health and Human Services,1988). Transdermal nicotine provides a stable source of nicotine, whilenew products, such as the nicotine nasal spray and inhaler, deliver a quickerbolus of nicotine to the brain that more closely matches what happens when acigarette is inhaled. Swallowed nicotine is poorly absorbed because of the highacidity of the gut.Nicotine inhaled in tobacco smoke enters the blood very rapidly, withuptake into the brain occurring within 1–2 minutes. After smoking, the actionof nicotine on the brain occurs very quickly. The rapid onset of effects after apuff is believed to provide optimal reinforcement for the development of drugdependence (U.S. Department of Health and Human Services, 1988). Theeffects of nicotine decline after it is distributed to other tissues. The distributionhalf-life, which describes the movement of nicotine from the blood and rapidlyperfused tissues to other body tissues, is approximately 9 minutes (U.S. Departmentof Health and Human Services, 1988).After absorption into the blood, which is at pH 7.4, about 69% of the nicotineis ionized and 31% is nonionized. Binding to plasma protein is less than5%. The drug is distributed to body tissues with a steady-state volume of distributionaveraging 180 liters. Spleen, liver, lungs, and brain have a high affinityfor nicotine, whereas the affinity of adipose tissue is very low (U.S. Departmentof Health and Human Services, 1988). Nicotine-binding sites or receptors inthe brain have been identified and differentiated as very-high-affinity, highaffinity,and low-affinity types (U.S. Department of Health and Human Services,1988). The most intense localization of labeled nicotine has been foundin the interpeduncular nucleus and medial habenula.Nicotine is extensively metabolized, primarily in the liver, but also to asmall extent in the lung. Renal excretion of unchanged nicotine depends onurinary pH and urine flow, and may range from 2 to 35% but typically accounts

120 III. SUBSTANCES OF ABUSEfor 5–10% of elimination (U.S. Department of Health and Human Services,1988).The relationship between the dose of nicotine and the resulting response(dose–response relationship) is complex and varies with the specific responsethat is measured. Nicotine is commonly thought of as an example of a drug thatin low doses causes ganglionic stimulation and in high doses causes ganglionicblockade (U.S. Department of Health and Human Services, 1988). At very lowdoses, similar to those seen during cigarette smoking, cardiovascular effectsappear to be mediated by the central nervous system, either through activationof chemoreceptor afferent pathways or by direct effects on the brainstem. Thenet result is sympathetic neural discharge, with an increase in blood pressureand heart rate. At higher doses, nicotine may act directly on the peripheral nervoussystem, producing ganglionic stimulation and the release of adrenalcatecholamine. With high doses or rapid administration, nicotine produceshypotension and slowing of heart rate, mediated by either peripheral vagal activationor direct central depressor effects (U.S. Department of Health andHuman Services, 1988).Humans and other species readily develop tolerance of the effects of nicotine.Studies of tolerance to nicotine on in vitro tissue preparations may be summarizedas follows: (1) With repeated dosing, responses diminish to nearly negligiblelevels; (2) after tolerance occurs, responsiveness can be restored byincreasing the size of the dose; and (3) after a few hours without nicotine,responsiveness is partially or fully restored (U.S. Department of Health andHuman Services, 1988). It is apparent that cigarette smokers reveal evidencefor both acute tolerance (tachyphylaxis) and chronic tolerance to nicotine.This is consistent with the fact that smokers increase their tobacco consumptionand intake of nicotine with experience (chronic tolerance). When smokersabstain for a while, the first few cigarettes they smoke produce a variety ofbodily symptoms. Thereafter, they quickly become less sensitive (acute tolerance).Tolerance may be related to an increase in central nicotine-binding sitesor to a decrease in the sensitivity of the sites (U.S. Department of Health andHuman Services, 1988).ACTIONS OF NICOTINE ON THE BRAINThe nicotine molecule is shaped like acetycholine (Benowitz, 2001). Nicotineactivates certain cholinergic receptors in the brain that would ordinarily beactivated by acetylcholine. By activating cholinergic receptors, nicotine enhancesthe release of neurotransmitters and hormones, including acetylcholine,norepinephrine, dopamine, vasopressin, serotonin, and beta-endorphin. Thecholinergic activation leads to behavioral arousal and sympathetic neural activation.The release of specific neurotransmitters has been specifically linked to

6. Tobacco 121particular reinforcing effects of nicotine. Enhanced release of dopamine, norepinephrine,and serotonin may be associated with pleasure, mood elavation,and appetite suppression. Release of acetycholine may be associated withimproved performance on behavioral tasks and improvement of memory, andthe release of beta-endorphin may be associated with the reduction of anxietyand tension (Benowitz, 2001).CLINICAL PRACTICE GUIDELINESPhysicians have a unique role to play in the anti-smoking arena (Sullivan,1991). Past reviews (Orleans, 1993), monographs (U.S. Department of Healthand Human Services, 1994b), and guidelines (American Psychiatric Association,1996) underscore the importance of physician intervention on smoking ina variety of medical settings. The Public Health Service–sponsored ClinicalPractice Guideline, Treating Tobacco Use and Dependence (Fiore et al., 2000),provides clinical and systems interventions that are intended to increase thelikelihood of successful quitting. The major findings and recommendations maybe summarized as follows:1. Tobacco dependence is a chronic condition that often requires repeatedintervention. However, existent effective treatments can produce longtermor even permanent abstinence.2. Because effective tobacco dependence treatments are available, everypatient who uses tobacco should be offered at least one of these treatments:• Patients willing to try to quit tobacco should be provided treatmentsidentified as effective.• Patients unwilling to try to quit tobacco use should be provided a briefintervention designed to increase their motivation to quit.3. It is essential that clinicians and health care delivery systems institutionalizethe consistent identification, documentation, and treatment of everytobacco user seen in a health care setting.4. Brief tobacco treatment is effective, and every patient who uses tobaccoshould be offered at least brief treatment.5. There is a strong dose–response relation between the intensity oftobacco counseling and its effectiveness. Treatments involving person-topersoncontact (via individual, group, or proactive telephone counseling) areconsistently effective, and their effectiveness increases with treatment intensity(e.g., minutes of contact).6. Three types of counseling and behavioral therapies were found to be especiallyeffective and should be used with all patients attempting tobacco cessation:

122 III. SUBSTANCES OF ABUSE• Provision of practical counseling (problem-solving/skills training).• Provision of social support as part of treatment (intratreatment socialsupport).• Help in securing social support outside of treatment (extratreatmentsocial support).7. Numerous effective pharmacotherapies for smoking cessation now exist.Except in the presence of contraindications, these should be used with allpatients attempting to quit smoking.Five first-line pharmacotherapies were identified that reliably increaselong-term smoking abstinence rates: bupropion SR (slow release), nicotinegum, nicotine inhaler, nicotine nasal spray, and nicotine patch. The guidelinesalso concluded that combining the nicotine patch (a passive form of dosingthat produces relatively stable levels of drug in the body) with a selfadministeredform of nicotine replacement (nicotine gum or nasal spray) ismore efficacious than a single form of NRT.Two second-line pharmacotherapies were identified as efficacious and maybe considered by clinicians if first-line pharmacotherpies are not effective:clonidine and nortriptyline.PREVENTION OF SMOKINGThe prevention of tobacco use in children and adolescents requires a multiprongedapproach that targets the social environment, as well as individualbehaviors (Bonnie, 2001; Lantz et al., 2000; Lynch & Bonnie, 1994; U.S.Department of Health and Human Services, 1994a). Individual behaviorchange strategies include school-based prevention programs, computer-basedsystems, and peer-based interventions (Lantz et al., 2000). Pediatricians andother health professionals also have an important role to play in preventingsmoking initiation (Hymowitz, Schwab, & Eckholdt, 2001). Sussman,Lichtman, Ritt, and Pallonen (1999) reported that average reductions in smokingonset among youth generated by school-based prevention programs wasabout 6%, with a range of 0 to 11%. Programs that focused on teaching youngpeople resistance skills to deal with social and other influences to smoke weremost successful and had a longer lasting impact (Lantz et al., 2000). At theenvironmental level, mass media campaigns and policies aimed at restrictingaccess to cigarettes, increasing the price of cigarettes, restricting cigaretteadvertising, and creating smoke-free facilities decrease smoking initiation inyoung people (Lantz et al., 2000).Community interventions target multiple systems, institutions, or channelssimultaneously to influence individual behaviors and community norms.

6. Tobacco 123The results of a small number of controlled trials of community interventionattest to their ability to have a positive effect on youth smoking behavior. Theeffectiveness of school-based interventions is enhanced when they are includedin a broad-based community effort, and the impact of community interventionsmay be enhanced if they are combined with strong advocacy, taxation, media,and policy interventions (Lantz et al., 2000).PSYCHOPHARMACOTHERAPYGeneral ConsiderationsThere are numerous approaches to smoking cessation and many comprehensivereviews of the literature (e.g., Hymowitz, 1999; Lando, 1993; Leventhal &Cleary, 1980; Schwartz, 1987). Although many approaches to smoking cessationhave been successful in the short run, few, if any, have proved satisfactoryin the long term. This is true for traditional group and individual counselingprograms, hypnosis and acupuncture, self-help stop-smoking strategies, multicomponentbehavioral interventions, and pharmacological therapies (Hunt &Bespalec, 1974; Hymowitz, 1999; Yudkin et al., 2003). The tendency of smokersto quit, relapse, and quit highlights the cyclic nature of the quitting processand serves as a reminder that as much care and effort must go into helpingsmokers remain cigarette-free as into helping them stop smoking in the firstplace.Youth Smoking CessationEfforts to help adolescents quit smoking have received relatively little attention.Studies suggest that teenagers who smoke on a daily basis; who wereunable to quit in the past for an extended period of time; who have parents whosmoke, particularly mothers, and a number of friends who smoke; who dopoorly in school and score high on a depression scale are least likely to quitsmoking (Burt & Peterson, 1998; Zhu, Sun, Billings, Choi, & Malarcher,1999). The more risk factors, the less likely adolescents are to quit (Zhu et al.,1999).Reviews of quit-smoking programs for adolescents painted a bleak picture(Burton, 1994; Digiusto, 1994; Sussman, et al., 1999). Retention and recruitmentof students were problematic, and end-of-group quit rates were modest.Many studies failed to use appropriate control groups, objective measures ofsmoking status, and long-term follow-up of graduates (Sussman et al., 1999).Teenage focus groups have provided insight into the nature of smoking cessationprograms that appeal to youth (Balch, 1998). Some suggestions were to (1)highlight the seriousness of quitting smoking before becoming an adult; (2)include mood control and stress management; (3) help teen smokers deal with

124 III. SUBSTANCES OF ABUSEsmoking peers; (4) avoid lecturing, preaching, or nagging; and (5) ensure confidentialityfrom parents.Sussman, Dent, and Lichtman (2000) designed an innovative school quitsmokingprogram that featured interactive activities, such as “games” and “talkshows,” alternative medicine techniques (i.e., yoga, relaxation, and meditation),and behavioral strategies for smoking cessation. Two hundred and fiftyninestudents enrolled in the program at 12 schools and another 76 studentsserved as “standard care” controls (smoking status surveyed at baseline and at 3months). Objective measures of cigarette smoking were used. Elective classcredit and class release time were offered for participation in the program.Only 54% of the students (n = 141) completed the program, and only 14%of them were abstinent for 30 days at the end of group. Comparable outcomedata for controls were not obtained, nor was the end-of-group quit rate based onan intent-to-treat analysis (students who did not complete the group were notincluded in the immediate outcome data).A total of 128 (49%) of the clinic enrollees were contacted at 3 months,including 40 (42%) of the clinic dropouts (those who did not complete four sessions).Forty-four (58%) standard care controls were successfully contacted.The 30-day quit rate (no smoking in the past 30 days) for students who completedthe program was 30%, compared to 16% for students assigned to thestandard care condition. This difference was statistically significant. An intentto-treatanalysis, which assumed that students who were not contacted atfollow-up still were smoking, yielded more modest, although still significantlydifferent, quit rates of 17% and 8% for the program and control conditions,respectively.Hurt and colleagues (2000) studied the effects of nicotine replacementpatch therapy plus minimal behavioral intervention on smoking cessation inadolescents who expressed a desire to stop smoking. Out of 101 adolescents, 71completed the entire 6 weeks of patch therapy. Biochemical tests confirmedthat 7-day point-prevalence smoking abstinence rates were 10.9% at 6 weeks(end of patch therapy), 5% at 12-week follow-up, and 5% at 6-month followup.These outcomes are much poorer than those obtained for adults in similarstudies.Adult Smoking CessationNonpharmacological ApproachesOf the many nonpharmacological approaches to smoking cessation, here,behavioral approaches are the most germane. They have undergone the mostextensive experimental study, are suitable for office and clinic-based physicianinterventions, and often are used in combination with pharmacological ap-

6. Tobacco 125proaches to smoking cessation (Fagerstrom, 1988; Hymowitz, 1999). Multicomponentbehavioral programs, whether in group, individual, or “self-help”formats, typically include a number of strategies (self-monitoring, stimulus–control procedures, behavioral contracting, alternative behaviors, aversive conditioning,relaxation training, diet and exercise, self-management skill trainingfor relapse prevention, etc.) to motivate smokers, to help them gain controlover smoking, and to eliminate smoking systematically from their behavioralrepertoire. Once smokers stop smoking, many of the very same behavioral skillsthat helped them quit smoking are used to help them prevent relapse. Schwartz(1987) reported that 1-year quit rates for multicomponent behavioral groupquit-smoking programs average 40%. Initial end-of-treatment quit rates may beconsiderably higher.The MRFIT employed diversified behavioral strategies for initial smokingcessation and long-term smoking abstinence (Hughes, Hymowitz, Ockene,Simon, & Vogt, 1981). The reported quit rates for special intervention (SI)men were 43.1% at year 1 and 50% at year 6. These quit rates were significantlysuperior to those for usual care (UC) participants (13% and 29% at years 1 and6, respectively). When serum thiocyanate, a breakdown product of hydrogencyanide, was used as an objective measure of smoking, the quit rate at year 6 forSI participants was reduced to 46% (Hymowitz, 1987).The Lung Health Study, like the MRFIT, was a large-scale, multicenter,multiyear study in which smokers were exposed to comprehensive behavioralinterventions for initial cessation and long-term follow-up (Anthonisen et al.,1994). In addition, SI participants in the Lung Health Study received NRT(nicotine gum, 2 mg). Five-year cross-sectional quit rates, confirmed by expiredair carbon monoxide and cotinine, were close to 40% for SI and 20% for UCparticipants, a highly significant difference.The MRFIT and the Lung Health Study generated excellent long-termsmoking cessation results. Each study featured a multicomponent treatmentpackage for initial smoking cessation, behavioral strategies for active relapse prevention,and comprehensive and sustained approaches to long-term abstinence.While few programs have the resources necessary to provide comparable sustainedintervention and follow-up, it is important to incorporate strategies tohelp successful quitters remain abstinent. Booster sessions, reunions, telephonecontact, hot lines, mailings, and the Internet have been tried with varyingdegrees of success (Hymowitz, 1999).Nicotine Replacement TherapyPharmacotherapies include several forms of NRT and several antidepressants,among which only bupropion SR has been sponsored and approved by the U.S.Food and Drug Administration (FDA; Sweeney, Fant, Fagerstrom, McGovern,

126 III. SUBSTANCES OF ABUSE& Henningfield, 2001). Four NRT medications have been approved by theFDA (gum, transdermal patch, nasal spray, and oral inhaler), and a lozenge hasrecently entered the U.S. market (Shiffman et al., 2002).Nicotine replacement medications enable the tobacco-dependent personto abstain from tobacco by replacing, at least partially, the nicotine obtainedfrom tobacco. As noted by Sweeney and colleagues (2001), there appear to beat least three major mechanisms by which NRT medications enhance smokingcessation. They (1) reduce either general withdrawal symptoms, or at leastprominent ones, enabling people to function normally while they learn to livewithout a cigarette; (2) reduce the reinforcing effects of tobacco-delivered nicotine;and (3) provide some effects for which the patient previously relied oncigarettes, such as sustaining desirable mood and attention states, and making iteasier to handle stressful or boring situations.The efficacy of NRT products for smoking cessation has been demonstratedin a number of placebo-controlled studies. The gum, transdermal patch,nasal spray, and oral inhaler yield initial and long-term quit rates that morethan double those generated by placebo products, and, when combined withbehavioral counseling and follow-up, quit rates as high as 40–50 after 1 yearhave been reported (Fiore et al., 2000). Physicians in a busy office setting, withminimal time available for counseling and follow-up, may generate 1-year quitrates as high as 10% (Hughes, Gust, Keenan, Fenwick, & Healey, 1989), andover-the-counter (OTC) sales of the gum, patch, and lozenge have markedlyincreased the number of quit-smoking attempts and the number of people usingNRT (Shiffman et al., 1997). Although a recent meta-analysis suggests thatOTC NRT products yield initial quit rates of the same magnitude as NRT productsprescribed by a physician, and twice the quit rate obtained by use of placeboproducts (Hughes, Shiffman, Callas, & Zhang, 2003), other analyses havequestioned the long-term efficacy of OTC NRT products (Pierce & Gilpin,2002). A survey in California showed that smokers who reported using NRTproducts to quit smoking were just as likely to relapse after 1 year as those whodid not use NRT products (Pierce & Gilpin, 2002; Walsh & Penman, 2000).In 20 cities that participated in COMMIT, 12.8% of smokers (1 out of 8)used the transdermal nicotine patch, making it the most popular method forstopping smoking (Cummings, Hyland, Ockene, Hymowitz, & Manley, 1997).By comparison, 1 out of 10 smokers used nicotine gum, 1 out of 13 attended astop-smoking program, 1 out of 16 went to a hypnotist or acupuncturist, and 1out of 20 used some other commercially available stop-smoking device. Amongsmokers who made an attempt to quit smoking, the likelihood of successfulquitting was more than twice as high among patch users than among nonusers.Among patch users, the highest quit rates were observed among those who usedthe patch between 1 and 3 months (Cummings et al., 1997).Compared to nonusers, patch users in COMMIT were more likely to befemale and white, to have higher annual incomes, to be more motivated to stop

6. Tobacco 127smoking, and to smoke more heavily. Among low-income smokers, nicotinepatch use was significantly higher among those who lived in a state where thepublic insurance program (i.e., Medicaid or MediCal) included the patch as abenefit (Cummings et al., 1997).Hall, Tunstall, Rugg, Jones, and Benowitz (1985) studied the effects nicotinegum and intensive behavioral treatment. They assigned 122 subjects to (1)intensive behavioral treatment, (2) nicotine gum (2 mg) in a low-contact treatment,or (3) intensive behavioral treatment plus nicotine gum. Gum was availablefor 6 months from the start of treatment. Subjects met in groups of five tosix with experienced psychologists serving as group leaders. The behavioraltreatment consisted of aversive smoking, relapse prevention skills training,relaxation training, and written exercises to increase commitment to stoppingsmoking. Group sessions were held 14 times in an 8-week period. The lowcontacttreatment had fewer sessions (four times over a 3-week period), paperand-pencilexercises on reasons for smoking, educational material, and groupdiscussions.Assessments were held at 0, 2, 12, 26, and 52 weeks. Reports of abstinencewere verified by measurement of expired air carbon monoxide and serumthiocyanate, as well as reports from significant others (Hall et al., 1985). Differencesbetween the combined condition and the other two conditions were significantat weeks 3, 12, and 26, but not at week 52. For the combined condition,abstinence rates were 95, 73, 59, and 44% at weeks 3, 12, 26, and 52.Corresponding abstinence rates for the low-contact condition were 81, 58, 47,and 37%. For the behavioral condition, the quit rates were 78, 47, 31, and 28%for weeks 3, 12, 26, and 52, respectively. Smokers with high blood cotinine levels(i.e., highly dependent smokers) were more likely to be helped by nicotinegum than were less dependent smokers (Hall et al., 1985).With NRT strongly endorsed as an effective therapy for smoking cessation,attention has shifted toward ways of enhancing its effectiveness, particularly forthe heavily addicted smokers. Options include increasing the dose of NRTproduct, extending the duration of use, and combination therapy (e.g., two ormore forms of NRT or NRT plus bupropion SR). For heavily addicted smokers,higher doses of nicotine gum (4 mg) led to higher quit rates than 2 mg gum(Herrara et al., 1995). In another study, the 21-mg nicotine patch yielded superiorquit rates than 14-mg and placebo patches (Transdermal Nicotine StudyGroup, 1991). However, no advantage was gained by using a 44-mg patch overa 21-mg patch (Jorenby et al., 1995).Sims and Fiore (2002) noted that extending the use of pharmacotherapybeyond the recommended time frame may be an effective strategy for helpingtobacco users achieve abstinence and for preventing relapse to tobacco use,especially for those who are highly nicotine dependent or concerned aboutweight gain. Their review suggests that long-term use is not harmful and is anacceptable alternative to continued smoking.

128 III. SUBSTANCES OF ABUSEAnother approach to enhancing efficacy entails combining an NRT medicationthat allows for passive nicotine delivery (e.g., transdermal patch) with aform of NRT that permits ad libitum nicotine delivery (e.g., gum, nasal spray,inhaler; Sweeney et al., 2001). The rationale for combining NRT medicationsis that smokers may need both a slow delivery system to achieve a constant concentrationof nicotine to relieve cravings and tobacco withdrawal symptoms,and a faster acting preparation that can be administered on demand for immediaterelief of breakthrough cravings and symptoms.Sweeney and colleagues (2001) identified five published studies that testedthe combined use of different nicotine delivery systems. All of the studies useda nicotine patch as one of the study medications, with four of the five studiessupplementing nicotine patch treatment with nicotine gum, and the fifth studysupplementing patch treatment with nicotine nasal spray. For two of the fivestudies, the suppression of nicotine withdrawal symptoms was the primary outcomeof interest, while the remaining three studies tested the impact of combinationtherapy on smoking abstinence rates. On the basis of their review,Sweeney and colleagues concluded that there are conditions under which combinationsof NRT products provide greater efficacy in relieving withdrawal andfostering cessation than monotherapy. However, the findings are not robust(mean odds ratio = 1.9; Fiore et al., 2000), and additional research is warrantedto understand better the magnitude and generality of the benefits of combinationtherapy.Bupropion SRBupropion SR is the first non-nicotine medication shown to be effective forsmoking cessation and approved by the FDA for that use (Fiore et al., 2000). Itsmechanism of action may be mediated by its capacity to block neural reuptakeof dopamine and/or norepinephrine. Bupropion SR is available exclusively as aprescription medication, with an indication for smoking cessation (Zyban) andan indication for depression (Wellbutrin) (Fiore et al., 2000).Hurt and colleagues (1997) conducted a double-blind, placebo-controlledtrial of bupropion SR for smoking cessation. Six hundred and fifteen subjectswere assigned randomly to receive placebo or 100, 150, or 300 mg of bupropionSR per day for 7 weeks. The target quit date was 1 week after the beginning oftreatment. Brief counseling was provided at baseline, weekly during treatment,and at 8, 12, 26, and 52 weeks. Self-reported abstinence was confirmed byexpired air carbon monoxide (≤10 ppm).At the end of 7 weeks of treatment, the rates of confirmed smoking cessationwere 19% for the placebo group and 28.8, 38.6, and 44.2% for the 100-,150-, and 300-mg bupropion SR groups, respectively. At 1 year, the respectiverates were 12.4, 19.6, 22.9, and 23.1% for the placebo, 100-, 150-, and 300-mgbupropion SR groups, respectively. The quit rates for the 150-mg group (p =

6. Tobacco 129.02) and the 300-mg group (p = .01)—but not the 100-mg group (p = .09)—were significantly higher than those for the placebo group (Hurt et al., 1997).Bupropion SR is effective for women and men (Gonzalez et al., 2002) andfor both blacks and whites (Ahluwalia, Harris, Catley, & Okuyemi, 2002).Bupropion SR minimizes weight gain associated with stopping smoking andreduces withdrawal symptoms (Hurt et al., 1997). Multivariate predictors ofsuccessful end-of-treatment outcomes include fewer cigarettes per day, longestduration quit in the past, and male gender (Dale et al., 2001).While bupropion SR may lower seizure thresholds and cause hypersensitivityreaction (Ferry & Johnston, 2003), clinical studies and 32 million patientexposures (9 million for smoking) show that it is generally well tolerated. Themost common adverse event in clinical trials or clinical practice is insomnia,which can also be a symptom of nicotine withdrawal. Tonstad and colleagues(2003) showed that bupropion SR was efficacious and safe for use with patientswith cardiovascular disease. One-year continuous abstinence rates forbupropion SR were more than double the rates obtained with placebo (22 vs.9%).Bupropion SR may be safely combined with NRT to enhance 12-monthquit rates (Gold, Rubey, & Harvey, 2002; Jorenby et al., 1999), although supportfor this strategy is weak. In one study, weight gain following the combinationtreatment was significantly less than with bupropion SR alone, althoughthe difference in 12-month quit rates (30.3 vs. 35.5%) did not achieve statisticalsignificance (Jorenby et al., 1999). In a study involving primary care smokingcessation clinics (Gold et al., 2002), the 6-month self-reported abstinencerate for nicotine patch alone was 14.8%, for bupropion SR alone, 27.7%, andfor patch plus bupropion SR, 34.4%. Quit rates for both forms of bupropion SRtreatments were significantly superior to patch treatment, although they werenot significantly different from one another.Hays and colleagues (2001) studied the efficacy of bupropion SR for preventionof smoking relapse. Participants (n = 784 healthy community volunteers)received open-label bupropion SR, 300 mg, for 7 weeks. Participants whowere abstinent throughout week 7 of open-label treatment were randomlyassigned to placebo or bupropion SR, 300 mg, for 45 weeks, and were subsequentlyfollowed for an additional year after the conclusion of the medicationphase.At the end of initial treatment, 58.8% of the participants were abstinent.The point prevalence smoking abstinence rates were significantly higher in thebupropion SR group than in the placebo group at weeks 52 (55.1 vs. 42.3%)and 78 (47.7 vs. 37.7%). The two groups did not differ at the final week offollow-up (week 104) (41.4 vs. 40.0%). The continuous abstinence rate washigher in the bupropion SR group than in the placebo group at study week 24(17 weeks after randomization) (52.3 vs. 42.3%), but did not differ betweengroups after week 24. The median time to relapse was significantly greater for

130 III. SUBSTANCES OF ABUSEbupropion SR recipients than for placebo recipients (156 vs. 65 days), andweight gain was significantly less in the bupropion SR group at study weeks 52(3.8 vs. 5.6 kg) and 104 (4.1 vs. 5.4 kg). Predictors of successful relapse prevention(in addition to assignment to bupropion SR treatment) were lower baselinesmoking rates, a Fagerstrom Tolerance Questionnaire score < 6, and initiationof smoking at an older age (Hurt et al., 2002).Hurt and colleagues (2003) studied the efficacy of bupropion SR (1) forpreventing relapse in adult smokers who quit smoking with transdermal nicotinepatch therapy and (2) for quitting smoking in smokers who failed to quiton the patch. At completion of nicotine patch therapy, nonsmoking participantswere assigned to bupropion SR or placebo for 6 months (relapse prevention),and smoking participants were assigned to bupropion SR or placebo for 8weeks of treatment. Of 578 subjects, 31% were abstinent at the end of nicotinepatch therapy. Of those not smoking at the end of initial patch treatment, 28and 25% were not smoking at 6 months (end of medication phase) forbupropion SR and placebo, respectively. For those still smoking at the end ofnicotine patch therapy, 3.1 and 0.0% stopped smoking with bupropion SR andplacebo, respectively. Hurt and colleagues concluded that bupropion SR neitherreduced relapse to smoking in smokers who stopped smoking with the nicotinepatch nor initiated abstinence among smokers who failed to stop smokingon the patch.REFERENCESAhluwalia, J. S., Harris, K. J., Catley, D., Okuyemi, K. S., & Mayo, M. S. (2002). Sustainedrelease bupropion for smoking cessation in African-Americans: A randomizedcontrolled trial. JAMA, 228, 468–474.Aitken, P. (1980). Peer group pressures, parental controls and cigarette smoking amongten- to- fourteen year olds. Br J Soc Clin Psychol, 19, 141–146.American Academy of Pediatrics Committee on Substance Abuse. (2001). Tobacco’stoll: implications for the pediatrician. Pediatrics, 107, 794–798.American Cancer Society. (1986). Facts and figures on smoking, 1976–1986 (PublicationNo. 5650-LE). New York: Author.American Cancer Society. (2003). Cancer facts and figures 2003. Atlanta: Author.American Lung Association. (2003). Key facts about tobacco use. Retrieved on April15, 2003, from www.lungusa.orgAmerican Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders(4th ed.). Washington, DC: Author.American Psychiatric Association. (1996). Practice guidelines for the treatment ofpatients with nicotine dependence. Am J Psychiatry, 153(Suppl), 1–31.American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders(4th ed., text rev.). Washington, DC: Author.Anthonisen, N. R., Connett, J. E., Kiley, J. P., Altose, M. D., Bailey, W. C., Buist, A.S., et al. (1994). Effects of smoking intervention and use of an inhaled anti-

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CHAPTER 7OpioidsSTEPHEN L. DILTS, JR.STEPHEN L. DILTSOpioids constitute the group of compounds whose pharmacological effectsduplicate those of morphine. They are commonly used medically as an adjunctto anesthesia, for the relief of pain, for the prevention of an abstinence syndrome,and for cough suppression. Opioids also are abused for their intoxicatingeffects.The history of opioid use goes back thousands of years in human history.The Ebers Papyri from approximately 7000 B.C. refer to the use of opium inchildren suffering from colic (Deneau & Mule, 1981). In the Victorian era, theuse of laudanum was socially acceptable. In the present day, opioids use is stringentlyregulated, especially in the United States; however, demand by addictsresults in the existence of a “black market” characterized by crime, disease, poverty,and loss of personal and social productivity. The sexually promiscuousintravenous heroin user is at high risk to contract and effectively spread thedeadly acquired immune deficiency syndrome (AIDS) virus, as well as venerealand other infectious diseases, such as hepatitis C. High overall death rates areassociated with opioid abuse, approximately 10–15 per 1,000 in the UnitedStates (Jaffe, 1989). The Drug Abuse Warning Network (Substance Abuse andMental Health Services Administration, 1995) indicates an alarming increasein the use of opioids, especially prescription drugs such as oxycodone.138

7. Opioids 139DEFINITIONSThe opioids are addicting; that is, they produce a well-defined syndrome ofrepeated self-administration over time, tolerance to the effects of the drug, andan abstinence syndrome when the drug is no longer available. “Cross-tolerance”refers to the ability of any drug in the opioid class to produce similar effects andto block the abstinence syndrome associated with opioids in general. The primaryeffects of opiates are mediated through their action at the opioid mu,kappa, and delta receptors. Morphine, codeine, and thebaine are naturallyoccurring phenanthrene alkaloids in opium, the milky exudate from the unripecapsule of the poppy plant, Papaver somniferum. Raw opium contains 4–21%morphine and 0.7–2.5% codeine, and is refined to produce these medically usefulproducts. In practice, most codeine is actually converted directly frommorphine, which also can be used to produce hydromorphone (Dilaudid).Thebaine, found in very small concentrations in raw opium, is similar to morphine.It is converted into medically useful compounds such as codeine,hydrocodone (Vicodin), oxycodone (Percodan, Percocet, Tylox), oxymorphone(Numorphan), nalbuphine (Nubain), and diacetylmorphine (heroin).Naloxone (Narcan) is also produced from morphine but lacks euphoric andanalgesic properties; its use in humans is discussed later in this chapter. Etorphine(M99), which is produced from thebaine, is a potent opioid useful mainlyin the immobilization of large animals. Raw opium, morphine, codeine, andthebaine are referred to as naturally occurring opioids or opiates, whereas thosecompounds mentioned previously, which are produced directly from these naturallyoccurring compounds, are called semisynthetic opioids or opiates.Attempts to synthesize opioid-like compounds have produced a variety ofagents that are chemically distinct from morphine yet seem to act via similarmechanisms and also exhibit cross-tolerance. These include meperidine(Demerol), propoxyphene (Darvon), methadone (Dolophine), and levo-alphaacetylmethadol (LAAM). Fentanyl (Sublimaze) and sufentanil (Sufenta) arevery potent short-acting opioids used mainly in anesthesia. Buprenorphine, apartial mu agonist, is useful in the treatment of heroin addiction. These compoundsare collectively referred to as the synthetic opioids.With the exception of methadone and LAAM, most opiates have shorthalf-lives. Extended release preparations of oxycodone (Oxycontin) and morphine(MSContin) have become increasingly popular in pain management,because they offer fewer peaks and troughs over 24 hours. Most opioids arelegitimately used medically for pain relief; however, the addicting properties ofopiates have prompted the search for a nonaddicting analgesic with the samepotent pain-relieving properties as the opioids; unfortunately, this has not cometo pass, and the following examples are known to produce dependence alongwith analgesia. Pentazocine (Talwin) and butorphanol (Stadol) produce anal-

140 III. SUBSTANCES OF ABUSEgesia in the opioid-free individual but are addicting, and when given to someonewho is opioid dependent produce an abstinence syndrome. The semisyntheticcompound nalbuphine, mentioned earlier, has similar properties.Tramadol (Ultram), a synthetic aminocyclohexanol, binds to mu opioid receptorsand also inhibits reuptake of norepinephrine and serotonin; there havebeen increasing reports of tramadol abuse.Despite their similarities, opioids may have varying effects on opioid receptors.For example, the mu receptor is occupied preferentially by the classicmorphine-like opioids, but butorphanol (Stadol) and nalbuphaine (Nubain)prefer the kappa receptor. Both receptors are highly specific, and an abstinencesyndrome mediated by the kappa receptor will not be relieved if a mu receptorcompound is administered. Like pentazocine, butorphanol, and tramadol,buprenorphine (Subutex) is a mixed opiate agonist–antagonist, with partial mureceptor agonism and full kappa agonism. Partial agonists show a “ceilingeffect”; unlike full agonists, dose escalation does not produce ever-increasingpharmacological effects. There are also compounds that bind selectively to thereceptor site, yet produce no agonistic action. These compounds are antagonisticin nature, because they occupy the receptor site and exclude agonist opioids;examples include naloxone (Narcan) and naltrexone (ReVia). These opioidantagonists, useful for the treatment of opioid intoxication and addiction, arediscussed later. Relative to full agonists, partial agonists may act as antagonists.Also of interest is the discovery and description of endogenous opioid substancesin humans, operating at the kappa receptor site along the spectrum fromagonistic to antagonistic function. To date, no endogenous mu receptor opioidhas been discovered (Jaffe, 1989).DIAGNOSISIn the framework provided by the fourth edition of the Diagnostic and StatisticalManual of Mental Disorders (DSM-IV-TR; American Psychiatric Association,2000), the problem of opioid misuse is divided into four categories, amongwhich there may be some overlap. Opioid intoxication and opioid withdrawalare specifically defined in DSM-IV-TR. Facility in making these diagnosesrequires a clear understanding of the clinical features associated with opioids, asdiscussed later in this chapter. In addition to intoxication or withdrawal, it isimportant to characterize the individual’s relationship to the use of opioids overtime.Initial assessment always includes a thorough history of the individual’ssubstance use over time, with corroboration from outside sources if possible.This corroboration of the individual’s history is essential because of the nearlyuniversal presence of denial in the nonrecovered substance abuser. Minimizationof the frequency and amounts of opioid use is common, as is the illu-

7. Opioids 141sion of control characterized by the often-heard phrase, “I can stop anytime Iwant to.” Progression in the pattern of usage is the rule, as the reinforcing qualitiesof the opioid and tolerance exert their powerful influence. Critical to theinitial assessment is an accurate answer to this question: “When did you last useand how much did you use?” With this information, the clinician can begin toassess the impact of intoxication or withdrawal upon the immediate clinicalpresentation. It is also necessary to understand the crises or events precipitatingcontact with the health care system to assess whether the patient has truly “hitbottom” or merely experienced a temporary loss of ability to obtain opioids.This information may be useful in predicting readiness to accept treatmentinterventions.A family history of substance abuse provides data reflective of the geneticinfluences in opioid dependence, as well as the contribution of learned behaviorand sanction of substance abuse within the family structure. This informationis particularly useful in planning a strategy for recovery and relapse prevention.Returning an individual to contact with family members and/or friendswho are still using opioids and other drugs will virtually guarantee a quickrelapse.Also important are inquiries into the individual’s functioning in the workplace,at home, and in the social arena. Trouble may occur in each area becauseof the competition between dependence-driven, drug-seeking behavior and thedemands of everyday living. It is important to ask specifically about legal difficulties,arrests, convictions, or restrictions of freedom (e.g., loss of professionallicensure).A medical review of systems in tandem with a thorough physical examination,including a neurological examination and a mental status examination,may reveal signs of intoxication or withdrawal, as outlined later. Stigmata ofopioid use, such as fresh or old needle marks (tracks) around superficial veins inthe extremities and neck, are readily observed. These often appear as increasedlines of pigmentation. There may be evidence of old and new skin abscesses,clotted or thrombosed veins, an enlarged and tender liver, swollen lymphnodes, a heart murmur caused by endocarditis, hypo- or hyperactive bowelsounds, and pupillary abnormalities, which depend on the stage of intoxicationor withdrawal. Significant weight loss is common, though weight gain is occasionallyreported.Useful laboratory studies include serum liver function studies, which mayshow inflammation in the form of elevated serum aspartate aminotransferase(AST), serum alanine aminotransferase (ALT), bilirubin, alkaline phosphatase,and reduction in total protein, clotting factors, and immunoglobulins.Blood urea nitrogen may also be elevated, though the meaning of this finding isunclear. Further testing may include hepatitis A, B, and C screening; humanimmunodeficiency virus (HIV) testing; complete blood count; and urine and/orserum analyses for the presence of opioids, cocaine metabolites, marijuana,

142 III. SUBSTANCES OF ABUSEalcohol, benzodiazepines, barbiturates, other stimulants, and hallucinogens. Ifpossible, the collection of urine samples should be actively observed to ensurethat the samples are not falsified in some manner by the individual. “Scams” foravoiding detection of illicit drugs in urine are diverse and imaginative: Somemen have provided “clean” urine from a small tube alongside the penis, andsome women have concealed a balloon of “clean” urine in the vagina to be laceratedwith a fingernail, while apparently positioning the specimen cup nearthe urethral meatus as the sample is collected.As evidence of opioid abuse or dependence grows, the clinician can mounta firm but respectful confrontation of the individual, who will frequently admitthe problem because he or she now recognizes that there may exist an opportunityfor treatment. The “addiction as an illness” concept can be useful at thiscritical juncture in the physician’s interactions with an opioid-dependent person.If the patient’s denial prevents engagement in treatment, leverage on hisor her behavior may be gained by involving significant others, employers, or thelegal system.CLINICAL FEATURES AND PHARMACOLOGYClinical features of opioid use are logically divided into three categories: intoxication,withdrawal, and overdose. These features are outlined in Tables 7.1, 7.2,and 7.3, respectively. The features listed in these tables are directly related tothe pharmacological actions of the opiates and are uniform in humans, with theoccasional exception of the individual who experiences an idiosyncratic reaction.TABLE 7.1. Signs of Opioid Intoxiciation1. Euphoria immediately following ingestion; profound relief from anxiety and tension.2. Apathy following euphoria.3. An initial mild-to-moderate burst of energy in the minutes following ingestion,ultimately replaced with psychomotor retardation.4. “Nodding,” a “twilight state” in between alertness and sleep, during which theindividual is quiescent but arousable.5. Pupillary constriction (miosis).6. Hypoactive bowel sounds.7. Slow regular respiration.8. Slurred speech.9. Impaired judgment, attention, concentration, and memory.10. Physical evidence of recent use, including needle marks, hyperemic nasal mucosa,if insufflation was the route of administration, and positive opioid blood or urinescreen.

TABLE 7.2. Opioid Withdrawal7. Opioids 143Stage I—begins within hours of last dose and peaks at 36–72 hours:1. Craving for the drug.2. Tearing (lacrimation).3. “Runny nose” (rhinorrhea).4. Yawning.5. Sweating (diaphoresis).Stage II—begins at 12 hours and peaks at 72 hours:1. Mild-to-moderate sleep disturbance.2. Dilated pupils (mydriasis).3. Loss of appetite (anorexia).4. “Goose flesh” or “cold turkey” (piloerection).5. Irritability.6. Tremor.Stage III—begins at 24–36 hours and peaks at 72 hours:1. Severe insomnia.2. Violent yawning.3. Weakness.4. Nausea, vomiting, and diarrhea.5. Chills and fever.6. Muscle spasms or “kicking the habit” (especially in the lower extremities).7. Flushing.8. Spontaneous ejaculation.9. Abdominal pain.TABLE 7.3. Opioid Overdose1. Signs of recent ingestion.2. Profoundly decreased respirations or apnea.3. Pale skin and blue mucous membranes.4. Pinpoint pupils, unless prolonged cerebral apnea has caused somebrain damage, in which case pupillary dilatation may occur.5. Pulmonary edema resulting in characteristic gasping and audiblerhonchi; occasional froth in the upper airway.6. Cardiovascular collapse.7. Cardiac dysrhythmias.8. Convulsions, especially with meperidine, propoxyphene, or codeine.9. Semicoma or coma.

144 III. SUBSTANCES OF ABUSEAnalgesia is the principal useful effect of the opioids. It seems not to matterwhether the pain is physical or emotional: Relief is significant. The addictionpotential of a given opioid appears to be at least partly related to the analgesicaffect. Analgesia from full opioid agonists increases in a dose-relatedmanner, to a point beyond which larger doses cause greater side effects but nogreater analgesia (Deneau & Mule, 1981). Contravening side effects includerespiratory depression, sedation, seizures, and loss of motor control. Heroin,morphine, and hydromorphone are among the best analgesics because of rapidabsorption into the central nervous system and a relatively higher threshold forside effects. Meperidine and codeine are less effective in this regard. Route ofadministration significantly affects analgesia. Parenteral use is the most efficient,because oral administration subjects the opioid to erratic absorption inthe gastrointestinal tract, as well as passage through the portal system beforereaching the central nervous system. Codeine and methadone are reliablyabsorbed orally; morphine and meperidine are not.Opioids are potent suppressors of the cough reflex, and this antitussiveaction is most often accomplished with codeine or hydrocodone. A related phenomenonis that of respiratory depression. Opioids cause the central respiratorycenter to become less sensitive to carbon dioxide, which in rising concentrationsordinarily stimulates breathing. The mechanism of death in acute opioidoverdose usually is respiratory arrest.Opioids have pronounced gastrointestinal effects. Initially the user mayexperience nausea and emesis due to central stimulation; however, this is followedby depression of the central structures controlling emesis, and evenemetic agents frequently fail to produce vomiting. The intestinal smooth muscleis stimulated to contract by opioids, thus reducing peristalsis. Although thisaction may be desirable in preventing loss of water through diarrhea, the relatedundesirable effect of constipation routinely appears with repeated administration.Smooth muscle contraction in the urinary bladder is also stimulated byopioids, sometimes resulting in an unpleasant sensation of nearly constant urinaryurgency. Although uterine muscle is not significantly affected by opioids,labor is frequently prolonged. Because opioids do cross the placental barrier,newborn infants can show all the adult signs of intoxication, withdrawal, andoverdose.Blood vessels in the periphery are generally dilated as a result of opioidinducedhistamine release; this sometimes causes a blush of the skin, with itching,especially in the face. By a separate mechanism, reflex vasoconstriction isinhibited, resulting in significant orthostasis. Some endocrine effects have alsobeen noted. Thyroid activity, output of gonadotropins, and adrenal steroid outputare all reduced. These effects are caused by opioid actions on the pituitarygland.

7. Opioids 145The concept of tolerance has been previously mentioned. Repeated administrationof opioids results in decreasing levels of euphoria and analgesiaover time. The user also becomes less affected by respiratory depression, nauseaand emesis, and impairment of consciousness. Less tolerance develops toorthostasis and very little to miosis, constipation, and urinary urgency; however,these side effects may be counteracted by the euphoric and analgesic propertiesof opioids, in which individuals remain aware of unpleasant physical sensationsbut insist that they are no longer bothered by these. Tolerance isreversed during periods of abstinence.Tolerance is the direct result of neuroadaptive change at the opioid receptorsite during a period of continuous occupation by an exogenous opioid. Astate of physical dependence is reached when removal of the opioid from itsreceptor site produces an abstinence syndrome. A more sudden removal of theopioid from its receptor site produces a more intense abstinence syndrome. Themost rapid removal of opioid from its receptor site is accomplished by theopioid antagonists, which selectively compete for the site but have no agonistproperties. Shorter acting opioids exit the receptor site more quickly than doopioids with longer half-lives. Thus, heroin and morphine produce intenseabstinence syndromes with relatively rapid onset and progression, whereasmethadone produces an abstinence syndrome of less overall intensity, but withslower progression through the stages of acute abstinence to resolution, which,for a short-acting drug such as heroin, arrives at 5–10 days. Abrupt methadonewithdrawal produces an abstinence syndrome that may not resolve for 14–21days. Following resolution of the acute abstinence syndrome, a more subtleabstinence syndrome may occur and last for many months. Symptoms includehyposensitivity to the respiratory stimulant effect of carbon dioxide, disturbedsleep, preoccupation with physical discomfort, poor self-esteem, and diminishedability to tolerate stress. Risk of relapse is higher during this period (Martin &Jasinski, 1969).COURSEMany complex factors influence the natural history of opioid addiction. Overall,the course is one of relapse and remission. Attempts to define opioid abusersas a group have been limited, because long-term contact with these frequentlyitinerant persons is difficult, and only a minority of opioid abusers can be studiedeffectively (i.e., those who elect to enter treatment). Given these obstaclesto accurate understanding, some generalizations can still be made. The vastmajority of active opioid abusers are between the ages of 20 and 50 years. Ageat first use is usually in the teens or 20s. Race, ethnicity, and socioeconomic statusvariables are important. Though opioid addiction affects persons from all

146 III. SUBSTANCES OF ABUSEgroups in the United States, black or Hispanic poor persons are overrepresented.True iatrogenic opioid dependence rarely persists to become chronic,although the risk exists for those with chronic, painful medical or surgical problems.Although men and women seek treatment in roughly equal numbers,women who are mothers of dependent children may benefit from a more favorableprognosis.Opioid addiction follows a relapsing and remitting course until middle age,when its relentless grip on the individual seems to abate slowly and spontaneously.Some experts have estimated 9 years as the average duration of activeopioid addiction (Jaffe, 1989). Criminal activity, usually in support of addiction,is very common during periods of active use. In periods of remission, criminalactivity drops off significantly. The overall death rate in opioid abusers isestimated to be as much as 20 times that of the general population. The proximatecause of death is usually overdose, use-related infections, suicide, homicide,or accidental death.Significant psychiatric comorbidity has been observed; depression and personalitydisorder are the most frequent diagnoses. Polysubstance abuse is commonin opioid addicts. Many are nicotine addicted, and many have seriousalcohol-related problems as well. Benzodiazepine use is common and probablyunderestimated, because it may not be specifically assayed in urine specimens.Sporadic use of cocaine and other stimulants is common, as is the use of marijuana.A few opioid addicts also use hallucinogens or inhalants.The medical complications of opioid abuse are many and diverse. Theystem most commonly from (1) the failure to use aseptic techniques duringinjection, (2) the presence of particulate contaminants in the injected solution,and (3) the direct pharmacological actions of the drug. The consequences ofinfection are the most frequently encountered medical complications of opioidabuse. Skin abscesses, lymphadenopathy, osteomyelitis, septic emboli in thelungs, endocarditis, septicemia, glomerulonephritis, meningitis, and brain abscessesare encountered with regularity when “dirty needles” are used. A lowlevelimmunodeficiency may exist in chronic opioid addicts, causing them to bemore susceptible to infectious processes such as tuberculosis, syphilis, malaria,tetanus, and hepatitis (Senay, 1983). HIV infection may result from sharingneedles with an infected individual. Risk of this complication is highest in thenortheastern United States, where a survey of opioid addicts in methadonetreatment programs showed seropositivity in 60% of those who reported sharingneedles (Jaffe, 1989). Fortunately, the percentage drops dramatically in mostother parts of the country, and aggressive efforts at education of both addictsand those who treat them in clinics and elsewhere have helped slow the spreadof this deadly virus.Addicts frequently inject opioid solutions contaminated with adulterantssuch as talc and starch; these substances are used to increase the bulk of theillicit powder, thus increasing profits for the drug dealer. Addicts mix the pow-

7. Opioids 147der with water, heat it, and use cotton or a cigarette filter to block the entry ofundissolved particles as the solution is drawn into the syringe. As a result, fibersenter the venous bloodstream and lodge in the lungs, where conditions becomefavorable for the development over time of pulmonary thrombosis (emboli ariseat distant sites), pulmonary hypertension, and right-side heart failure. Opioidabusers are at further risk of compromised pulmonary function if they use cigarettesand marijuana, as they often do. The antitussive effect of opioids alsocompromises pulmonary function, contributing to frequent pneumonia andother respiratory tract infections.A number of lesions may occur in the central nervous system of those personswho have survived overdoses that featured anoxia and coma. The residualeffects of such trauma include partial paralysis, parkinsonism, intellectualimpairment, personality changes, peripheral neuropathy, acute transversemyelitis, and blindness.Psychiatric comorbidity caused by opioid dependence occurs most frequentlyin the form of depression. When depression is observed during therecovery period, treatment with antidepressants and psychotherapy is indicatedand frequently helpful if the individual is abstinent from illicit drug use.Dysphoria is common during with withdrawal interval, and is not helped byantidepressants, but rather by appropriate treatment of withdrawal symptoms.The following disorders also are seen in association with opioid dependence:1. Bipolar disorder.2. Antisocial personality disorder.3. Anxiety disorders.4. Other personality disorders, including paranoid, schizoid, schizotypal,histrionic, narcissistic, borderline, dependent, obsessive–compulsive,and mixed.5. Delirium and dementia (rare).6. Schizophrenia (very rare).Mood disorders may be diagnosable in many opioid addicts (Mirin, Weiss,Michael, & Griffin, 1989). Major depression is the most common mood disorder,diagnosed at almost 16% (Brooner, King, Kidorf, Schmidt, & Bigelow,1997); it may have preceded the onset of drug abuse as chronic, episodic lowgradedepression or dysthymia, and a full-blown major depressive episode maydevelop in the stressful and traumatic context of opioid addiction. Depressionoccurs more frequently in women than in men. Depression coexisting withopioid dependence is more strongly associated with a history of concomitantpolydrug abuse. More attention is being paid to the complicating presence ofattention-deficit/hyperactivity disorder (ADHD; King, Brooner, Kidorf, Stoller,& Mirsky, 1999).

148 III. SUBSTANCES OF ABUSEOf the personality disorders, antisocial personality disorder is the mostcommonly diagnosed and can be seen in as many as 25% of opioid abusers seekingtreatment; this is noted in men the vast majority of the time (Brooner et al.,1997). It is inaccurate to assume that drug-seeking behavior learned duringyears of addiction is responsible for the high percentage of antisocial personalitiesamong opioid addicts. Antisocial personality disorder can be reliably diagnosedhistorically in most individuals at a young age, prior to the onset ofopioid dependence. The relationship between opioid abuse and antisocial personalityis complicated and appears to be influenced by a non-sex-linkedgenetic factor. When antisocial personality and opioid dependence are foundtogether, the treatment course is frequently challenging, and the overall outcomeis poor with regard to adequate length of time in treatment, relapse, criminalbehavior during treatment, and ability to establish rapport with a therapistor counselor. The one exception appears to be the antisocial addict who alsohas a diagnosable depression. This group responds much better to treatment, ona par with the average opioid addict without significant psychiatric comorbidity(Woody, McLellan, Luborsky, & O’Brien, 1985).Anxiety disorders, such as panic disorder, obsessive–compulsive disorder,generalized anxiety disorder, and phobia, are seen in approximately 10% ofopioid addicts. Members of this group are typically somewhat younger in ageand higher in socioeconomic status, and their drug use histories are not asextensive.Delirium, dementia, and psychotic disorders such as schizophrenia, mania,and psychotic depression are not usually seen in opioid clinic populations. Thepresence of both a DSM-IV Axis I diagnosis (depression or an anxiety disorder)and an Axis II diagnosis (a personality disorder) in the same opioid-dependentindividual is frequently observed; the proportion of such patients may approach50% in clinic populations (Khantzian & Treece, 1985).TREATMENTThe various nonpharmacological treatment modalities used to treat other typesof substance abusers are also useful in treating opioid addicts, and are discussedin Chapter 19. The focus of this chapter is on pharmacotherapy of situationscommonly found in the context of opioid use, including overdose, withdrawal,detoxification, and maintenance.IntoxicationThe management of opioid overdose is best accomplished in a medical facilitywith the availability of sophisticated expertise and technology. These can bebrought to bear on the potential “worst-case scenario,” for example, opioid

7. Opioids 149overdose in a pregnant female with septicemia, pulmonary edema, and coma. Inaddition to intensive physiological support needed in opioid overdose, the useof an opioid antagonist can be life saving. Naloxone is the drug of choice,because it does not further depress respiratory drive (Berger & Dunn, 1986). Aregimen of 0.4–0.8 mg, administered intravenously several times over thecourse of 20–30 minutes, is usually effective. If after 10 mg of naloxone there isno improvement in the patient’s condition, one must question the diagnosis ofopioid overdose. Other drugs may be involved, or other central nervous systemprocesses may exist. One also must remember that the action of naloxonealmost always will be shorter than the action of the opioid, necessitating closeattention to the reemergence of the opioid’s physiological effects (Wilford,1981). The use of opiate antagonists in tolerant individuals will precipitate opiatewithdrawal.WithdrawalThe opioid withdrawal syndrome can easily be suppressed by administering anyopioid with significant same-receptor agonism as the drug that originally producedthe addiction. However, it is more useful to prevent opioid withdrawalsymptoms pharmacologically with a nonaddicting drug. This approach furthersthe goals of detoxification and abstinence. When circumstances force addicts totreat their withdrawal symptoms without opioids, they most commonly usealcohol and/or benzodiazepines. The main disadvantage to this approach is thatbecause of the lack of cross-tolerance between opioids and alcohol/benzodiazepines,blockade of withdrawal symptoms requires the ingestion of largeamounts of these sedatives to achieve suppression. Clonidine, a presynapticalpha 2agonist originally marketed as an antihypertensive, represents an effectiveand safer alternative for the treatment of opiate withdrawal symptoms(Koob & Bloom, 1988; O’Connor et al., 1995). It can partially suppress many(but not all) elements of opioid withdrawal, so that the risk of immediaterelapse is reduced (Jasinski, Johnson, & Kocher, 1985). Clonidine is most effectivefor those motivated persons who are involved in their overall treatmentprogram and are using small amounts of opioid (Kleber et al., 1985). Outpatientswho are on less than 20 mg of methadone per day and detoxifying at ratesapproaching 1 mg per day make ideal candidates for the adjunctive use ofclonidine. These individuals can be given 0.1 to 0.3 mg up to three or fourtimes a day throughout the withdrawal period, with good effect. Sometimesonly small amounts of clonidine (on the order of 0.1 mg per day) may be useful,to be administered at the time of day that is most difficult for the patient.Clonidine is not generally useful beyond 2 weeks after the last dose of methadone(Gold, Pottash, Sweeney, & Kleber, 1980). A transdermal delivery system(Catapres-TTS), which is active over a 7-day period, is useful in the outpatientsetting, because the indiscriminate use of large amounts of clonidine by the

150 III. SUBSTANCES OF ABUSEindividual can be avoided, thus limiting the risk of adverse reactions (Spencer& Gregory, 1989). Hypotension and bradycardia are major side effects ofclonidine, and can be profound. Lethargy is also common, but this effect can beuseful at night.In a hospital setting, clonidine has been used in concert with abstinenceand an opioid antagonist to produce tolerable withdrawal and detoxification ina short period (5–6 days) for persons on methadone doses of 50 mg or less; variousprotocols exist (Charney, Heninger, & Kleber, 1986). This treatment canbe complicated by delirium and/or psychosis (Brewer, Rezae, & Bailey, 1988).The treatment involves sudden cessation of opioid ingestion, precipitation ofan acute abstinence syndrome with an opioid antagonist, and aggressive treatmentof the withdrawal symptoms with large doses of clonidine throughout theday and benzodiazepines at night. Over the 5- to 6-day course, the clonidineand opioid blocker are tapered. Naltrexone with buprenorphine has been usedsuccessfully (Cheskin, Fudala, & Johnson, 1994; Gerra et al., 1995), and thiscombination produces the shortest and least severe withdrawal interval. Benzodiazepinesare not routinely used after the second or third night, and there is arisk of synergistic respiratory suppression in the coadministration of benzodiazepinesand full or partial opiate agonists. A more time-consuming approachwould involve abstinence not precipitated suddenly by an opioid blocker andmore aggressive use of clonidine than would be practical in an outpatient setting.These approaches are appropriate for those individuals who are highlymotivated to become drug-free quickly in a controlled manner, for reasonsrelated to employment or to impending incarceration.It is generally recognized that abrupt withdrawal from opioids is almostalways followed by relapse. The risk of relapse is less with a rational plan fordetoxification, using decreasing amounts of an opioid over time. In this way,the withdrawal syndrome is minimized, rendering the individual more responsiveto other, nonpharmacological therapies during this high-risk phase of treatment.In the United States, the usual first step toward detoxification is toswitch the addicted individual to a longer acting opioid. Methadone is theobvious choice, with a half-life of 15–25 hours in comparison to 2–3 hours formorphine, heroin, and many other commonly available opioids. In additionto methadone, LAAM was approved in 1993 as a maintenance treatmentagent for opioid dependence; however, because of growing awareness of lifethreateningarrhythmias, it is no longer used. Generally speaking, for every 2mg of heroin, 1 mg of methadone may be substituted. The same is true for 4 mgof morphine, 20 mg of meperidine, 50 mg of codeine, and 12 mg of oxycodone.Other equivalencies are available in standard pharmacology texts.Usually, it is not possible to know how much heroin a user is actuallyadministering in a 24-hour period because of the impure nature of the productavailable on the street. Experience shows that an initial dose of 20–30 mg ofmethadone will block most withdrawal symptoms in moderate to heavy users

7. Opioids 151who may inject from four to 12 or more times in 24 hours. For those who injecttwo to three times per day, a starting dose of 10–20 mg of methadone is usuallysufficient. Methadone may be given every 24 hours, and the dose may beadjusted daily up or down by 5- to 10-mg increments, based on observablesymptoms of withdrawal or intoxication. The peak plasma levels from methadoneoccur between 2 and 6 hours after ingestion. Over time, methadonebecomes tissue-bound throughout the body, creating a buffer against significantwithdrawal in those persons who occasionally miss a daily dose. This phenomenonalso facilitates a smooth detoxification over time as daily dosage is reduced.Stabilization on methadone can usually be accomplished with 20–50 mg daily.Detoxification may then begin. Federal law allows the use of opiates for detoxificationonly when doses are dispensed directly by the provider. Of course,methadone may only be dispensed for the treatment of opiate addiction by alicensed clinic.For the hospitalized patient, federal law allows the administration of opiatesfor a maximum of 3 days, or longer as required, if the patient is primarilyadmitted for a general medical condition. Any opiate may be selected, but commonchoices are methadone, buprenorphine, or propoxyphene.Regulations at the various levels of government historically mandated thatoutpatient detoxification be accomplished within 21 days. Unfortunately, thisperiod was too short for all but the most minimally addicted individuals and frequentlyresulted in relapse. Fortunately, the regulations have been liberalized,largely because of recognition that HIV/AIDS is spread very rapidly amongintravenous drug abusers who share needles. Changes in the regulations areintended to allow more addicts to enter and stay in treatment. As a practicalmatter, 30 days is the minimum amount of time required for successful detoxification,and often 45 days or more may be needed; relapse still is a definite risk.For those individuals with long abuse histories and high doses of opioids, 6months or more may be required. Veteran opioid users are extremely sensitiveto even small reductions in their daily dose of methadone. The critical stage ofdetoxification occurs below 20 mg of methadone daily, and the use of clonidineis helpful in blocking withdrawal symptoms. In some individuals, detoxificationis successful, but symptoms of insomnia, malaise, irritability, fatigue, gastrointestinalhypermotility, and even premature ejaculation may persist for months.Clonidine is less effective in this situation.Ultrarapid detoxification (URD) under anesthesia, which has received agreat deal of recent attention and controversy, is not generally accepted as costeffectivein the long term but may be useful in special cases (Hensel & Kox,2000). Naltrexone maintenance, which probably is underutilized as a generaltreatment technique, has been utilized in follow-up after URD (Rabinowitz,Cohen, & Atias, 2002).Acupuncture may be helpful in detoxification, as well as maintenance,although scientific studies are limited (Otto, 2003).

152 III. SUBSTANCES OF ABUSEMaintenanceAfter detoxification, relapse prevention must be actively addressed with whatevertreatment interventions are available.Unfortunately, a large percentage of addicts seem unable to tolerate acutewithdrawal, to succeed at controlled detoxification, or to remain drug free.Methadone maintenance may then become the treatment of choice. Administeredon a once-a-day schedule, methadone in appropriate doses blocks opioidwithdrawal, thus reducing compulsive drug-seeking behavior and use. The individualmay then focus energy and attention on more productive behaviors.Indications for the use of methadone maintenance include (1) a history ofchronic, high-dose opioid abuse; (2) repeated failures at abstinence; (3) historyof prior successful methadone maintenance; (4) history of drug-related criminalconvictions or incarcerations; (5) pregnancy, especially first and third trimesters;and (6) HIV seropositivity.Relative contraindications to methadone maintenance include (1) age lessthan 16 years, (2) the expectation of incarceration within 30–45 days, and (3)history of abuse of methadone maintenance, including diversion of methadoneto “the street” and failure to cease illicit use despite adequate doses.The administration of methadone, as noted earlier, is heavily regulated byFederal and state governments. Specific requirements must be met by individualsand clinics offering this service. Generally, after the individual’s history andphysical condition are assessed, methadone dosing begins according to the protocolpreviously described. A period of 4–10 days may be required to stabilizethe patient at an appropriate dose. When stabilization has occurred, the individual’sillicit drug use should cease, as evidenced by regular, monitored urinalysisshowing only methadone. Methadone maintenance programs that maintainan overall average dose of 60–100 mg a day yield consistently better resultsin decreasing illicit opioid use. Doses in excess of 120 mg a day are seldomneeded (Gerstein, 1990). A pitfall here is that individuals may supplementtheir maintenance dose with “black market” methadone. Urinalyses will not behelpful in detecting this behavior, since quantification techniques are not generallyemployed. Dosage requirements should not change after stabilization,unless something has occurred to change the body’s absorption, metabolism,distribution, or excretion of methadone. Emesis within 20–30 minutes after theoral ingestion of methadone is an obvious example of disruption to absorption.Metabolism of methadone may be increased by the use of phenytoin, rifampin,barbiturates, carbamazepine, and some tricyclic antidepressants, all of whichcan precipitate withdrawal symptoms by reducing methadone plasma levels.Concealed regular use of other opiates in addition to methadone will result inthe user’s asking for more methadone, because the development of tolerancehas outpaced current stable dosing. Abusive use of alcohol and/or benzodiazepineswith methadone maintenance will also cause individuals to request

7. Opioids 153more methadone, possibly because of enhanced hepatic metabolism and/or significantwithdrawal symptoms from these agents that do not share crosstolerancewith methadone. Administering disulfiram with methadone is a commonand highly useful therapeutic approach.Some individuals report that heavy labor with much perspiration reducesthe effectiveness of methadone in a 24-hour period. This phenomenon is usuallyeasily addressed with a small increase in dose, unless the individual is notbeing truthful. After months or years of methadone maintenance, most individualsare able to tolerate a slow taper of a few milligrams per week or month. Forthose persons who become suspicious or psychologically unstable as their dose islowered, a “blind” detoxification schedule may be used, in which the individualnever knows the exact amount of methadone he or she is receiving.Pregnancy is a special situation for which continued methadone maintenanceis recommended, because any withdrawal symptoms place the fetus atrisk for spontaneous abortion (Finnegan, 1979). In addition, relapse to streetdrugs after detoxification also places the fetus at risk. Therefore, maintenanceat a level of 20 mg is the safest plan. Slow detoxification down to this level canbe achieved safely during the second trimester.Other agents may be useful in maintenance of opioid users. Safety, regulatory,and political concerns unfortunately have limited the availability of methadonemaintenance, so that a significant number of opiate dependent individualswho might benefit from this therapy fail to receive it. Because of theseproblems, the federal government in 2003 approved buprenorphine for use inthe treatment of opiate withdrawal and maintenance. As previously discussed,buprenorphine is a long half-life (24 hours), mixed opiate agonist–antagonist.A dose of 8–16 mg of sublingual buprenorphine (Subutex) administered dailyfor 2–4 days can be extremely effective in ameliorating withdrawal symptoms(Bickel et al., 1988). For maintenance treatment, this same dose of sublingualbuprenorphine (in combination with naltrexone to prevent street value, marketedas Suboxone) has been shown to be equivalently effective to methadoneand LAAM in preventing relapse (Johnson et al., 2000; Mattick et al., 2003;Petitjean et al., 2001). Unlike methadone and LAAM, buprenorphine may beprescribed in the general office setting by practitioners specially qualifiedthrough the Drug Enforcement Agency. Currently, candidates for qualificationare those practitioners who are either subspecialty boarded in addiction psychiatry,or who have received 8 hours of training through the American Academyof Addiction Psychiatry or the American Society of Addiction Medicine.A pharmacological agent in the form of an opioid antagonist can be a usefuladjunct in relapse prevention. A long-acting antagonist such as naltrexone(ReVia) is effective in blocking the euphoric effects of opioids and ultimatelyleads to the extinction of operantly conditioned drug-seeking behaviors. Naltrexoneis given orally in the opioid-free individual three times a week in dosesof 50–150 mg, and it blocks the effects of relatively large doses of opioids (John-

154 III. SUBSTANCES OF ABUSEson & Strain, 1999). This adjunctive therapy works best in the context ofongoing treatment and support. Its administration should be monitored overtime, because compliance with voluntary, unsupervised self-administration ofnaltrexone is notoriously poor. Length of treatment with this agent is a therapeuticissue having mainly to do with the individual’s ability to embrace a drugfreelifestyle consistently over time. Because of the significant risk of developinghepatitis during naltrexone treatment, monitoring of liver function tests isimportant.Psychosocial TreatmentsAlthough this chapter has presented only pharmacotherapies for opioid addiction,it is crucial that psychosocial interventions be used to help these patientschange their lifestyles. It is generally accepted that escape from drug seekingand the accompanying antisocial impulses requires a change in deeply rootedbehavioral patterns. Individual and group psychotherapy may be useful inapproaching this goal. Contingency management may be very helpful (Robles,Stitzer, Strain, Bigelow, & Silverman, 2002). The various 12-step programssuch as Narcotics Anonymous are also useful adjuncts to treatment and facilitatesignificant degrees of change. For those persons who continue to relapse inless restrictive treatment settings, a “therapeutic community” may be the appropriatenext step (O’Brien & Biase, 1981); these nonhospital, community-based,24-hour, live-in programs are geared to subject the addict to continuous treatmentpressure for as long as 1 or 2 years. Personal freedom is severely curtailed,and community rules are rigorously enforced. The goal is to use nonviolent buthighly confrontational tactics, in the context of peer pressure, for the purposeof breaking down denial and exposing destructive attitudes and behaviors thatformerly led to drug use (Rosenthal, 1989). A growth process may then occur,allowing the individual to achieve a degree of personal integrity that is unrelatedto the former identity of drug abuser. When successful, this type of personaltransformation can lead to permanent recovery. However, this form oftreatment requires total commitment, which many opioid addicts are unable tomake; thus, the dropout rate is high. As with any treatment modality, selectionof appropriate candidates leads to greater success.REFERENCESAmerican Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders(4th ed., text rev.). Washington, DC: Author.Berger, P. A., & Dunn, M. J. (1986). The biology and treatment of drug abuse. In S.Arieti (Ed.), American handbook of psychiatry (Vol. 8, pp. 811–822). New York:Basic Books.

7. Opioids 155Bickel, W. K., Stitzer, M. L., Bigelow, G. E., Liebson, I. A., Jasinski, D. R., & Johnson,R. E. (1988). A clinical trial of buprenorphine: Comparison with methadone inthe detoxification of heroin addicts. Clin Pharmacol Ther, 43, 72–78.Brewer, C., Rezae, H., & Bailey, C. (1988). Opioid withdrawal and naltrexone inductionin 48–72 hours with minimal drop-out, using a modification of thenaltrexone–clonidine technique. Br J Psychiatry, 153, 340–343.Brooner, R. K., King, V. L., Kidorf, M., Schmidt, C. W. Jr., & Bigelow, G. E. (1997).Psychiatric and substance use comorbidity among treatment-seeking opioid abusers.Arch Gen Psychiatry, 54, 71–80.Charney, D. S., Heninger, G. R., & Kleber, H. D. (1986). The combined use ofclonidine and naltrexone as a rapid, safe, and effective treatment of abrupt withdrawalfrom methadone. Am J Psychiatry, 143, 831–837.Cheskin, L. J., Fudala, P. J., & Johnson, R. E. (1994). A controlled comparison ofbuprenorphine and clonidine for acute detoxification from opioids. Drug AlcoholDepend, 36, 115–121.Deneau, G. A., & Mule, S. J. (1981). Pharmacology of the opiates. In J. H. Lowinson &P. Ruiz (Eds.), Substance abuse: Clinical problems and perspectives (pp. 129–139).Baltimore: Williams & Wilkins.Finnegan, L. P. (Ed.). (1979). Drug dependency in pregnancy: Clinical management ofmother and child. Rockville, MD: National Institute on Drug Abuse.Gerra, G., Marcato, A., Caccavari, R., Fontanesi, B., Deisignore, R., Fertonani, G., etal. (1995). Clonidine and opiate receptor antagonists in the treatment of heroinaddiction. J Subst Abuse Treat, 12, 35–41.Gerstein, D. R. (1990). The effectiveness of treatment. In D. R. Gerstein & H. J. Harwood(Eds.), Treating drug problems (Vol. 1, pp. 132–199). Washington, DC:National Academy Press.Gold, M. S., Pottash, A. C., Sweeney, D. R., & Kleber, H. D. (1980). Opiate withdrawalusing clonidine. JAMA, 243(4), 343–346.Hensel, M., & Kox, W. J. (2000). Safety, efficacy, and long-term results of a modifiedversion of rapid opiate detoxification under general anesthesia: A prospectivestudy in methadone, heroin, codeine, and morphine addicts. Acta AnaesthsiolScand, 44(3), 326–333.Jaffe, J. H. (1989). Psychoactive substance use disorders. In H. I. Kaplan & B. J. Sadock(Eds.), Comprehensive textbook of psychiatry (5th ed., pp. 642–698). Baltimore: Williams& Wilkins.Jasinski, D. R., Johnson, R. E., & Kocher, T. R. (1985). Clonidine in morphine withdrawal:Differential effects on signs and symptoms. Arch Gen Psychiatry, 42, 1063–1066.Johnson, R. E., Chutuape, M. A., Strain, E. C., Walsh, S. L., Stitzer, M. L., & Bigelow,G. E. (2000). A comparison of levomethadyl acetate, buprenorphine, and methadonefor opioid dependence. N Engl J Med, 343, 1290–1297.Johnson, R. E., & Strain, E. C. (1999). Other medications for opioid dependence. In E.C. Strain & M. L. Stitzer (Eds.), Methadone treatment for opioid dependence(pp. 281–321). Baltimore: Johns Hopkins University Press.Khantzian, E. J., & Treece, C. (1985). DSM-III psychiatric diagnosis of narcotic addicts:Recent findings. Arch Gen Psychiatry, 42, 1067–1071.

156 III. SUBSTANCES OF ABUSEKing, V. L., Brooner, R. K., Kidorf, M. S., Stoller, K. B., & Mirsky, A. F. (1999). Attentiondeficit hyperactivity disorder and treatment outcome in opioid abusers enteringtreatment. J Nerv Ment Dis, 187(8), 487–495.Kleber, H. D., Riordan, C. E., Rounsaville, B., Kosten, T., Charney, D., Gaspari, J., etal. (1985). Clonidine in outpatient detoxification from methadone maintenance.Arch Gen Psychiatry, 42, 391–394.Koob, G. F., & Bloom, F. E. (1988). Cellular and molecular mechanisms of drugdependence. Science, 242, 715–723.Martin, W. R., & Jasinski, D. R. (1969). Physiological parameters of morphine dependencein men: Tolerance, early abstinence, protracted abstinence. J Psychiatr Res, 7,9–17.Mattick, R. P., Ali, R., White, J. M., O’Brien, S., Wolk, S., & Danz, C. (2003).Buprenorphine versus methadone maintenance therapy: A randomized doubleblind trial with 405 opioid-dependent patients. Addiction, 98, 441–452.Mirin, S. M., Weiss, R. D., Michael, J., & Griffin, M. L. (1989). Psychopathology insubstance abusers: Diagnosis and treatment. Am J Drug Alcohol Abuse, 14, 139–157.O’Brein, W. B., & Biase, D. V. (1981). The therapeutic community: The family-milieuapproach to recovery. In J. H. Lowinson & P. Ruiz (Eds.), Substance abuse: Clinicalproblems and perspectives (pp. 303–316). Baltimore: Williams & Wilkins.O’Connor, P. G., Waugh, M. E., Carroll, K. M., Rounsaville, B. J., Diagkogiannis, I. A.,& Schottenfeld, R. S. (1995). Primary care-based ambulatory opioid detoxification:The results of a clinical trial. J Gen Intern Med, 10, 255–260.Otto, K. C. (2003). Acupuncture and substance abuse: A synopsis, with indications forfurther research. Am J Addict, 12(1), 43–51.Petitjean, S., Stohler, R., Deglon, J. J., Livoti, S., Waldvogel, D., Uehlinger, C., &Ladenwig, D. (2001). Double-blind randomized trial of buprenorphine and methadonein opiate dependence. Drug Alcohol Depend, 62, 97–104.Rabinowitz, J., Cohen, H., & Atias, S. (2002). Outcome of naltrexone maintenance followingultra rapid opiate detoxification versus intensive inpatient detoxification.Am J Addict, 11(1), 52–56.Robles, E., Stitzer, M. I., Strain, E. C., Bigelow, G. E., & Silverman, K. (2002).Voucher-based reinforcement of opiate abstinence during methadone detoxification.Drug Alcohol Depend, 65(2), 179–189.Rosenthal, M. S. (1989). The therapeutic community: Exploring the boundaries. Br JAddict, 84, 141–150.Senay, E. C. (1983). Substance abuse disorders in clinical practice. Littleton, MA: JohnWright/PSG.Spencer, L., & Gregory, M. (1989). Clonidine transdermal patches for use in outpatientopiate withdrawal. J Subst Abuse, 6, 113–117.Substance Abuse and Mental Health Services Administration. (1995, November). Preliminaryestimates from the Drug Abuse Warning Network (Advance Report No. 11).Washington, DC: Author.Wilford, B. B. (1981). Drug abuse for the primary care physician. Chicago: AmericanMedical Association.Woody, G. E., McLellan, A. T., Luborsky, L., & O’Brien, C. P. (1985). Sociopathy andpsychotherapy outcome. Arch Gen Psychiatry, 42, 1081–1086.

Marijuana, Hallucinogens,and Club DrugsCHAPTER 8DAVID MCDOWELLHallucinogens consist of a disparate group of psychoactive substances, andinclude 3,4-methylenedioxyamphetamine (MDMA), hallucinogens, ketamine,and marijuana. They differ in terms of administration, mechanism of action,and effect. In many cases, they are used by groups of younger people and aretaken in various combinations with each other and other classes of substances,usually in social settings (often at “raves” [see Bellis, Hale, Bennett, Chaudry,& Kilfoyle, 2000] or other parties). At some of these events, a substantialmajority of rave participants are using MDMA, ketamine, gamma-hydroxybutyricacid (GHB), or other drugs, such as marijuana and D-lysergic aciddiethylamide (LSD). In addition, at times inhalants are used at these events(Lee & McDowell, 2003; McDowell & Kleber, 1994; Winstock, Griffiths, &Stewart, 2001). Polysubstance might be considered the norm at such events,with over 80% of participants using more than one substance (Boys, Lenton, &Norcross, 1997; Winstock et al., 2001). Although the demographics and settingsof use have changed, these substances remain significant clinical problems.MARIJUANAMarijuana refers to the dried-out leaves, flowers, stems, and seeds of the hempplant, Cannabis sativa. The plant is a common weed that grows freely in mostareas of the world. Marijuana, also known as cannabis, is also probably the most157

158 III. SUBSTANCES OF ABUSEcommonly used, abusable substance in the world, with the U.N. World DrugReport (1997) estimating 140 million daily users. It is most frequently smokedin small, hand-rolled cigarettes called “joints” (Schwartz, 2002). Alternatively,users employ regular pipes or water pipes called “bongs.” The resin from theflowering tips, hashish, is more potent and may also be smoked (Abel, 1980).Marijuana can also be ingested; usually this occurs when it’s baked into lipidrichfoods, such as brownies.Peak popularity occurred in the late 1970s, then steadily declined until1992. Since that time, marijuana’s use has been on the rise, and whether itscurrent level of use has reached a plateau phase is still a subject of debate. Marijuanahas many purported uses; in recent years, the debate over its controversialrole as a medicine has been revived.HistoryMarijuana has been used since antiquity, and it can be found in numerousancient texts. The oldest known reference to marijuana is in a 15th-centuryB.C. Chinese text on herbal remedy (Walton, 1938). Also, Assyrian cuneiformtablets from 650 B.C. that contain references to people smoking marijuana “aregenerally regarded as obvious copies of much older texts,” according to Walton.Although archeological findings in Berlin, Germany, suggest that marijuanawas in Western Europe by 500 B.C., an exact date or extent of use is unknown.However, hemp-based clothing was widespread in central and southern Italy,and the intoxicating effects of marijuana were also recorded in Renaissancetexts. In Europe, it was quite popular in 19th-century high society. In theUnited States, in the beginning of this century, it was popular principally in theWest and was mostly associated with ethnic groups and jazz musicians. Marijuana’ssocial stigma, epitomized in the now-popular classic cult film ReeferMadness, led Congress to enact the Marijuana Tax Act of 1937 (Bonnie &Whitebread, 1974). This legislation calls for the requirement of a federallyapproved stamp for commerce with marijuana. No such stamps were everissued, however.Marijuana, considered benign by many, became more popular as a mainstreamdrug in late the1960s, coinciding with the growing drug subculture. Itspeak use was in 1979, when approximately 51% of high school seniors admittedto having tried it (Johnson, O’Malley, & Bachman, 2002). Perhaps due to thepublic’s exposure to individuals who used the drug frequently and suffered lethargyand impairment from it, as well as pressure from the newly emerging law indrugs, marijuana use declined substantially through the 1980s, bottoming out at22% in 1992 (Johnson et al., 2002). The mid-1990s, however, saw substantialincrease in the popularity of the drug, with 1996 being the peak year for 8thgraders, and 1997 for 10th and 12th graders. Coinciding with this resurgence ofdrug use, mainstream iconographic representations of the marijuana plant also

8. Marijuana, Hallucinogens, and Club Drugs 159began appearing on numerous articles of clothing (from such companies aswww.happyhippie.com or www.hempstyle.com), worn by both adolescents andadults, thereby attesting to widespread renewed interest among marijuana users.Mechanism of ActionMarijuana smokers usually inhale deeply, with the user keeping the smoke inhis or her lungs for as long as possible. This allows for 25–50% of the delta-9-tetrahydrocannabinol (THC) in the marijuana cigarette to be absorbed. THCis the most potent, but by no means the only, active ingredient in marijuana.THC is the psychoactive substance of most studies, and the one that most literatureagrees is responsible for its psychoactive property. THC is to marijuana asnicotine is to tobacco. The THC level in the blood is quickly distributedthroughout the body, especially in areas with high fat content, such as the brainand testes for men. THC then leaches out, and small levels of the drug can bedetected in the bloodsteam. This effect lasts for 2–4 days in a naive user and aslong as 2 months in a heavy daily user. It should be noted that though the urinetest would be positive in such a person, the marijuana would not be intoxicating,unless the person had used additional doses. As with other drugs of abuse, itis the rise in concentration of THC that is intoxicating, and this residualamount that leaches out into the bloodsteam probably does not have mucheffect on the user.While the effects of the drug can be felt almost immediately, usually heraldedby the giggles of the new initiator, the peak effect occurs after about 20minutes. The user feels a mild euphoria, an alternation of sensory acuity, and adistortion of time perception. These effects gradually diminish over the next 3–4 hours. For persons who ingest marijuana, the effects also begin in 20–30 minutesbut peak at about 2 hours. The effects of the orally ingested drug usuallylast for up to 8 hours. Most users of the oral form cite it as reinforcing, butdescribe the subjective effect as “heavy.” The molecular bases of THC’s actionsare only now being understood. It has a number of physiological properties thatact like a barbiturate, and it has anticonvulsant activity, as well as opioid properties,causing weak analgesia and antidiarrheal action. In addition, it suppressesrapid eye movement (REM) nondream sleep. Smokers of marijuana usuallyreport an increase in nonrestorative sleep. It increases brain limbicstimulation and is thought to activate the pleasure/reward system in the brain.It is for this reason that it is an addictive agent.In recent years, a specific receptor in the mammalian and hence thehuman brain has been discovered and, in fact, cloned (Sugiura & Waku, 2002).There are at least two subtypes of this receptor. Along with it, a natural ligandin marijuana, anandamide, has been identified. Substances of abuse mimic moleculesthat naturally occur in the brain. Such compounds (the naturally occurringones), called ligands, have an effect on the receptors to which they have an

160 III. SUBSTANCES OF ABUSEaffinity. This effect may be to stimulate, to inhibit, or a variety of in-betweeneffects. The natural ligand for marijuana is called anandamide, and its receptoris the anandamide receptor. Interestingly, the term “anandamide” is derivedfrom the Hindi word for bless. At present, pharmaceutical companies have synthesizedboth agonists and antagonists to the receptor. Much research has beenconducted to identify the properties of these compounds, but it is still unclearwhat function they serve in mammalian and human brains. Cannabinoid receptorshave been described in various regions of the brain, with the greatest abundancein the basal ganglia and hippocampus, areas involved with memory function.The hemp plant synthesizes at least 400 chemicals, of which more than 60are cannabinoid. Pyrolyzing the plant can create even more molecules. Very littleis known about the vast majorities of these molecules or their effects onhuman. The most psychologically and physiologically active compound isTHC. In the pyrolyzed form, it actually becomes delta-11-tetrahydrocanbonol.This molecule is believed to account for most of marijuana’s effects. There are,however, numerous compounds whose effects remain completely unknown. Forinstance, it is known that marijuana use raises the seizure threshold overall andmakes it more difficult to have a seizure (Zagnoni & Albano, 2002). THCalone decreases the seizure threshold. This property of marijuana, therefore, isnot the result of THC, but rather some other cannabinoid. The two most abundantcannabinoids are cannabinol and cannabidiol. Much research is currentlyunderway regarding the possible use of marijuana in clinical or other settings.Physiological EffectsCannabis intoxication commonly heightens the user’s sensitivity to externalstimuli, thus making colors seem brighter and smells more pungent. It also distorts,sometimes severely, the user’s sense of time. The term “temporal disintegration”(Mathew, Wilson, Humphreys, Lowe, & Weithe, 1993) has beencoined to describe this slowing of subjective time after use of marijuana. Inaddition, at least in low doses, marijuana causes mild euphoria and feelings ofrelaxation. It is also know to increase appetite. There is some controversy overwhether individuals intoxicated with cannabis pose a hazard, as they seem to beattracted to thrill-seeking behavior and are usually subdued. Some people haveargued that individuals who smoke marijuana are less likely to drive fast; however,reaction time to complex and unforeseen situations is slowed, and musclestrength and hand–eye coordination is decreased. Because it delays reactiontime, alters time perception, and for many other reasons, marijuana must beconsidered a danger to those who would operate a motor vehicle or use complexmachinery or equipment, thus putting themselves and others in danger.At higher dose levels and with chronic patterns of use, cannabis caninduce panic attacks (Deas, Gerding, & Hazy, 2000). This is especially com-

8. Marijuana, Hallucinogens, and Club Drugs 161mon in first-time users or in older experimenters who have not used marijuanafor a long time. Hypervigilance, sometimes resembling frank paranoia, is seenwith higher doses. Cannabis-induced psychosis is rare but does occur, especiallyin countries where heavy smoking is more common and the THC concentrationof the plant is higher (Chopra & Smith, 1974). The term “hemp insanity”refers to this type of psychosis. The question of whether the drug causes longtermpsychotic disorders is more difficult to answer. Clearly, first-break psychoticepisodes are commonly associated with marijuana ingestion, but again,whether they are causal is a matter of debate. More probably, individuals whoare prone to psychosis are attracted to the drug. In a population that is prone topsychosis, such as individuals with schizophrenia, marijuana is a risk factor forrelapse and psychosis (Arseneault, Cannon, Witton, & Murray, 2004; Verdoux,Gindre, Sorbara, Tournier, & Swendsen, 2003).Much has been written about the amotivational syndrome, and it hasremained a controversial entity (Lynskey & Hall, 2000). It is marked by apathy,poor concentration, social withdrawal, and loss of interest in achievements(Solowij, 1998). Because research in the topic is contradictory, it isunclear at this time whether marijuana induces amotivational attitudes andbehavior or causes permanent, irreversible impairment in cerebral function.However, the general consensus is that it likely does not cause permanentcognitive damage. Still, individuals who are chronic users tend to smoke marijuanaoften and in high doses; cannabis has a long half-life, and users can bethought to be chronically under the influence of marijuana or “stoned.” Somarijuana clearly causes impairment in the acquisition of short-term memory,at least for the time an individual is intoxicated, although there is evidenceof specific residual effects (Block, 1996; Pope & Yurgelun-Todd, 1996;Schwartz, 1991). If an individual, especially a young person, is “stoned”nearly all the time, his or her accumulation of knowledge will be seriouslyimpaired (Lynskey & Hall, 2000; Solowij, Michie, & Fox, 1995). If theintoxication continues long enough during critical growing time, it may havepermanent consequences. This is the most dangerous and insidious aspect ofmarijuana use. A high school student who is constantly “stoned” will notlearn to the degree to which he or she is capable of functioning. For manypeople, this will lead to a lifetime deficit that can never be completelyrepaired.TreatmentMarijuana withdrawal has been demonstrated in laboratory animals, as well asin humans, and is now well documented. Chronic heavy users of cannabis mayexperience some withdrawal in the form of irritability, general discomfort, disruptedsleep, and decreased appetite (Budney, Moore, Vandrey, & Hughes,2003). This syndrome is not as painful as that with heroin, as dangerous as that

162 III. SUBSTANCES OF ABUSEwith alcohol, or as long-lasting as that with cocaine. It may contribute torelapse in some individuals.The clinician is confronted with a wider range of marijuana users. At oneend is the individual who uses the drug only rarely, but whose use is detected ona routine drug screen and brought to the clinician’s attention, perhaps for anevaluation. Brief assessment, to make sure the problem is not more serious thanit appears, is always necessary in this case. Subsequent follow-up, to ensure thatthe initial impression was correct, is part of a thorough assessment. In thisinstance, the user is usually embarrassed and repentant, and has no objection tofuture monitoring. Users who do not have a problem with marijuana do nothave a problem giving it up. They may be able to use it in the future, once theyhave demonstrated the capacity for voluntary nonuse.On the other end of spectrum is the person, most predictably the adolescent,who uses the drug both daily and heavily. In this case, the individual mayneed much more intensive rehabilitation and may need to be admitted to a residentialdrug treatment facility. In any case, the clinician must be alert to anyunderlying comorbid condition and treat it appropriately. Many researchersbelieve that marijuana is administered as a form of self-medication (Marmor,1998).The comorbid conditions that have been suggested to be associated withmarijuana use range from the personality disorders to psychotic spectrum illness.In certain personality disorders, the drug’s sedating and anxiolytic propertiesmay be used to reduce painful affects. In some mode disorders, marijuanamay be a form of self-medication for agitation, even manic or hypomanic states.This hypothesis is still quite intriguing and controversial; at the present time,there is only anecdotal and circumstantial evidence for its existence.In recent years, there has been increased interest in “medicinal marijuana”(Iversen & Snyder, 1999) as an advocacy issue for such conditions as glaucoma(American Academy of Opthalmology, 1992; Hepler & Petrus, 1976; NationalEye Institute, 1997), epilepsy (Feeney, 1976), nausea and other symptoms associatedwith cancer and chemotherapy (Kris et al., 1996; Maurer, Henn,Dittrich, & Hofmann, 1990; Nelson et al., 1994; Sallan, Zinberg, & Frei, 1975;Tramer et al., 2001; Vinciguerra, Moore, & Brennan, 1988). In general, thereare better and safer agents for such medical conditions. Marijuana may, however,have some use, and the issue has been subject to much debate within thepublic arena, such as California voters’ passing of the Compassionate Use Act(Proposition 215) (Marmor, 1998). Although the possible medicinal benefits ofmarijuana have been a matter of perennial debate within the medical communityas well (Grinspoon & Bakalar, 1995; Kassirer, 1999), with articles andcommentary frequently appearing in the Journal of the American Medical Associationand the New England Journal of Medicine, the issue has yet to havebeen satisfactorily resolved through sound, scientifically methodical research(National Institutes of Health, 1997).

8. Marijuana, Hallucinogens, and Club Drugs 163MDMAMDMA has many names, but is perhaps best known as Ecstasy. It is sometimesclassified as a stimulant and does have similar properties to the amphetamines,although it also has some unique effects that distinguish it (Hermle et al., 1993;Shulgin, 1986). MDMA was legal in this country until 1985, when it was madea Schedule I drug. Prior to that, its use was unregulated and therefore legal.The primary appeal of MDMA is its psychological effect, a dramatic andconsistent ability to induce a profound feeling of attachment and connection inthe user. The compound’s street name is perhaps a misnomer; the Los Angelesdrug dealer who coined the term “Ecstasy” originally wanted to call the drug“Empathy,” but asked, “Who would know what that means?” (Eisner, 1968).MDMA has long been known to damage brain serotonin (5-HT) neuronsin laboratory animals (McCann & Ricaurte, 1993; Montoya, Sorrentino, Lucas,& Price, 2002). Although a minority of researchers disagree with the conclusion,it has become increasingly apparent over the past decade that MDMA isneurotoxic to humans. Furthermore, the neurotoxicity has real and functionalimplications (McCann, Eligulashvili, & Ricaurte, 2000; Montoya et al., 2002;Morgan, 2000; Sprague, Everman, & Nichols, 1998). Ecstasy use is associatedwith sleep, mood, and anxiety disturbances, elevated impulsiveness, memorydeficits, and attention problems. Many of these disturbances appear to be permanentand seem likely to depend on the overall amount of MDMA consumedover time, but may be caused by as little as a single dose (Rodgers, 2000; Turner& Parrott, 2000).HistoryA synthetic process for the creation of MDMA was patented in 1914 by Merckin Darmstadt, Germany (Shulgin, 1990). MDMA was not, as is sometimesthought, intended as an appetite suppressant. It was most likely developed as anexperimental compound. Except for a minor chemical modification mentionedin a patent in 1919, there is no other known historical record of MDMA untilthe 1950s. At that time, the United States Army experimented with MDMA.The resulting information was declassified and became available to the generalpublic in the early 1970s. These findings consisted primarily of a number ofLD 50(median lethal dose) determinations for a variety of laboratory animals.Humans probably first used MDMA in the late 1960s. It was discovered asa recreational drug by free-thinking individualists (New Age seekers), peoplewho liked its properties of inducing feelings of well-being and connection(Watson & Beck, 1986). MDMA does induce feelings of warmth and connectedness,and using this rationale, its use was promulgated by therapists in the1970s (Shulgin, 1990). Before the compound became illegal in 1985, it wasused extensively for this purpose (Beck, 1990).

164 III. SUBSTANCES OF ABUSEAlthough for an organic chemist, the synthesis of MDMA is reasonablysimple, most supplies in the United States are imported and then distributed byorganized crime networks. Its price, usually $25–40 for a 125-mg tablet, theamount producing the sought-after effect in most intermittent users (Green,Cross, & Goodwin, 1995), has remained remarkably stable over the past twodecades. This high price makes adulteration attractive to the criminal element.Such adulteration can be dangerous when the substance used is something thatis physiologically dangerous. Paramethoxymethamphetamine (PMA) has beensold as MDMA, and in those unfortunate enough to consume both substances,appears to be highly dangerous.Physiological EffectsMDMA is almost exclusively available in pill form. Often the pills are stampedwith clever images. The usual single dose is 100–150 mg. The onset of effectbegins about 20–40 minutes after ingestion and is experienced with immediacy.Often this “rush” is accompanied by nausea and an urgent need to defecate(disco dump).The plateau stage of drug effects lasts 3–4 hours. The principal desiredeffect, according to most users, is a profound feeling of relatedness to the restof the world. Most users experience this feeling as a powerful connection tothose around them, as well as to the universe (Leister, Grob, Bravo, &Walsh, 1992). Although the desire for sex can increase, the ability to achievearousal and orgasm is greatly diminished in both men and women (Buffum &Moser, 1986). MDMA has thus been termed a sensual, not a sexual, drug.The prescription drug sildenafil (Viagra) may be taken in order to counteractthis effect, and may be sold along with MDMA (Weir, 2000); the successormedications involving sexual enhancement can be expected to be used inthis manner. The array of physical effects and behaviors produced by MDMAis remarkably similar across mammalian species (Green et al., 1995) andincludes mild psychomotor restlessness, bruxism, trismus, anorexia, diaphoresis,hot flashes, tremor, and piloerection (Peroutka, Newman, & Harris,1998).Aftereffects associated with MDMA are common and can be pronounced.People using MDMA once, or on multiple occasions, may experience any numberof symptoms, including lethargy, anorexia, decreased motivation, sleepiness,depression, and fatigue. Combining MDMA with PMA has been associatedwith a number of serious adverse events and deaths (Ling, Marchant,Buckley, Prior, & Irvine, 2001). Another acute adverse event, hyponatremia,followed by seizure and coma, appears be a result of the law of unintended consequences.The “harm reduction” admonition of advising MDMA users toadopt the strategy of ingesting copious amounts of water prior to and while takingMDMA appears, in some instances, to have backfired and has caused these

8. Marijuana, Hallucinogens, and Club Drugs 165severe physiological adverse events (Ajaelo, Koenig, & Snoey, 1998; Holmes,Banerjee, & Alexander, 1999).Severe, immediate effects appear to be rare, but they do occur: alteredmental status, convulsions, hypo- or hyperthermia, severe changes in bloodpressure, tachycardia, coagulopathy, acute renal failure, hepatotoxicity, rhabdomyolysis,and death have all occurred (Demirkiran, Jankovic, & Dean, 1996;Khalant, 2001). There are numerous case reports of a single dose of MDMAprecipitating severe psychiatric illness. MDMA probably induces a range ofdepressive symptoms and anxiety in some individuals; for that reason, peoplewith affective illness should be specifically cautioned about the dangers ofusing MDMA (Cohen, 1998; McCann, Ridenour, Shaham, & Ricaurte, 1994;McDowell, 1998).Mechanism of ActionMDMA is a “dirty drug,” affecting many neurotransmitter systems. It is primarilyserotonergic, and its principal mechanism of action is as an indirect serotonergicagonist (Ames & Wirshing, 1993; Rattray, 1991; Sprague et al., 1998).The drug’s effects, and side effects (an arbitrary distinction), including anorexia,psychomotor agitation, difficulty in achieving orgasm, and profoundfeelings of empathy, can be explained as a result of the flooding of the serotoninsystem (Beck & Rosenbaum, 1994). After ingestion, MDMA is taken up by theserotonin cells through active channels, effecting the release of serotoninstores. MDMA also blocks reuptake of serotonin, and this contributes to itslength of action. Although it inhibits the synthesis of new serotonin, this doesnot contribute to the intoxication phase, but it may contribute to sustainedfeelings of depression reported by some users and to a diminished magnitude ofsubjective effects when the next dose is taken within a few days of the first dose.Most people who use MDMA on a regular basis tend not to increase theiruse as time goes on (Cohen, 1998; Peroutka, 1990). Because of its mechanismof action (the drug depletes serotonin stores and inhibits synthesis of new serotonin),subsequent doses produce a diminished high and a worsening of thedrug’s undesirable effects, such as psychomotor restlessness and teeth gnashing.MDMA users most typically become aware of the benefits of periodic, even rareuse. First-time users are often instant advocates of MDMA, only to have theirenthusiasm dampen with time. An adage about Ecstasy captures this succinctly:“Freshmen love it, sophomores like it, juniors are ambivalent, and seniors areafraid of it” (Eisner, 1993).MDMA’s effects may be arbitrarily divided into short- and long-term categories(McKenna & Peroutka, 1990). The short-term effects presumably resultfrom the acute release of serotonin and are associated with decreases in serotoninand 5-hydoxyindoleacetic acid (5-HIAA), and in tryptamine hydroxylase(TPH) activity. The long-term effects are manifested by a steady, slow decrease

166 III. SUBSTANCES OF ABUSEin serotonin and 5-HIAA after initial recovery, persistently depressed TPHactivity, and a decrease in serotonin terminal density (Demirkiran et al., 1996;Ricaurte, McCann, Szabo, & Scheffel, 2000). 5-HIAA levels most typicallyrecover to baseline levels within 24 hours.NeurotoxicityThe most important individual and public health danger posed by the widespreaduse of MDMA is the likelihood that it causes the permanent destructionof serotonin axons in humans who use it. The ingestion of MDMA in laboratoryanimals causes a decrease in the serum and spinal fluid levels of 5-HIAA ina dose-dependent fashion (McCann et al., 2000; Shulgin, 1990) and damagesbrain serotonin neurons (Burgess, McDonoghoe, & Gill, 2000; McCann &Ricaurte, 1993; Montoya, Sorrentino, Lucas, & Price, 2002). The dosage necessaryto cause permanent damage to most rodent species is many times greaterthan that normally ingested by humans (Shulgin, 1990). In nonhuman primates,the neurotoxic dosage approximates the recreational dosage taken byhumans (McCann & Ricaurte, 1993). A recent study by Ricaurte and McCann(2001), which reported an alarmingly small dose necessary for the neurotoxicityto occur, has subsequently been retracted due to a human error in the laboratory(Walgate, 2003). Nevertheless, like its close structural relative methylenedioxyamphetamine(MDA, or “Eve”), MDMA has been found to damageserotonin neurons in all animal species tested to date (McCann, Slate, &Ricaurte, 1996), and the same is likely to occur in humans.MDMA produces a 30–35% drop in serotonin metabolism in humans(McCann et al., 1994). Even one dose of MDMA may cause lasting damage tothe serotonin system. There are many reports of individuals with lasting neuropsychiatricdisturbances after MDMA use (Cohen, 1998; Creighton, Black, &Hyde, 1991; McCann & Ricaurte, 1991; Schifano, 1991). Such damage mightbecome apparent only with time or under conditions of stress. Users with noinitial complications may manifest problems over time (McCann et al., 1996).For obvious reasons of safety and ethics, human studies are more difficultto execute, and those that are done offer legitimate and ample room for criticism.The bulk of evidence that MDMA is neurotoxic in humans is indirect butconvincing (Burgess et al., 2000; Green et al., 1995). This evidence includesmetabolite studies, which quantify the levels of serotonin and metabolites inpopulations of Ecstasy users. An increasing number of investigations demonstratethat metabolite levels of serotonin are much lower in chronic users, evenwhen abstinent for long periods of time. The difficulties of the studies notwithstanding,the available clinical evidence suggests that repeated ingestion ofhigh doses of MDMA produces long-term reductions in serotonergic activityand degeneration of serotonergic terminals in humans (Montoya et al., 2002).

8. Marijuana, Hallucinogens, and Club Drugs 167Extensive cognitive studies in individuals using MDMA, though rife withmethodological problems, show a consistent pattern of cognitive dysfunctionseen in the frontal cortex and the hippocampus. This phenomenon is consistentwith that found in animals exposed to MDMA (Fox, Parrott, & Turner,2001; Montoya et al., 2002). Psychiatric problems, such as depression, anxiety,panic, increased impulsiveness, and sleep disturbances, are significantly higherin MDMA users, even when users are abstinent and the last use is remote. In asymposium (“Is MDMA a Human Neurotoxin?”), Turner and Parrott (2000)concluded: “Novel studies . . . confirmed and extended the range of cognitive,behavioral, EEG, and neurological deficits, displayed by drug-free Ecstasy users.Moreover, these deficits often remained when other illicit drug use was statisticallycontrolled. In conclusion: If MDMA neurotoxicity in humans is a myth,then it is a myth with a heavy serotonergic component.” A recent study byRicaurte, Yuan, Hatzidiitrious, Cord, and McCann (2002) implicated MDMAas causal of dopaminergic neurotoxicity as well. The involvement of the dopaminesystem has important implications in terms of increased vulnerability to avariety of motor and cognitive functions. Some of the more dramatic results ofthe work of Ricaurte have recently been thrown into doubt and are controversial,but the basic results of his and others’ work are still considered consistent.This is a general chapter dealing with all aspects of club drugs and MDMA. Thereader is directed to several excellent and extensive reviews of the particularsubject of MDMA and neurotoxicity (McCann et al., 2000; Montoya et al.,2002; Verkes et al., 2001).TreatmentThe treatment of MDMA abuse may be divided into the treatment of acute reactionsto the drug and the treatment of those who abuse the drug chronically.Urgent TreatmentsFatalities from Ecstasy use and overdose, although rare, do occur. Becausepolydrug use is the norm in many of the venues where Ecstasy is popular (Lee &McDowell, 2003), it is sometimes difficult to ascertain the contribution ofMDMA versus those other substances. Fatalities can be caused by hyperpyrexia,rhabdomyolysis, intravascular coagulopathy, hepatic necrosis, cardiac arrhythmias,cerebrovascular accidents, as well as by a variety of behaviors associatedwith confusion and impaired judgment (Khalant, 2001).Ecstasy has many chemical similarities to amphetamine, and drug detectionproducts may indicate a positive presence of amphetamine after use.MDMA intoxication or overdose may be suspected in any individual with alterationsof sensorium, hyperthermia, muscle rigidity, and/or fever. Because the

168 III. SUBSTANCES OF ABUSEdrug is used in specific settings and by specific subgroups, the level of suspicionshould take into account the user and the circumstance involved. If an individualpatient has been to a rave, or to some club event, this should raise the clinician’ssuspicion that MDMA was ingested. In addition, the clinician shouldhave a high degree of suspicion that the patient may have taken multiple drugs.Drugs that may have been substituted for Ecstasy tablets, such as ephedrine,Ma-Huang (herbal ecstasy), and caffeine, should be considered.Tachycardia, agitation, tremor, mydriasis, and diaphoresis may occur withMDMA intoxication. Ecstasy ingestion may mimic LSD or other classic hallucinogeningestion. In addition, MDMA overdose may mimic the ingestion ofan anticholinergic agent (Shannon, 2000). Anticholinergic agents induce dry,hot skin, however; this result is in contrast to MDMA, which, except in thecase of dehydration, causes diaphoretic skin.Ecstasy overdose would most likely involve the ingestion of multiple dosesand also occur in an environment that induced dehydration. MDMA overdoseor toxic reaction is a diagnosis by exclusion. Supportive measures, such as effectivehydration using intravenous fluids and lowering the temperature of thepatient with cooling blankets or an ice bath, are often necessary. Standard gastriclavage should be employed (Schwartz & Miller, 1997). Physical restraintmay be necessary for agitated patients but should be used sparingly. Benzodiazepinesare the preferred choice as sedating agent (Shannon, 2000). Hypertensionoften resolves with sedation. If it persists, nitroprusside, or a calciumchannelblocker, is preferred over a beta-blocker, which may worsen vasospasmand hypertension (Holland, 2001).Nonurgent TreatmentMDMA ingestion may be associated with a number of adverse psychiatricsymptoms, notably, anxiety, panic, and depression. These symptoms usuallysubside in a matter of hours or days. Support and reassurance are often all that isneeded. If the symptoms are severe, brief pharmacotherapy to alleviate symptomsis recommended.Although classical physiological dependence on MDMA does not occur,some individuals use the drug compulsively. For these people, the standardarray of treatments, based on a thorough assessment of internal and externalresources, should be employed.Adolescents are frequent users of MDMA and the population most likelyto present with this as the drug causing the most problems for them (McDowell& Spitz, 1999). Furthermore, they are more likely to be involved with the subculturethat is enmeshed with MDMA, and that views the drug as harmless atworst, and life-transforming at best (Beck & Rosenbaum, 1994; Winstock et al.,2001). Clinicians are cautioned against adopting a knee-jerk, negative attitudethat may inadvertently preclude the initiation of a therapeutic alliance.

8. Marijuana, Hallucinogens, and Club Drugs 169KETAMINESpecial K, Super K, Vitamin K, or just plain K, are all names for the nonanalgesicanesthetic ketamine. Ketamine was first manufactured in 1965. Veterinariansand pediatric surgeons still legally manufacture it, primarily for therapeutic use;recent crackdowns on the illegal distribution of ketamine from these sourceshave led to the increased smuggling of it from foreign sources. The recreationaluse of ketamine probably began in the 1960s and was first described in detail byLilly (1978). Since that time, its popularity has continued to rise (Cooper,1996; Dotson, Ackerman, & West, 1995; Graeme, 2000).Ketamine is classified as a dissociative anesthetic. As this classificationimplies, the drug causes a dose-dependent dissociative episode, with feelings offragmentation, detachment, and what one user has described as “psychic/physical/spiritualscatter.” Use of ketamine imparts a disconnection from awarenessof stimuli from the general environment. This includes but is not limited topain.HistoryKetamine was first manufactured in 1965 at the University of Michigan andmarketed under the name of Ketalar. It is most commonly available in 10-ml(100 mg/ml) liquid-containing vials (Fort Dodge Laboratories, 1997). It is aclose chemical cousin of phencyclidine, also known as PCP or angel dust. PCPhas physiological properties that made it advantageous as an anesthetic. PCPdoes not cause the kind of cardiac arrhythmias and respiratory depression inherentin classical anesthetics. PCP also had a number of severe limitations as ananesthetic, most significantly, that it causes a high degree of psychotic and violentreactions (National Institute on Drug Abuse, 1979). These effects occur atan alarmingly high rate (50%) and may persist for as long as 10 days (Crider,1986; Meyer, Greifenstein, & DeVault, 1959). Ketamine produces minimal cardiacand respiratory effects, and its anesthetic and behavioral effects remit soonafter administration (Moretti, Hassan, Goodman, & Meltzer, 1984; Pandit,Kothary, & Kumar, 1980). The medication continues to have therapeutic usefulness,principally with children and animals.Since the 1970s, ketamine has been a drug used for “recreational” purposes.Although the distinction is by no means complete, ketamine users clusterinto two distinct subtypes. The first type uses ketamine in a solitary fashion;the second type uses the drug in a social setting, although the effects of the drugdo not promote sociability. These are the young clubgoers and “ravers” (Weir,2000). Ketamine is especially popular at circuit parties and thus a favorite of gayurbanites (Lee & McDowell, 2003).Ketamine is commercially available as a liquid. About 90% of ketaminecomes from diverted veterinary sources (National Institute on Drug Abuse,

170 III. SUBSTANCES OF ABUSE2002). The liquid form is easily evaporated into a powder, the form in which itis most often sold. Ketamine can be administered in a variety of ways. At clubs,most people snort lines of the powder. Ketamine may also be dabbed on thetongue or mixed with a liquid and imbibed.Physiological EffectsKetamine has been studied extensively in humans. It is a noncompetitive N-methyl-D-aspartate (NMDA) antagonist (Curran & Monaghan, 2001). Recreationalusers of ketamine report feeling anesthetized and sedated in a dosedependentmanner (Krystal et al., 1994). Ketamine can influence all modes ofsensory function (Garfield et al., 1994; Óye, Paulsen, & Maurset, 1992). Attypical dosages, ketamine distorts sensory stimuli, producing illusions (Garfieldet al., 1994). In higher than typical dosages, hallucinations and paranoid delusionscan occur (Malhotra et al., 1996).Ketamine substantially disrupts both attention and learning. In humanresearch subjects, ketamine affects the ability to modify behavior, to learn newtasks, and to remember (Curran & Monaghan, 2001; Krystal et al., 1994). Therecreational dosage of ketamine is approximately 0.4 mg/kg, and the anestheticdosage is almost double that. The median lethal dose (LD 50) is nearly 30 timesthe anesthetic dosage, which makes overdose from ketamine very rare.One dose of ketamine creates a “trip” that lasts about 1 hour (Delgarno &Shewan, 1996). Larger doses last longer and have a more intense effect(Malhotra et al., 1996). The user feels physical tingling, followed by a feelingof removal from the outside sensory world. Tolerance develops rapidly toketamine, and dependence, though rare, is well known. Flashbacks have beenreported, and their incidence may be higher than with many other hallucinogens(Siegel, 1984). Ketamine works in a dose-dependent fashion. Mild dosesinvolve an autistic stare and a paucity of thinking. Higher doses result in the K-hole phenomenon, which is characterized by social withdrawal, autistic behavior,and an inability to maintain a cognitive set. Such individuals may bedescribed as zombie-like (Gay Men’s Health Crisis, 1997).Mechanism of ActionKetamine is chemically similar to PCP but has important differences (Jansen,1990). Ketamine binds to the NMDA receptor complex on the same site asPCP, located inside the calcium channel. It works by inhibiting several ofthe excitatory amino acid neurotransmitters (Cotman & Monaghan, 1987;Hampton et al., 1982). Ketamine works globally, affecting numerous neurotransmittersystems, but its action, as an NMDA antagonist, is likely the causeof its schizotypal and dissociative symptoms. NMDA blockade causes anincrease in dopamine release in the midbrain and prefrontal cortex as well

8. Marijuana, Hallucinogens, and Club Drugs 171(Bubser Keseberg, Notz, & Griffiths, 1992), and this is likely the cause of itsability to reinforce and cause dependence. Furthermore, persisting memory deficitshave been demonstrated (Curran & Monaghan, 2001).TreatmentThe most dangerous effects of ketamine are behavioral. Individuals maybecome withdrawn, paranoid, and physically sloppy. In the event of dealingwith an individual who is intoxicated on ketamine, the physician must treatthe individual symptomatically. Calm reassurance and a low-stimulation environmentare usually most helpful. The patient should be placed in a part of theclinic or emergency room with the least amount of light and stimulation. Ifnecessary, the patient may be given benzodiazepines to control the associatedanxiety (Graeme, 2000). Neuroleptics should be avoided, because the sideeffectprofile may cause discomfort and possibly exacerbate the patient’s agitatedstate.Ketamine is an addictive drug. There are numerous reports of individualswho have become dependent on the drug and use it daily (Galloway et al.,1997; Jansen, 1990). Such dependence should be treated in the same manner asany other chemical dependence. The clinician should do a careful evaluation inorder to discern other psychological conditions. These should be dealt with inthe most clinically expeditious manner.HistoryGHBGHB was first synthesized in the mid-1970s by Dr. H. Laborit, a Frenchresearcher interested in exploring the effects of gamma-aminobutyric acid(GABA) in the brain. Laborit was attempting to manufacture a GABA-likeagent that would cross the blood–brain barrier (Vickers, 1969). During the1980s, GHB was widely available in health food stores. It came to the attentionof authorities in the late 1980s as a drug of abuse, and the Food and DrugAdministration (FDA) banned it in 1990, after reports of several poisoningswith the drug (Chin, Kreutzer, & Dyer, 1992). In the past decade, it hasbecome more widely known as a drug of abuse associated with nightclubs andraves.GHB is known as “liquid Ecstasy,” and in Great Britain as GBH, or “grievousbodily harm.” It can be found, occurring naturally, in many mammaliancells. In the brain, the highest amounts are found in the hypothalamus andbasal ganglia (Gallimberti et al., 1989). It is likely that it is itself a neurotransmitter(Galloway et al., 1997). GHB is closely linked to GABA and is both aprecursor and a metabolite of GABA (Chin et al., 1992).

172 III. SUBSTANCES OF ABUSEIn the 1970s, GHB was available commercially as a sleep aid. It has somedemonstrated therapeutic efficacy, particularly in the treatment of narcolepsy(Lammers et al., 1993; Mamelak, Scharf, & Woods, 1986; Scrima, Hartman,Johnson, Thomas, & Hiller, 1990). In 1990, after reports indicated that GHBmight have contributed to the hospitalization of several California youth, theFDA banned it. GHB has an extremely small therapeutic index, and as little asdouble the euphorigenic dose may cause serious central nervous system (CNS)depression. In recent years, it has been associated with numerous incidents ofrespiratory depression and coma. Increasing numbers of deaths have beenlinked to GHB (Li, Stokes, & Woeckner, 1998).The legal status of GHB is complicated. Recently, GHB, under the brandname Xyrem, was classified as a Schedule III controlled substance, but with specialregulations. The company that makes and markets the medication hasdeveloped a rigorous system that makes Xyrem available to patients from a singlespecialty pharmacy. Both physicians and patients must receive an educationprogram from the manufacturer, Orphan Medical, before obtaining Xyrem.Orphan Medical has worked closely with the FDA, the Drug EnforcementAdministration (DEA), and law enforcement agencies to develop strict distributionand risk-management controls designed to restrict access to Xyrem tothe intended patient population (Tunnicliff & Raess, 2002). Illicit use ofXyrem is subject to penalties reserved for Schedule I drugs.Most of the GHB sold in the United States is of the bootleg variety, manufacturedby nonprofessionals. In fact, it is relatively easy to manufacture, andInternet sites devoted to explaining the process can be found readily, althoughthey are sometimes cleverly concealed.Physiological EffectsGHB is ingested orally, absorbed rapidly, and reaches peak plasma concentrationsin 20–60 minutes (Vickers, 1969). The typical recreational dosage is0.75–1.5 g; higher dosages result in increased effects. The high lasts for no morethan 3 hours and reportedly has few lasting effects. Repeated use of the drug canprolong its effects.Users of the drug report that GHB induces a pleasant state of relaxation andtranquility. Frequently reported effects are placidity, mild euphoria, and anenhanced tendency to verbalize. GHB, like MDMA, has also been described as asensual drug. Its effects have been likened to alcohol, another GABA-like drug(McCabe, Layne, Sayler, Slusher, & Bessman, 1971). Users report a feeling ofmild numbing and pleasant disinhibition. This effect may account for the reportsthat GHB enhances the experience of sex. The dose–response curve for GHB isexceedingly steep. The LD 50is estimated at perhaps only five times the intoxicatingdosage (Vickers, 1969). Furthermore, the drug has synergistic effects withalcohol and probably other drugs as well. Therefore, small increases in the

8. Marijuana, Hallucinogens, and Club Drugs 173amount ingested may lead to significant intensification of the effects and to theonset of CNS depression. Overdose is a real danger. Users who drink alcohol,which impairs judgment and with which synergy is likely, are at greater risk.The most commonly experienced side effects of GHB are drowsiness, dizziness,nausea, and vomiting. Less common side effects include weakness, loss ofperipheral vision, confusion, agitation, hallucinations, and bradycardia. Thedrug is a sedative and can produce ataxia and loss of coordination. As dosesincrease, patients may experience loss of bladder control, temporary amnesia,and sleepwalking. Clonus, seizures, and cardiopulmonary depression can occur.Coma and persistent vegetative states, and death may result from overdose(Chin et al., 1992; Gallimberti et al., 1989; Takahara et al., 1977; Vickers,1969).Mechanism of ActionSeveral lines of evidence support the hypothesis that GHB is a neurotransmitter.GHB temporarily suppresses the release of dopamine in the mammalianbrain. This is followed by a marked increase in dopamine release, accompaniedby the increased release of endogenous opioids (Hechler, Goebaille, & Maitre,1992). GHB also stimulates pituitary growth hormone (GH) release, althoughthe mechanism by which GHB stimulates GH release is not known. Dopamineactivity in the hypothalamus stimulates pituitary release of GH, but GHBinhibits dopamine release as it stimulates GH release. While GH is beingreleased, serum prolactin levels also rise in a similar, time-dependent fashion.GHB has several different actions in the CNS, and some reports indicate that itantagonizes the effects of marijuana (Galloway et al., 1997). The consequencesof these physiological changes are unclear, as are the overall health consequencesfor individuals who use GHB.TreatmentGHB is not detectable by routine drug screening; thus, history is that muchmore important. Clinicians should remember to ask about GHB use, especiallyin younger people, for whom it has become a drug of choice. In cases of acuteGHB intoxication, physicians should provide physiological support and maintaina high index of suspicion for intoxication with other drugs. A recentreview (Li et al., 1998) suggested the following features for the management ofGHB ingestion with a spontaneously breathing patient:1. Maintain oxygen supplementation and intravenous access.2. Maintain comprehensive physiological and cardiac monitoring.3. Attempt to keep the patient stimulated.4. Use atropine for persistent symptomatic bradycardia.

174 III. SUBSTANCES OF ABUSE5. Admit the patient to the hospital if he or she is still intoxicated after 6hours.6. Discharge the patient if he or she is clinically well in 6 hours (withplans for follow-up, and a suggestion that therapy may be appropriate).Patients whose breathing is labored should be managed in the intensive careunit. Most patients who overdose on GHB recover completely, if they receiveproper medical attention.Individuals may develop physiological dependence on GHB. The symptomsare similar to those of alcohol withdrawal: anxiety, tremor, insomnia, and“feelings of doom,” which may persist for several weeks after cessation of use(Galloway et al., 1997). There is anecdotal evidence, such as the proliferationof support groups and help lines for GHB-dependent individuals, that the numbersof GHB-dependent individuals is rising.The complex symptoms suggest that benzodiazepines may be useful intreating GHB withdrawal. Because data are lacking, clinicians must exercisetheir most prudent judgment regarding what will be most helpful in a given situation.HALLUCINOGENSHallucinogens produce a wide range of effects depending on the properties, dosage,and potency of the drug, the personality and mood of the drug taker, andthe immediate environment. Visually, perception of light and space is altered,and colors and detail take on increased significance. If the eyes are closed, thedrug taker often sees intense visions of different kinds. Nonexistent conversations,music, odors, tastes, and other sensations are also perceived. The sensationsmay be either very pleasant or very distasteful and disturbing. The natureof this effect is often random and not predictable. The drugs frequently alter thesense of time and cause feelings of emptiness. For many individuals, the separationbetween self and environment disappears, leading to a sense of oneness orholiness.The effects, sometimes referred to as a “trip,” can last from an hour to a fewdays. “Bad trips,” full of frightening images, monsters, and paranoid thoughts,are known to have resulted in accidents and suicides. Flashbacks (unexpectedreappearances of the effects) can occur months later.Physiologically, the drugs act as mild stimulants of the sympathetic nervoussystem, causing dilation of the pupils, constriction of some arteries, a risein blood pressure, and increased excitability of certain spinal reflexes. Manyhallucinogenic drugs share a basic chemical structural unit, the indole ring,which is also found in the nervous system substance serotonin. Mescaline haschemical similarities to both the indole ring and the adrenal hormone epineph-

8. Marijuana, Hallucinogens, and Club Drugs 175rine. This suggests that, like most psychoactive substances, hallucinogensmimic the action of naturally occurring biological entities (McDowell & Spitz,1999).LSDLysergic acid diethylamide is an alkaloid synthesized from lysergic acid, which isfound in the fungus ergot (Claviceps purpurea). It is perhaps the most famousand well known hallucinogenic drug that intensifies sense perceptions and produceshallucinations, mood changes, and changes in the sense of time. It alsocan cause restlessness, acute anxiety, and, occasionally, depression. Althoughlysergic acid itself is without hallucinogenic effects, LSD, one of the most powerfuldrugs known, is weight for weight 5,000 times as potent as the hallucinogenicdrug mescaline and 200 times as potent as psilocybin. LSD is usuallytaken orally from little squares of blotter paper, gelatin “windowpanes,” or tinytablets called “microdots.” The period of its effects, or “trip,” is usually 8 to 12hours. Unexpected reappearances of the hallucinations, called “flashbacks,” canoccur months after taking the drug. The drug does not appear to cause psychologicalor physical dependence. It can cause psychological dependence in someindividuals (Koesters, Rogers, & Rajasingham, 2002). The danger of LSD isthat its effects are unpredictable, even in experienced users. These individualsmay act in dangerous ways. This is termed behavioral toxicity.HistoryLSD was developed in 1938 by Arthur Stoll and Albert Hofmann, Swiss chemistshoping to create a headache cure. Hofmann accidentally ingested some ofthe drug and discovered its hallucinogenic effect. On his ride home by bicycle,he began to experience the beginnings of what would be a 2-day-long nightmarish“bad trip.”In the 1960s and 1970s, LSD was used by millions of young people inAmerica; its popularity waned as its reputation for bad trips and resulting accidentsand suicides became known. In 1967, the federal government classified itas a Schedule I drug (i.e., having a high abuse potential and no accepted medicaluse), along with heroin and marijuana. In the early 1990s, it again becamepopular, presumably because of its low cost. It is produced in clandestine laboratories(Graeme, 2000).InhalantsInhalants are substances whose chemical vapors can be intentionally inhaled toproduce psychoactive effects. These are used by a variety of individuals, usuallyadolescents. According to the 2002 National Survey on Drug Use and Health,

176 III. SUBSTANCES OF ABUSE4.4% of youth ages 12–17 used inhalants in the past year, compared to 0.5% ofadults. Inhalants are often found in legal and easily obtained products.Inhalants are generally classified into four different groups:1. Volatile solvents, which include glue, paint thinner, and gasoline. Thestreet names for these are air blast, discorama, hippie crack, moon gas,oz and poor man’s pot.2. Aerosols, which include hair spray and spray paint.3. Gases, which include nitrous oxide and ether. Nitrous oxide is knownas laughing gas or whippets.4. Nitrites, which include amyl, butyl, and isobutyl nitrites.EffectsThe instant, short-lived high produced after directly inhaling these substances(called huffing) produce an instant, short-lived euphoria, along with disinhibition,impaired judgment, slurred speech, lethargy, nervous system depression,and, in extreme cases, unconsciousness.Prolonged use may result in neurological impairment and damage to theheart, lungs, and other vital organs. Death may be the result, usually from heartfailure, but can also be the result of asphyxiation, suffocation, choking, orbehavioral toxicity (CESAR, 2004).CONCLUSIONMDMA, ketamine, and GHB are by no means the only drugs found at clubs,raves, or circuit parties. They are, however, the most emblematic. Attendeesalso use more traditional drugs, such as LSD and other hallucinogens. Marijuanais perennially popular, and alcohol use is also common. Furthermore,each week seems to bring a report of some “new” drug of abuse. Often this is justan older, well-known drug, packaged differently or with a new name, but theeffect on a new generation of users will be just as devastating.Drugs such as these are being increasingly used at clubs, often in combination,and often by very young people. This is cause for concern for several reasons.The younger a person is when he or she begins to use drugs, and the moreoften he or she uses them, the more likely he or she is to develop serious problemswith these or other substances. In the future, we are likely to see more andmore use of such drugs and the problems that come with their use.When the evidence of MDMA’s neurotoxicity was lacking, and whatresearch existed on GHB and marijuana was not as compelling, individualsconcerned with the public’s safety could afford to be less alarmed. The mount-

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Cocaine and StimulantsCHAPTER 9MICHELLE C. ACOSTADEBORAH L. HALLERSIDNEY H. SCHNOLLETHNOGRAPHYNational-level prevalence studies indicate that after a period of recent decline,cocaine use may be rising again, especially among adults. Importantly, cocaineuse has recently begun to increase again, with 0.9 million new users in 2000.Data from the 2001 National Household Survey on Drug Abuse (NHSDA;Substance Abuse and Mental Health Services Administration, 2001b) indicatethat 1.7 million Americans, or 0.7% of the population age 12 and older, arecurrent cocaine users, and that past year use increased significantly for bothpowder cocaine (1.5–1.9%) and crack cocaine (0.3–0.5%). Users were morelikely to be young adults ages 18–25 (1.9%) than youth ages 12–17 (0.4%) oradults 26 years and older (0.6%). NHSDA data show that current cocaine useamong young adults (ages 18–25) grew significantly, from 1.4% in 2000 to1.9% in 2001, with significant increases in past year use from 4.4 to 5.7% forpowder cocaine and 0.7 to 0.9% for crack. For adults age 26 and older, currentuse was relatively stable (0.4% in 2000 and 0.6% in 2001). However, past yearuse for adults ages 26–34 rose slightly for both powder cocaine (2.1–2.7%) andcrack (0.4–0.6%). A similar 2000 to 2001 trend was found for current use inadults age 35 and older, with powder cocaine use increasing from 0.7 to 0.9%and crack use increasing from 0.2 to 0.3%. Current cocaine use also increasedsignificantly among men (0.7% in 2000 to 1.0% in 2001), while women’s userates stayed approximately the same (0.4–0.5%). In addition, current cocaineuse in 2001 was inversely correlated with educational status and was higher184

9. Cocaine and Stimulants 185among the unemployed (3.6%) than among the employed (1.8%). Becausesocioeconomically disadvantaged persons are still a minority population,cocaine users are more often white, employed, and high school graduates(Johanson & Schuster, 1995).Unlike adult levels of use, national-level prevalence studies indicate thatadolescent (ages 12–17) levels of cocaine use appear stable and may be declining.According to NHSDA data, adolescents reported that past year cocaineuse dropped from 1.7% in 2000 to 1.5 % in 2001, while past year crack useremained the same (0.4%). In 2001, the past year prevalence of cocaine useamong youth ages 12–17 years was higher among Hispanic males (0.9%) andwhite females (0.6%) and males (0.4%) than among blacks (0.1%) and femaleHispanics (.1%). The Monitoring the Future study (MTF; Johnston, O’Malley,& Bachman, 2003) demonstrated that past year rates for powder cocaine appearsimilar (1.9% in 2001 and 1.8% in 2002) for eighth graders, 10th graders (3.0%in 2001 and 3.4% in 2002), and 12th graders (4.4% in 2001 and 2002). Crackcocaine use appeared stable for eighth (1.7% in 2001 and 1.6% in 2002) and12th graders (2.1% in 2001 to 2.3% in 2002), but increased significantly for10th graders (1.8% in 2001 to 2.3% in 2002).Consistent with overall growth in cocaine use, the Drug Abuse WarningNetwork (DAWN; Substance Abuse and Mental Health Services Administration,2001a) reports that cocaine continues to be the most frequently mentionedillicit substance reported by hospital emergency departments (EDs)nationwide. The most recent data available regarding the consequences ofcocaine use reveal rising ED mentions and declining treatment admissions.Data from DAWN show that the estimated number of cocaine-related EDmentions increased significantly, from 174,881 in 2000 to 193,034 in 2001. Infact, reports of cocaine were present in 30% of the ED drug episodes during2001 and part of 2002. ED cocaine mentions in 2001 increased 10% from 2000.In a large study conducted in New York City, the rate of overdose deaths forcocaine increased from 1993 to 1998, with cocaine being involved in 69.5% offatal overdoses. The majority of overdose death rates were attributed to drugcombinations of opiates, cocaine, and alcohol. Accidental overdose deaths variedby racial and ethnic group, with overdose deaths among blacks due primarilyto cocaine, and overdose deaths among Latinos and whites due to opiateswith cocaine (Coffin et al., 2003).Treatment Episode Data Set (TEDS; Substance Abuse and Mental HealthServices Administration, 2002) data also reveal the use of cocaine in combinationwith other illegal drugs. Marijuana, methamphetamine, and heroin werethe secondary drugs of abuse most often mentioned in 1999 TEDS admissionsfor which cocaine was identified as the primary substance of abuse. Admissionsfor cocaine taken by routes other than smoking were more likely to be whitemales (29%), followed by black males (23%), white females (18%), and blackfemales (12%). Admissions for smoked cocaine were more likely to be black

186 III. SUBSTANCES OF ABUSEmales (34%), followed by black females (25%), white males (18%), and whitefemales (14%).Consistent with NHSDA data, both DAWN ED and TEDS data indicatethat the average age of cocaine users is increasing. DAWN data show significantincreases between 2000 and 2001 in ED cocaine mentions for patients age35 and older and for patients age 55 and older. TEDS data further indicate thatin 1999, most cocaine-related treatment admissions were in the 35–39 age category,whereas in 1998, most cocaine-related treatment admissions were in the30–34 age category.The number of Drug Enforcement Administration (DEA) arrests involvingcocaine dropped from 15,767 in 2000 to 12,847 in 2001, and data from theU.S. Sentencing Commission (USSC) show that the percentages of federaldrug sentences involving powder and crack cocaine were nearly unchangedfrom 2000 to 2001. Data from the Arrestee Drug Abuse Monitoring (ADAM;U.S. Department of Justice, 2001) program demonstrated that a median of29.1% of adult male arrestees and 30.7% of adult female arrestees tested positivefor cocaine at arrest in 2001. A median of 18.9% of adult male arresteesand 28.5% of adult female arrestees reported using crack cocaine at least oncein the year before being arrested. ADAM data indicate that powder cocaine inadult male arrestees decreased from 13.4% in 2000 to 12.5% in 2001, whilecrack cocaine in adult male arrestees increased from 17.5% in 2000 to 18.9% in2001. However, National Drug Threat Survey (U.S. Department of Justice,2003) data show that 33.1% of state and local law enforcement agenciesnationwide identify cocaine as their greatest drug threat; 8.2% identify powdercocaine as their greatest drug threat, while 24.9% identify crack cocaine astheir greatest drug threat. In both major urban areas, including Philadelphiaand New York City, and rural areas (i.e., St. John Parish, Louisiana), between31 and 40% of homicide victims tested positive for antemortem cocaine use(Clark, 1996; McGonigal et al., 1993; Tardiff et al., 1994).PREPARATION AND ROUTES OF ADMINISTRATIONCocaine is the most potent stimulant of natural origin. It is a benzoylmethylecgonine,an ester of benzoic acid and a nitrogen-containing base.Cocaine occurs naturally in the leaves of Erythroxylon coca and other species ofErythroxylon indigenous to Peru, Bolivia, Java, and Columbia. There are severalbasic routes to cocaine administration: chewing the leaves, cocaine sulfate(paste), cocaine hydrochloride, freebase cocaine, and crack cocaine. SouthAmerican natives who chew coca leaves experience diminished hunger andfatigue, and an improved sense of well-being without evidence of chronic toxicityand dependence. However, other preparations and routes of administrationof cocaine have a more rapid onset of action and are more problematic.

9. Cocaine and Stimulants 187Cocaine sulfate (paste) is the intermediate form between the coca leaf andthe finished cocaine hydrochloride crystal. The smoking of coca paste, popularlyknown as “pasta” or “bazooka,” is prevalent in South America andalso occurs in some parts of the United States. This results in a gray to whiteor dull brown powder, with a slightly sweet smell, that is 40–85% cocaine sulfate.Cocaine hydrochloride is a stable, hydrophilic salt. Thus, it is frequentlysnorted (insufflation) or “tooted” in “lines” or “rails” about one-half to 2 incheslong and one-eighth of an inch thick. Users pour the powdered cocaine onto ahard surface such as a mirror, glass, or slab of marble, and arrange it into lineswith a razor blade, knife, or credit card. One line is snorted into each nostril viaa rolled bill, straw, miniature coke spoon, or a specially grown fingernail. A singlegram of cocaine produces about 30 lines averaging 10–35 mg of powder. Theactual amount of cocaine hydrochloride present in each line depends on thepurity of the drug. Absorption through the nasal mucosa is relatively modestdue to a small surface area and the fact that cocaine is vasoconstrictive.The bioavailability of intranasal cocaine is about 60%. Peak plasma levelsoccur over a range of 30–120 minutes (Barnett, Hawks, & Resnick, 1981).Cocaine is a topical anesthetic and causes numbness of the nose during snorting.Nasal congestion, with stuffiness and sneezing, may occur after snortingcocaine due to both vasoconstrictive properties and contaminants in the preparation.Users may flush out the inside of the nose with a saltwater mixture aftera round of snorting, and they commonly employ decongestants and antihistaminesto relieve symptoms.Cocaine can also be injected intravenously: “shooting” or “mainlining.”The cocaine hydrochloride is mixed with water in a spoon or bottle cap to forma solution. Unlike heroin, cocaine hydrochloride may not need to be heated toenter solution. “Kicking” or “booting” refers to drawing blood from the veinback into the syringe and reinjecting it with each cocaine mixture. Injectiondrug users feel that this produces a heightened drug sensation or “rush,” despitethe lack of a pharmokinetic basis. Following intravenous administration, usersachieve peak plasma levels almost instantaneously.Freebase cocaine is obtained by extracting cocaine hydrochloride with analkali, such as buffered ammonia, then mixing it with a solvent, which is usuallyether. The solvent fraction is separated and volatilized, leaving very smallamounts of residual freebase material. Cocaine freebase is most often smoked ina special freebase glass pipe with a small bowl, into which the freebase cocaineis placed, or in a water pipe with a fine stainless steel screen on which thecocaine is vaporized. Cigarettes are rarely used, because only a small amount ofcigarette smoke actually enters the lungs, wasting valuable cocaine. Cocainehydrochloride is soluble in water and has a melting point of 195°C. In contrast,cocaine freebase is lipid-soluble and has a vaporizing point of 98°C. Thus,cocaine freebase vapors can be smoked, readily crossing the blood–lung barrier

188 III. SUBSTANCES OF ABUSE(DePetrillo, 1985), resulting in nearly immediate peak plasma levels that areachieved at a rate similar to that of injecting cocaine hydrochloride.“Crack” or “rock” is cocaine that has been processed from cocaine hydrochlorideto a freebase for smoking. To prepare crack cocaine for injection, thecrack cocaine is dissolved in water or alcohol, either by heating the solution orby acidifying it. The resultant viscous solution, which is too thick for use instandard insulin syringes, requires a larger bore needle. Because these needlesare considerably harder to obtain, the incidence of needle sharing, along withthe risk of HIV infection, is greater.In the United States, popular street names for cocaine include toot, snow,blow, flake, white lady, snowbirds, paradise, and white. Adulterants commonlyfound in illicitly purchased cocaine include inert substances such as talc, flour,cornstarch, and various sugars (lactose, inositol, sucrose, maltose, and mannitol).Local anesthetics such as procaine, lidocaine, tetracaine, and benzocainemay be added to replace or enhance the local anesthetic effect of cocaine.Cheaper stimulants, including amphetamines, caffeine, methylphenidate, ergotamine,aminophylline, and strychnine (“death hit”), may also be added tothe preparation. Quinine may be added for taste, and other compounds such asthiamin, tyramine, sodium carbonate, magnesium silicate, magnesium sulfate,salicylamide, and arsenic (Lombard, Levin, & Weiner, 1989) may be found.Crack and cocaine are also used frequently in conjunction with tobacco cigarettesand cigars (bananas, coolies, geek joints), 3,4-methylenedioxymethamphetamine(MDMA; “bumping up”), heroin (snow balls, speed balls, smokinggun, dynamite), marijuana (woolas, lace, Sherman stick, champagne,caviar), and amphetamines (snow seals).Contaminants may include bacteria, fungi, and viruses. Users frequentlytake cocaine in combination with other drugs, citing the need to take the edgeoff the abrupt effects and “crash” from cocaine. Intravenous injection of heroinand cocaine mixed together is called “speedballing,” and ingesting alcohol inconjunction with cocaine may be referred to as “liquid lady.” Any drug combinationis possible, and other opioids and depressants, as well as hallucinogens,phencyclidine (PCP), and marijuana, are all frequently used in conjunctionwith cocaine.COCAETHYLENESimultaneous cocaine and alcohol use produces enhanced euphoria, comparedto either substance alone (Farre et al., 1993). This enhanced effect has beenattributed to pharmacokinetic factors, such as more rapid absorption and higherplasma concentrations (up to 30% increase) of cocaine (McCance-Katz et al.,1993). Typically, when cocaine and ethanol use coincide, the normal hydrolysisof cocaine to benzoylecgonine by hepatic carboxyesterase enzymes is inhib-

9. Cocaine and Stimulants 189ited, allowing higher levels of cocaine to remain in the body. A portion of thiscocaine undergoes hepatic microsomal transesterification and is converted tococaethylene (Andrews, 1997; Jatlow et al., 1991). Cocaethylene has very similarbehavioral and toxicological effects to cocaine, but these effects last muchlonger (cocaethylene’s plasma half-life is three to five times that of cocaine;Jatlow et al., 1991). Cocaethylene causes significant sustained increases inheart rate and blood pressure, myocardial infarctions, arrhythmias, and decreasesin heart functioning, possibly due its inhibitory effects on potassiumchannels in the heart (O’Leary, 2002). In addition, cocaethylene is associatedwith seizures, liver damage, and immune compromise in adults (Andrews,1997). Additional toxicological aspects, such as the effects on the exocrinepancreas, remain unexplored (Jatlow et al., 1991).NEUROTRANSMITTERS ANDBEHAVIORAL PHARMACOLOGYCocaine is both a stimulant of the central nervous system (CNS) and a localanesthetic, with large abuse liability due to its reinforcing properties. It iswidely believed that the cocaine reward system is the mesocorticolimbic pathway,which originates in the ventral tegmental area (VTA) and projects tonumerous areas of the forebrain, including the frontal cortex, hippocampus,amygdala, and the striatum (including the nucleus accumbens and the caudateputamen) (Koob, 1992). Recent work examining neurochemical turnoverrates suggests that discrete subpopulations of dopamine, serotonin, glutamate,and gamma-aminobutyric acid (GABA)–releasing neurons are responsible forcocaine reward. Data suggest that dopamine in the nucleus accumbens, VTA,septum, lateral hypothalamus, and brainstem; glutamate in the nucleus accumbensand VTA; and serotonin in the medial hypothalamus are implicatedin cocaine reward. In addition, surprising findings in the cerebral cortex haveincluded noradrenergic and GABA activation of the somatosensory and anteriorcingulate cortices, and glutamate activation of the posterior cingulate andentorhinal and visual cortices in response to cocaine administration (Smith,Koves, & Co, 2003).Cocaine acts on these brain pathways by blocking the reuptake of dopamine,serotonin, and norepinephrine by binding to their respective neuronaltransporters (DAT, SERT, NET), thereby increasing the synaptic concentrationof these neurotransmitters. In addition, cocaine is responsible for indirecteffects in the glutamate, GABA, and opioid systems, and for activating thestress response in the hypothalamic–pituitary–adrenal (HPA) axis. Researchhas just begun to elucidate the complex interplay of these direct and indirecteffects on both the rewarding and aversive aspects of cocaine use. However,evidence generally suggests that dopamine plays a key role in cocaine reward,

190 III. SUBSTANCES OF ABUSEand the many other neurotransmitter systems impact cocaine reward by actingon dopamine.Corticotropin-releasing factor (CRF) modulates the HPA axis response tostressors. The HPA axis may be implicated in cocaine self-administration, particularlyregarding relapse in cocaine use. Inhibition of circulating corticosteronedecreases intravenous cocaine self-administration in rats. In addition,data suggest that corticosterone secretion does not play a major role in cocaineinducedreinstatement. However, a minimal level is necessary to achieve bothstress-induced and cue-induced cocaine reinstatement, demonstrating an involvementof the HPA axis in the relapse of cocaine use (Goeders, 2002).Intoxication/OverdoseCLINICAL FEATURESWith intoxication, cocaine blocks monoamine neuronal reuptake, initiallyleading to increased dopamine serotonin and norepinephrine availability atreceptor sites. This stimulation of the endogenous pleasure center results ineuphoria, increased energy and libido, decreased appetite, hyperalertness, andincreased self-confidence when small initial doses of cocaine are taken. Exaggeratedresponses such as grandiosity, impulsivity, hyperawareness of the environment,and hypersexuality may also occur. The acute noradrenergic effects ofsmall doses of cocaine include a mild elevation of pulse and blood pressure.Insomnia results from both increased dopamine and norepinephrine concentrations,and decreased serotonin synthesis and turnover.Higher doses of cocaine are accompanied by increasing toxicity. Not onlyis there intensification of the “high,” but anxiety, agitation, irritability, confusion,paranoia, and hallucinations may also occur. Sympathomimetic effectsinclude dizziness, tremor, hyperreflexia, hyperpyrexia, mydriasis, diaphoresis,tachypnea, tachycardia, and hypertension. These symptoms can be accompaniedby a sense of impending doom and may have important ramifications inoverdose situations. Overdose complications may become manifest as muscletwitching, rhabdomyolysis, convulsions, cerebral infarction and hemorrhage,cardiac ischemia and arrhythmias, and respiratory failure.More than any other stimulant, acute intoxication with cocaine is characterizedby convulsions and cardiac arrhythmias. Death may be caused by peripheralautonomic toxicity and/or paralysis of the medullary cardiorespiratory centers(Gay, 1982).Chronic UseIn contrast to acute intoxication, chronic cocaine administration results inneurotransmitter depletion. This is evidenced by a compensatory increase in

9. Cocaine and Stimulants 191postsynaptic receptor sensitivity for dopamine and noradrenaline, increasedtyrosine hydroxylase activity (a major enzyme in norepinephrine and dopaminesynthesis), and hyperprolactinemia. These are expected results for a negativefeedback system. Chronic use is also associated with volume losses in theprefrontal cortex and nucleus accumbens. In addition, striatal dopamine responseis significantly lower in cocaine abusers during withdrawal than incocaine nonabusers. Furthermore, lower levels of dopamine receptors in thestriatum are associated with lower metabolism in the orbitofrontal cortex andanterior cingulate gyrus in cocaine-addicted subjects (Goldstein & Volkow,2002).Clinical features of chronic cocaine use include depression, fatigue, poorconcentration, loss of self-esteem, decreased libido, mild parkinsonian features(myoclonus, tremor, bradykinesis), paranoia, and insomnia. Tolerance to thestimulant effects of cocaine, particularly the anorexic effects, develops rapidly.However, repeated phasic use of low-dose cocaine can lead to enhanced sensitivityand potentiation of motor activity, including exaggerated “startle” reactions,dyskinesias, and postural abnormalities. Increased stereotypical behaviorand a toxic psychosis can occur after repeated cocaine use. The eliminationhalf-life of cocaine is under 1 hour by the intravenous route, and just over 1hour by the intranasal route. The physiological and subjective effects dueto cocaine correlate well with plasma levels (Javaid, Fischman, Schuster,Dekirmenjian, & Davis, 1978), although, with repeated use, pharmacodynamictachyphylaxis does occur. Cocaine euphoria is of short duration, with a 10- to20-second “rush,” followed by 15–20 minutes of a lower level of euphoria andthe subsequent onset of irritability and craving. Cocaine users who try to maintainthe euphoric state readminister the drug frequently, until their supply disappears.Cocaine binges average 12 hours but can last as long as 7 consecutivedays.WithdrawalA withdrawal syndrome, often referred to as the “crash,” consists of strong craving,electroencephalograph abnormalities, depression, alterations in sleep patterns,hypersomnolence, and hyperphagia (Jones, 1984). However, becauseabrupt discontinuation of cocaine does not cause any major physiologicalsequelae, cocaine is stopped and not tapered or substituted by a cross-tolerantdrug during medically supervised withdrawal. Following the resolution of intoxicationand acute withdrawal symptoms, there is a 1- to 10-week period ofchronic dysphoria, anergia, and anhedonia. Relapses frequently occur, becausethe memory of cocaine euphoria is quite compelling in contrast to a bleak backgroundof intense boredom. If patients can remain abstinent from illicit moodalteringdrugs during this period, the dysphoria gradually improves. Thereafter,intense cocaine craving is replaced by episodic craving that is frequently trig-

192 III. SUBSTANCES OF ABUSEgered by environmentally conditioned cues during an indefinite extinctionphase.Abuse and AddictionThe National Institute on Drug Abuse (NIDA) estimates that of the 30 millionAmericans who have tried cocaine intranasally, 20% become regular users and5% develop compulsive use or addiction (Gawin & Ellinwood, 1988). Whethera given recreational cocaine user will become chemically dependent is difficultto predict. Abusers report that controlled use becomes compulsive either whenthey attain increased access to cocaine and therefore escalate their dosage, orwhen they switch to a more rapid route of administration (e.g., from intranasaladministration to intravenous injection or smoking freebase or crack).With recreational use, the cocaine user’s initial experience of elation andheightened energy, with increased sexuality and self-esteem, appears to be freeof negative consequences. Abusers may experience occasional problems associatedwith their drug use. Unlike dependence on alcohol or opiates, cocainedependence is frequently characterized by binge use. With chronic and increaseduse, there is increased drug toxicity, dysphoria, and depression. Theaddict has irresistible cravings for cocaine. He or she focuses on pharmacologicallybased cocaine euphoria despite progressive inability to attain this stateand adverse physical, psychological, and social sequelae. Loved ones areneglected, responsibility becomes immaterial, financial hardships occur, andnourishment, sleep, and health care are ignored.GENETIC FACTORSStudies in rodents suggest that genetic variation influences several aspects ofthe response to cocaine, including preference, stimulant effects, and sensitization(Miner & Marley, 1995; Schuster, Yu, & Bates, 1977). Cocaine dependencein probands specifically increased the risk of cocaine dependence in siblings(Bierut et al., 1998).One large-scale twin study of substance use and abuse in male U.S. veteransfound that genetic factors played a substantial etiological role in stimulantabuse (Tsuang et al., 1996). However, the effects were generally nonspecific,indicating that the same characteristics that place an individual at risk forcocaine abuse also put that individual at risk for other substance abuse. A secondstudy focusing specifically on cocaine use, abuse, and dependence wasconducted in over 800 pairs of female–female twins ascertained from thepopulation-based Virginia Twin Registry (Karkowski, Prescott, & Kendler,2000). Cocaine use, abuse, and dependence were all found to be strongly influencedby both shared environmental influences and genetic factors, with

9. Cocaine and Stimulants 193heritabilities ranging from 69 to 81%. However, both the environmental andgenetic factors appeared nonspecific. A third, large-scale twin study examinedlifetime history of use and abuse/dependence of cocaine and other drugsin 1,196 male–male twin pairs ascertained by the Virginia Twin Registry(Kendler, Jacobson, Prescott, & Neale, 2003). Ultimately, one must concludethat while cocaine use, abuse, and dependence seem to be strongly influencedby genetic factors, evidence for a cocaine-specific genetic effect is currentlylacking.PSYCHIATRIC COMORBIDITY AND SEQUELAEMore than one-half of all cocaine abusers meet criteria for a current psychiatricdiagnosis and nearly three-fourths for a lifetime psychiatric diagnosis (Ziedonis,Rayford, Bryant, Kendall, & Rounsaville, 1994). The most common comorbidpsychiatric diagnoses among cocaine abusers include alcohol dependence,affective disorders, anxiety disorders, and antisocial personality disorder(Kleinman et al., 1990; Marlowe, Husband, Lamb, & Kirby, 1995; Mirin,Weiss, Griffin, & Michael, 1991; Rounsaville et al., 1991; Weiss, Mirin, Griffin,Gunderson, & Hufford, 1993). For most cocaine users, co-occurring psychiatricdisorders (including agoraphobia, alcohol abuse, alcohol dependence,depression, posttraumatic stress disorder (PTSD), simple phobia, and socialphobia) precede cocaine use (Abraham & Fava, 1999; Shaffer & Eber, 2002).The most frequent co-occurring substance use disorder is alcoholism; 29%of cocaine abusers have a current alcoholism diagnosis, and 62% a lifetime alcoholismdiagnosis (Rounsaville et al., 1991). These findings are alarming consideringthat individuals with comorbid cocaine and alcohol use disorders manifesta more severe form of cocaine dependence, and comorbid alcohol abuse is associatedwith poorer retention in treatment and poorer treatment outcomes forboth disorders (Brady, Sonne, Randall, Adinoff, & Malcolm, 1995). Cocaineuse disorders also are common among opioid abusers. In addition, 66% ofmethadone-maintained patients abuse cocaine (Kosten, Rounsaville, & Kleber,1987), and 75% of the heroin addicts admitted to methadone programs identifycocaine as their secondary drug of abuse (New York State Division of SubstanceAbuse Services, 1990). A national survey of 15 clinics (General AccountingOffice, 1990) revealed continued cocaine use in as many as 40% of patientsafter 6 months of treatment. Marijuana is also commonly misused amongcocaine-dependent patients. Studies have found that 25–70% of cocainedependentpatients also abuse marijuana (Higgins, Budney, Bickel, & Badger,1994). Similarly, 80.5% of cocaine-dependent patients smoke tobacco cigarettes(Patkar et al., 2002), and the heavier the tobacco smoking, the heavierthe use of cocaine (Henningfield, Clayton, & Pollin, 1990). In addition,cocaine-dependent individuals who smoke tobacco report an earlier age of

194 III. SUBSTANCES OF ABUSEonset and more frequent use of cocaine than cocaine-dependent individualswho do not smoke (Budney, Higgins, Hughes, & Bickel, 1993).Non-substance-related Axis I disorders are also common among cocaineaddicts. The rates for current depressive disorders vary between 11 and 55%(Carroll et al., 1994; Griffin, Weiss, Mirin, & Lange, 1989; Haller, Knisely,Dawson, & Schnoll, 1993), whereas those for lifetime depression range from 40to 60% (Kleinman et al., 1990). Bipolar depression appears to be overrepresentedamong cocaine users. In a large, community-based sample, 42.1%of cocaine abusers were found to have bipolar disorder (Karam, Yabroudi, &Melhem, 2002). Because of the specific actions and effects of cocaine, it issometimes difficult to determine whether depression is independent of cocaineuse or the result of chronic self-administration. However, depression that predatesdrug use or persists beyond the 1–2 weeks characteristic of cocaine withdrawalmay indicate a coexisting disorder. Also, if a cocaine abuser becomesacutely depressed or suicidal after ingesting only very small amounts of the drug,a primary depressive disorder may be indicated (Kosten et al., 1987). In mostcases of comorbid depression and cocaine use, depression precedes cocaine useby an average of 7 years (Abraham & Fava, 1999). Panic disorder is prevalentamong cocaine abusers, and the literature contains a number of case reports ofindividuals who developed panic disorder following cocaine use (Aronson &Craig, 1986; Bystritsky, Ackerman, & Pasnau, 1991). Among 122 cocainedependentoutpatients, 30.2% of women and 15.2% of men met DSM criteriafor PTSD (Najavits et al., 1998). Furthermore, in a large epidemiological study,rates of PTSD among cocaine-dependent individuals were 10 times higher thanamong non-cocaine-dependent individuals. Findings suggest that cocaine dependenceis a risk factor for PTSD, because it usually precedes the trauma andplaces individuals in situations where traumatic events are more likely to occur(Cottler, Compton, Mager, Spitznagel, & Janca, 1992).Attention-deficit/hyperactivity disorder (ADHD) is an important comorbidcondition. In a large longitudinal study, approximately 21% of adults withADHD were cocaine dependent, compared to 10% of agemate controls (Lambert& Hartsough, 1998). Studies indicate that between 12 and 35% of cocaineaddicts meet childhood criteria for ADHD (Carroll & Rounsaville, 1993;Levin, Evans, & Kleber, 1998; Rounsaville et al., 1991). Compared to cocaineabusers without comorbid ADHD, those with ADHD are more likely to bemale and to also meet criteria for conduct disorder and antisocial personalitydisorder. Cocaine abusers with ADHD evidence earlier age of onset of use,more frequent and severe use, more alcoholism, and more prior treatment episodes.Men who score high on an ADHD measure also report more use ofcocaine for the purpose of self-medication (Horner, Scheibe, & Stine, 1996).Although somewhat controversial, several case reports suggest that stimulants(e.g., magnesium pemoline, and methylphenidate) can be successfully used totreat patients with comorbid cocaine abuse and ADHD (Khantzian, Gawin,

9. Cocaine and Stimulants 195Kleber, & Riordan, 1984; Weiss, Pope, & Mirin, 1985). This treatment effectappears to be selective, because non-ADHD cocaine abusers derive no apparentbenefit from stimulants but do manifest cross-tolerance (Gawin, Riordan, &Kleber, 1985).Studies conducted with both inpatients and outpatients with schizophreniashow prevalence of cocaine use falling between 20 and 93% (Regier et al.,1990; Rosenthal, Hellerstein, Miner, & Christian, 1994; Schwartz, Swanson, &Hannon 2003; Ziedonis & Fischer, 1996). Cocaine-abusing persons with schizophreniahave fewer negative signs (Lysaker, Bell, Beam-Goulet, & Milstein,1994), but more depression and anxiety at the time of hospital admission(Serper, Alpert, Richardson, & Dickson, 1995); at posttreatment, no differencesin negative signs or mood are observed, suggesting that differences resultfrom the effects of cocaine. Persons with schizophrenia who abuse cocaine haveincreased morbidity, evidenced by higher rates of hospitalization, greatersuicidality, and the need for higher doses of neuroleptics than both users ofother drugs and nonusers (Seibyl, Satel, Anthoy, & Southwick, 1993). Cocaineuse may itself induce noxious psychiatric effects, some of them psychotic innature. Bruxism, picking at the face and body, and other stereotypical or repetitiousbehaviors may occur. Cocaine hallucinosis may include visual, tactile,auditory, and olfactory hallucinations, along with delusions. Cocaine users mayalso perceive “cocaine bugs” on their skin, as well as visual “snow lights.” In lesssevere cases, the user is aware that the hallucinations and delusions are not real.However, in more severe cases, individuals may show a full-blown toxic psychosiswith extreme paranoia, hypervigilance, and ideas of persecution. This toxicpsychosis can potentially lead to unusual aggressiveness, damaged property, andhomicidal or suicidal behavior. Fortunately, these effects are generally limitedto the time of cocaine intoxication.Comorbid Axis II disorders are even more prevalent than Axis I disorders,with rates of personality disorders in cocaine abusers ranging from 30 to 75% ininpatient samples (Kleinman et al., 1990; Kranzler, Satel, & Apter, 1994; Weisset al., 1993). Cocaine addicts with personality disorders tend to have greaterpsychiatric severity than those without personality disorders and are also atgreater risk for both anxiety and mood disorders (Bunt, Galanter, Lifshutz, &Castaneda, 1990; Stone, 1992). Among cocaine-abusing outpatients, 48% haveat least one personality disorder, whereas 18% have two or more (Barber, Frank,Weiss, & Blane, 1996). Even more compelling, 65% of those with a comorbidAxis II diagnosis have a Cluster B disorder, antisocial and borderline personalitydisorder (BPD) being the most frequent. Patients with BPD have higher levelsof polysubstance and cocaine dependence, and also have more personalitydisorders such as avoidant, antisocial, and dependent personality disorder(Kranzler et al., 1994; Nurnberg, Rifkin, & Doddi, 1993). For cocaine abusersin intensive outpatient treatment, the rates of co-occurring personality disordersare quite high; three-fourths meet criteria for at least one Axis II diagnosis

196 III. SUBSTANCES OF ABUSEand more than one-third have two or more (Haller et al., 1993; Marlowe et al.,1995). Males are more likely to have comorbid alcohol dependence, stimulantdependence, antisocial personality disorder, and narcissistic personality disorder,whereas females are more likely to be diagnosed with mood disorders andBPD. It is important to evaluate patients routinely for Axis II disorders at pointof treatment entry and to design drug treatment programs that provide adequateattention to these comorbid conditions.Unfortunately, psychiatric comorbidity has negative implications for symptomexpression, prognosis, medical compliance, and services utilization (Bartelset al., 1993; Moos, Mertens, & Brennan, 1994; Moos & Moos, 1995; Pristach &Smith, 1990). It is important for substance abuse and mental health cliniciansto become aware of patterns of comorbidity among their patients and todevelop treatment plans that address dual disorders simultaneously. Awarenessof subtypes of cocaine abusers may help to guide treatment in both pharmacologicaland psychological intervention.MEDICAL COMPLICATIONSDirect Results of Cocaine UseMedical consequences of acute and chronic cocaine abuse may be categorizedas those caused directly by cocaine, those due to adulterants, and those relatedto route of administration. The most common direct medical consequences ofcocaine use include cardiovascular and CNS difficulties.Cocaine use may account for up to 25% of cases of acute myocardialinfarction among patients 18–45 years of age (Weber, Hollander, Murphy,Braunwald, & Gibson, 2003). Upon acute administration, cocaine increasesblood pressure and heart rate, primarily through an action on the sympatheticnervous system. Through its pharmacological effect at alpha- and betaadrenergicreceptors, cocaine may increase oxygen demand of the myocardiumby increasing blood pressure and heart rate. Cocaine also suppresses thebaroreflex response and vagal tone, further contributing to its effects on heartrate. At the same time that cocaine is increasing the workload on the heart, itinduces coronary artery vasoconstriction and platelet aggregation, potentiallyleading to coronary spasm and/or cardiac ischemia (Schrank, 1993). In addition,cocaine use is also associated with significantly decreased coronary bloodflow velocity, leading to increased microvascular resistance. Slow coronary fillingmay also suggest the possibility of cocaine use in patients in whom it wasnot otherwise suspected (Kelly, Sompalli, Sattar, & Khankari, 2003). At higherdoses, cocaine can depress ventricular function and slow electrical conductionin the heart. Both these effects appear to be mediated by cocaine’s localanesthetic action. Cocaine may potentiate catecholamine activity, impactingvoltage-dependent sodium ion channels related to local anesthetic properties.

9. Cocaine and Stimulants 197When cocaine is administered repeatedly over a short period of time, acute tolerancecan develop to the sympathomimetic effects of cocaine. In contrast, theeffects of cocaine mediated by its local anesthetic action do not appear bluntedby anesthesia or susceptible to acute tolerance. In addition to the effects ofcocaine alone, the metabolites of cocaine may also contribute to cocaine’sacute and chronic cardiovascular toxicity, and both licit and illicit drugs used incombination with cocaine might potentially alter its cardiovascular effects(Schindler, 1996).With chronic administration, higher cocaine doses appear to induce tolerance,while lower doses may induce sensitization to cocaine’s sympathomimeticeffects. Chronic cocaine use is associated with multiple cardiovascular conditions,including myocardial infarction, aortic dissection, left ventricularhypertrophy, arrhythmias, sudden death, and cardiomyopathy (Frishman, DelVecchio, Sanal, & Ismail, 2003).CNS manifestations of cocaine exposure include seizures, status epilepticus,cerebral hemorrhage, and transient ischemic attacks. Cocaine may producehyperpyrexia through direct effects on thermoregulatory centers. Depressionof the medullary centers may result in respiratory paralysis, and suddendeath may be caused by respiratory arrest, myocardial infarction or arrhythmia,or status epilepticus (Cregler & Mark, 1986). Migraine-like headaches havebeen associated with cocaine withdrawal and may be linked to serotonin dysregulation(Satel & Gawin, 1989). Rhabdomyolysis is a complication ofcocaine use. When it is accompanied by acute renal failure, severe liver dysfunction,and disseminated intravascular coagulation, the fatality rate is high(Roth, Alarcon, Fernandez, Preston, & Bourgoignie, 1988).Other difficulties associated with chronic cocaine use include weight loss,dehydration, nutritional deficiencies (particularly of vitamins B 6, C, and thiamine),and endocrine abnormalities. Neglect of self-care may be evident,including dental caries and periodontitis exacerbated by bruxism. Addicts maymedicate their pain with cocaine or other mood-altering drugs and seek medicalattention only after prolonged existence of their problem(s).Adulterants also play a role in the development of medical complications.Local anesthetics and stimulants may increase cocaine’s inherent toxicity byincreasing the risk of hypertension and cardiovascular complications. Sugars,though relatively benign, may encourage development of bacteria that becomesproblematic when injected intravenously.Other complications of cocaine may be due to the route of administration.Intestinal ischemia caused by vasoconstriction and reduced blood flow in themesenteric vasculature from catecholamine stimulation of alpha receptors hasbeen reported after oral cocaine ingestion (Texter, Chou, Merrill, Laureton, &Frohlich, 1964). Emergency room patients have required surgical correction oftheir intestinal perforations, after smoking crack cocaine. The chronologicalrelationship between crack consumption and gastrointestinal perforation indi-

198 III. SUBSTANCES OF ABUSEcates that crack may induce ischemic events, causing intestinal ruptures insome people (Muniz & Evans, 2001).Gastroenterological exposure to cocaine has been studied among drugsmugglers, among whom a 58% mortality rate has occurred when swallowedcocaine packets have ruptured (McCarron & Wood, 1983), or among thosewho swallow cocaine for other reasons. If a packet ruptures, causing severecocaine intoxication, immediate laparotomy for removal of the packets is thebest treatment option (Schaper, Hofmann, Ebbecke, Desel, & Langer, 2003).The treatment for those who swallow cocaine may be less clear, but each grouprequires medical attention.Complications of intranasal administration include loss of sense of smell,atrophy and inflammation, and necrosis and perforation of the nasal septum.Snorting cocaine may anesthetize and paralyze the pharynx and larynx, causinghoarseness and predisposing the person to aspiration pneumonia (Estroff &Gold, 1986). Recurrent snorting of cocaine may result in ischemia, necrosis,and infections of the nasal mucosa, sinuses, and adjacent structures.In terms of pulmonary effects, pneumomediastinum and cervical emphysemahave been reported after smoking cocaine due to alveolar rupture withprolonged deep inspiration and Valsalva’s maneuver (Aroesty, Stanley, &Crockett, 1986). Other respiratory complications of inhaling or smokingfreebase cocaine include abnormal reductions in carbon monoxide diffusingcapacity (Itkonen, Schnoll, & Glassroth, 1984), granulomatous pneumonitis(Cooper, Bai, Heyderman, & Lorrin, 1983), pulmonary edema (Allred & Ewer,1981), thermal airway injury, pulmonary hemorrhage, hypersensitivity reactions,interstitial lung disease, obliterative bronchiolitis, asthma, and persistentgas-exchange abnormalities (Laposata & Mayo, 1993). Respiratory manifestationsinclude shortness of breath, cough, wheezing, hemoptysis, and chest pains.Severe respiratory difficulties have been reported in neonates of abusing mothers.Inhalation of hot cocaine vapors may also result in bilateral loss of eyebrowsand eyelashes (Tames & Goldenring, 1986), and preparation of freebasecocaine with solvents such as ether may result in accidental burns and explosions.Complications of intravenous cocaine use are multiple and include skinabscesses, phlebitis and cellulitis, and septic emboli resulting in pneumonia, pulmonaryabscesses, subacute bacterial endocarditis, ophthalmological infections,and fungal cerebritis (Wetti, Weiss, Cleary, & Gyori, 1984). Injected talc and silicatemay cause granulomatous pneumonitis with pulmonary hypertension, as wellas granulomata of the liver, brain, or eyes (Estroff & Gold, 1986). Hepatitis B,hepatitis C, and delta agent are all too frequently by-products of intravenous drugabuse. In the past several years, concomitant with the increase in HIV infection,there has been an increase in pneumonia, endocarditis, tuberculosis, and hepatitisdelta and other sexually transmitted diseases in drug users (see Chapter 19 onHIV and addictions for more information on cocaine and HIV/AIDS).

9. Cocaine and Stimulants 199OBSTETRIC AND DEVELOPMENTAL EFFECTSIn the United States, more than 100,000 babies are exposed prenatally tococaine each year (Office of the Inspector General, 1990). Increasing evidenceindicates that prenatal cocaine exposure is associated with negative perinataloutcomes, including premature delivery, low birthweight, microcephaly, newbornbehavioral abnormalities, and possible long-term cognitive and developmentaldifficulties (Singer et al., 2002). However, the impact of cocaine on thedeveloping fetus is difficult to ascertain, because no confined, homogeneous,syndromic pattern of malformations has been identified, and because the mechanismsby which cocaine impacts on the unborn child are complex; maternalcocaine use may have both indirect and direct effects on a developing fetus(Vidaeff & Mastrobattista, 2003).Indirect effects of maternal cocaine use include negative health consequencesfor mothers, which then impact their pregnancies. Women usingcocaine are more likely to suffer arrhythmias, cardiac ischemias, and hemorrhagicstrokes. In addition, they may develop pregnancy complications similarto preeclampsia, including hypertension, headaches, blurred vision, and placentalabruption, as well as vascular damage and uterine vasoconstriction, leadingto problems such as spontaneous abortion and premature delivery (Church &Subramanian, 1997). Poor maternal weight gain and increased energy demandsare another common effect of cocaine use in pregnant women, often leading todecreased birthweights and poorer prenatal nutrition (Church et al., 1991).In addition to indirect effects, cocaine readily crosses the placental barrierand can thereby directly influence the unborn child (Moore, Sorg, Miller, Key,& Resnik, 1986; Volpe, 1992). Due to the fetus’s immature metabolic systems,the drug is poorly metabolized, increasing its half-life (Chasnoff & Schnoll,1987). Research has also shown that maternal intake of cocaine results inincreased fetal systolic blood pressure, decreased uterine blood flow, anddecreased fetal oxygenation (Moore et al., 1986), which may also negativelyimpact child outcomes.Cocaine may directly affect early embryonic development by disruptingenergy-producing mechanisms for cell metabolism and impact later fetal developmentby crossing the placenta, causing vascular disruption and changes inneurochemistry. Vascular disruption during a critical developmental periodmay be responsible for problems such as limb reduction deformities, intestinalatresia, fetal edema, necrotizing enterocolitis, intracranial hemorrhage, stroke,porencephaly, and other cocaine-related problems (Vidaeff & Mastrobasttista,2003).A stable, negative, cocaine-specific effect on language functioning wasfound through age 7, after controlling for sex, age, prenatal exposure to alcohol,marijuana and tobacco, and over 20 other medical and demographic factors(Bandstra et al., 2002). Similarly, Azuma and Chasnoff (1993) reported lower

200 III. SUBSTANCES OF ABUSEIQ scores (though still in the normal range) on the Stanford–Binet for childrenprenatally exposed to cocaine in combination with other drugs; this study alsoidentified mediating variables such as home environment, head circumference,and child behavior. In addition, a large study found that cocaine-exposed childrenwere twice as likely to be significantly delayed developmentally throughoutthe first 2 years of life and were twice as likely to require intervention as thenoncocaine polydrug-exposed comparison group. These cognitive delays werenot due to exposure to other drugs or to covariates. Furthermore, poorer cognitiveoutcomes were related to higher levels of prenatal cocaine exposure(Singer et al., 2002). In addition to cognitive delays, 2-year-olds who had beenprenatally exposed to both PCP and cocaine were found to utilize less matureplay strategies and to evidence less sustained attention, more deviant behaviors,and poorer quality interactions with caregivers (Beckwith et al., 1994).In summary, findings on the consequences of prenatal cocaine exposurerelative to child development are inconsistent. Early concerns about severe,permanent neurobehavioral deficits appear to have been exaggerations; however,evidence remains that prenatal exposure to cocaine may contribute to thedevelopment of more mild or subtle neurobehavioral difficulties, such as poorerlanguage functioning. In studying this population, it will be essential forresearchers to control for confounding factors such as age, race, socioeconomicstatus, and other drug use; this is especially true, because some studies havefound environmental factors to be equal even more important determinants offunctioning.ASSESSMENTInitial evaluation of the cocaine abuser begins with a medical, psychiatric, andpsychosocial history, as well as a physical examination. Confirming and augmentingthe patient’s history through collateral reports of family members andsignificant others is often helpful. On an emergency basis, the following laboratorytests need to be considered, based on the patient’s clinical presentation:complete blood count, chemical profile (SMA-12), urinalysis, urine and/orblood toxicology, electrocardiogram, and chest X-ray. Indications for acute hospitalizationinclude (1) serious medical or psychiatric problems either caused bythe stimulant drugs or independently coexisting, and (2) concurrent dependenceon other drugs, such as alcohol or sedative hypnotics, necessitating a moreclosely supervised withdrawal. A validated, widely accepted tool to assess addictionseverity specifically to cocaine has not yet been developed. However,DSM-IV-TR (American Psychiatric Association, 2000) diagnostic criteria forcocaine intoxication, withdrawal, delirium, delusional disorder, dependence,and abuse are based on the symptoms described in this chapter. Evaluation to

9. Cocaine and Stimulants 201guide addiction treatment needs to address a variety of issues, including the dosage,patterns, chronicity, and method of cocaine use; other drug use; antedatingand drug-related medical, social, and psychological problems; the patient’s cognitiveability and social skills; and the patient’s knowledge, motivation, attitude,and expectations of treatment (Washton, Stone, & Hendrickson, 1988).Additional factors indicating increased severity of addiction that may necessitateinpatient treatment include chronic smoking of freebase or intravenouscocaine use, the demonstrated inability to abstain from use while in outpatienttreatment, and the lack of family and social supports.Once the patient is stabilized and assigned to an appropriate level of care, amore detailed medical, psychiatric, and psychosocial history and physical examinationshould be performed. Patient motivation and readiness for change mayenhance retention and positive treatment outcomes. The search for evidence ofmedical, neuropsychological, and psychiatric sequelae should be stressed, aswell as consequences of self-neglect. The following laboratory tests shouldbe considered supplements to those obtained previously on an acute carebasis: pulmonary function testing with diffusing capacity of carbon monoxide(DLCO, DCO) in smokers of freebase and crack cocaine, and purified proteinderivative (PPD) tubercular skin testing with controls; rapid plasma reaginagglutination test (RPR; syphilis serology); hepatitis B surface antigen and hepatitisC antigen; and HIV serology in intravenous users. Because these patientsgenerally have poor follow-up rates, immunizations should be given, and generalpreventive health maintenance should be performed at this time as well.OverdoseTREATMENTIn the case of a massive cocaine overdose, patients are likely to present withadvanced cardiorespiratory distress and seizures. Treatment is performed in anemergency setting, with attention to cardiac function, and with an eye to thepresence of other substances. The principles of resuscitation, along with theadministration of thiamine, glucose, and naloxone (Narcan), are necessary(Goldfrank & Hoffman, 1993).IntoxicationIntoxicated persons who seek assistance with less severe cocaine complicationsare more likely to present with panic, irritability, hyperreflexia, paranoia, hallucinations,and stereotyped repetitive movements. Assurance in a calm,nonthreatening environment is a prerequisite for successful patient management.Psychosis can be treated with haloperidol, although caution is necessary,

202 III. SUBSTANCES OF ABUSEbecause this medication can lower the seizure threshold. Monoamine oxidaseinhibitors are contraindicated, because they block cocaine degradation. Infectiousdiseases and other complications need to be treated appropriately. Sodiumnitroprusside, phentolamine, and calcium channel blockers are effective therapiesfor hypertension. Propranolol is controversial due to resultant unopposedalpha-receptor stimulation.WithdrawalBenzodiazepines may ameliorate the “crash” or early phase withdrawal fromcocaine. However, the high abuse potential of benzodiazepines limits theirtherapeutic value (Kosten, 1988). The most serious complication of early withdrawalis depression, with the potential for suicide. Patients must be watchedclosely when manifesting depression and agitation. If symptoms of depressiondo not remit within 10 days to 2 weeks, despite relative normalization of sleeppatterns, underlying major depression requiring psychiatric intervention is suggested.In addition, repeated exposure to cocaine followed by withdrawal leadsto an activation of the neuroendocrine stress response, which may increase susceptibilityto infection during the initial stages of withdrawal (Avila, Morgan,& Bayer, 2003).Pharmacological Treatment of Chronic Cocaine AddictionClinical researchers have tried to identify drugs to reduce cocaine craving andprevent relapse. Numerous drugs looked promising in initial open-label trialsbut did not prove efficacious in subsequent placebo-controlled studies. Thesepharmacological treatments have included dopaminergic agonists (e.g., monamineoxidase inhibitors, amantadine, mazindol, methylphenidate, pemoline,bromocriptine, L-dopa, and pergolide), neurotransmitter precursors (L-tyrosine,L-tryptophan, and multivitamins with B complex), carbamazepine, and antidepressants,including desipramine and fluoxetine. In a meta-analysis examining45 clinical trials examining mostly antidepressants, carbamazepine, and dopamineagonists, no significant impact of drug treatment was found, regardless ofthe type of drug or dose used (Lima, Soares, Reisser, & Farrell, 2002).Clinical trials with bupropion, olanzapine, naltrexone, buprenorphine, andother drugs are ongoing. As our understanding of the neurobiological basis ofcocaine addiction becomes further refined, new pharmacological strategies areemerging. Potential targets include specific dopamine, serotonin, and otherreceptor subtypes, neuroendocrine peptides (i.e., CRF), and biogenic aminetransporters, including the dopamine reuptake transporter. These pharmacotherapiesand the potential development of a vaccine to prevent cocaine fromreaching its CNS site of action are covered in Chapter 26.

9. Cocaine and Stimulants 203Cognitive, Behavioral, and Nonpharmacological TreatmentsCocaine disorders have proven to be refractory to both psychological and pharmacologicaltreatment. Consequently, considerable energy has been directedtoward developing and testing the efficacy of new psychotherapeutic approachesin the treatment of cocaine use disorders. Many of these therapieshave been adapted from ones originally developed to treat alcoholism. Oneapproach that has received attention is cognitive-behavioral relapse prevention(Marlatt & Gordon, 1985). Relapse prevention strives to teach the addict howto recognize high-risk situations and deal with these using cognitive strategiesthat have been well rehearsed. Relapse prevention recognizes that with achronic disorder such as addiction, relapses and remissions are expected. Whena relapse occurs, more intense treatment and cognitive restructuring are necessaryto help prevent a “slip” from escalating. Reminding patients of their priorprogress, focusing on making the “slip” an isolated event, and maximizing thelearning value of this experience are constructive ways of handling the situation.The literature on efficacy of relapse prevention in the treatment ofcocaine dependence is mixed. In a review of 24 randomized clinical trials ofrelapse prevention for drug abuse (including cocaine), Carroll (1996) concludedthat relapse prevention is superior to no treatment, although superiorityto other active therapies is less evident.Cognitive behavioral therapy (CBT) is also an effective treatment forcocaine addiction, and improves comorbid psychosocial problems (Carroll,2000). In addition, CBT has demonstrated higher retention rates and improvedcompliance compared to other forms of individual and group therapy (Crits-Christoph et al., 1999). However, recent findings indicate that patients withcognitive impairments are more likely to drop out of CBT (Aharonovich,Nunes, & Hasin, 2003).A somewhat different approach has been taken by researchers studying therole of conditioned cues or “reminders” of cocaine use (O’Brien, Childress,Arndt, & McLellan, 1988); this approach attempts to extinguish conditionedresponses to these cocaine cues, thereby reducing the chances for relapse.Desensitization training requires that patients be repeatedly exposed to drugstimuli, then given the opportunity to deal with them in real-life situations.Behavioral rehearsal is key to being prepared to deal with the drug-laden situationsthat exist outside the protection of the treatment center. In one study(O’Brien, Childress, McLellan, & Ehrman, 1990), 30 drug-free cocaine addictswere repeatedly exposed to cocaine cues within a controlled setting. Subjectsreported experiencing strong physiological arousal, including cocaine craving,highs, and withdrawal in response to exposure. However, by the sixth hour ofextinction (repeated nonreinforced exposure to cocaine cues), highs and withdrawalwere no longer reported and, by the 15th hour, craving was no longer

204 III. SUBSTANCES OF ABUSEexperienced. Despite the strong extinction of arousal, these effects diminishedover time, unless they were reinforced with repeated cue exposure sessions.Voucher-based reinforcement strategies have also shown considerablepromise (Higgins, Budney, Bickel, & Foerg, 1994; Higgins et al., 1995, 2000).Higgins and colleagues (1994) demonstrated that voucher incentives (in combinationwith comprehensive behavioral intervention) enhanced retention inthe 24-week-long treatment program both for patients receiving interventions(75%) and those receiving behavioral therapy only (40%). In addition, those inthe voucher group had greater continuous abstinence and evidenced greaterimprovements on the Addiction Severity Index (ASI) Drug and Psychiatricscales than those not receiving vouchers. Subsequent follow-up assessmentsindicated that these gains were maintained 6 months after treatment (Higginset al., 1995), and as much as 15 months after treatment (Higgins et al., 2000).Other studies of contingent vouchers have yielded similarly positive outcomesin cocaine-dependent outpatients (Kirby, Marlowe, Festinger, Lamb, & Platt,1998; Silverman et al., 1996). In addition, a study by Rawson and colleagues(2002) compared contingency management (vouchers), CBT, a combinationof the two, and a “no-cocaine-treatment condition,” which consisted of methadonemaintenance for heroin addiction only in patients with heroin andcocaine dependence. They found that contingency management was associatedwith significantly higher levels of cocaine abstinence than were the CBT orcontrol interventions. However, the CBT group showed improvement at the 6-and 12-month follow-up points that was congruent with the contingency managementgroup.Unfortunately, not all substance abusers are motivated to change theirdrug use behavior; this is particularly true of patients with comorbid psychiatricdisorders, who may be overwhelmed by their multiple problems and prior treatmentfailures (Martino, McCance-Katz, Workman, & Boozang, 1995; Ziedonis& Fischer, 1996). Motivational enhancement therapy (MET), or motivationalinterviewing (MI), a nonconfrontational approach developed by Miller andRollnick (1991), was originally designed for working with problem drinkers. Innumerous trials, the principles of MI have been shown to be effective, sometimesafter only one or two sessions (Bien, Miker, & Tonigan, 1993; Brown &Miller, 1993). Because of promising results with alcoholics, MET/MI is currentlybeing adapted for use with drug abusers, including those with cocainedependence and psychiatric comorbidity. MET/MI works in tandem with thestages-of-change model of Prochaska, DiClemente, and Norcross (1992). Themodel postulates five distinct stages: precontemplation, contemplation, action,maintenance, and relapse. These stages can be assessed via paper-and-pencilinstruments, such as the University of Rhode Island Change Assessment(URICA). Different therapeutic strategies are employed, based on the patient’sdesignated stage of change. MET/MI represents a clear departure from traditionaldrug abuse counseling strategies. Because acceptance of the addict iden-

9. Cocaine and Stimulants 205tity is considered unimportant, patients are less likely to manifest overt resistance.Rather than emphasize powerlessness, this approach assumes that peoplehave within themselves the capacity to change. Although the efficacy of MET/MI for cocaine abusers has yet to be proven, it would appear that its uniquefocus on readiness should, at minimum, help patients to engage in other formsof therapy. In addition, a few studies have begun to support the use of MET/MIfor treatment of cocaine abuse and dependence. In a small study examining 27female workers with concurrent cocaine or heroin dependence, MI significantlyreduced the women’s cocaine use (Yahne, Miller, Irvin-Vitela, & Tonigan,2002). Similarly, compared to patients who only underwent a detoxificationprogram, patients who also received MI were more likely to be abstinentfrom cocaine following detoxification and demonstrated higher abstinencerates throughout the following relapse prevention treatment. Inaddition, MI was more effective for those patients with lower initial motivation(Stotts, Schmitz, Rhoades, & Grabowski, 2001). Finally, Brown and colleagues(1998) showed that, compared to patients who received meditation/relaxation,patients who received MI had better retention in treatment, though no differenceswere found in overall cocaine use. The researchers also found that MIpatients who initially reported less motivation for change had higher rates ofabstinence at follow-up than did MI patients reporting more motivation forchange at baseline. These findings suggest that MET/MI strategies may be mosteffective for patients who come into drug treatment with low motivation.The approaches described (i.e., relapse prevention, cue exposure/desensitization,contingency management, and motivational interviewing) are somewhattechnical and require specific training and supervision. Research-basedinterventions such as these appear to be the wave of the future, and most can beadapted for use in community-based programs. Frequently, treatment of cocainedependence takes place within the context of a comprehensive drug treatmentprogram. Although therapeutic modalities may be the same as for other drugabusers (e.g., education, and individual and group therapy), the intensity oftreatment must be greater. Emphasis must be placed on the acquisition of skillsthat will enable the cocaine abuser to have more internal control, greater selfefficacy,and reduced likelihood of relapse. This means that treatment musthave multiple “practical” components.The first goal of treatment is to interrupt recurrent binges or daily use ofcocaine and overcome drug craving. For patients who do not have serious psychiatriccomorbidity, a structured outpatient program can be attempted prior tophysically removing the person from the drug-using environment for treatmentin a residential setting. While attempting to initiate abstinence, treatmentshould include daily or multiple weekly contacts and urine monitoring, with asmany external controls as possible. Explicit practical measures to limit exposureto stimulants and high-risk situations should be individualized but mightinclude monitoring and support by drug-free “significant others,” discarding

206 III. SUBSTANCES OF ABUSEdrug supplies and paraphernalia, breaking off relationships with dealers anddrug-using comrades, limiting finances, changing one’s telephone number and/or geographic location, and structuring one’s time during all waking hours.Instead of simply replacing cocaine’s central role in one’s existence, emphasizinglifestyle changes such as stress reduction, wellness, exercise, and leisureactivities is important. This may be more difficult for persons of lower socioeconomicgroups and/or those with an earlier onset of addiction. These personslack the knowledge, experience, and resources to make these changes. Suchpatients may need linkage to other social services and habilitation, in additionto the rehabilitation just discussed. The involvement of significant others inthe treatment of cocaine use disorders can have a positive impact. For instance,Higgins, Budney, Bickel, and Badger (1994) recently showed that patients whohad family involvement were 20 times more likely to complete treatment.Finally, supportive therapies, including self-help groups, may provide positiverole models, group spirituality, and the backing needed to assist in change. SpecialCocaine Anonymous (CA) groups may be beneficial in addressing issuespertinent to cocaine’s strong reinforcing properties and associated lifestyle. Onthe other hand, CA meetings may have detrimental effects by continuing tofoster a sense of cocaine separatism.METHAMPHETAMINEAccording to the NHSDA (Substance Abuse and Mental Health ServicesAdministration, 2001b), approximately 4% of the population (8.8 million people)have tried methamphetamine in their lifetime. Emergency department(ED) mentions of methamphetamine in 2001 (15,000 mentions) were not significantlydifferent from mentions in 1994, 1999, or 2000. However, there wasan increase and subsequent decline of ED mentions in 1997 (Substance Abuseand Mental Health Services Administration, 2001a). The highest rates of useare seen in patients 26–29 years of age, followed by patients ages 18–25; 39% ofmethamphetamine admissions were patients 20–29 years old. In addition,TEDS data reveal that 80% of ED mentions were white (Substance Abuse andMental Health Services Administration, 2002). Rates of use are highest inHawaii, San Francisco, San Diego, Phoenix, Seattle, Denver, Los Angeles, and,Minneapolis (Substance Abuse and Mental Health Services Adimnistration,2001b).D-Methamphetamine hydrochloride is a stimulant that produces manysubjective effects similar to those of cocaine, although its 10- to 12-hour halflifeis 6–30 times as long as the 20- to 120-minute duration of cocaine (Gold,Miller, & Jonas, 1992). Its street names include crank, chalk, go-fast, crystal,and crystal meth. Methamphetamine can be snorted, taken orally, injectedintravenously, or inhaled, but it must be purified before it can be smoked. The

9. Cocaine and Stimulants 207purified form of the d-isomer, often called “ice” or “glass,” is frequently sold aslarge crystals that are smoked. The freebase form of methamphetamine is a liquidat room temperature. Rocks are made by melting, cooling, and cutting themethamphetamine crystals, which is often done in an aluminum turkey roastingpan. Methamphetamine can be smoked by inhaling it from a straw placedon aluminum foil or inhaling it through a glass pipe. Methamphetamine pipesdiffer from those for crack cocaine, because the drug vaporizes at a much lowertemperature (Cook, 1991). Methamphetamine is heated by holding a lighterunder a large glass ball at the end of the pipe. A finger placed over a hole on thetop of the pipe regulates airflow.Methamphetamine elevates blood pressure, speeds heart rate, raises bodytemperature, dilates pupils, reduces food intake, and diminishes sleep. Lowdoses initially are associated with increased alertness, energy, and vigilance.Higher doses produce intoxication symptoms, including euphoria, enhancedself-esteem, and increased sexual pleasure. Even higher doses result in anxiety,irritability, tremors, paranoia, and stereotypical behavior. Tolerance (needingmore drug to achieve a given effect) or sensitization (needing less drug toachieve a given effect) may occur upon continued methamphetamine exposure.Different drug effects may have varying rates of either tolerance or sensitization(Lukas, 1997). Tolerance to methamphetamine euphoria occurs more quicklythan tolerance to its tachycardic or anorexic effects. Being more prone to seizuresand psychosis after repeated dosing with methamphetamine is an exampleof sensitization (Koob, 1997). Methamphetamine toxicity can affect manyorgan systems. Methamphetamine cardiotoxicity is related to catechol excess,and may result in myocardial infarction and/or arrhythmias. Pulmonary hypertension,rhabdomyolysis, acute renal failure, heightened immunosuppression,and idiosyncratic liver necrosis are a few of the morbidities associated withmethamphetamine use. Paranoid delusions occur in more than 80% of the casesof toxic psychosis. Acute lead poisoning is also a risk for methamphetamineusers, because lead acetate is often used as a reagent in its production. Prenatalexposure to methamphetamine is associated with pregnancy complications,prematurity, problems with reflexes, irritability, and congenital deformities.Finally, injecting methamphetamine places users (increasingly, gay male populations)at increased risk for HIV and hepatitis B and C.Methamphetamine enters the nerve terminal via the synaptic or membranetransporter, then enters the storage vesicles through vesicular transporters,forcing out neurotransmitters such as dopamine and norepinephrine. Methamphetamineis basic and disrupts the acidic interior of the synaptic vesicles,inactivating the proton pump necessary to transport dopamine back inside thevesicle. The dopamine in the cytoplasm undergoes autooxidation, which producestoxic peroxides, oxygen radicals, and hydroxylquinones, which can causedamage in such dopamine-rich areas of the brain as the ventral tegmentum andsubstantia nigra (Seiden, 1991; Seiden & Sabol, 1996). Dopamine and seroto-

208 III. SUBSTANCES OF ABUSEnin, and their precursor enzymes tyrosine hydroxylase, and tryptophan hydroxylase,are depleted, which in turn affects levels of the major metabolites ofthese transmitters, their receptors, and their reuptake transporters. Methamphetaminealso affects serotonergic, noradrenergic, and glutamatergic systemsthrough interactions with dopamine transporters, monoamine transporters, andN-methyl-D-aspartate (NMDA) receptors. Nitric oxide may have a role inmethamphetamine-induced behavioral sensitization and neurotoxicity.Chronic methamphetamine abuse can lead to psychotic behavior (particularlyparanoia), visual and auditory hallucinations, and violent behavior.Chronic methamphetamine users also demonstrate deficits in attention, verbalmemory, abstract reasoning, task shifting, and spatial abilities (Simon etal., 2000). Animal studies have demonstrated that chronic administration ofmethamphetamine decreases striatal concentrations of dopamine and dopaminemetabolites in several regions of the brain (Nordahl, Salo, & Leamon,2003).Other than symptomatic treatment of drug-induced sequelae, there are nospecific pharmacological treatments for methamphetamine addiction (Lukas,1997). Continued progress in understanding the neurobiological basis for methamphetamineaddiction, as well as medication development initiatives aimed atcocaine and other drugs, may benefit methamphetamine pharmacotherapy inthe future. Nonpharmacological therapies for methamphetamine addiction aresimilar to those for other chemical dependencies but need to take into accountmethamphetamine’s longer duration of action, withdrawal period, and potentiallylonger recovery phase. In addition, methamphetamine users may experienceparanoia, psychotic symptoms, and protracted depression and anhedonia,making them more difficult to treat than the standard drug treatment population.Regarding nonpharmacological treatment, methamphetamine usersand cocaine users respond similarly to manualized behavioral and cognitivebehavioraltreatment strategies (Shoptaw, Rawson, McCann, & Obert, 1994).In addition, new behavioral treatments under development show promise. TheMatrix Program, a multisite, Center for Substance Abuse Treatment (CSAT)–funded drug treatment program, demonstrated significantly reduced methamphetamineuse from pretreatment levels in a follow-up sample 2–5 yearsposttreatment (Rawson et al., 2002). However, continuing high rates of dropoutand relapse in this population indicate a need for further treatment researchfor this difficult population.CONCLUSIONOver the past 15 years, much has changed with regard to the use and our understandingof both amphetamines and cocaine. Most notably, cocaine depend-

9. Cocaine and Stimulants 209ence now appears to be differentially affecting poor, minority individuals wholive in the inner city. This same population is overrepresented in the AIDSpopulation. This confluence is not surprising, because both sex risk (includingsex workers) and needle risk are associated with chronic use of cocaine. Ittherefore appears that these two epidemics are interconnected in a way thatdeserves close attention.At the same time, there may be reason for cautious optimism with regardto the long-term effects of prenatal exposure to cocaine. Some of the earlyclaims of devastating physical consequences to “crack babies” have proven tobe exaggerated; experts in the perinatal addiction field now consider that manyfactors (e.g., poverty, poor maternal nutrition/health, smoking, and exposure toviolence) combine to influence development. Molecular mechanisms of developmentalneuroadaptation are at the same time beginning to be studied. In thefuture, we hope to understand better the physiological basis for the observedclinical events.In the basic sciences area, we have come to understand more about theinteractions of various neurotransmitters, drug reinforcement, and the rewardpathway. Receptors are being subtyped and cloned. Signal transduction pathways,with their longer range on protein synthesis and genetic regulation, arebeing explored. We are beginning to make inroads in our understanding of sensitizationand tolerance. Although pharmacological treatments for cocaineaddiction have not yet proven successful in clinical trials, there are many excitingnew avenues of pursuit. These prospects for pharmacological interventionare based on the remarkable advances in neuroscience being made in thisdecade.Researchers also have been hard at work testing psychotherapeutic solutionsto this complex problem. Cocaine dependence should not be viewed inisolation from other psychiatric conditions and life problems. Rather, we mustconsider how best to address the problem in the presence of other psychoactivesubstance use and non-substance-use Axis I and Axis II disorders. Dependingon the larger clinical picture, successful treatment may require multiple orhighly select therapies that are matched to the patient’s pathology and adaptivestrengths and resources. It is clear that a “one size fits all” approach to treatmentof cocaine dependence is inappropriate; instead, an array of assessment tools isnecessary to determine patient needs, along with a menu of cost-effective andreadily available therapeutic strategies. Although American Society of AddictionMedicine (Hoffman, Halikas, Mee-Lee, & Weedman, 1991) criteria facilitatepatient placement in an appropriate treatment setting based on addictionseverity, they provide little guidance in terms of specific interventions to bedelivered within those settings. Clinical research aimed at developing therapiesfor specific subtypes of cocaine addicts in a variety of settings is the most promisingapproach we now have.

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Sedatives/Hypnoticsand BenzodiazepinesCHAPTER 10ROBERT L. DUPONTCAROLINE M. DUPONTThe sedatives and the hypnotics, especially the benzodiazepines, are widelyused in medical practice in the treatment of anxiety, insomnia, epilepsy, and forseveral other indications (Baldessarini, 2001). The combination of abuse byalcoholics and drug addicts, and the withdrawal symptoms on discontinuationleads to the view that these are “addictive” drugs (DuPont, 2000; Juergens &Cowley, 2003). The pharmacology and the epidemiology of sedatives andhypnotics are reviewed in this chapter, which focuses on the needs of the clinician.A sedative lowers excitement and calms the awake patient, whereas a hypnoticproduces drowsiness and promotes sleep. The nonbenzodiazepine sedativesgenerally depress central nervous system (CNS) activity in a continuum,depending on the dose, beginning with calming and extending progressively tosleep, unconsciousness, coma, surgical aesthesia, and, ultimately, to fatal respiratoryand cardiovascular depression. Sedatives share this spectrum of effectswith many other compounds, including general anesthetic agents, a variety ofaliphatic alcohols, and ethyl alcohol. At lower doses, sedatives can causeimpaired cognitive and motor functioning (including staggering and slurredspeech). Sedation is a side effect of many other medicines, including antihistaminesand neuroleptics.The benzodiazepines resemble the other sedatives, except that they do notproduce surgical anesthesia, coma, or death, even at high doses, except when219

220 III. SUBSTANCES OF ABUSEcoadministered with other agents that suppress respiration. The benzodiazepinescan be antagonized by specific agents that do not block the effects ofother sedatives. The benzodiazepine antagonists do not produce significanteffects in the absence of the benzodiazepines. These properties distinguish thebenzodiazepines from the other sedatives and produce a margin of safety thathas led to the widespread use of benzodiazepines (Charney, Minie, & Harris,2001).The National Comorbidity Survey (NCS) found that 17.2% of the populationhad an anxiety disorder in the past 12 months, and 24.9% had a lifetimehistory of anxiety disorder (DuPont, Dupont, & Rice, 2002; Kessler et al.,1994). These studies establish that the anxiety disorders are the most prevalentclass of mental disorders over a 12-month period of time (DuPont, 1995). Usingthe standard human capital approach to estimate the social costs of illnesses in1994, the anxiety disorders produced a total social cost of $65 billion (DuPontet al., 2002). Of this total, the cost of all treatments was only $15 billion,whereas $50 billion was due to lost productivity as a result of the often seriouslydisabling nature of the anxiety disorders. For comparison, using the same methodology,the costs of all mental illnesses in 1994 was $204 billion, of which themood disorders—including depression and bipolar disorders—totaled $42 billionand schizophrenia totaled $45 billion.The benzodiazepines were introduced in 1960s as comparatively problemfreecompared to the barbiturates, which they rapidly replaced. Their popularityreached unprecedented levels in the early 1970s. However, a powerful backlash,labeled the “social issues,” emerged, which caused a drop in the use of benzodiazepinesduring the 1980s, even though there was a rise in the prevalence ofthe disorders for which they are used (DuPont, 1986, 1988).As the benzodiazepines became more controversial, and as various regulatoryapproaches were employed to limit their use in medical practice, there wasa danger that clinicians would revert to the older and generally more toxic sedativesand hypnotics, which, in the era of the benzodiazepines, had becomeunfamiliar (Juergens & Cowley, 2003). Thus, there is more than historicalinterest in looking at these earlier sedatives, because for some younger medicalpractitioners, they are new medicines. The use of sedatives and hypnotics forthe treatment of anxiety and insomnia in patients with addiction to alcoholand other drugs entails additional risks, especially when benzodiazepines areused (Handelsman, 2002).For more than three decades, the federal government has tracked the ratesof self-reported, nonmedical use of a variety of drugs within the United States,primarily in two surveys—one of high school seniors (Monitoring the Future[MTF]), and the other of Americans 12 years of age and older (National HouseholdSurvey on Drug Abuse [NHSDA]) (U.S. Department of Health andHuman Services, 2001, 2002). The NHSDA separately tracks the use of “tran-

10. Sedatives/Hypnotics and Benzodiazepines 221quilizers” and “sedatives” while the MTF survey tracks “tranquilizers” and “barbiturates.”Neither survey identifies “benzodiazepines” specifically. In general,the trends over this extended period of time show a steady rise in nonmedicaluse, peaking in the late 1970s, followed by a low point in the early 1990s. Thiswas followed by a subsequent upturn in the levels of use that continued into2001. In 2000, the NHSDA estimated the total number of use Americans, 12years of age and older, who had used a tranquilizer nonmedically during theprior 30 days as 788,000, down from 950,000 the prior year (U.S. Departmentof Health and Human Services, 2001). Most of the people who had used abenzodiazepine nonmedically had done so only a few times in their lifetimes.Nonmedical benzodiazepine use, which is different from, and far less commonthan medical use of the benzodiazepines, is a small but significant part of theoverall nonmedical drug problem in the nation.DISTINGUISHING MEDICAL AND NONMEDICALUSE OF BENZODIAZEPINESA series of national surveys tracking the medical use of the benzodiazepinesshowed that their use peaked in 1976 and by the late 1980s had fallen about25% off that peak rate (DuPont, 1988). A 1979 survey of medical use of thebenzodiazepines (near the peak of benzodiazepine use in the United States),showed that 89% of Americans ages 18 years and older had not used a benzodiazepinewithin the previous 12 months. Of those who had used a benzodiazepine,most (9.5% of all adults) had used the benzodiazepine either less thanevery day or for less than 12 months, or both, whereas a minority (1.6% of theadult population) had used a benzodiazepine on a daily basis for 12 months orlonger. This long-term user group was two-thirds female; 71% were age 50 orolder, and most had chronic medical problems, as well as anxiety (DuPont,1988).Of those with anxiety disorders in a large community sample, three-fourthswere receiving no treatment at all, including not using a benzodiazepine. The1.6% of the population who are chronic benzodiazepine users can be comparedto the 17% of the population suffering from anxiety disorders at any 12-monthperiod. This statistic led many observers to conclude that not only are benzodiazepinesnot overprescribed but they also may actually be underprescribed,because of the reluctance of both physician and patients to use these medicines(Mellinger & Balter, 1981).To understand the place of the benzodiazepines in contemporary medicalpractice, it is important to separate appropriate medical use from inappropriate,nonmedical use. Five characteristics distinguish medical from nonmedical useof all controlled substances, including the benzodiazepines.

222 III. SUBSTANCES OF ABUSE1. Intent. Is the substance used to treat a diagnosed medical problem, suchas anxiety or insomnia, or is it used to get high (or to treat the complications ofnonmedical use of other drugs)? Typical medical use of a benzodiazepine orother controlled substance occurs without the use of multiple nonmedicaldrugs, whereas nonmedical use of the benzodiazepines is usually polydrug abuse.Although alcoholics and drug addicts sometimes use the language of medicineto describe their reasons for using controlled substances nonmedically, “selfadministration”or “self-medication” of an intoxicating substance outside theordinary practice boundaries of medical care is a hallmark of drug abuse(DuPont, 1998).2. Effect. What is the effect of the controlled substance use on the user’slife? The only acceptable standard for medical use is that it helps the user live abetter life. Typical nonmedical drug use is associated with deterioration in theuser’s life, even though continued use and denial of the negative consequencesof this use are nearly universal.3. Control. Is the substance use controlled only by the user, or does a fullyknowledgeable physician share the control of the drug use? Medical drug use iscontrolled by the physician, as well as the patient, whereas typical nonmedicaluse is solely controlled by the user.4. Legality. Is the use legal or illegal? Medical use of a controlled substanceis legal. Nonmedical drug use of controlled substances, including benzodiazepines,is illegal.5. Pattern. What is the pattern of the controlled substance use? Typicalmedical use of controlled substances is similar to the use of penicillin or aspirin,in that it occurs in a medically reasonable pattern to treat an easily recognizedhealth problem other than addiction. Typical use of nonmedical drugs (e.g.,alcohol, marijuana, or cocaine), in contrast, takes place at parties or in othersocial settings. Medical substance use is stable and at a moderate dose level.Nonmedical use of a controlled substance is usually polydrug abuse at high and/or unstable doses (Juergens & Cowley, 2003).DRUG DEPENDENCE VERSUS PHYSICAL DEPENDENCESubstance use disorder is a mental disorder defined in the fourth revised editionof the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR; AmericanPsychiatric Association, 2000). It includes out-of-control drug use, useoutside social and medical sanctions, continued use despite clear evidenceof drug-caused problems, and a drug-centered lifestyle. Physical dependence(including withdrawal on discontinuation), in contrast to addiction, is a pharmacologicalphenomenon in which the user experiences a specific constellationof symptoms for a relatively short period when use of the substance is abruptlydiscontinued. Physical dependence may, but often does not, accompany sub-

10. Sedatives/Hypnotics and Benzodiazepines 223stance use disorder (abuse or dependence). The appropriate treatment foraddiction, or substance use disorder, is usually long-term, specialized additionaltreatment followed by prolonged participation in one of the 12-step programsand/or other ongoing support and care. The appropriate treatment for physicaldependence, in clear contrast, is gradual dose reduction to permit biologicaladaptation to lower doses of the dependence-producing substance, leading tozero dosing.A patient who seeks to continue using a medicine because it is helpful isno more demonstrating “drug-seeking behavior” than is a patient who findseyeglasses helpful in the treatment of myopia demonstrating “glasses-seekingbehavior” if deprived of a corrective lens. Drug abuse and drug dependence arecharacterized by use despite problems caused by that use (loss of control) and bydenial (and dishonesty)—neither of which is seen in appropriate medical treatment(DuPont & Gold, 1995).Precisely the same confusion of medically trivial physical dependence withserious substance use disorder (addiction) occurs in regard to the use of opiatesin the treatment of severe pain. Many patients and many physicians undertreatsevere pain, because they are unable to distinguish physical dependence, thebenign pharmacological fact of neuroadaptation in medical patients, from theabuse of opiates by drug addicts, a malignant biobehavioral disorder (Savage,2003).MEDICAL USE AND ABUSEThe benzodiazepines are among the most widely prescribed psychotropic medicinesin the world. The World Health Organization (1988) labeled them“essential drugs” that should be available in all countries for medical purposes.Of the widely used psychotropic drugs, they are the least likely to cause anyadverse effects, including serious medical complications and death.Workplace drug testing is usually limited to identification of marijuana,cocaine, morphine–codeine, amphetamine–methamphetamine, and phencyclidine(PCP). However, benzodiazepines and barbiturates may be added to thetest panel. Laboratory positive test results for patients with legitimate prescriptionsfor benzodiazepines and barbiturates are reported to employers by medicalreview officers (MROs) as negative, as are other laboratory results that reflectappropriate medical treatment with other controlled substances (MacDonald,DuPont, & Ferguson, 2003).Several important health concerns about benzodiazepine use that are unrelatedto addiction have been expressed, especially about the long-term use ofbenzodiazepines, including the effects on the brain, the possibility of cerebralatrophy associated with prolonged benzodiazepine use, and other problems,such as memory loss and personality change (American Psychiatric Associa-

224 III. SUBSTANCES OF ABUSEtion Task Force on Benzodiazepine Dependence, Toxicity and Abuse, 1990;Golombok, Moodley, & Lader, 1988). The evidence for these problems is bothpreliminary and disputed, except for the well-studied acute effect of benzodiazepineson memory, which has no clinical significance for most patients.PHARMACOLOGYIn this section, the sedatives and hypnotics are divided for convenience intothree groups: barbiturates, “other sedatives and hypnotics,” and benzodiazepines.We also discuss the newer agents, which are alternatives to the benzodiazepines.BarbituratesBarbital was introduced into medical practice in 1903, and phenobarbital, in1912. Their rapid success led to the development of over 2,000 derivatives ofbarbituric acid, with dozens being used in medical practice. The only sedativesto precede the barbiturates were the bromides and chloral hydrate, both ofwhich were in widespread use before the end of the 19th century.The most commonly used barbiturates today are amobarbital (Amytal),butabarbital (Butisol), mephobarbital (Mebaral), pentobarbital (Nembutal),secobarbital (Seconal), and phenobarbital (Luminal). The first five have anintermediate duration of action, whereas the last, phenobarbital, has a longduration of action. Short-acting barbiturates are used as anesthetics, but not inoutpatient medicine.Barbiturates reversibly suppress the activity of all excitable tissue, with theCNS being particularly sensitive to these effects. Except for the antiepilepticeffects of phenobarbital, there is a low therapeutic index for the sedative effectsof the barbiturates, with general CNS depression being linked to the desiredtherapeutic effects. The amount of barbiturates that can cause a fatal overdoseis well within the usual size of a single prescription. A common problem withthe medical use of the barbiturates for both sedation and hypnosis is the rapiddevelopment of tolerance, with a common tendency of medical patients to raisethe dose on chronic administration. The barbiturates affect the gammaaminobutyricacid (GABA) system, producing both a cross-tolerance to othersedating drugs, including alcohol and the benzodiazepines, and a heightenedrisk of fatal overdose reactions (Charney et al., 2001).Other Sedatives and HypnoticsOver the course of the 20th century, several medicines with diverse structureswere used as sedatives and hypnotics. In general, the pharmacological proper-

10. Sedatives/Hypnotics and Benzodiazepines 225ties of these medicines resembled the barbiturates. They produced profoundCNS depression, with little or no analgesia. Their therapeutic index was lowand their abuse potential was high, similar to the barbiturates. Chloral hydrate(Noctec), ethchlorvynol (Placidyl), ethinamate (Valmid), glutethimide(Doriden), meprobamate (Miltown, Equanil), methyprylon (Noludar), andparaldehyde (Paral) belong in this class of seldom-used medicines that do nothave a useful place in contemporary medical practice.Despite the continued widespread use of antihistamines to treat insomnia,the Food and Drug Administration (FDA), noting the prominent sedativeside effects encountered in the administration of antihistamines (includingdoxylamine, diphenhydramine, and pyrilamine), concluded that theantihistamines are not consistently effective in the treatment of sleep disorders.Tolerance rapidly develops to the sedating effects of these medicines,and the antihistamines can produce paradoxical stimulation. In addition, theantihistamine doses currently approved for the treatment of allergies are inadequateto induce sleep. Antihistamines used to treat sleep disorders can producedaytime sedation because of their relatively long half-lives (Charney etal., 2001).The use of sedating antidepressants such as Desyrel (trazodone) and Elavil(amitriptyline) to treat insomnia at dose levels lower than are effective for thetreatment of depression, such as the use of sedating antihistamines for this indication,is clinically problematic, since these agents may be both less effectiveand more likely to produce undesirable side effects (especially in producing daytimesedation) than the use of benzodiazepines in this indication (Mendelson etal., 2001).BenzodiazepinesThe benzodiazepines were recognized in animal experiments in the 1950s fortheir ability to produce “taming” without apparent sedation. Cats, which areextremely sensitive to even small electrical shocks, were obviously sedatedwhen given enough alcohol or barbiturates to prevent anxious avoidancebehavior of impending shocks. In contrast, when given benzodiazepines, thecats appeared normal in all of their behavior, except that they did not show theexaggerated anticipatory sensitivity to mild electrical shocks that they showedprior to treatment with benzodiazepines.Chlordiazepoxide (Librium), the first benzodiazepine used in clinical practice,was introduced in 1961. More than 3,000 additional benzodiazepines havebeen synthesized, of which about 50 have been used clinically (Baldessarini,2001). Several of the benzodiazepines, including alprazolam (Xanax), diazepam(Valium), lorazepam (Ativan), and clonazepam (Klonopin) are among not onlythe most widely prescribed medicines for anxiety but are also the most frequentlyprescribed medicines worldwide.

226 III. SUBSTANCES OF ABUSEThe identification of the benzodiazepine receptors in 1977 began the modernera of benzodiazepine research, establishing this class as the best understoodof the psychiatric medicines. GABA receptors are membrane-bound proteinsdivided into three subtypes, GABA-A, GABA-B, and GABA-C receptors. TheGABA-A receptors are composed of five subunits that together form the chloridechannel, which primarily mediates neuronal excitability (seizures), rapidmood changes, and clinical anxiety, as well as sleep. GABA-B receptors mediatememory, mood, and analgesia. The role of the GABA-C receptors remainsunclear. The effects of benzodiazepines are reversed by benzodiazepine antagonists,one of which—flumazenil—is used clinically to reverse rapidly the effectsof benzodiazepine overdoses (Charney et al., 2001). The benzodiazepine receptors,part of the GABA system, are found in approximately 30% of CNS synapsesand in all species above the level of the shark, demonstrating their fundamentalbiological importance.There are pharmacological differences among the individual benzodiazepinesthat have clinical significance. The differences between the benzodiazepinesresemble the differences between the individual medicines in two othermajor classes of psychotropic medicines: antipsychotics and antidepressants.Although there are many overlapping effects within each class, there are alsoimportant differences among the medicines in each class, so that the medicineswithin a class cannot be used interchangeably. These pharmacological differencesamong the benzodiazepines include the rapidity of onset (distributionalhalf-life), persistence of active drug and/or metabolite in the body (eliminationhalf-life), major metabolic breakdown pathways (conjugation vs. oxidation),and specific molecular structure (e.g., alprazolam has a unique triazolo ring thatmay account for some differences in its clinical effects) (Charney et al., 2001).Table 10.1 summarizes these differences for the most widely used benzodiazepines,along with clinically important pharmacological characteristics as theyrelate to the use and abuse of the benzodiazepines (Chouninard, Lefko-Singh,& Teboul, 1999). Benzodiazepines may produce some clinically relevant effectsby mechanisms that do not involve GABA-mediated chloride conductance(Burt & Kamatchi, 1991). The benzodiazepines have only a slight effect onrapid eye movement (REM) sleep, but they do suppress deeper, stage 4 sleep.Although this effect is probably of no clinical significance in most settings,diazepam has been used to prevent “night terrors” that arise in stage 4 sleep.Speed of OnsetThe most important distinction among the benzodiazepines in the substanceabuse context is the speed of onset, which determines abuse potential (Griffiths& Werts, 1997). Those benzodiazepines with a slow onset (because they areeither slowly absorbed or they must be metabolized to produce an active substance)have a relatively lower abuse potential. Those that rapidly reach peak

TABLE 10.1. Pharmacological Characteristics of BenzodiazepinesDrug Trade nameOnset of actionafter oraladministrationRate ofmetabolismMetabolizedprimarily by liveroxidationActivemetabolitesEliminationhalf-life(hours)Maximumusual dose(mg/day)Used primarily to treat anxietyAlprazolam Xanax Intermediate Intermediate Yes Yes 12–15 4100ChlordiazepoxidehydrochlorideLibrium Intermediate Long Yes Yes 5–3010–15Clonazepam a Klonopin Fast Long Yes No 26–30 2Clorazepate a dipotassium Tranxene Fast Long Yes Yes 36–200 60Diazepam a,b Valium Fast Long Yes Yes 20–50 40Halazepam Paxipam Intermediate Long Yes Yes 50–100 160Lorazepam Ativan Intermediate Short No No 10–14 6Oxazepam Serax Slow Short No No 5–10 60Prazepam Centrax Slow Long Yes Yes 36–200 60Used primarily to treat insomniaEstazolam ProSom Fast Short Yes No 10–24 2Dalmane Intermediate Long Yes Yes 40–100 30FlurazepamhydrochlorideQuazepam Doral Fast Long Yes Yes 20–120 30Temazepam Restoril Intermediate Short No Yes 8–12 30Triazolam Halcion Intermediate Short Yes No 2–5 0.25Approved to treat epilepsy.Approved as muscle relaxant.ab227

228 III. SUBSTANCES OF ABUSEbrain levels after oral administration are relatively more likely to produceeuphoria, and are therefore more likely to be abused by alcoholics and drugaddicts. Diazepam has a relatively rapid onset of action and is therefore amongthe most effective producers of euphoria. In contrast, the more slow-actingbenzodiazepines, such as oxazepam (Serax) and prazepam (Centrax), appear tohave lower abuse potentials.Clorazepate and prazepam, with inactive parent compounds, are also lesslikely to be abused for their euphoric effects because of slower onset of action.Oxazepam and the other slower onset benzodiazepines, like phenobarbital comparedto other barbiturates and codeine compared to other opiates, appear tohave relatively low abuse potentials.The relative rapidity of onset of diazepam does not mean that it is morelikely than other benzodiazepines to lead to abuse by medical patients who haveno addiction history. None of the benzodiazepines, including diazepam, arereinforcing for patients who do not have a history of addiction. On the otherhand, the pharmacology of the benzodiazepines suggests that, for patients witha history of addiction to alcohol and other drugs, diazepam may be more likelyto be abused than oxazepam, clorazepate, or prazepam (Griffiths & Weerts,1997).Some serious students of the pharmacology of benzodiazepines believe thatabuse is no more likely for diazepam than for oxazepam (Woods, Katz, &Winger, 1988). Addicts’ greater liking for diazepam in some studies, in thisview, is the result of the dose: Raise the dose of oxazepam in the double-blindstudies, and the liking scores of oxazepam are indistinguishable from those ofdiazepam. In contrast, other well-respected researchers are convinced that diazepam,lorazepam, and alprazolam have greater abuse potential—not solelybecause of dosage factors—because of their more rapid absorption and penetrationof the blood–brain barrier due to greater lipid solubility (Griffiths &Sannerud, 1987).Metabolic PathwaysThe metabolic pathways of the various benzodiazepines are important clinically,because those benzodiazepines that are metabolized by oxidation in theliver may alter the effects of other drugs. This is illustrated by the “boosting”effect of some benzodiazepines when used by methadone-maintained patients.Although the pharmacology of this effect is not well understood, it appears thatsimultaneous use of a benzodiazepine (e.g., diazepam or alprazolam) that competeswith methadone for oxidative pathways in the liver produces higher peaklevels of methadone in the blood (and brain) shortly after methadone is administered.Thus, prior use of some benzodiazepines may enhance brain reward foran hour or so after oral methadone dosages.Benzodiazepines that have conjugation as the major metabolic pathway are

10. Sedatives/Hypnotics and Benzodiazepines 229not dependent on liver functioning, so they are less likely to raise methadoneplasma levels or to build up plasma levels of the active benzodiazepine inpatients who have compromised liver functioning, including alcoholics and theelderly. The benzodiazepines metabolized by conjugation include lorazepam,oxazepam, and temazepam. Thus, because these are less “liked” by methadonemaintainedpatients and may be better choices for these patients and forpatients with compromised liver functioning, a benzodiazepine is to be used.Oxazepam is both a slow-onset and a conjugated benzodiazepine, making itperhaps the best choice for methadone-maintained patients who are treatedwith a benzodiazepine. On the other hand, oxazepam has a short eliminationhalf-life, which means it must be taken three or four times a day for continuoustherapeutic effects. Oxazepam is no less likely to produce physical dependence(including difficulties on discontinuation) than any other benzodiazepine.Oxazepam is a widely used benzodiazepine in Europe (but not in the UnitedStates, where it is commonly abused by drug addicts and alcoholics). Thus,whatever benefit oxazepam may possess for alcoholics and drug addicts comparedto other benzodiazepines is relative and not absolute (DuPont, 1988).PersistencePersistence of a benzodiazepine (or an active metabolite) in the body is importantclinically, because it governs the rapidity of onset of withdrawal symptomsafter the last dose for people who have used benzodiazepines for prolonged periods.The benzodiazepines with shorter elimination half-lives are more likely toproduce early and pronounced withdrawal symptoms on abrupt discontinuation,whereas those with longer elimination half-lives generally produce moredelayed and somewhat attenuated withdrawal symptoms. In general, alprazolam,lorazepam, and oxazepam are more rapidly eliminated than are clorazepate,diazepam, flurazepam, and prazepam. Thus, the benzodiazepines with shorterelimination half-lives are more likely to produce acute withdrawal on abruptcessation after prolonged use. Clonazepam has a longer elimination half-lifethan alprazolam or lorazepam, so it is less likely to produce interdose withdrawalsymptoms and is more appealing as a withdrawal agent (for the same reason,methadone and phenobarbital are attractive as agents in opiate withdrawal andsedative–hypnotic withdrawal).When discontinuing treatment with a benzodiazepine abruptly, the speedof onset and the severity of symptoms are greater for benzodiazepines withshorter elimination half-lives (e.g., alprazolam or lorazepam) than for thosewith a longer half-life (such as clonazepam). However, abrupt discontinuationis not an appropriate medical treatment for benzodiazepine discontinuationafter prolonged, everyday use. When short-acting benzodiazepines are withdrawngradually over several weeks or longer, they do not produce more symptomsof withdrawal than do longer acting benzodiazepines (Sellers et al., 1993).

230 III. SUBSTANCES OF ABUSEAlthough a long half-life may be beneficial in reducing the speed of onsetand severity of benzodiazepine withdrawal on abrupt discontinuation, it can bemore problematic in other situations. An increase in motor vehicle crashinvolvement was found in elderly persons using long half-life benzodiazepines,whereas use of shorter half-life benzodiazepines showed no increase in the probabilityof crashes in elderly persons compared to same-age persons who did notuse a benzodiazepine (Hemmelgarn, Suissa, Huang, Boivin, & Pinard, 1997;Wang, Bohn, Glynn, Mogun, & Avom, 2001).ReinforcementThree additional aspects of benzodiazepine pharmacology are relevant to thetreatment of addicted patients: reinforcement, withdrawal, and tolerance.Reinforcement is the potential for these medicines to be abused or “liked” byalcoholics and drug addicts. In controlled studies, benzodiazepines are not reinforcingor “liked” by either normal or anxious subjects. For example, normaland anxious subjects, given a choice between placebos and benzodiazepines,more often choose the placebo in double-blind acute dose experiments, regardlessof the specific benzodiazepine given. In contrast, subjects with a history ofaddiction in double-blind studies prefer benzodiazepines—especially at highdoses—to placebos. Studies have demonstrated that people with a history ofaddiction show a greater preference for intermediate-acting barbiturates andstimulants, as well as narcotics, than for benzodiazepines. Thus, the benzodiazepinesare reinforcing for alcoholics and drug addicts (though not for anxiouspeople or for people who do not have a history of addiction). The benzodiazepinesare relatively weak reinforcers compared to opiates, stimulants, andbarbiturates among alcoholics and drug addicts.This research confirms the common clinical observation that benzodiazepinesare rarely drugs of choice among addicted people for their euphoriceffects (DuPont, 1984, 1988). Although it remains unclear why alcoholics anddrug addicts react differently to the benzodiazepines than do normal or anxioussubjects, this phenomenon exists with all abused drugs. It is not limited to thebenzodiazepines. Normal subjects in double-blind studies do not generally“like” abused drugs, including stimulants, narcotics, and even alcohol. Peoplewho are not addicted to alcohol and other drugs do not like the feeling of beingintoxicated. Whether addicted people learn to like the intoxicated feeling orwhether they have some innate (perhaps genetically determined) differencethat explains this characteristic response to alcohol and controlled substancesremains an unanswered question of great importance to the prevention ofaddiction.When it comes to the outpatient treatment of anxiety in patients withactive addiction (e.g., current or recent abuse of alcohol or other drugs), the useof a controlled substance, including benzodiazepines, is generally contraindi-

10. Sedatives/Hypnotics and Benzodiazepines 231cated. A number of alternative treatments for anxiety are available, includingnonpharmacological treatments, antidepressants, and buspirone (Buspar), anonsedating antianxiety medicine with no abuse potential. As a general principle,the use of psychotropic medicines, whether controlled (e.g., benzodiazepines)or noncontrolled substances (e.g., antidepressants or antipsychotics), isunlikely to produce a therapeutic benefit for the actively using addicted patient.Stable abstinence is required for these antianxiety medicines to produce therapeuticresults.For patients who have been stable in recovery (including recovering alcoholics)and need treatment for anxiety, it is advisable not to use benzodiazepines,unless the physician can be sure that the patient uses the benzodiazepineonly as prescribed and in the absence of any nonmedical drug use,including alcohol use. For many recovering people, successful use of benzodiazepinesin the treatment of their anxiety disorders has not threatened theirsobriety. We have seen many more patients in recovery who do not want to useany controlled substance and have done well with their anxiety problems, withoutusing a benzodiazepine (Ciraulo et al., 1996; Sattar & Bhatia, 2003).If a benzodiazepine is to be administered to a recovering person, it may beprudent to use one of the slow-onset medicines (e.g., oxazepam, clorazepate, orprazepam) and to include a family member, as well as the sponsor from a 12-step fellowship in the therapeutic alliance, to help ensure that there is no abuseof the benzodiazepine or any other drug, including alcohol.WithdrawalAll of the medicines that influence the GABA system show cross-tolerance andsimilar withdrawal patterns. Because of cross-tolerance within this class of sedativesand hypnotics, an alcoholic or barbiturate addict can be withdrawn undermedical supervision using a benzodiazepine. For the same reason, phenobarbitalcan be used to manage benzodiazepine withdrawal (Wesson, Smith, & Ling,2003). Compared to other benzodiazepines, however, alprazolam withdrawalmay be inadequately covered by substitution. Alprazolam detoxification shouldinclude an estimation of daily use and a slow withdrawal over a period of weeks.Clonazepam has been found to be helpful in this condition.The sedatives/hypnotics withdrawal syndrome, including the potential forwithdrawal seizures on abrupt discontinuation, is also a phenomenon of thisclass of medicines, which argues against abrupt discontinuation of any of thesemedicines after daily use for more than a few weeks. Cessation of use of thebenzodiazepines, along with the other sedatives and hypnotics, can cause withdrawalseizures, because they are potent antiepilepsy drugs that raise the seizurethreshold. Medicines that raise the seizure threshold, when abruptly discontinued,produce a rebound drop in the seizure threshold that may cause seizures,even in people who have not previously had an epileptic seizure.

232 III. SUBSTANCES OF ABUSESome recovering people believe that they are more likely to have withdrawalsymptoms when they discontinue a benzodiazepine, even if it has beentaken within medical guidelines. Research on the topic suggests that this is notthe case, but this often contentious issue is best dealt with as an unresolvedquestion in clinical practice.ToleranceTolerance is rapid, and all but complete, to the sedative and to the euphoriceffects of the benzodiazepines on repeated administration at a steady dose levelfor even a few days. This rapidly developing tolerance for both sedation andeuphoria/reward is seen clinically when these medicines are used to treat anxiety.Patients often experience sedation or drowsiness when they take their firstfew benzodiazepine doses, but within a few days of steady dosing, the symptomsof sedation lessen and, for most patients, disappear.By contrast, tolerance to the antianxiety and antipanic effects of benzodiazepinesis nonexistent. Medical patients who are not alcoholics or drugaddicts, and who use a benzodiazepine to treat chronic anxiety, obtain substantialbeneficial effects at standard, low doses. They do not escalate their benzodiazepinedoses beyond common therapeutic levels, even after they have takenbenzodiazepines every day for many years.This distinction between the rapid tolerance to the sedating and theeuphoric effects and the absence of tolerance to the antianxiety effects ofbenzodiazepines is important for the clinician. Patients who use benzodiazepinesto get high typically add other substances and escalate their benzodiazepinedose over time. This commonly observed pattern reflects the existence oftolerance to the euphoric effects of benzodiazepines among addicted people. Incontrast, typical medical patients using benzodiazepines for their antianxietyeffects take them at low and stable doses, without the addition of other drugs,including alcohol.Some patients who use benzodiazepines daily, even after a long time, doescalate their dose beyond the usually prescribed level, add other drugs (especiallyalcohol), and/or have a poor clinical response to the benzodiazepine use(inadequate suppression of anxiety). Usually, but not always, these patientshave a personal and a family history of addiction to alcohol and other drugs.These same patients sometimes have unusual difficulty in discontinuing theiruse of benzodiazepines. This group of problems with long-term benzodiazepineuse is commonly seen in treatment programs for alcoholics and drug addicts,reinforcing the view in the addiction field that benzodiazepines are ineffective,problem-generating medications, especially after long-term use. Although thispattern of problems exists, it is, in our experience, uncommon in the typicalmedical or psychiatric practice dealing with anxious patients who do not have ahistory of addiction. Nevertheless, when it occurs, the best response is discon-

10. Sedatives/Hypnotics and Benzodiazepines 233tinuation of benzodiazepine use. For some patients, this requires inpatient treatment.IDENTIFICATION OF PROBLEMSAMONG LONG-TERM BENZODIAZEPINE USERSPhysicians frequently encounter patients, or family members of patients, whoare concerned about the possible adverse effects of long-term use of a benzodiazepinein the treatment of anxiety or insomnia. In helping to structure thedecision making for such a patient, we use the Benzodiazepine Checklist(DuPont, 1986; see Table 10.2). There are four questions to be answered:1. Diagnosis. Is there a current diagnosis that warrants the prolonged use ofa prescription medicine? The benzodiazepines are serious medicines that shouldonly be used for serious illnesses.2. Medical and nonmedical substance use. Is the benzodiazepine dose thepatient is taking reasonable? Is the clinical response to the benzodiazepinefavorable? Is there any use of nonmedical drugs, such as cocaine or marijuana? Isthere any excessive use of alcohol (e.g., a total of more than four drinks a week,or more than two drinks a day)? Are other medicines being used that candepress CNS functioning?3. Toxic behavior. Is the patient free of evidence of slurred speech, staggering,accidents, memory loss, or other mental deficits or evidence of sedation?4. Family monitor. Does the family confirm that there is a good clinicalresponse and no adverse reactions to the patient’s use of a benzodiazepine?Because people who abuse drugs deny drug-caused problems and often lie toTABLE 10.2 Benzodiazepine Checklist for Long-Term Use1. Diagnosis. Is there a current diagnosis that warrants the prolonged use of aprescription medicine?2. Medical and nonmedical substance use. Is the dose of the benzodiazepine the patient istaking reasonable? Is the clinical response to the benzodiazepine favorable? Is thereany use of nonmedical drugs, such as cocaine or marijuana? Is there any excessive useof alcohol (e.g., a total of more than four drinks a week, or more than two drinks aday)? Are there other medicines being used that can depress the functioning of theCNS?3. Toxic behavior. Is the patient free of evidence of slurred speech, staggering, accidents,memory loss, or other mental deficits or evidence of sedation?4. Family monitor. Does the family confirm that there is a good clinical response and noadverse reactions to the patient’s use of a benzodiazepine?Standard for continued benzodiazepine use: a “yes” to all four questions.

234 III. SUBSTANCES OF ABUSEtheir doctors, and because many family members are concerned about longtermbenzodiazepine use, we generally ask that a family member come to theoffice at least once with the patient who is taking a benzodiazepine for a prolongedperiod. This gives us an opportunity to confirm with the family member,while the patient is present, that benzodiazepine use produces a therapeuticbenefit without problems. If there is a problem of toxic behavior or abuse ofother drugs, we are more likely to identify it when we speak with the patient’sfamily members; if not, we have an opportunity to educate and reassure boththe patient and family members when they are seen together.Most patients without a history of addiction produce four “yes” answers tothese four questions. Even a single “no” answer deserves careful review and maysignal the desirability of discontinuation of the benzodiazepine. After completionof the Benzodiazepine Checklist, if there is clear evidence that long-termbenzodiazepine use is producing significant benefits and no problems, and if thepatient wants to continue using the benzodiazepine (which is, in our experience,a common set of circumstances for chronically anxious patients), then wehave no hesitancy in continuing to prescribe a benzodiazepine, even for thepatient’s lifetime.On the other hand, many anxious patients, even when they have goodresponses without problems, want to stop using benzodiazepines. Other patientsdo not want to stop using a benzodiazepine, but they do show signs of poor clinicalresponse or trouble with the use of a benzodiazepine. In either case, discontinuationis in order, and it is an achievable goal.Some critics of benzodiazepines, including Stefan Borg and Curtis Carlsonof St. Goran’s Hospital in Stockholm, Sweden (Allgulander, Borg, & Vikander,1984), have expressed concerns about the possibility that benzodiazepine usemay lead to alcohol problems in patients without a prior history of alcoholabuse, especially in women. The simple advice to a long-term medical user of abenzodiazepine is not to use alcohol, or to use alcohol only occasionally andnever more than one or two drinks in 24 hours. Most anxious patients who donot have a prior history of addiction either do not use alcohol at all or use itonly in small amounts. The Benzodiazepine Checklist helps the physician, thepatient, and the patient’s family identify any problems (including alcoholabuse) at early stages, thus facilitating constructive interventions.LONG-TERM DOSE AND ABUSEOne clinical observation helps the physician identify people who have addictionproblems among anxious benzodiazepine users. Most anxious medical usersof benzodiazepines have used these medicines at low and stable doses over time,often for many years, with good clinical responses. Dose is a critical and distin-

10. Sedatives/Hypnotics and Benzodiazepines 235guishing variable in long-term benzodiazepine use. People who are addicted toalcohol and other drugs commonly abuse benzodiazepines in high and unstabledoses; anxious patients who are not addicted do not. People with active addiction(e.g., who currently use illegal drugs and/or abuse alcohol) seldom report agood clinical response to low and stable doses of benzodiazepines.We use a simple assessment of dose level: If the patient’s typical benzodiazepinedose level is stable at or below one-half the ordinary clinical maximumdose of the prescribed benzodiazepine as recommended in the Physicians’Desk Reference (PDR; Medical Economics Data Production, 2003) or in thepackage insert approved by the FDA for the prescribed benzodiazepine, we callthis the “green light” benzodiazepine dose zone. Thus, patients whose dailybenzodiazepine dose is stable at or less than 2 mg of alprazolam, 20 mg of diazepam,5 mg of lorazepam, 4 mg of clonazepam, or 60 mg of oxazepam are in therelatively safe or green-light zone.The “red light,” or danger, zone is above the FDA-approved maximumdaily dose (e.g., above 4 mg of alprazolam or 40 mg of diazepam). Except in thetreatment of panic, when doses up to two or three times the FDA maximum forchronic anxiety are occasionally needed, it is unusual to see an anxious nonalcohol-or non-drug-abusing patient taking benzodiazepine doses that are thishigh. Most panic disorder patients, after a few months of treatment, are able todo well (with good panic suppression) in the green light zone, without the physicianor the patient making any effort to limit or restrict the benzodiazepinedose level. If vigilance and control are required by the physician to limit thebenzodiazepine dose to levels below the maximum recommended doses, this is apoor prognostic sign and a signal that addiction to alcohol and other drugs maybe a confounding comorbid disorder.One common clinical challenge is to see a patient, a family member, orsometimes a physician or therapist who is concerned about “tolerance” and“addiction,” because the patient feels compelled to raise the dose of the benzodiazepineover time. In our experience, such worries among patients who lack apersonal history of addiction to alcohol or other nonmedical drugs are usuallythe result of underdosing with the benzodiazepine rather than evidence ofaddiction. Although some patients with such a presentation are more comfortabletaking no medicine at all, most need education about the proper dose ofthe benzodiazepine. Once the benzodiazepine dose is raised to an ordinary therapeuticlevel (e.g., well within the green light zone), patients usually feel muchbetter in terms of their symptoms of an anxiety disorder and have no inner pressureto raise the benzodiazepine dose further.Within the addicted population, several patterns of benzodiazepine abusehave been identified. The most common pattern is the use of a benzodiazepineto reduce the adverse effects of the abuse of other, more preferred drugs. Typicalis the suppression of a hangover and other withdrawal phenomena from alcoholuse with a benzodiazepine. Patients waking up in the morning after an alcoholic

236 III. SUBSTANCES OF ABUSEbinge may take 10–40 mg or more of diazepam, for example, “just to face theday.”Other common nonmedical patterns are to use benzodiazepines (oftenalprazolam or lorazepam) concomitantly with stimulants (often cocaine ormethamphetamine) to reduce the unpleasant experiences of the stimulant use,and/or to use benzodiazepines (often triazolam [Halcion]) to treat the insomniathat accompanies stimulant abuse.Benzodiazepines are occasionally used as primary drugs of abuse, in whichcase they are typically taken orally at high doses. Addicted patients report usingdoses of 20–100 mg or more of diazepam, or the equivalent doses of otherbenzodiazepines, for example, at one time. Such high-dose oral use is oftenrepeated several times a day for long periods or on binges. Although, in ourexperience, such primary benzodiazepine abuse without simultaneous use ofother drugs is unusual, it does occur.Daily use of benzodiazepines, even when there is no dose escalation and noabuse of alcohol or other nonmedical drugs has led to controversy. Clinicalexperience has shown that even over long periods of daily use, benzodiazepinestypically do not lose their efficacy and do not produce significant problems formost patients. An example of this experience was a study of 170 adult patientstreated for a variety of sleep disorders continuously with a benzodiazepine for 6months or longer over a 12-year period. The study found sustained efficacy,with low risk of dose escalation, adverse effects, or abuse (Schenck &Mahowald, 1996).Discontinuation of Benzodiazepine UseDiscontinuation of sedatives and hypnotics, including the benzodiazepines, canbe divided into three categories: (1) long-term low-dose benzodiazepine use, (2)high-dose benzodiazepine abuse and multiple drug abuse, and (3) high-doseabuse of nonbenzodiazepine sedatives and hypnotics (especially intermediateactingbarbiturates). The first group of patients can usually be discontinued onan outpatient basis. Some of the second and even the third group can be treatedas outpatients, but most will require inpatient care. Inpatient discontinuationtoday with managed care is generally reserved for patients who fail at outpatientdiscontinuation and for those who demonstrate acutely life-threatening lossof control over their drug use. The pharmacological management of inpatientbenzodiazepine withdrawal from nontherapeutically high doses of thesemedicines is covered in standard texts dealing with inpatient detoxification(Wesson et al., 2003).With respect to withdrawal from benzodiazepines in the context of addictiontreatment, the most common problem that addiction treatment professionalsexperience is that some of their patients who take benzodiazepines also sufferfrom underlying anxiety disorders and panic attacks. When these patients

10. Sedatives/Hypnotics and Benzodiazepines 237stop taking a benzodiazepine, they experience a short-term rebound increase inthese distressing symptoms. These rebound symptoms, including panic attacks,are difficult for the patients and their physicians to separate from withdrawalsymptoms, because they are similar and the time course is also similar, withboth types of symptoms occurring at low benzodiazepine doses and peaking duringthe first or second drug-free week.There is evidence that most patients who take benzodiazepines at prescribeddose levels can discontinue using them with quite moderate symptoms ifthe dose reduction is gradual (Busto, Simpkins, & Sellers, 1983; Rickels,Schweizer, Csanalosi, Case, & Chung, 1988). One study found that about halfof long-term benzodiazepine users could stop with no withdrawal symptoms(Tyrer, Rutherford, & Huggett, 1981). However, some patients who stopbenzodiazepine use, especially after use for many years, do have either prolongedor severe withdrawal symptoms (Noyes, Garvey, Cook, & Perry, 1988).About one in three medical patients with long-term use of a benzodiazepinehave clinically significant withdrawal symptoms, even after gradual tapering,and about one in eight patients stopping a benzodiazepine will have prolongedand/or severe symptoms (DuPont, 1988). In any case, discontinuation symptoms(except for abrupt cessation, which can produce seizures and is not indicated)from benzodiazepines are “distressing but not dangerous” (DuPont et al.,1992; Sellers et al., 1993).There are a number of useful publications on the diagnosis and treatmentof chronic anxiety (Davidson, 2003; DuPont, Spencer, & DuPont, 2004; Ross,1994; Spencer, DuPont, & DuPont, 2004). The benzodiazepines can be used totreat either acute or chronic anxiety, as well as the panic attacks that are commonlyassociated with anxiety disorders. The benzodiazepines can be usedeither as needed or every day, and they can be used either alone or with othermedicines, most often with antidepressants (Davidson, 1997).Although all of the benzodiazepines are now off patent, there has been arecent interest in the development of new delivery mechanisms for the twomost widely used benzodiazepines (Stahl, 2003). Alprazolam is now available inan extended release formulation, Xanax XR. It has the advantage of sloweronset of action, which reduces initial sedation in the hour or two after administration.Slower onset of action also lowers the abuse potential of Xanax XR,since it is the rapid onset of action that triggers the brain reward that addictsseek. This new formulation of alprazolam permits once-a-day, or at most twicea-day,dosing and reduces the risk of “clock watching,” which may be seen withfrequent dosing throughout the day. This new formulation of alprazolam may bea significant improvement over the three to four times a day dosing required forthe immediate release alprazolam.Clonazepam has been reformulated for sublingual administration for easyadministration without swallowing a pill. This new product is called KlonopinWafers. In the new formulations of these two benzodiazepines, the manufactur-

238 III. SUBSTANCES OF ABUSEers have moved in opposite directions to maximize two different therapeuticeffects. Xanax XR has a slower onset and longer duration of action to smooththe brain level of alprazolam for 24-hour-a-day effectiveness. Sublingual clonazepamhas been reformulated to overcome the problems some patients haveswallowing pills.Newer Sedative and Hypnotic AgentsIn recent years, a variety of alternatives to the benzodiazepines have becomeavailable to treat both anxiety and insomnia. Buspirone (Buspar) has beenshown to reduce anxiety in generalized anxiety disorders, but it does not suppresspanic attacks, and is not used as a primary treatment of obsessive–compulsive disorder. Buspirone is not abused by alcoholics and drug addicts,and it does not produce withdrawal symptoms on abrupt discontinuation. Likethe antidepressants, buspirone requires several weeks of daily dosing to produceantianxiety effects, which are less dramatic from patients’ point of view thanare the effects produced by the benzodiazepines (Sussman & Stein, 2002).The antidepressants as a class have been shown to possess antipanic andantianxiety effects opening a new range of uses for these medicines in the treatmentof anxiety disorders. The selective serotonin reuptake inhibitors (SSRIs)have emerged as the first-line treatment for many anxiety disorders (Davidson,2003; DuPont, 1997; Jefferson, 1997). Although the earlier antianxiety andanti-insomnia medicines focused exclusively on the benzodiazepine receptors inthe GABA system, the recognition of the importance of serotonin andnorepinephrine neurotransmitters in the management of anxiety and insomnia,and the success of buspirone, have stimulated a search for a new generation ofantianxiety medicines that are not controlled substances (e.g., they are notabused by alcoholics and drug addicts). Recognition of the withdrawal symptomsassociated with abrupt discontinuation of some antidepressants (especiallythose with shorter half-lives and more anticholinergic properties) have shownthat withdrawal is not limited to controlled stubstances (DuPont, 1997).Two nonbenzodiazepine hypnotic agents have been introduced. Zolpidem(Ambien) and Zaleplon (Sonata) are rapid-onset, short duration of action medicinesthat act on the benzodiazepine receptors of the GABA system. Theyhave been shown to reduce insomnia. They have largely replaced the benzodiazepinesas hypnotic medicines, although they lack the anxiolytic, anticonvulsant,and muscle-relaxant properties of the benzodiazepines (Scharf,Mayleben, Kaffeman, Krall, & Ochs, 1991). Zolpidem and zaleplon are reinforcingto alcoholics and drug addicts, underscoring the fact that the abusepotential of both drugs appears to be similar to that of benzodiazepines. Bothmedicines impair memory and performance of complex tasks in ways that aresimilar to the acute effects of benzodiazepines. They do not affect stage 4 sleep,as do the benzodiazepines.

10. Sedatives/Hypnotics and Benzodiazepines 239Both zaleplon and zolpidem are effective in relieving sleep-onset insomnia,and both have been approved by the FDA for use up to 7–10 days at a time.Both medicines clinically appear to have sustained hypnotic activity over longerperiods of time. Zolpidem has a half-life of about 2 hours, which is consistentwith therapeutic activity over a typical 8 hours of sleep. Zaleplon has a 1-hour half-life that offers the possibility of dosing in the middle of the night forbroken sleep. For this reason zaleplon is approved for use both at bedtime andin midsleep periods of insomnia.In recent years, the antiepilepsy medicines, including valproate (Depakote)and gabapentin (Neurontin), have been used as augmenting agents in thetreatment of anxiety (Lydiard, 2002).REFERENCESAllgulander, C., Borg, S., & Vikander, B. (1984). A 4–6 year follow-up of 50 patientswith primary dependence on sedative and hypnotic drugs. Am J Psychiatry, 141,1580–1582.American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders(4th text rev. ed.). Washington, DC: Author.Baldessarini, R. J. (2001). Depression and anxiety disorders. In J. G. Hardman & L. E.Limbird, (Eds.), Goodman and Gilman’s, the pharmacological basis of therapeutics(10th ed., pp. 447–483). New York: McGraw-Hill.Burt, D. R., & Kamatchi, G. L. (1991). GABA receptor subtypes: From pharmacologyto molecular biology. FASEB, 5, 2916–2923.Busto, U., Simpkins, J., & Sellers, E. M. (1983). Objective determination of benzodiazepineuse and abuse in alcoholics. Br J Addict, 48, 429–435.Charney, D. S., Minic, S. J., & Harris, R. A. (2001). Hypnotics and sedatives. In J. G.Hardman & L. E. Limbird, (Eds.), Goodman and Gilman’s, the pharmacological basisof therapeutics (10th ed., pp. 399–427). New York: McGraw-Hill.Chouninard, G., Lefko-Singh, K., & Teboul, E. (1999). Metabolism of anxiolytics andhypnotics: Benzodiazepines, buspirone, zopliclone, and zolpidem. Cell Mol Neurobiol,19, 533–552.Ciraulo, D. A., Sarid-Segal, O., Knapp, C., Ciraulo, A. M., Greenblatt, D. J., & Shader,R. I. (1996). Liability to alprazolam abuse in daughters of alcoholics. Am J Psychiatry,153, 956–958.Davidson, J. (2003). The anxiety book. New York: Penguin/Putnam.Davidson, J. R. T. (1997). Use of benzodiazepines in panic disorder. J Clin Psychiatry,58(Suppl. 2), 26–31.DuPont, R. L. (1984). Getting tough on gateway drugs: A guide for the family. Washington,DC: American Psychiatric Press.DuPont, R. L. (1986). Benzodiazepines: The social issues. Rockville, MD: Institute forBehavior and Health.DuPont, R. L. (Ed.). (1988). Abuse of benzodiazepines: The problems and the solutions.Am J Drug Alcohol Abuse, 14(Suppl 1), 1–69.

240 III. SUBSTANCES OF ABUSEDuPont, R. L. (1995). Anxiety and addiction: A clinical perspective on comorbidity.Bull Menninger Clin, 59(Suppl A), A53–A72.DuPont, R. L. (1997). The pharmacology and drug interactions of the newer antidepressants.Essential Psychopharmacology, 2, 7–31.DuPont, R. L. (1998). Addiction: A new paradigm. Bull Menninger Clin, 62, 231–242.DuPont, R. L. (2000). The selfish brain: Learning from addiction (rev. ed.). Center City,MN: Hazelden.DuPont, R. L., DuPont, C. M., & Rice, D. P. (2002). Economic costs of anxiety disorders.In D. J. Stein & E. Hollander (Eds.), Textbook of anxiety disorders (pp. 365–374). Washington, DC: American Psychiatric PressDuPont R. L., & Gold, M. S. (1995). Withdrawal and reward: implications for detoxificationand relapse prevention. Psychiatr Ann, 25, 663–668.DuPont, R. L., Spencer, E. D., & DuPont, C. M. (2004). The anxiety cure: An eight stepprogram for getting well (rev. ed.). New York: Wiley.DuPont, R. L., Swinson, R. P., Ballenger, J. C., Burrows, G. D., Noyes, R., Rubin, R. T.,Rifkin, A., & Pecknold, J. C. (1992). Discontinuation effects of alprazolam afterlong-term treatment of panic-related disorders. J Clin Psychopharmacol, 12, 352–354.Golombok, S., Moodley, P., & Lader, M. (1988). Cognitive impairment in long-termbenzodiazepine users. Psychol Med, 18, 365–374.Griffiths, R. R., & Sannerud, C. A. (1987). Abuse of and dependence on benzodiazepinesand other anxiolytic/sedative drugs. In H. Meltzer, B. S. Bunney, & J. T.Coyle (Eds.), Psychopharmacology: The third generation of progress (pp. 1535–1541).New York: Raven Press.Griffiths, R. R., & Weerts, E. M. (1994). Benzodiazepine self-administration in humansand laboratory animals: Implications for problems of long-term use and abuse. Psychopharmacology,134, 1–37.Handelsman, L. (2002). Anxiety in the context of substance abuse. In D. J. Stein & E.Hollander (Eds.), Textbook of anxiety disorders (pp. 441–448). Washington, DC:American Psychiatric Press.Hemmelgarn, B., Suissa, S., Huang, A., Boivin, J.-F., & Pinard, G. (1997). Benzodiazepineuse and the risk of motor vehicle crash in the elderly. JAMA, 278, 27–31.Jefferson, J. W. (1997). Antidepressants in panic disorder. J Clin Psychiatry, 58(Suppl 2),20–25.Juergens, S. M., & Cowley, D.S. (2003). The pharmacology of benzodiazepines andother sedative–hypnotics. In A. W. Graham, T. K. Schultz, M. F. Mayo Smith, &R. K. Ries (Eds.), Principles of addiction medicine (3rd ed., pp. 119–139). ChevyChase, MD: American Society of Addiction Medicine.Kessler, R. C., McGonagle, K. A., Zhao, S., Nelson, C. B., Hughes, M., Eshleman, S., etal. (1994). Lifetime and 12-month prevalence of DSM-III-R psychiatric disordersin the United States: Results from the National Comorbidity Survey. Arch GenPsychiatry, 51, 8–19.Lydiard, R. B. (2002). Pharmacotherapy for panic disorder. In D. J. Stein & E. Hollander(Eds.), Textbook of anxiety disorders (pp. 257–273). Washington, DC: AmericanPsychiatric Press.MacDonald, D. I., DuPont, R. L., & Ferguson, J. L. (2003). The role of the medicalreview officer. In A. W. Graham, T. K. Schultz, M. F. Mayo Smith, & R. K. Ries

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242 III. SUBSTANCES OF ABUSEville, MD: Substance Abuse and Mental Health Services Administration, Office ofApplied Studies.Wang, P. S., Bohn, R. L., Glynn, R. J., Mogun, H., & Avom, J. (2001). Hazardousbenzodiazepine regimes in the elderly: Effects of half-life, dosage, and duration onrisk of hip fracture. Am J Psychiatry, 158, 892–898.Wesson, D. R., Smith, D. E., & Ling, W. (2003). Pharmacologic interventions forbenzodiazepine and other sedative–hypnotic addiction. In A. W. Graham, T. K.Schultz, M. F. Mayo Smith, & R. K. Ries (Eds.), Principles of addiction medicine (3rded., pp. 721–735). Chevy Chase, MD: American Society of Addiction Medicine.World Health Organization. (1988). The use of essential drugs: Third report of the WorldHealth Organization expert committee (WHO Technical Report Series No. 770).Geneva: Author.

PART IVSPECIAL POPULATIONS

CHAPTER 11Polysubstance Use, Abuse,and DependenceRICHARD N. ROSENTHALPETROS LEVOUNISDEFINING MULTIPLE SUBSTANCE USEDiagnostic ApproachesChanges in Diagnostic Criteria from DSM-III to DSM-IV-TR“Polysubstance dependence” originated in the DSM nomenclature only in1987, with the introduction of the third revised edition of the Diagnostic Manualof Mental Disorders (DSM-III-R; American Psychiatric Association, 1987).Prior to this, in DSM-III (American Psychiatric Association, 1980, p. 179),there was the diagnostic category of “mixed substance abuse,” in which criteriafor diagnosing substance abuse were met, but either the substances could not beidentified or the abuse involved “so many substances that the clinician prefers”to treat them as a combination rather than define a specific disorder for eachsubstance” (italics added). In addition, in DSM-III, there was an attempt to createclinically meaningful diagnostic categories with respect to dependence onmultiple substances, hence the diagnoses “dependence on a combination ofopioid and other non-alcoholic substances,” an early nod to the high prevalenceof use of multiple substances among heroin users, and “dependence on acombination of substances, excluding opioids and alcohol.” In parallel with theDSM-III diagnosis for multiple substance abuse, each of these multiple dependencecriteria was made only if the substances could not be identified, or thedependence involved so many substances that the clinician preferred to treatthem as a combination rather than define a specific disorder for each substance.245

246 IV. SPECIAL POPULATIONSThis concept is what underlies the typical, non-DSM use of the term “polysubstancedependence.” In DSM-III-R, the concept of polysubstance dependencewas formally introduced: The imprecise DSM-III concept of “so many” substanceswas dropped in favor of a threshold number of substances, and clinician“preference” was eliminated as an option to making such diagnoses. DSM-III-Rpolysubstance dependence stipulates that the person meets criteria due torepeated use of at least three categories of substances as a group over 6 months,excluding caffeine and nicotine, but does not fulfill dependence criteria for anyspecific substance (American Psychiatric Association, 1987, p. 185).In DSM-IV, the concept of polysubstance dependence is more specific(American Psychiatric Association, 1994). However, the DSM-IV versionsallow for two different ways to interpret the diagnosis. The first diagnostic conceptof polysubstance dependence in DSM-IV is: at least 3 groups of substancesrepeatedly used by the patient during 12 months that, as a group, meet criteriafor dependence, but in which there is no specific drug that independently qualifiesfor substance dependence. As in all recent versions of the DSM, any substancefor which the patient satisfies criteria for dependence should be giventhat diagnosis independently of other substances used. A second, more exclusiveDSM-IV concept of polysubstance dependence is: three or more classes ofdrugs used by the patient without dependence on any one drug, but the sum ofthe criteria met for all drugs used is three or more. The definition of “polysubstancedependence” has been clarified somewhat in DSM-IV-TR (AmericanPsychiatric Association, 2000). However, there are still two interpretationspossible with the DSM-IV-TR related to polysubstance dependence. Oneschema focuses on episodes of indiscriminate use of a variety of substances thateach meet one criterion, but when added together meet three or more dependencecriteria; the other is that full dependence criteria are only met when thedrug classes used are grouped together as a whole (First & Pincus, 2002). Thatstated, as defined by DSM-IV, polysubstance dependence is a relatively rare disorder,and the formal diagnosis is used infrequently by clinicians and researchers(Schuckit et al., 2001).Clinicians and researchers use the term “polysubstance dependence” morefrequently as shorthand for patients for whom the DSM-IV criteria would suggestthat the patient fulfills independent dependence criteria for several differentsubstances. Conway, Kane, Ball, Poling, and Rounsaville (2003) call thisconstruct “polysubstance involvement.” According to DSM-IV (American PsychiatricAssociation, 1994, 2000), a patient should have a diagnosis of substancedependence for each substance for which the person meets criteria.Because there is room for misinterpretation between the formal DSM-IV conceptof polysubstance dependence and the more frequently used broad conceptof use of multiple substances that is also described as “polysubstance dependence,”in this chapter we use the convention “multiple substance use disorders”(SUDs) to denote the latter, broad concept, reserving the former for cases inwhich a formal DSM-based diagnosis has been made. “Multiple SUD” here

11. Polysubstance Use, Abuse, and Dependence 247denotes that the identified subject or sample has two or more formal SUD diagnoses,at least meeting criteria for substance abuse, or meets it by reasonableproxy, such as seeking treatment. “Multiple substance dependence” means thatthe identified subject or sample meets formal or reasonable proxy criteria fortwo or more substance dependence disorders.“Polysubstance Abuse”Although there was a diagnostic category of “mixed substance abuse” in DSM-III (American Psychiatric Association, 1980, p. 179), there is no diagnosisof polysubstance abuse in DSM-IV-TR (American Psychiatric Association,2000). There may not be many people who abuse multiple substances over timewith clinically significant impact, for whom no one substance is sufficient tomake formal abuse criteria. This is because one needs only to satisfy one of thefour DSM-IV criteria to pass the threshold for a substance abuse diagnosisrelated to that particular substance. However, it is conceivable that one couldmeet a criterion for substance abuse based on use of multiple substances, but noton one in particular. For example, a person could have two arrests for drivingunder the influence, one for alcohol and the other for cannabis, in the sameyear.Descriptive ApproachesPolydrug Use or Polysubstance UseMost broadly, the literature frequently describes “polydrug use” or “polysubstanceuse.” This nondiagnostic designation generally describes the use ofmultiple substances rather than framing the use and its effects in clinical terms,which is the intent of diagnosis. As such, polydrug use describes, at minimum,the use of multiple substances, whether licit or illicit. In the treatment researchliterature, “polydrug use” is often used to describe the lifetime number of drugsregularly used to a threshold SUD, in addition to the index substance (Ball,Carroll, Babor, & Rounsaville, 1995; Feingold, Ball, Kranzler, & Rounsaville,1996). However, in other than addiction or mental health treatment settings,the expressions “polysubstance use” or “polysubstance abuse” are frequentlymeant to describe the use by subjects of as few as two substances, such ascocaine and alcohol, alcohol and cannabis, or opiates and cocaine (Ross,Kohler, Grimley, & Bellis, 2003). In a more differentiated conceptualization,the use of multiple substances that cause impairment is frequently described as“polydrug abuse.”In an effort to further distinguish patterns of use, Grant and Hartford(1990) framed “polydrug use” either as simultaneous, which is the use of multipledrugs at the same occasion, or concurrent, which is the use of differentsubstances on different occasions. Use of different substances is common

248 IV. SPECIAL POPULATIONSin patients with alcohol dependence or substance dependence (Caetano &Weisner, 1995), the majority of whom use substances simultaneously (Staines,Magura, Foote, Deluca, & Kosanke, 2001). Longitudinal studies in communitysamples are able to discriminate between simultaneous and concurrent polydruguse, but a differential impact upon subsequent health outcomes including psychologicaldistress, physical symptoms, and services utilization has not beenidentified (Earleywine & Newcomb, 1997).EPIDEMIOLOGYReaders of the research and clinical addiction literature face a problem in understandingwhat is meant by terms used to describe multiple SUDs in a specificsample population. These terms are variously given as “polysubstance abuse,”“polydrug abuse,” “polyaddiction,” and “multiple-drug dependence.” As statedearlier, “polysubstance abuse” in a narrow DSMs-IV sense, is relatively unlikely tooccur, especially in clinical settings, where patients are likely to meet criteria forseveral SUD diagnoses. On the other hand, the terms “polysubstance abuse” and“polydrug abuse” are frequently used by clinicians and researchers as descriptors ofmultiple drug use in populations of patients who have an index diagnosis of substancedependence, such as opioid dependence, and who meet at least DSM substanceabuse criteria for the other substances.The use of differing phraseology to describe use of multiple drugs is notlimited to the domain of mental health, and addiction clinicians and researchers.Cause of death statements from medical examiners and coroners often useterms such as “polydrug toxicity,” “polypharmacy,” “multiple drug poisoning,”and “polypharmaceutical overdose” to describe multiple-drug-induced deaths(Cone et al., 2003).Population-Based StudiesWhen considered in community samples, the presence of an SUD diagnosis elevateslifetime risks of additional SUD diagnoses (Regier et al., 1990). This istrue with most classes of abused drugs. For example, the risk for a nonalcoholSUD is elevated among both males and females with alcohol dependence. Inthe National Comorbidity Survey (NCS), more than 40% of individuals witha DSM-III-R alcohol dependence had, excluding nicotine dependence, cooccurringdrug abuse or dependence (Kessler et al., 1997). Between 13 and 18%of those with alcohol abuse will also have a co-occurring lifetime drug use disorder(NCS; Kessler et al., 1997). Lifetime drug use disorder was also present in21.5% of subjects (odds ratio [OR] = 7.1) with an alcohol use disorder identifiedin the Epidemiologic Catchment Area survey (ECA; Regier et al., 1990).In addition, among individuals with a nonalcohol substance use disorder in theECA study, 47.3% also had a lifetime alcohol use disorder. Excluding nicotine

11. Polysubstance Use, Abuse, and Dependence 249dependence, which was not surveyed in the ECA, individuals with cocaineabuse/dependence have the strongest risk (84.8%; OR = 36.3) of any groupwith an SUD for an additional alcohol use disorder (Regier et al., 1990). In theECA, the associated use disorder for barbiturates, opiates, amphetamines, andhallucinogens demonstrates an OR for an additional lifetime alcohol use disorderof 10.0 or more (Regier et al., 1990).However, if one tries to understand the temporal relationship betweenclasses of substances used, lifetime diagnoses do not easily allow for the attributionthat the use of multiple substances was temporally coemergent. Therefore,using this threshold to determine multiple-substance abuse may lower its specificity,thus overestimating its prevalence. Past-year prevalence rates are morelikely than lifetime rates to provide higher specificity for identifying personswith concurrent multiple-substance use in a subpopulation identified as havingtwo or more SUDs. Unfortunately, few national surveys have presented pastyeardata on substance use comorbidity. However, data from the 11th, 12th,and 13th National Household Surveys on Drug Abuse (NHSDA; n = 87,915)offer an important source of epidemiological data on drug-related symptoms ofdependence, using criteria that can be used to approximate DSM-IV currentSUDs (Kandel, Chen, Warner, Kessler, & Grant, 1997).AdolescentsAdolescent substance users are a subgroup who have been identified as high riskfor concurrent polysubstance use, and with that, progression to hazardous use,abuse, or dependence (Brook, Brook, Zhang, Cohen, & Whiteman, 2002).Compared with older age groups, younger users in treatment settings are morelikely to report polydrug use (Substance Abuse and Mental Health ServicesAdministration [SAMHSA], 2003b). The NHSDA oversamples subjects whoare from 12 to 34 years old, offering community substance use data on adolescentswho are not typically covered in other national surveys (Kandel et al.,1997). Although males overall are more likely than females to use or be dependentupon alcohol, cannabis, or cocaine, Kandel and colleagues (1997), usingNHSDA data to determine abuse and dependence by proxy, demonstrated thatthese gender differences for rates of use and of dependence rates among usersare largely attenuated among adolescents. Adolescent girls who use alcohol orillicit drugs are at higher risk for dependence than adolescent boys, and amongfemale users of alcohol, cannabis, or cocaine, the rates of dependence are thehighest in adolescents compared with older age groups (Kandel et al., 1997).Clinical SamplesIn treatment samples, multiple SUDs are common but typically underdiagnosed(Ananth, Vandeater, Kamal, & Brodsky, 1989; Rosenthal, Hellerstein, &Miner, 1992). In general, the risk for comorbid substance use and other mental

250 IV. SPECIAL POPULATIONSdisorder diagnoses is increased when comparing clinical to community samples,and the highest rates of comorbid mental disorders–SUDs are typically found ininstitutional populations, including psychiatric units, substance abuse programs,and jails and prisons (Hien, Zimberg, Weisman, First, & Ackerman,1997; Jordan, Schlenger, Fairbank, & Caddell, 1996; Kokkevi & Stefanis, 1995;Regier et al., 1990). This is due in part to the selection bias that those mostlikely admitted to treatment programs are people with impairment due to theirdrug use. Because of higher severity, they are at higher risk for an additionalsubstance use diagnosis than other drug users.Comorbidity of various substance use and other mental disorders tends tocluster among certain subsets of the general population, such that more thanhalf of the lifetime alcohol, drug, and mental disorders diagnoses can be foundamong about 14% of the population (Kessler et al., 1994). In any year, almost59% of the community sample with an alcohol, drug, or other mental (ADM)disorder meet criteria for three or more lifetime ADM disorders (Kessler et al.,1994). Therefore, compared to the community, treatment settings that aggregatethose with SUDs are also most likely to cohort people at the highest riskfor multiple SUDs. This is borne out in large-scale family genetics studies. Forexample, in the Collaborative Study on the Genetics of Alcoholism (COGA),among 1,212 subjects with definite alcohol dependence, recruited from addictiontreatment centers, 62% had an additional diagnosis of cannabis and/orcocaine dependence (Bierut et al., 1998).Treatment Episode Data Set (TEDS) data over the period 1992–2001 consistentlyrevealed that about half of treatment admissions have reported multipleSUDs (SAMHSA, 2003b). This means that in addition to the index substancefor which the patient was admitted to treatment, a substantial portion ofpatients are also abusing other substances. The SAMHSA-sponsored NationalSurvey of Substance Abuse Treatment Services (NSSATS) demonstrated thatof the 1,123,239 people receiving treatment in 13,720 responding facilities in2002, 48% were being treated for abuse or dependence on both alcohol and atleast one other substance (SAMHSA, 2003a). Thirty-one percent were intreatment for drug use disorders only, while the remaining 21% were in treatmentfor alcohol use disorders only. Similarly, data from the 2001 TEDSrevealed that 54% of all persons admitted to substance abuse treatmentreported multiple substance use, and approximately 42% of all admissionsreported problems with both alcohol and drugs (SAMHSA, 2003b). Alcoholand opiates were reported more often as primary substances than as secondarysubstances (TEDS; SAMHSA, 2003b). The most commonly reported secondarysubstances were alcohol, marijuana/hashish, and cocaine.Multiple Substance Use DisordersThe increased risk of comorbidity among treatment-seeking populations overthat of the general population has clinical implications for the outcome of treat-

11. Polysubstance Use, Abuse, and Dependence 251ment (Rosenthal & Westreich, 1999). Patients with multiple SUDs have greaterdifficulty achieving remission in intensive addiction treatment (Ritsher, Moos,& Finney, 2002). In addition, a history of multiple substance use predicts relapseto drugs in addiction treatment follow-up studies (Walton, Blow, & Booth,2000). Among patients in treatment for SUDs in a 2-year follow-up study byWalton and colleagues (2000), subjects (n = 241) self-reported their current primarysubstances of choice. Forty-one percent indicated alcohol as the sole drug ofabuse. Among the 59.1% who were polysubstance users, the drugs of choice werealcohol, 79.1%; cocaine, 72.7%; marijuana, 48.2%; opiates, 16.5%; sedatives,13.7%; stimulants, 8.6%; heroin, 9.4%; and hallucinogens, 5.0%.Nicotine and Multiple Substance Use DisordersNicotine dependence has not been traditionally thought of in the context oftreating drug abuse problems, even among clinicians trained in addiction treatment.Consequently, when multiple SUDs are discussed, they usually do notinclude whether the person referred to is a habitual smoker. Nonetheless, over90% of patients in methadone maintenance treatment are current tobaccosmokers, a reasonable proxy for nicotine dependence (Clemmey, Brooner,Chutuape, Kidorf, & Stitzer, 1997). Similarly, 90% of patients in alcoholisminpatient treatment are current smokers (Beatty, Blanco, Hames, & Nixon,1997). Thus, even among patients identified as having only one current SUD,these individuals are, in fact, multiply drug dependent.Multiple Substance Use among AlcoholicsThe concurrent abuse of alcohol and drugs is a significant problem. Alcoholand drug use disorders frequently overlap, and there are high rates of nonalcoholSUDs among patients in treatment for alcohol use disorders (Beatty etal., 1997). In the 2001 TEDS sample, 72% of all persons admitted to treatmentreported alcohol as a primary or secondary substance; 22% of addiction treatmentadmissions reported primary drug abuse with secondary alcohol abuse, and20% reported primary alcohol abuse with secondary drug abuse (SAMHSA,2003b).Multiple Substance Use among Injecting Heroin UsersInjection drug use is highly correlated with use of multiple substances. Injectingheroin users frequently use multiple drugs in addition to nicotine, such as alcohol,benzodiazepines, cannabis, and amphetamines, and there do not appear tobe differences between treatment and nontreatment samples with regard to thenumber of either lifetime or current dependence diagnoses (Darke & Ross,1997; Dinwiddie, Cottler, Compton, & Abdallah, 1996; Kidorf, Brooner, King,Chutuape, & Stitzer, 1996). Darke and Ross (1997) recruited a nonrandom

252 IV. SPECIAL POPULATIONSsample of 222 Australian heroin injectors, half of whom were in methadonetreatment, and found that they had used a mean of 5.3 different classes of substancesin the prior 6 months, and 40% had three or more current DSM-III-Rdependence diagnoses. Injecting drugs increases the risk for comorbid substancedependence. Dinwiddie and colleagues (1996) found elevated lifetime rates ofalcohol, amphetamine, sedative/hypnotic opiate and hallucinogen dependenceamong injecting drug users (IDUs) compared to non-IDUs with a substantialdrug use history.Severity of psychopathology also appears to be highly associated with multiplesubstance use. Compared to users of cocaine alone, compulsive simultaneoususers of cocaine and heroin (“speedball”) have higher Minnesota MultiphasicPersonality Inventory (MMPI) scores on depression and trait anxiety, with moresevere psychopathology (Malow, West, Corrigan, Pena, & Lott, 1992). With frequentuse of this combination, cocaine abusers who are using opiates to reduce thejitters and “crash” of intravenous cocaine use likely increase the risk of heroindependence in this population (Levin, Foltin, & Fischman, 1996).Darke and Ross (1997) demonstrated in a sample of Australian heroininjectors that heroin use is correlated strongly with not only multiple substanceuse but also comorbid psychiatric disorders. Among IDUs, the extent and severityof non-substance-related psychopathology is a strong and linear predictor ofthe extent of multiple substance dependence. The prevalence of current moodand/or anxiety disorders was about 55%, with 25% having both a current moodand anxiety disorder—in each case, clearly greater than prevalence in the generalpopulation (Darke & Ross, 1997; Kessler et al., 1994). Darke and Ross alsofound a significant positive correlation between the number of lifetime drugdependence diagnoses and the number of lifetime comorbid psychiatric diagnosesin IDUs, and a similar positive correlation (p

11. Polysubstance Use, Abuse, and Dependence 253more likely to meet dependence criteria than men (Kandel et al., 1997). Inexamining gender effects in opioid dependence, in a study of heroin users, theredid not appear to be a gender-based difference in risk for dependence on multiplesubstances, which may be related to the equivalent risk of mental disordersin this subpopulation (Darke & Ross, 1997). In the general population, thereare clear gender differences in the risk for anxiety and mood disorders, with therelative risk for females about double that for males (Kessler et al., 1994). However,in multiple-substance-dependent IDUs, there appears to be no differenceby gender in either the lifetime prevalence of mood and anxiety disorders or thecurrent prevalence of anxiety disorders. Only the rate of current depressive disordersis significantly elevated for females over males (Darke & Ross, 1997).PERSONALITY CORRELATESIn community samples, 28.6% of individuals with a current alcohol use disorderhave at least one personality disorder, and 47.7% of those with a current druguse disorder have at least one personality disorder (Grant et al., 2004). Furthermore,of individuals with at least one personality disorder, 16.4% had a currentalcohol use disorder and 6.5% had a current drug use disorder. Personality disordersare associated with poorer treatment outcome for patients with alcoholdependence and those with drug dependence (Helzer & Pryzbeck, 1988;Rounsaville, Dolinsky, Babor, & Meyer, 1987). In various treatment settings,patients with SUDs screened with standard instruments meet criteria for personalitydisorders, with 57–73% having at least one personality disorder diagnosis,and 35–50% having at least two personality disorder diagnoses (Kleinmanet al., 1990; Kranzler, Satel, & Apter, 1994; Marlowe et al., 1995; Rounsavilleet al., 1998; Skinstad & Swain, 2001). Personality disorder diagnoses are associatedwith an increased risk of multiple substance use in IDUs (Darke, Williamson,Ross, Teesson, & Lynskey, 2004).Categorical Personality DisordersThe “Cluster B” personality disorders (antisocial, borderline, narcissistic, andhistrionic), as described in DSM-IV, demonstrate elevated rates of SUDs (Mors& Sorensen, 1994). Conversely, in patients with SUDs, there is an elevatedrate of Cluster B personality disorders, and multiple-substance-dependentpatients are more likely to be diagnosed with Cluster B personality disordersthan non-multiple-substance-dependent subjects (Skinstad & Swain, 2001).For example, in 370 patients with heterogenous SUDs, Rounsaville and colleagues(1998) found that 57% had an DSM-III-R personality disorder diagnosis,of which 45.7% were Cluster B, including 27% with antisocial personalitydisorder (ASPD) and 18.4% with borderline personality disorder (BPD).

254 IV. SPECIAL POPULATIONSAntisocial Personality DisorderThe risk of ASPD among drug-dependent individuals in community samples is29 times that of the general population, and rates of ASPD among IDUs rangebetween 35 and 71% (Darke et al., 2004; Dinwiddie et al., 1996; Regier et al.,1990). ASPD appears to be a risk factor for multiple substance dependence. Forexample, patients who meet dependence criteria for both cocaine and alcoholhave higher psychiatric severity and are more likely to have ASPD thanpatients with cocaine dependence only (Cunningham, Corrigan, Malow, &Smason, 1993). Among clinical populations, sociopathy among substance abusersis associated with high treatment dropout and poorer treatment outcome(Leal, Ziedonis, & Kosten, 1994; Woody, McLellan, Luborsky, & O’Brien,1985). Tómasson and Vaglum (2000) followed 100 treatment-seeking alcoholicswith ASPD for 28 months in a European study: Forty-seven percent of thecohort had multiple SUDs and more prior admissions, and they were more frequentlyinvolved in fights. The route of drug administration also is associatedwith elevated risk of ASPD. Compared to non-IDUs with a substantial drug usehistory, rates of ASPD are elevated in IDUs (Dinwiddie et al., 1996). Increasedsocial deviance is a factor that likely increases risk of access to hard drugs. However,the specific contribution of ASPD to SUD risk is less clearly delineated.Recent family genetics studies suggest that familial aggregation of SUD islargely independent of ASPD (Bierut et al., 1998; Merikangas et al., 1998).Borderline Personality DisorderAlthough ASPD has been the personality disorder that is traditionally diagnosedin patients with SUDs and is typically believed to be responsible for thehigher risk of self- and other-harmful behaviors in this population, recent evidencesuggests that some proportion of the risk for multiple substance use, aswell as suicide attempts and psychiatric severity, is associated with BPD (Darkeet al., 2004). Trull, Sher, Minks-Brown, Durbin, and Burr (2000) reviewed 26studies of the comorbidity of BPD and SUD, and found rates of BPD thatranged from 5 to 65%. Much of the variability between studies was due to differentinstruments used and populations studied. However, the rate across studieswas 57.4%; thus, it is clear that the prevalence of BPD is elevated amongpatients with SUDs (Trull et al., 2000). BPD is present in 18–34% of cocaineabusers in treatment settings and among 46% of injection heroin users in andout of treatment (Darke et al., 2004; Kleinman et al., 1990; Kranzler, Satel, &Apter, 1994; Marlowe et al., 1995). In a recent study of injection heroin users,46% of the sample met criteria for BPD, including 38% who also met criteriafor comorbid ASPD, yet there appeared to be little increased risk for harmfulbehaviors among IDUs with ASPD compared to those without ASPD (Darkeet al., 2004).

Dimensional Approaches11. Polysubstance Use, Abuse, and Dependence 255In addition to the increased rates of SUD in persons with categorically definedpersonality disorders compared to controls, there are personality dimensionsthat may be predictive of increased risk for SUDs. Moreover, those with multipleSUDs tend to have more severe personality pathology, as measured ondimensional constructs, than users of single substances, independent of drug ofchoice (McCormick, Dowd, Quirt, & Zegarra, 1998; Pedersen, Clausen, &Lavik, 1989). Multiple-substance-dependent individuals tend to have highlevels of two personality characteristics particularly related to behavioraldisinhibition—impulsivity and sensation seeking (see review in Conway et al.,2003). Those with multiple substance dependence score lower in measures ofbehavioral inhibition (constraint) than those who prefer to use alcohol,cocaine, or cannabis singly (Conway, Swendson, Rounsaville, & Merikangas,2002).ImpulsivityImpulsivity/disinhibition appears to be a major factor in both SUD and BPD.Though impulsivity is associated with polysubstance use (O’Boyle & Barratt,1993), and in addition to the risks for polysubstance abuse attributable to BPD,as described earlier, impulsivity appears more highly elevated in comorbidBPD–SUD than with either disorder alone (Kreudelbach, McCormick, Schulz,& Grueneich, 1993; Morgenstern, Langenbucher, Labouvie, & Miller, 1997).As such, impulsivity may explain some of the increased risk in substance userswith BPD for polydrug use and its sequelae. In an analysis of the associationbetween personality and substance use in a nonclinical population screened foralcohol or personality disorders, partialling out trait impulsivity significantlyreduced the correlation between BPD or ASPD and the risk for SUD, suggestingthat at least part of the association between SUD and personality may bedue to underlying personality traits such as impulsivity (Casillas & Clark,2002). On the balance, increased morbidity in polysubstance abusers might alsobe explained by a constitutional insensitivity to negative feedback from theenvironment. Multiple SUD subjects’ poor performance on the Gambling Tasksuggests a heightened tendency to continue reinforced behavior in the contextof increasingly negative consequences (Grant, Contoreggi, & London, 2000).Novelty SeekingA related personality trait that has been consistently linked with the vulnerabilityto development of SUD is novelty seeking or sensation seeking. Amongchildren, those with higher sensation seeking are more likely to declare anintention to use alcohol and to have symptoms of substance abuse as adults

256 IV. SPECIAL POPULATIONS(Cloninger, Sigvardsson, & Bohman, 1988; Webb, Baer, & McKelvey, 1995).Generally, persons with SUD exhibit higher levels of this trait compared tothose without SUD, whether they are alcoholics or abusers of other substances(Conway et al., 2002). Moreover, users of multiple substances tend to haveeven higher levels of sensation seeking, such that the greater the involvementin multiple substance dependence, the greater the behavioral disinhibition(Conway et al., 2003; Pedersen et al., 1989). Conversely, the high sensationseekers among cocaine-dependent persons are more likely to have multipleSUD (Ball, Carroll, & Rounsaville, 1994). Conway and colleagues (2003) demonstratedthat the number of lifetime substance dependence diagnoses among325 individuals in addiction treatment was positively and linearly associatedwith broad psychological measures of behavioral disinhibition. Compared topatients who were dependent on one substance, those who were dependent ontwo or more substances had higher scores on several different instruments usedto rate behavioral undercontrol. All other things being equal (e.g., access, economicstatus), the more disinhibited a person with a vulnerability to substancedependence, the more likely the thresholds for contact with multiple drugs willbe breached, and the vulnerability linked to use of multiple drugs.Other CharacteristicsMultiple-substance-dependent patients in treatment report lower mean levelsof self-efficacy and higher mean levels of temptation regarding substance use incomparison to alcohol-only-dependent patients (Edens & Willoughby, 1999).In addition to the increased impulsivity and sensation seeking compared tonon-multiple-drug SUD patients, multiple SUD patients score higher on allmeasures of hostility and aggression (McCormick & Smith, 1995).Typologic ApproachesAnother important development in elucidating the relationship between patternsof substance use, and both categorical and dimensional approaches tomeasuring personality is the recognition of characteristic patterns, typicallygrouped into two broad categories among substance abusers, designated TypesA and B (Ball, Kranzler, Tennen, Poling, & Rounsaville, 1998). Earlier classificationsystems in reference to alcoholism had a similar typology, variouslyreferred to as Types 1 and 2 (Cloninger, 1987), which developed out of measuresin family genetic studies, or Types A and B (Babor et al., 1992), developedthrough cluster analyses of a somewhat broader set of patient characteristics.Feingold and colleagues (1996), using a schema analogous to that of Babor andcolleagues (1992), replicated the A-B classification in 521 subjects chosen fromthe community, inpatient, and outpatient drug treatment programs, or outpatientpsychiatric treatment programs. Subjects were grouped by presence of

11. Polysubstance Use, Abuse, and Dependence 257alcohol, cocaine, marijuana, or opiate abuse or dependence. The authors founda consistent 60:40 ratio of Type A to Type B for each of the drug groups, suggestingclusters of personality characteristics that are independent of drug ofchoice. Similarly, in 370 patients attending treatment for alcoholism, cocaine,or opiate dependence, Ball and colleagues (1998) replicated the A-B classificationand also found a 60:40 Type A to Type B ratio. Type A substance abusershad less multiple drug use, as well as an older age of onset, fewer years of heavyuse, less family history of substance abuse, less impulsivity, and less severe substanceabuse. Type B substance abusers tended to be more severe than type Aabusers, scoring higher on the personality dimensions of neuroticism, noveltyseeking, and harm avoidance. They also had a higher prevalence of multiplesubstance abuse, an earlier age of onset, more childhood psychiatric symptoms,higher incidence of all Cluster B personality disorders, and more frequent familyhistory of substance abuse (Ball et al., 1998). The Type B profile is quitecommon in methadone patients, in whom there is a greater prevalence ofASPD than in the general population (Brooner, King, Kidorf, Schmidt, &Bigelow, 1997; Rounsaville et al., 1991).Compared to drug abusers who are categorized as Type A, Type B is predictiveof having multiple SUDs. This is an important refinement in the assessmentof drug abusers; since multiple SUD does not occur in non-substance-abusingpopulations, this distinction gives some predictive power in the target subpopulationof those with SUD. As described earlier, ASPD in persons with SUDis predictive of multiple SUDs, IDU, and higher severity, and an earlier studyfound that ASPD was one of the best predictors of Type B membership amongcocaine abusers (Ball et al., 1995). However, Ball and colleagues (1998) foundthat the basis for Type A and Type B distinctions in personality dimensions anddisorders among the 370 patients in their study remained much the same whenthe cluster analysis was controlled for presence of ASPD. The typological distinctionis not just of heuristic value—Type B patients have more severe SUDs andrelapse more quickly after addiction treatment as compared with Type A patients(Babor et al., 1992; Ball et al., 1995). In addition, the more frequent family historyof SUD and early onset in Type B patients is consistent with a stronger geneticcomponent compared with late-onset Type A patients.GENETIC AND FAMILY STUDIESVulnerability to substance abuse has general genetic, familial, and nonfamilialenvironmental factors, as well as factors that appear to be specific to a particularclass of substances. A family history of substance abuse is one of the strongestrisk factors for development of a SUD (Merikangas et al., 1998). Studies havedemonstrated that there are genetic influences on the risk for substance abuse(Tsuang et al., 1996) and that, at least among men, abusing one category of

258 IV. SPECIAL POPULATIONSdrug is associated with a marked increase in the probability of abusing otherclasses of drugs (Tsuang et al., 1998). One of the strongest predictors for presenceof an SUD is the presence of another SUD (Bierut et al., 1998).Much of the evidence for the heritability of the general and specific vulnerabilityfor SUD is taken from studies of familial aggregation. Bierut and colleagues(1998) compared siblings of probands with alcohol dependence andthose of a control group for the presence of lifetime SUDs. Siblings of alcoholicprobands were not only more likely to have a lifetime alcohol use disorder, butthey also had an increased risk of cannabis, cocaine, and nicotine dependence.Fifty percent of the alcohol-dependent siblings of alcohol-dependent probandshad an additional diagnosis of cannabis and/or cocaine dependence. What iscompelling with respect to understanding the risk for multiple substancedependence is that the siblings of cannabis-dependent probands had an increasedrisk of cannabis dependence, siblings of cocaine-dependent probandshad an increased risk for cocaine dependence, and siblings of habitual smokerswere at higher risk for nicotine dependence (Bierut et al., 1998). In anotherstudy, Tsuang and colleagues (1998) demonstrated that there is a general drugabuse vulnerability factor with genetic, family, and nonfamily environmentalcomponents that is shared across all drugs of abuse, in addition to genetic factorsthat appear to be unique for most classes of drug abuse. So although thereappear to be nongenetic general and specific factors for familial transmission ofvulnerability to SUDs, multiple SUDs among probands render increased vulnerabilityto multiple SUDs in relatives, at least through both drug-specific andcommon genetic factors.NEUROPSYCHOLOGICAL IMPACTOF MULTIPLE SUBSTANCE USE DISORDERSAs compared with non-polysubstance-using drug abusers, those with multipleSUDs demonstrate the greatest degree of chronic neuropsychological impairmentand recover the least function with long-term abstinence (Beatty et al.,1997; Medina, Shear, Schafer, Armstrong, & Dyer, 2003). This may be due inpart to the increased cumulative exposure of the brain to drugs and alcohol:Multiple substance users tend to use as much of a particular substance (e.g.,alcohol or cocaine) as those who use only alcohol or cocaine (Selby & Azrin,1998). Selby and Azrin (1998) conducted a comprehensive neuropsychologicalbattery with 355 prison inmates classified by DSM-IV criteria into four groups:those with alcohol use disorders, cocaine use disorders, multiple SUDs, and nohistory of SUD. The multiple SUDs and the alcohol groups demonstrated significantimpairment on most measures compared to the cocaine or no-druggroups, but the multiple SUDs group performed worse than the cocaine alone,alcohol alone or no SUD groups on measures of short-term memory, long-term

11. Polysubstance Use, Abuse, and Dependence 259memory, and visual motor ability. Beatty and colleagues (1997) found analogousresults in their neuropsychological evaluation of spatial cognition in multipleSUD and non-multiple-SUD inpatient alcoholics who had at least 3weeks of sobriety. Multiple SUD patients had significant impairment of geographicalknowledge requiring place localization, over and above the impairmenton all other measures of visuospatial perception, construction, learning,and memory that all of the alcoholics had compared to controls. After 3 weeksof sobriety, alcoholics with multiple SUD compared to alcoholics without multipleSUD also demonstrate greater memory deficits in tests of recall (Bondi,Drake, & Grant, 1998). The heavy cocaine users among the alcoholics had theworst deficits, suggestive of subcortical dysfunction due to small vessel infarcts.Subjects with multiple SUDs also demonstrated impaired decision makingthrough poor performance on the Gambling Task compared to non-drugusingcontrols (suggesting dysfunction of the ventromedial prefrontal cortex[Bechara, 1999; Grant et al., 2000]).Given the neuropsychological effects of multiple SUDs, it is important torecognize that the baseline cognitive function also has a role in vulnerability tomultiple SUDs. Premorbid intellectual functioning is a predictor of drug use:Compared to matched non-drug-using controls, multiple substance users weredemonstrated to have lower fourth-grade Iowa Test composite and individualscores on Vocabulary, Reading, Language, Work–Study Skills, and Mathematicstests (Block, Erwin, & Ghoneim, 2002)SPECIAL POPULATIONSOpioid Dependence and Opioid Maintenance TreatmentPolydrug use is the norm among heroin users. In a study of 329 primary heroinusers by Darke and Hall (1995), the most prevalent drugs used during the preceding6 months were tobacco (94%), cannabis (84%), alcohol (78%), benzodiazepines(64%), amphetamines (42%), cocaine (24%), and hallucinogens(22%); the mean number of drug classes used was 5.2. However, it appears thatas they grow older, illicit drug users reduce their range of drugs: Age is inverselycorrelated in IDUs with the number of current dependence diagnoses, andyoung males who are not in treatment, and who inject amphetamines, are athigher risk for polysubstance use (Darke & Hall, 1995; Darke & Ross, 1997).Cocaine UseThe use of cocaine by patients in methadone or buprenorphine maintenancetreatment programs has been reported to be as high as 73% in a sample of 1038newly admitted patients in 15 methadone clinics in New York City (Magura,Kang, Nwakeze, & Demsky, 1998). Contrary to popular belief, the simulta-

260 IV. SPECIAL POPULATIONSneous use of intravenous heroin and cocaine (“speedball”) does not result in anovel set of experiences, nor does it reinforce the effects of either drug whenused alone, especially when cocaine and heroin are used in high doses.Cocaine, however, has been shown to alleviate some symptoms of opioid withdrawal,and as such may be used in a self-medicating pattern, as mentioned earlier(Leri, Bruneau, & Stewart, 2003).CannabisCannabis use among patients in methadone treatment programs has recentlybeen investigated in an attempt to answer the practical question of whethercannabinoid-positive urine toxicology examinations predict poor treatmentoutcome. Both a recent Israeli study (Weizman, Gelkopf, Melamed, Adelson,& Bleich, 2004) and a review of three U.S. studies (Epstein & Preston, 2003)suggest that cannabis use is not a risk factor for treatment outcome ofmethadone-maintained outpatients. The authors concluded that cannabinoidpositiveurines do not need to be a major focus of clinical attention.OverdoseIn examining both fatal and nonfatal heroin overdoses, the majority of casesinvolve simultaneous use of alcohol, benzodiazepines, and tricyclic antidepressants(TCAs), such that the toxicology of heroin overdose is probably bestdescribed as “polydrug toxicity” (Darke & Hall, 2003; Darke & Zador, 1996). Infatal heroin overdoses, alcohol has been used more than 50% of the time(Darke & Hall, 2003). The mechanism of action for the overdose appears to bethe synergistic effect of the various depressants on the central nervous system,leading to respiratory collapse. This is further collaborated by autopsy findingsof an inverse relationship between alcohol and morphine blood concentrations;in the presence of alcohol, lower levels of morphine are sufficient to result indeath (Darke & Hall, 2003). In a study by Darke and Ross (2000) in Sydney,Australia, both fatal and nonfatal heroin overdoses were linked to concomitantuse of TCAs but not selective serotonin reuptake inhibitors (SSRIs), despitethe fact that heroin users in Australia predominantly use SSRIs instead ofTCAs.Adolescents, Club Drugs, and the Rave SceneA recent review of the literature revealed that club drug use [MDMA (3,4-methylenedioxymethamphetamine), ketamine, and GHB (gamma-hydroxybutyricacid)] has reached epidemic proportions and is particularly problematicamong adolescents with psychiatric illness, including mood and anxiety disor-

11. Polysubstance Use, Abuse, and Dependence 261ders, as well as attention-deficit/hyperactivity disorder. Although club drugsoriginally got their name from nightclubs and raves, adolescents and youngadults now use club drugs in both club and nonclub settings (Rosenthal &Solhkhah, in press). Overall, studies of typical MDMA users reveal high ratesof multiple drug use (Parrott, Milani, Parmar, & Turner, 2001; Parrott, Sisk, &Turner, 2000; Rodgers, 2000; Schifano, Di Furia, Forza, Minicuci, & Bricolo,1998). Among treatment seekers, heavy MDMA use is associated with increasedpsychopathology (Parrott et al., 2000; Schifano et al., 1998). In additionto use of alcohol and cannabis, the heavier the MDMA use, the morelikely is the co-use of stimulants and hallucinogens (Scholey et al., 2004).MDMA as a sole drug of abuse is an uncommon phenomenon; thus, it is a reasonableproxy for abuse of multiple substances (Rodgers, 2000).Raves are large, all-night dance parties, where people come together to useclub drugs and “feel like a closely knit family” in what is sometimes called“marching to the beat of Ecstasy.” Raves started in England in the early 1980sand have since spread throughout the United States, Europe, South America,and Australia in major urban centers and on college campuses. Adolescents andyoung adults are particularly drawn to raves, where they feel free to hug, laugh,talk, scream, and dance to “techno” or “house” music under laser lights and theeffects of drugs, primarily MDMA (Cohen, 1998). Rave participants oftendescribe looking for a “trance-induced” state or “euphoric transcendence,”while smiling, touching, and loving each other in a completely nonviolent setting(Tyler, 1995). Interestingly, a recent study from the Netherlands found anegative association between substance dependence and violent offending (butnot criminal recidivism) among a sample of incarcerated male Dutch adolescents(Vreugdenhil, Van Den Brink, Wouters, & Doreleijers, 2003).Heroin use has been rising among adolescents and young adults, possiblybecause heroin is now so pure that people can easily sniff or smoke it. Anextensive review of descriptive studies of young heroin users revealed, in a patternsimilar to that of adult heroin users, substantial multiple substance use andpsychiatric comorbidity (Hopfer, Khuri, Crowley, & Hooks, 2002). The sameauthors also reviewed different treatments of adolescents who use heroin,including therapeutic communities and methadone maintenance, and foundthat length of time in treatment, regardless of modality, was the best predictorof patient outcome (Hopfer et al., 2002).Club Drugs and the Circuit SceneCircuit parties are large-scale dance events, primarily for gay men, where use ofmultiple drugs is prevalent. Participants often travel from all over the country,and sometimes overseas, to attend these large gatherings that bring togetherseveral thousand gay men. MDMA, ketamine, GHB, cocaine, methamphet-

262 IV. SPECIAL POPULATIONSamine and alcohol are the most frequently used substances. Recent studies byMansergh and colleagues (2001), Mattison, Ross, Wolfson, Franklin, andSan Diego HIV Neurobehavioral Research Center Group (2001), and Lee,Galanter, Dermatis, and McDowell (2003) indicate high rates of simultaneousdrug use at circuit parties; the average number of substances ingested byresponders on the day of the circuit party studied by Lee and colleagues was 2.4,with a range of 0 to 7. Most people report that using drugs during a circuit partyenhances the dancing experience, relieves inhibitions, and improves sex. Othersdescribe multiple substance use as self-medication for depressed mood, anxiety,social isolation, or stress associated with living with HIV disease or AIDS.Some participants report a synergistic effect between drugs, as in the case of theMDMA and ketamine combination; some users believe that it results in a moreintense “high,” while others feel that ketamine prolongs the effect of MDMA.Multiple Substance Use and HIV RiskMultiple substance use at circuit parties has recently become a great concern inthe gay community, in the context of the crystal methamphetamine epidemicand the rising incidence of HIV transmission among young gay men in largeurban environments. A study of 428 young gay and bisexual men under the SanFrancisco Young Men’s Health Study (Greenwood et al., 2001) found polydrugusers to be more likely to be HIV seropositive (OR = 2.05) or of unknown HIVstatus (OR = 2.78). The common link between HIV seropositivity and multiplesubstance use has not been demonstrated, but given the preceding discussion, itis reasonable to suspect that an important personality factor may be involved,such as behavioral dyscontrol in the form of impulsivity or sensation seeking.When disinhibiting drugs such as alcohol and GHB are taken concert, a personwho has high trait impulsivity is even more likely to engage in risky behavior.For example, Cook and colleagues (2001) identified gay men recently infectedwith syphilis in Liverpool, United Kingdom, and found that 61% had usedGHB as an aphrodisiac in the context of unprotected sex.The association of multiple substance use and HIV raises medical concernsboth in terms of HIV transmission and HIV treatment. Sexual disinhibitionand increased risk of HIV transmission have been correlated to substance use,and particularly to stimulants, not only in the gay community but also in a varietyof other settings (Levounis, Galanter, Dermatis, Hamowy, & De Leon,2002). These findings support the hypothesis that multiple substance use maydirectly result in increased rates of unsafe sex and HIV seroconversion. In termsof HIV treatment, club drugs such as MDMA and GHB interact with proteaseinhibitors, resulting in dangerously high levels of the club drugs (Harrington,Woodward, Hoofon, & Horn, 1999). Furthermore, patients often fail to adhereto complicated HIV pharmacological regimens during intoxication with orwithdrawal from a variety of different drugs of abuse (Lee et al., 2003).

11. Polysubstance Use, Abuse, and Dependence 263TREATMENT CONSIDERATIONSAt its simplest, treatment of patients with chronic multiple SUDs requires afocus upon each disorder separately, in addition to providing patients with acoherent overall rationale and approach to addiction treatment. Although multipleSUDs have a net negative impact on treatment outcome, Abellanas andMcLellan (1993) have shown that patients with multiple SUDs report generallysimilar motivation for change across drugs of abuse, meaning that theirdesire to modify their substance use remains consistent across substances. Anadditional issue is the specific impact of other substance use upon recovery for aparticular SUD. Treatment is thus best constructed with a bottom-up approach,using evidence-based approaches where available (Rosenthal, 2004), ratherthan assuming that optimal treatment should be largely psychotherapeutic orpharmacotherapeutic. For example, there is a clear evidence base for the useof methadone as an agonist therapy for stabilization of opioid dependence(Ciraulo, 2003). However, there is not good evidence that an adequate dose ofmethadone for treating opioid dependence will suffice in treating cocaine abuseor dependence. Since there is no approved pharmacotherapy for cocaine usedisorders at present, the optimal therapy should come from the behavioraltreatments, which also have an evidence base. As such, the approach to treatingpatients with opioid dependence and cocaine dependence should have bothpharmacotherapeutic and psychotherapeutic components.In the acute setting, multiple SUDs present the treatment team with significantchallenges. Given a patient’s complicated history of recent and chronicuse of multiple substances, the clinician in the emergency room or detoxificationunit often struggles to make treatment priorities out of a constellation ofsigns and symptoms that may be the result of intoxication or withdrawal from anumber of substances. Given the frequent occurrence of multiple substance usediagnoses (particularly between alcohol and other drugs), any attempt to attributeobserved findings associated with comorbid substance use to a single substance,or class of substances, is often difficult, if not impossible. Intoxicationfrom stimulants may result in psychotic symptoms, but so does withdrawal fromsedatives. Lethargy is not only a classic sign of opioid intoxication but also aconsequence of stimulant withdrawal. A patient who currently uses both benzodiazepinesand crystal methamphetamine, and presents with seizures, may beeither acutely intoxicated with methamphetamine or suffering from severebenzodiazepine withdrawal, or both. Furthermore, the serious psychosocialcomplications of multiple SUDs add significantly to the difficulty in treatingthe already confusing biological manifestations of the illness. As in the case ofrelapse prevention, the successful management of acute multiple substance userelies primarily upon identification and treatment of each intoxication andwithdrawal syndrome separately. For example, patients with serious withdrawalfrom heroin and alcohol typically require both opioid agonists (e.g., methadone

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CHAPTER 12Co-Occurring Substance Use Disordersand Other Psychiatric DisordersALISA B. BUSCHROGER D. WEISSLISA M. NAJAVITSDetermining better ways to identify and treat individuals with co-occurringsubstance use disorders (SUDs) and other psychiatric disorders has becomeincreasingly important from clinical, research, and policy perspectives. Severalobservations have driven this imperative: (1) Co-occurring SUDs with otherpsychiatric disorders are prevalent (Kessler et al., 1996; Regier et al., 1990) andassociated with worse clinical and functional outcomes than either SUDs orother psychiatric disorders alone (Mueller et al., 1994; Ritsher, McKellar,Finney, Otilingam, & Moos, 2002); (2) many people with these co-occurringdisorders do not receive adequate treatment (Substance Abuse and MentalHealth Service Administration, 2002); and (3) compared to psychiatricpatients without co-occurring SUDs, patients with a dual diagnosis tend to usemore costly treatments, such as emergency and hospital care (Dickey & Azeni,1996; Mark, 2003). Together, these observations have led to the developmentof specific new treatments designed or adapted for this population—althoughthis research is at an early stage.Within SUD populations, multiple substance use disorders are common(Kessler et al., 1997; Regier et al., 1990). While these individuals can also beconsidered “dually diagnosed,” this chapter focuses exclusively on patients whohave an SUD plus a (non-SUD) co-occurring Axis I or II psychiatric disorder.271

272 IV. SPECIAL POPULATIONSAdditionally, non-SUD Axis I and II psychiatric disorders are here referred tosimply as “psychiatric disorders” to distinguish them from substance use disorders.In this chapter, we review psychosocial and psychopharmacological treatmentsfor dual-diagnosis populations. While increasing methodological rigor isbeing employed in many of these studies, this research is still at an early stage.Thus, some of the available evidence is from pilot or noncontrolled trials.When evidence from blinded and/or controlled trials is not available for a particulartreatment, we review the level of evidence that is available.EPIDEMIOLOGYStudies in SUD and psychiatric treatment-seeking populations (McLellan &Druley, 1977; Ross, Glaser, & Germanson, 1988; Rounsaville et al., 1991)have suggested high prevalence rates of co-occurring SUDs and psychiatricdisorders. However, treatment-seeking samples may not be representative ofcommunity populations, since they tend to have higher rates of comorbidityand may have more severe manifestations of the disorder for which they areseeking treatment. Thus, epidemiological studies of prevalence rates in communitypopulations are important in assessing the true comorbidity prevalencerate.The two largest U.S. psychiatric epidemiological studies to date, theEpidemiologic Catchment Area (ECA) study (Regier et al., 1990) and themore recent National Comorbidity Survey (NCS; Kessler et al., 1996) demonstratethat co-occurring SUDs and psychiatric disorders are prevalent in communitypopulations. Methodological advancements of the NCS included anexpanded scope of the community sample (e.g., the ECA sampled from withinfive U.S. communities, whereas the NCS sampled nationally representativehouseholds), and an advanced version of the Diagnostic and Statistical Manual ofMental Disorders (i.e., DSM-III-R [American Psychiatric Association, 1987]).Also, while both studies surveyed most of the more common psychiatric disorders,the ECA did not include posttraumatic stress disorder (PTSD), whereasthe NCS did. Neither epidemiological survey included Axis II disorders otherthan antisocial personality disorder (ASPD). Despite these limitations and differencesbetween the two studies, their results were often qualitatively similar,although the magnitude of their estimates differed somewhat at times. Amongpersons with psychiatric disorders, the ECA estimated that 30% had a cooccurringSUD. The prevalence varied by diagnosis, however; co-occurringSUDs were most common in individuals with ASPD, followed by those withbipolar I disorder. In SUD populations, the ECA and the NCS estimated thatover half will experience Axis I or II psychiatric disorders in their lifetime.These lifetime estimates do not merely reflect rare or historical periods in an

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 273individual’s history; the 12-month comorbidity prevalence rate of these disorderswas also quite high. For example, the NCS estimated that over 33% ofthose with bipolar disorder would experience an SUD within 12 months, followedby nearly 20% of those with major depression and 15% of those with ananxiety disorder.THE ASSOCIATION BETWEEN DUAL DIAGNOSISAND TREATMENT OUTCOMEIn both SUD and psychiatric treatment-seeking populations, dually diagnosedpatients typically experience worse outcomes than their “singly diagnosed”peers (Ritsher et al., 2002; Schaar & Oejehagen, 2001). However, there arespecific populations in which the evidence regarding this is mixed, such as theseverely and persistently mentally ill (SPMI) (Farris et al., 2003; Gonzalez &Rosenheck, 2002) and ASPD populations (Cacciola, Alterman, Rutherford, &Snider, 1995; Kranzler, Del Boca, & Rounsaville, 1996). The effect of otherpsychiatric disorders on SUD outcomes may vary by SUD type. For example,co-occurring major depression appears to predict worse alcohol outcomes(Brown et al., 1998; Greenfield et al., 1998), while there is less evidence for itspredicting worse cocaine outcomes (McKay et al., 2002; Rohsenow, Monti,Martin, Michalec, & Abrams, 2002).There is also evidence (albeit somewhat inconsistent) that gender mayplay a role in mediating the effect of co-occurring psychiatric disorders onSUD outcome. Major depression in men has been associated with worseSUD outcome (Compton, Cottler, Jacobs, Ben-Abdallah, & Spitznagel, 2003;Rounsaville, Dolinsky, Babor, & Meyer, 1987), although this is not a consistentfinding (Kranzler et al., 1996; Powell et al., 1992). In contrast, some studiessuggest that female gender has been associated with similar or better SUD outcomesamong patients with co-occurring psychiatric disorders (Compton et al.,2003; Rounsaville et al., 1987), except for phobia, which was associated in onestudy with worse SUD outcome in women (Compton et al., 2003). Finally,ASPD in men has been associated with worse outcomes (Compton et al., 2003;Kranzler et al., 1996); although, the evidence in women has been mixed(Compton et al., 2003; Rounsaville et al., 1987).THE RELATIONSHIP BETWEEN SUBSTANCE ABUSEAND PSYCHOPATHOLOGYWhile determining which disorder is primary in dually diagnosed populationscan be useful in clinical research, it may provide little benefit in the clinicalmanagement of these patients. Patients with two disorders typically require

274 IV. SPECIAL POPULATIONStreatment for both; the exception is patients who present with temporary psychiatricsymptoms caused by the substance use or its withdrawal.Meyer (1986) suggests considering six possible ways in which substance useand other psychopathology may be related:1. Psychopathology may be a risk factor for SUDs. As described previously,studies of patient and community samples have shown that the risk of having aco-occurring SUD is elevated in persons with psychiatric disorders. For example,dopaminergic dysfunction in patients with schizophrenia has been hypothesizedto increase their risk of SUDs—particularly cocaine use disorders (Greenet al., 1999; Smelson, Losonczy, Kilker, et al., 2002). Another theory, widelyknown as the “self-medication hypothesis” (Khantzian, 1989, 1997), suggeststhat psychopathology leads patients to use substances in an attempt to decreaseunwanted psychiatric symptoms. For example, a patient with insomnia due toPTSD nightmares may use alcohol or marijuana to induce sleep. Althoughresearch has not found direct connections between particular psychopathologicalsymptoms and specific substances (rather, patients tend to misuse a widevariety of substances to “treat” a range of symptoms), the general principle is animportant one. It is discussed in more detail in the next section.2. Psychiatric disorders and co-occurring SUDs may serve to modify the courseof each other in terms of symptomatology, rapidity of onset, and response to treatment.Also described earlier, there is considerable evidence that comorbidity isassociated with worse outcomes. Additionally, there is evidence that patientswith schizophrenia and co-occurring SUDs do not respond as well as thosewithout SUDs to similar doses of first-generation antipsychotic medications(Bowers et al., 1990).3. Psychiatric symptoms may result from chronic intoxication. Drug and alcoholuse can result in a variety of psychiatric symptoms, such as depression, anxiety,euphoria, psychosis, and dissociative states. Most such symptoms disappear,however, within hours (e.g., cocaine-induced paranoia) (Satel, Southwick, &Gawin, 1991) to weeks (e.g., alcohol-induced anxiety or depression) (Brown,Irwin, & Schuckit, 1991; Brown & Schuckit, 1988).4. Long-term substance use can lead to psychiatric disorders that may not remit.Alcohol-induced long-term cognitive changes, such as those seen in alcoholinducedpersisting dementia, exemplify one way in which chronic use of a substancecan create enduring change.5. Substance abuse and psychopathological symptoms may be meaningfullylinked. Some individuals may use alcohol or drugs in ways that enhance theirpsychiatric symptoms. For example, patients with ASPD may use alcohol orcocaine, seeking disinhibition and aggression, and patients with bipolar disordermay use cocaine or other stimulants to augment a euphoric mood (Weiss,1986l; Weiss et al., 1988).

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 2756. The SUD and psychiatric disorder are unrelated. The presence of two disorderswithin an individual does not imply a causal link. For example, bothalcohol dependence and depressive disorders are common in the general population;many people with both disorders are not depressed because they drink,nor do they drink because they are depressed. Brunette, Mueser, Xie, and Drake(1997) studied the relationship between severity of substance abuse and severityof schizophrenic symptoms in patients dually diagnosed with both disorders,and found weak relationships and no consistent patterns of relationshipsbetween the two sets of symptoms.The “Self-Medication Hypothesis”One potential explanation for the increased prevalence rate of co-occurringSUDs among patients with psychiatric disorders has been the “self-medicationhypothesis” (Khantzian, 1985, 1997), which postulates that certain drugs may beparticularly reinforcing because of particular patients’ specific psychopathology.Two fundamental assumptions underlie this hypothesis: first, that substancesare abused to relieve psychological pain, not just to create euphoria; andsecond, that there is specificity between patients’ “drug of choice” preferenceand the specific intolerable emotions or symptoms that they are attempting toalleviate. For example, patients with social anxiety may be drawn to alcohol todecrease their symptoms, while patients who are prone to violence and angeroutbursts may prefer the calming effects of opioids to the potentially disinhibitingeffects of alcohol.A major criticism of the self-medication hypothesis has been its heavy relianceon anecdotal data from patients in psychotherapy and the relative paucityof empirical studies testing it (Aharonovich, Nguyen, & Nunes, 2001). Additionally,intoxicants may produce very different effects acutely compared to theeffects of chronic administration. Studies of individuals with heroin (Meyer& Mirin, 1979), cocaine (Post, Kotin, & Goodwin, 1974), and alcohol(Mendelson & Mello, 1966) use disorders have observed a dichotomy betweenthe acute effects of these drugs in producing euphoria or tension relief and thechronic or high-dose effects in producing dysphoria. Several researchers havesought to test empirically the self-medication hypothesis in larger samples. Theresults have tended not to support the specificity of using a particular addictivesubstance to alleviate specific psychopathology or mood states (Aharonovich etal., 2001; Weiss, 1992a). However, while not necessarily a validation of thetheory that patients use addictive substances to alleviate certain mood states,there is evidence that treating a co-occurring psychiatric disorder (Cornelius etal., 1997; Greenfield et al., 1998) and remission of its symptoms (Hasin, Tsai,Endicott, & Mueller, 1996) can improve SUD outcomes.

276 IV. SPECIAL POPULATIONSOther TheoriesWeiss (1992b) suggests three additional mechanisms by which psychopathologycan make an individual more vulnerable to SUDs.1. Psychopathology may interfere with an individual’s judgment or ability toappreciate consequences. Individuals with psychiatric disorders may be more vulnerableto SUDs, because impaired judgment is often present in many psychiatricsyndromes and can interfere with the ability or willingness to understand orchange one’s behavior. For example, severely depressed patients may haveinsight regarding the destructive effect of their drinking but may continue todrink due to the pessimism about the possibility and value of change that ispart of their depressive disorder. Similarly, the recklessness, irritability, andgrandiosity of patients who are manic or hypomanic may interfere with theircapacity to appreciate the harmful nature of their substance use.2. Psychopathology may accelerate the process of substance dependence by leadingto more dysphoria during either chronic use or early abstinence. It is possible thatpatients with underlying psychopathology may experience more dysphoria fromchronic substance use or more severe withdrawal symptoms when discontinuingdrugs or alcohol. Although this potential mechanism has received little study,there is some evidence that cocaine abusers with major depression compared tococaine abusers without depression may report more severe mood symptomsduring abstinence (Gawin & Kleber, 1986).3. Psychopathology may reinforce the social context of drug use. Some patientswith severe psychiatric illness may be drawn to a drug-using subculture, becausethey feel it facilitates socialization or a new peer group. For example, somepatients with schizophrenia have described using substances to socialize or beaccepted by peers, even though substances increased the risk of psychosis(Drake, Osher, & Wallach, 1989; Spencer, Castle, & Michie, 2002).Thus, multiple possible motivations and causes contribute to the initiationand maintenance of problematic alcohol and drug use in patients with psychiatricdisorders.DIAGNOSING PSYCHIATRIC DISORDERS IN PATIENTSWITH SUBSTANCE USE DISORDERSThe task of determining whether a patient is suffering from a substanceinduceddisorder or an independent psychiatric disorder can be complicated.Substances of abuse can cause a wide range of psychiatric symptoms. Cliniciansevaluating such patients need to determine whether the disturbance

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 277is independent of substance use or related to intoxication or withdrawal.For example, when examining a patient who has a long history of alcoholdependence and depressive symptoms, it can be difficult to determinewhether the depressive symptoms result from the direct pharmacologicaleffects of alcohol, the many losses experienced as a result of the alcohol use,feelings of discouragement about the inability to stop drinking, or an independentmood disorder. Other etiologies, such as metabolic disturbances,head trauma, and personality disorders, must also be considered in the differentialdiagnosis of depressive symptoms in alcohol-dependent patients (Jaffe& Ciraulo, 1986).Given these considerations, one could ideally establish diagnostic rules toassist in determining whether a psychiatric syndrome is due to substance use orrepresents a separate and independent disorder. For example, some cliniciansmay establish a rule that a patient must be abstinent from alcohol and drugs forat least 4 weeks before they can make a diagnosis. Unfortunately, one does notalways have the luxury of observing such lengthy abstinent periods (either byhistorical report or in the present) to assess this. In such circumstances, guidelines,as opposed to strict rules, can be helpful. For example, several studieshave indicated that for alcoholics with major depression, treating the depressioncan have a positive impact on drinking (Cornelius et al., 1997; Greenfieldet al., 1998). Thus, while DSM-IV-TR (American Psychiatric Association,2000) criteria for substance-induced mood disorder suggest at least 4 weeks ofobservation during abstinence before a clinician can diagnose an independentpsychiatric disorder, it also recommends that clinicians should diagnose an independentdisorder if the symptoms are qualitatively or quantitatively not whatone would expect, given the amount and duration of the substance use. Certaindisorders, such as eating disorders and PTSD, can be diagnosed readily, even inthe context of substance use or withdrawal, since their symptoms do not closelyresemble substance-related syndromes. Indeed, for a diagnosis such as PTSD,which tends to be underdiagnosed in SUD patients, the greater danger is todelay diagnosis; waiting for a period of abstinence may prevent needed treatmentfor the co-occurring disorder (Najavits, 2004).Finally, clinicians should consider whether the patient’s symptoms arewhat would be expected upon discontinuation of the abused substance. If thereis considerable overlap between the observed symptoms and what one wouldexpect from the drug discontinuation syndrome, then the clinician should waituntil either (1) the symptoms resolve, or (2) the symptoms no longer are consistentwith what one would expect from drug cessation (i.e., the syndrome onewould expect to see after 1 week vs. 1 month of alcohol abstinence). Alternatively,if there is little overlap between the symptoms observed and theexpected abstinence syndrome (e.g., bulimia nervosa in an opioid-dependentpatient), then the diagnosis can be made without waiting.

278 IV. SPECIAL POPULATIONSDIAGNOSING SUBSTANCE USE DISORDERSAMONG PATIENTS SEEKING TREATMENTFOR PSYCHIATRIC DISORDERSCo-occurring SUDs are often overlooked in patients seeking treatment for psychiatricdisorders. The first step in the accurate diagnosis of SUDs is to systematicallyask the patient about the presence of substance use. Structured clinicalassessments have been demonstrated to improve detection of SUDs comparedto routine assessment in outpatient SPMI (Breakey, Calabrese, Rosenblatt,& Crum, 1998) and inpatient (Albanese, Bartel, Bruno, Morgenbesser, &Schatzberg, 1994) populations; they have also outperformed urine toxicologytesting (Albanese et al., 1994). Unfortunately, the increasing acuity of patientson inpatient units and the demanding time constraints of outpatient psychiatricpractice (Woodward, Fortgang, Sullivan-Trainor, Stojanov, & Mirin, 1991)may pose challenges to the systematic assessment of SUDs. In one outpatientstudy, adding the 4-item CAGE (Cut Down, Annoyed, Guilty, Eye-Opener;Ewing, 1984) questionnaire improved the sensitivity of detecting SUDs from62% to 97% in an SPMI population (Breakey et al., 1998). However, selfreportalone, without urine toxicology, can also lead to underdetection of substanceuse (Claassen et al., 1997; Shaner et al., 1993).Finally, contingencies play an important role in patients’ willingness to selfreportsubstance use. If patients are repeatedly encouraged to be honest in theirself-reports, and if they are told (and more importantly, if they believe) that therewill be no negative consequences of reporting use (e.g., being discharged from atreatment program or reported to a probation officer or employer), then they aremore likely to be forthcoming in reporting their use. If, however, they are concernedthat there will be negative consequences, then they are less likely to do so.Thus, self-reports of substance use in an emergency room, where a patient isunlikely to know the clinician and will probably not believe (whether it is true ornot) that there will be no negative consequences for disclosing use, are likely to besuspect. However, in an outpatient treatment setting, where a patient has anopportunity to build a relationship with a clinician or treatment team, and perhapssees other patients self-disclosing and benefiting from that disclosure, selfreportsare likely to be more valid (Weiss, 1998).TREATMENT OF DUALLY DIAGNOSED PATIENTSA Heterogeneous PopulationSince “dually diagnosed” patients comprise a heterogeneous population, it followsthat their treatment should perhaps reflect that heterogeneity (Weiss,Mirin, & Frances, 1992); a “one size fits all” approach therefore will likely

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 279not be optimal. However, providing group treatments tailored to patientswith some degree of diagnostic homogeneity (e.g., patients with bipolar disorderand SUDs) can be a difficult strategy to implement if one is unable torecruit a large enough clinical population for these groups. Similarly, evenwithin diagnostically homogeneous groups, considerable heterogeneity in illnessseverity and functioning may still exist. Ries, Sloan, and Miller (1997)have suggested a conceptual approach that divides dually diagnosed patientsinto four major subgroups, according to the severity (i.e., major or minor) ofeach disorder. Although this is a somewhat crude way to classify patients, itmay be helpful in developing an outpatient group treatment program fordually diagnosed patients.An additional consideration is that not all patients are similar in terms ofinsight regarding their SUD, nor are they similarly ready to address it. Thus,patients who are undecided whether or not to address their substance use maydo better in a group focused on resolving that issue, as opposed to a group inwhich all participants are actively engaged in treatment and making lifestylechanges to support sobriety. We know of no studies, however, that have testedthis idea empirically. It is possible, for example, that having a mix of patientseverity levels in one group allows patients the opportunity to learn from thosefurther along in their recovery. This is a central principle of Alcoholics Anonymous(AA), and appears to have strong anecdotal support. Treatments thatfocus on particular dual diagnoses (e.g., bipolar SUD patients) also have notbeen directly compared to more general thematic groups (e.g., dual diagnosisgroups that are more general, encompassing a wide variety of diagnoses). Thus,it remains an empirical question how the known heterogeneity of such patientsshould best be addressed within the realistic constraints of specific clinical settings.Sequential, Parallel, and Integrated Treatment ModelsThere are three major models in which dually diagnosed patients are treated:sequential, parallel, and integrated treatment. Each is discussed below.In sequential treatment, the more acute condition is treated first, followed bythe less acute co-occurring disorder. The same staff may treat both disorders, orthe less acute disorder may be treated after transfer to a different program orfacility. For example, a manic patient with a cocaine use disorder needs moodstabilization before initiating substance abuse treatment. Conversely, a patientwith major depression and alcohol withdrawal delirium is not in a position todiscuss treatment adherence to antidepressant medication. Instead, this issue isbest addressed when the patient is more stable. Although sequential treatmenthas the advantage of providing an increased level of attention to the moreacute disorder, a typical disadvantage of this model is that patients are often

280 IV. SPECIAL POPULATIONStransferred to a different treatment team to address the less acute disorder, andthe interrelationship between the two disorders may never be adequatelyaddressed.In parallel treatment, both disorders are treated simultaneously, but not bythe same treatment team. For example, a patient may receive treatment for anSUD in an addiction treatment program and for a psychiatric disorder in amental health clinic. Typically, staff members of each program are very wellversedin their own area of expertise, but not in the other. However, majorcross-training efforts on dual diagnosis have improved this situation in the pastdecade. The different treatment programs may also have different treatmentphilosophies, which may be confusing to the patient (Mueser, Bellack, &Blanchard, 1992; Ridgely, Goldman, & Willenbring, 1990). For example, insubstance abuse treatment programs, clinicians may attribute psychiatric symptoms(e.g., depression and anxiety) to substance use; when a patient attempts toobtain relief, they may view this as “drug-seeking” behavior. Alternatively, staffin psychiatric programs may tend to minimize the importance of substance useand not stress its potential negative consequences.Unfortunately, patients treated in parallel or sequential programs oftenreceive different experiences based on the treatment settings they enter. Thetwo different programs may provide patients with different feedback on therelationship between their substance use and psychological symptoms. Patientsin these situations are then left to attempt to integrate these sometimes disparateapproaches themselves. In these circumstances, patients may be accused of“manipulating” and “splitting staff” when they present information obtained inone program that is contradictory to the other.In integrated treatment, the management of both disorders occurs in onetreatment setting, and the same clinicians, or team of clinicians, manage bothillnesses. Integrated treatment has received increasing interest of researchersand clinicians, fostered by the belief that it is more effective than the othertreatment models described earlier.INTEGRATED PSYCHOSOCIAL TREATMENTSFOR DUALLY DIAGNOSED PATIENTSIntegrated psychosocial treatments have been developed for diverse patientpopulations with co-occurring SUDs and psychiatric disorders. Here, we reviewthe scope of psychiatric patient populations for which treatments have beendeveloped, followed by a review of specific treatment modalities. While thisliterature has advanced overall in terms of randomized study designs andmanualized treatments, it remains hampered by the limited number of studiesand small sample sizes. Thus, while these treatments appear promising, furtherstudy is needed.

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 281Severely and Persistently Mentally Ill PopulationsSeveral investigators have examined integrated treatments for SPMI adults.Effectiveness trials by Drake and colleagues have obtained more success indecreasing substance use (Drake et al., 1998; McHugo, Drake, Teague, & Xie,1999) and hospitalization (McHugo et al., 1999) than in diminishing psychiatricsymptoms (Drake, Yovetich, Bebout, Harris, & McHugo, 1998; Drake et al.,1998) or improving functional status or quality of life (Drake et al., 1997).However, these interventions did not compare patients randomized to differenttreatments. Rather, treatment clinics were assigned to administer one interventionversus another. A recent review of the prospective, controlled trials ofintegrated treatment programs for SPMI dually diagnosed individuals (Jeffery,Ley, McLaren, & Siegfried, 2003) concluded that methodological flaws precludeddetermining whether one particular integrated treatment model is moreeffective than another, or whether integrated treatment in general is superior tononintegrated treatment for this population. Despite this, much enthusiasmremains for integrated treatment in SPMI populations (Drake et al., 2001). Ofnote, a recent trial not included in the review approached integrating treatmentfor dually diagnosed SPMI patients from a different psychosocial treatmentperspective and found positive results. Rather than integrating treatmentfrom the perspective of intensive case management and/or housing (as in thestudies discussed earlier), patient and caregiver dyads were randomized to routinecare versus additional integrated treatment that included motivationalinterviewing, cognitive-behavioral therapy (CBT), and a family or caregiverintervention for dual-diagnosis patients with schizophrenia. The interventionwas associated with improvements in general functioning, psychotic symptoms,and SUD outcomes (Barrowclough et al., 2001). Thus, this field continues toevolve and develop creative new treatments that are being tested with increasingmethodological rigor.Other Psychiatric PopulationsIn non-SPMI populations, integrated treatment models have also been developedfor other patient subpopulations with psychiatric disorders and SUDs suchas bipolar disorder (Weiss et al., 2000), personality disorders (Ball, 1998;Linehan et al., 2002), and anxiety disorders such as PTSD (Brady, Dansky,Back, Foa, & Carroll, 2001; Najavits, Weiss, Shaw, & Muenz, 1998), obsessive–compulsive disorder (Fals-Stewart & Schafer, 1992), and social phobia (Randall,Thomas, & Thevos, 2001). With the exception of social phobia, for whichintegrated CBT for social phobia and alcohol use disorders has yielded worseanxiety and drinking outcomes compared to group CBT geared toward alcoholrelapse prevention alone (Randall et al., 2001), preliminary evidence suggeststhat these new treatments are generating some positive results.

282 IV. SPECIAL POPULATIONSSpecific Treatment ModalitiesPsychosocial treatments with the potential for broad applicability across severaldual-diagnosis populations have also been developed. With the exception ofcognitive therapy, most originated in the addiction literature but have demonstratedsome efficacy in treating both disorders when adapted specifically fordually diagnosed populations. Below, we briefly describe several of the morecommon psychosocial interventions studied in populations with co-occurringSUDs and psychiatric disorders.Cognitive-behavioral therapy (CBT), developed by Beck, Rush, Shaw, andEmery (1979), has been adapted for the treatment of substance abuse (Beck,Wright, Newman, & Liese, 1993). When adapted to specific dually diagnosedpopulations (e.g., PTSD), additional techniques include the identification ofcognitive distortions associated with both disorders (e.g., getting high now as a“reward” for having been deprived in the past), identifying meanings of substanceuse in the context of PTSD (e.g., as revenge against an abuser), andteaching new coping skills (e.g., setting boundaries) (Najavits et al., 1996).Relapse prevention therapy (RPT), developed by Marlatt and Gordon (1985),is a form of CBT that focuses on understanding the process of relapse in order toprevent it. RPT can be used as an adjunctive therapy or as a treatment in and ofitself. When modified to address dually diagnosed individuals, preventingrelapse from both disorders is emphasized. For example, RPT modified forpatients with co-occurring bipolar disorder and SUDs (Weiss, Najavits, &Greenfield, 1999; Weiss et al., 2000) teaches patients about triggers for bothsubstance use and bipolar disorder (e.g., erratic sleep behaviors, associating withthe wrong people, nonadherence to one’s medication regimen).Motivational interviewing (MI), developed by Miller and Rollnick (1991,2002), utilizes theory derived from several psychotherapeutic models: systems,client-centered, cognitive-behavioral, and social psychology. MI is also calledmotivational enhancement, because it is often a brief treatment conducted inas few as two sessions, sometimes aimed at helping the patient accept other psychotherapy(e.g., CBT). Guidelines for modifying MI in dually diagnosedpatients with psychotic disorders have been published (Carey et al., 2001;Martino et al., 2002). Recent randomized pilot trials of MI in diverse duallydiagnosed populations suggest that it may improve the likelihood of making thetransition to outpatient treatment (Swanson, Pantalon, & Cohen, 1999),improve SUD outcomes (Graeber et al., 2003), and decrease psychiatric hospitalization(Daley & Zuckoff, 1998).The transtheoretical stages-of-change model (Prochaska, DiClemente, &Norcross, 1992, 1994) describes a sequential process of five stages of change inrecovery for patients with SUDs: precontemplation, contemplation, preparation,action, and maintenance. Osher and Kofoed (1989) have articulated amodel similar to stages of change for dually diagnosed patients with severe psy-

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 283chiatric disorders. Adaptations to the stages-of-change model for SPMI dualdiagnosispopulations have also been developed, and some have been empiricallytested for reliability and validity (Carey, Carey, Maisto, & Purnine, 2002;Velasquez, Carbonari, & DiClemente, 1999) with promising results (Carey etal., 2002; Ziedonis & Trudeau, 1997). Pilot work of a family interventionadapted from the stages-of-change model for this population has also shownpromise (Mueser & Fox, 2002).Twelve-step drug counseling derives directly from the principles of AA andhas been adapted for use by professional alcohol and drug counselors (a necessaryadaptation, since AA was designed as a self-help group not led by professionals).Two types of treatment emphasize these principles: individual drugcounseling (Mercer & Woody, 1999) and 12-step facilitation (TSF) (Nowinski,Baker, & Carroll, 1995). TSF is used by all of the studies described below. Severaltrials have compared outcomes of dually diagnosed patients treated withTSF groups with outcomes among those treated with various other psychosocialtreatments (i.e., CBT, RPT, dialectical behavioral therapy [DBT], or behavioralskills group) (Brooks & Penn, 2003; Fisher & Bentley, 1996; Jerrell &Ridgely, 1995; Linehan, 1993; Linehan et al., 2002; McKay et al., 2002;Ouimette, Gima, Moos, & Finney, 1999). Among them, only one foundimproved SUD outcomes in TSF versus the comparison integrated treatment(Brooks & Penn, 2003). However, in that study, the TSF group also experiencedworsening health and employment status, and psychiatric hospitalization,compared to the group of patients receiving integrated treatment.Contingency management (CM) interventions reinforce behavior that meetsspecific, clearly defined, and observable goals (Petry, 2000) such as abstinence(Higgins et al., 1994), medication adherence (Liebson, Tommasello, &Bigelow, 1978), therapy attendance (Helmus, Rhodes, Haber, & Downey,2001), or completion of treatment goals (Petry, Martin, Cooney, & Kranzler,2000). Recent empirical evaluations using CM as an adjunctive treatment indually diagnosed populations suggest that it may offer some benefit in attendance,but its impact on SUD outcomes has been mixed (Helmus, Saules,Schoener, & Roll, 2003; Sigmon, Steingard, Badger, Anthony, & Higgins,2000).SELF-HELP GROUPSAND DUALLY DIAGNOSED INDIVIDUALSAs in other substance-using populations (Miller, Ninonuevo, Klamen, Hoffmann,& Smith, 1997; Ritsher et al., 2002), self-help group attendance has been associatedwith improved substance use outcomes in dually diagnosed populations(Brooks & Penn, 2003; Ritsher et al., 2002). Whether this is a reflection of selfhelpgroups’ improving outcomes directly or a self-selection bias (i.e., patients

284 IV. SPECIAL POPULATIONSattending self-help groups may be more likely to remain abstinent because theyare more motivated) is unclear.Despite the fact that self-help groups are both free of charge and geographicallyaccessible (Kurtz, 1997), many dually diagnosed patients do not attendthese meetings (Noordsy, Schwab, Fox, & Drake, 1996). Some clinicians maybe reluctant to recommend self-help groups to dually diagnosed patientsbecause of concerns that self-help group members might express negative attitudestoward psychotropic medication (Humphreys, 1997). However, recentresearch indicates that, while this sometimes occurs (Noordsy et al., 1996), it isnot prevalent (Meissen, Powell, Wituk, Girrens, & Arteaga, 1999). Moreover,official AA literature states that psychiatric medication, when legitimatelyprescribed, is appropriate (Alcoholics Anonymous, 1984). When educatingpatients about the interaction between psychiatric symptoms, drug and alcoholuse, and medications, clinicians should inform patients that while some selfhelpgroup members may criticize the use of medications, this contradicts officialAA policy.Clinicians may also be concerned that these groups only focus on SUDs(Humphreys, 1997) and may therefore not be as helpful to patients who arestruggling with other psychiatric disorders. Recent research suggests that somepatients and AA contacts (i.e., persons listed in the AA directories as experiencedmembers) agree (Meissen et al., 1999; Noordsy et al., 1996). However, byencouraging patients to focus on obtaining what AA and similar groups offer,and not expecting AA to provide services outside of its stated mission, clinicianscan help dually diagnosed patients to take advantage of these groups.To address some of these concerns, several dual-focus self-help groups haveemerged for participants with co-occurring SUDs and psychiatric disorders(e.g., Double Trouble in Recovery, Dual Recovery Anonymous, and Dual DisordersAnonymous) (Magura et al., 2003). Similar to the literature on self-helpgroups in the SUD population, positive associations have been found betweenattendance at dual-focus self-help groups and abstinence (Magura et al., 2003)as well as psychiatric/quality-of-life (Magura, Laudet, Mahmood, Rosenblum, &Knight, 2002) outcomes. Again, whether this is a result of self-selection biasregarding the characteristics of patients who attend these meetings or not isunclear. It is important to consider that the literature on dual-focus self-helpgroups is an emerging one and is even slimmer than the literature on integratedpsychosocial treatments. Further study is needed before conclusions regardingtheir effectiveness can be drawn.General Treatment Themes for Dually Diagnosed PatientsBecause of the limitations of the empirical literature described earlier regardingpsychosocial treatments, it may be helpful to draw on general recommendations

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 285provided by various writers on this subject (Bellack & DiClemente, 1999;Carey, 1995; Drake et al., 2001; Drake & Mueser, 2000; Najavits et al., 1996;Rounsaville & Carroll, 1997; Ziedonis, Williams, Corrigan, & Smelsen, 2000).Although treatment modalities differ, some common themes can help guide clinicianswho must decide how to intervene with their patients. The suggestionsare as follows:• Be empathic and provide support for the difficulty of living with two disorders,but also provide limit setting.• Assist patients in setting a goal to stop drug or alcohol use. Explorepatients’ perceptions of the relationship between their substance use andtheir psychiatric disorders. As part of this process, also explore the longerterm relationship between the two (e.g., an individual may reportdrinking to reduce social anxiety and feel initially better, but then mayfeel worse the following day) and discuss the advantages of a drug-freelife.• Educate patients and their family members about the symptoms of bothdisorders and the causal connections between them.• Monitor symptoms of both disorders (including the use of biologicalmeasures such as urine screens for substance use when indicated).• Monitor adherence to medications, since nonadherence is a significantrisk for relapse.• To improve functioning and foster the rewards of abstinence, assistpatients in developing social, relationship, or vocational skills.• Attend to patient safety, including attention to human immunodeficiencyvirus (HIV) and suicidal ideation (both of which have beenfound to be increased in dually diagnosed patients [Mahler, 1995; Weiss& Hufford, 1999]).• Have available resources to refer patients to self-help groups for each disorder.• Discuss with patients what to do and whom to call in case of emergency.• Provide positive reinforcement for improvements, however small, ineach disorder.• For patients who have had significant periods of recovery, acknowledgethese successes and, in a positive way, ask them how they accomplishedit. Doing so reminds patients of prior successes and can mitigate the feelingsof hopelessness and discouragement that often accompany relapse.• Take a relapse history to help identify triggers to relapse (e.g., discontinuingmedications or treatment, engaging in high-risk behaviors suchas socializing where alcohol is present).• Expect occasional breaks in treatment attendance, and engage in activeoutreach.

286 IV. SPECIAL POPULATIONSPHARMACOTHERAPY FOR DUALLY DIAGNOSED PATIENTSDuring the past decade, the literature regarding when to prescribe pharmacotherapyfor dually diagnosed patients has changed considerably. Previous consensusin the field reflected reluctance to prescribe psychotropic medicationsin these populations. However, this consensus was based on earlier, methodologicallyflawed studies. For example, older studies examining the use ofantidepressants in alcoholics often did not use standardized methods to assessthe depressed population, had inadequate dosing or duration of antidepressants,and sometimes measured mood or drinking outcomes, but not both(Ciraulo & Jaffe, 1981). More recent studies have demonstrated that pharmacotherapycan improve outcomes for the psychiatric disorder and sometimesfor the SUD as well (Greenfield et al., 1998; Schubiner et al., 2002).Still, it is important also to incorporate psychosocial treatments directed atimproving substance use outcomes when treating dually diagnosed patients.The literature on treatments for specific psychiatric disorders is reviewedbelow.Major DepressionNunes and Levin (2004) performed a meta-analysis of antidepressant medicationefficacy for the treatment of co-occurring depression and SUD. The resultsindicated that in this patient population, the efficacy of antidepressants is comparableto that seen in patients with depression alone. Studies that required atleast 1 week of abstinence before treating the depression yielded larger effectsizes and lower placebo response, suggesting that requiring even at least 1 weekof abstinence before initiating medication treatment can successfully screen outtransient depressive symptoms. Also, studies that exhibited better depressionoutcomes as a result of antidepressants also showed decreased quantity of substanceuse. However, rates of sustained abstinence or SUD remission were lowacross studies, highlighting the importance of treatment directed at the SUD aswell when treating these patients.Bipolar DisorderAlthough face validity would suggest that stabilizing mania or hypomania inpatients with bipolar disorder would improve impulse control and judgment,and therefore lead to decreases in substance use, the literature is thin regardingthe efficacy of mood stabilizing medications on bipolar and SUD outcomes. Anopen pilot trial by Gawin and Kleber (1984) suggested that lithium may beeffective in reducing cocaine use in patients with cyclothymia and cocaineabuse. However, an open trial of lithium in patients with bipolar spectrum disordersand cocaine abuse (Nunes, McGrath, Wager, & Quitkin, 1990) demon-

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 287strated little efficacy in mood or cocaine outcome measures. An open label trialwith valproate in patients with bipolar disorder and SUD (Brady, Sonne,Anton, & Ballenger, 1995) resulted in improvement in mood and substance usemeasures. Additionally, open-label trials of lamotrigine (Brown, Nejtek, Perantie,Orsulak, & Bobadilla, 2003) and quetiapine (Brown, Nejtek, Perantie, &Bobadilla, 2002) in patients with bipolar disorder and cocaine dependence suggestthat these medications may be associated with improved mood symptomsand cocaine craving, although not with significant reductions in cocaine use.Since there have been no double-blind, placebo-controlled studies assessing theefficacy of mood stabilizers or antipsychotic medications in adults with bipolardisorder and SUDs, the results of these open trials can be seen as preliminary atbest. However a double-blind, placebo-controlled, 6-week trial of lithium inadolescents with bipolar disorder and substance dependence (Geller et al.,1998) found lithium to be efficacious for outcomes in both disorders.SchizophreniaUnfortunately, the literature on the pharmacological treatment of patients withschizophrenia and SUDs is limited to retrospective or open-label prospectivestudies, some of which lack a comparison group. For example, an open trial ofdesipramine added to antipsychotic treatment in an integrated dual-diagnosisrelapse prevention program has shown promise in reducing cocaine use andimproving psychiatric symptoms (Ziedonis, Richardson, Lee, Petrakis, & Kosten,1992). Additionally, preliminary reports suggest that there may be a potentialbenefit of second-generation antipsychotic medications such as clozapine(Buckley, Thompson, Way, & Meltzer, 1994; Drake et al., 2000; Zimmet,Strous, Burgess, Kohnstamm, & Green, 2000), olanzapine (Littrell, Petty,Hilligoss, Peabody, & Johnson, 2001), and risperidone (Smelson, Losonczy,Davis, et al., 2002) in improving substance use outcomes in populations withco-occurring schizophrenia. Clozapine has been hypothesized to be uniquelybeneficial: Its unique pharmacological receptor activity may correct underlyingreward system deficits of patients with schizophrenia and SUDs (Green,Zimmet, Strous, & Schildkraut, 1999; LeDuc & Mittleman, 1995). Additionally,when administered in low doses (50 mg or less) to normal volunteers,clozapine has been shown to attenuate the subjective high and rush associatedwith cocaine, as well as its pressor effect (Farren et al., 2000).Despite these encouraging findings, there is evidence from normal studyvolunteers that low-dose clozapine may increase cocaine blood levels and causenear-syncope (Farren et al., 2000). However, to our knowledge, there are nocase reports or studies documenting clinically significant syncopal episodes inpatients with schizophrenia and stimulant use disorders who are prescribedclozapine. Thus, while the introduction of second-generation antipsychoticsare encouraging in their potential to improve SUD outcomes in this dually

288 IV. SPECIAL POPULATIONSdiagnosed population, well-designed controlled trials are needed to establishsafety, tolerability, and efficacy in this population.Anxiety DisordersThe use of benzodiazepines in populations with SUDs and co-occurring psychiatricdisorders is controversial. This issue has been explored almost exclusivelyin populations with anxiety and alcohol use disorders. The prevalence of benzodiazepineuse among patients with alcohol use disorders is greater than in thegeneral population but comparable to psychiatric disorder populations (Ciraulo,Sands, & Shader, 1988). Clinicians are often understandably concerned thatprescribing benzodiazepines to these patients may lead to either a worsening ofthe alcohol use disorder, the development of a benzodiazepine use disorder, orpotentiation of the benzodiazepine effect when combined with alcohol. Preliminaryevidence from case reports (Adinoff, 1992) and a prospective naturalisticstudy (Mueller, Goldenberg, Gordon, Keller, & Warshaw, 1996) suggests thatthere may be a carefully selected subpopulation of patients with co-occurringalcohol use and anxiety disorders for whom long-term prescription of benzodiazepinemay not affect sobriety or result in benzodiazepine misuse. However,it may not improve outcomes either. For example, a retrospective naturalisticstudy of veterans with PTSD and SUD found that physicians were less likely toprescribe benzodiazepines for those with SUD (Kosten, Fontana, Sernyak, &Rosenheck, 2000). While those with prescribed benzodiazepines did not haveworse outcomes, chronic benzodiazepine treatment (independent of a cooccurringSUD) did not improve anxiety or social functioning in these patientseither. Similarly, Brunette, Noordsey, Xie, and Drake (2003) followed SPMIpatients with SUDs annually for 6 years and found that the rate of benzodiazepineprescribing was high (up to 63%) but not associated with differences insubstance use remission, hospitalization, or, interestingly, reductions in anxietyor depression. Also, unsurprisingly, patients prescribed benzodiazepines weremore likely to abuse them than those who were not. While controlled trials areneeded to explore these issues more fully, the findings from these reports addfurther to concerns that the long-term use of benzodiazepines in these populationsperhaps offers the risk of abuse or dependence without great potential forclinical benefit.Another pharmacological alternative in this population is buspirone,which does not have abuse potential. Thus far, there have been three doubleblind,placebo-controlled studies of buspirone in patients with alcohol dependenceand anxiety—generalized anxiety disorder (GAD) (Tollefson, Montague-Clouse, & Tollefson, 1992), GAD and “other nonpanic anxiety” (Malcolm etal., 1992), or “anxious alcoholics” (Kranzler et al., 1994). Two of the studiesfound buspirone to be associated with improvements in anxiety and alcohol useoutcomes (Kranzler et al., 1994; Tollefson et al., 1992). Although there have

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 289been concerns that buspirone’s antianxiety effect is more limited in patientswith a prior history of benzodiazepine use (Schweizer, Rickels, & Lucki, 1986),a pooled analysis of eight placebo-controlled randomized trials of patients withGAD (DeMartinis, Rynn, Rickels, & Mandos, 2000) found that patients witheither remote (defined as at least 1 month duration) or no prior benzodiazepinetreatment experienced improved anxiolysis, fewer adverse events, and clinicalimprovement similar to that with benzodiazepines compared to patients withrecent benzodiazepine treatment. Thus, patients who have not received benzodiazepinesfor at least 1 month may benefit from buspirone.Attention-Deficit/Hyperactivity DisorderAlthough stimulants have been the most extensively studied treatment foradult attention-deficit/hyperactivity disorder (ADHD) (Levin, Evans, & Kleber,1999), there are concerns that they may worsen the course of the SUDs or besubject to abuse themselves in dually diagnosed populations (Gawin, Riordan,& Kleber, 1985). At the same time, it has also been observed that a childhoodhistory of ADHD worsens outcomes for cocaine dependence (Carroll &Rounsaville, 1993). Therefore, improving a patient’s difficulties with inattentionand hyperactivity may have beneficial effects on substance abuse as well(Levin et al., 1999). Consistent with this, prospective studies of children whoreceived stimulant treatment for ADHD indicate that stimulants have a protectiveeffect against future development of SUDs as an adult (Wilens, 2001).Although not as well-studied as stimulants, nonstimulant medications thatlack abuse potential are possible alternatives in the treatment of ADHD. In adultpopulations, only bupropion (Wilens et al., 2002), desipramine (Wilens et al.,1996), and atomoxetine (Michelson et al., 2003) have undergone double-blind,placebo-controlled study and demonstrated effectiveness in the treatment ofhyperactivity and inattention. However, none of these trials included patientswith active SUDs. To our knowledge, the only published trials of antidepressantsas treatment for ADHD in populations with a current co-occurring SUD are asingle-blind trial of bupropion for adult ADHD and cocaine abuse (Levin, Evans,McDowell, Brooks, & Nunes, 2002), and an open-label study of venlafaxine inpatients with ADHD and alcohol use disorder (Upadhyaya, Brady, Sethuraman,Sonne, & Malcolm, 2001). Both showed improvements in hyperactivity andinattention, as well as improved substance use outcomes. However, these resultsneed to be replicated in larger, more rigorous studies.Clinical trials of methylphenidate in adults with ADHD and a history ofcocaine use disorders have also shown promising results. Both open-labeltrials of long-acting methylphenidate (Castaneda et al., 2000; Levin, Evans,McDowell, & Kleber, 1998) and a double-blind, placebo-controlled study ofregular methylphenidate (Schubiner et al., 2002) in adults with ADHDand cocaine dependence have all been consistent in that ADHD symptoms

290 IV. SPECIAL POPULATIONSimproved, and no escalation of the stimulant dose was observed. However,while the open trial by Levin and colleagues (1998) indicated reductions incocaine craving and use, Schubiner and colleagues (2002) found no evidence ofimproved cocaine outcomes in their double-blind, placebo-controlled trial.Pemoline is a stimulant thought to have lower abuse potential than methylphenidate.However, there are no controlled trials of pemoline in this population,and its increased risk of hepatotoxicity, while small, makes its safety inthis population unclear (Levin, Evans, & Kleber, 1999). Despite limited evidencethat stimulants may be safely used in this population to treat ADHDwithout worsening SUD outcomes (and perhaps improving them), their use inthese patients remains controversial.What to Do When the Pharmacological Treatmentfor the Co-Occurring Psychiatric Disorder Has Abuse PotentialAs evidenced in numerous studies, treating a co-occurring psychiatric disordercan often have positive outcomes in both reducing substance use and helpingthe specific psychiatric disorder for which it is prescribed. However, what if thepharmacological treatment has the potential to worsen or create a new SUD?This dilemma is often considered in treating patients who suffer with SUDs andco-occurring anxiety disorders or ADHD, when clinicians ask themselves, “Is itsafe to prescribe stimulants/benzodiazepines for this patient?”Pharmacotherapies that do not have abuse potential should be consideredfirst-line treatments before prescribing stimulants or benzodiazepines in thesepopulations (Ciraulo & Nace, 2000; Levin et al., 1999), and it is important thatpatients receive adequate trials (i.e., dose and duration) of these medicationsbefore they are abandoned. Psychosocial treatments with demonstrated efficacyshould also be tried before prescribing an abusable medication. For example,CBT has demonstrated efficacy for anxiety disorders (Beck et al., 1993) andshould be explored before prescribing a benzodiazepine. If these first-line treatmentsfail to improve the anxiety or ADHD symptoms adequately, then the followingguidelines are suggested when prescribing stimulants or benzodiazepinesin these patient populations (Ciraulo & Nace, 2000; Levin et al., 1999):• Select preparations that limit the potential for abuse. Medications with longerhalf-lives or sustained-release preparations have lower abuse potentialand are therefore preferable in these populations. Select as low adose as possible. For benzodiazepines, avoid as-needed-basis prescribingin lieu of a fixed dosing schedule. Limit the number of pills given witheach prescription, and keep a log of the pills prescribed. Frequent patientcontact can help the clinician assess whether the medication is helpful,as well as whether it is being overused.• Use objective measures to document improvements. For example, using a

12. Co-Occurring Substance Use Disorders and Other Psychiatric Disorders 291standardized assessment such as the Adult Behavior Checklist (Murphy& Barkley, 1996) or the Beck Anxiety Inventory (Beck, Epstein, Brown,& Steer, 1988) can help document improvements (or lack thereof).• Monitor substance use. Patients should be asked about alcohol and druguse, and other sources of information (urine screens, collateral informationfrom family members) should be strongly considered.• Enlist family members in supporting and monitoring the patient. Verify theefficacy and appropriate use of the medication with family members.• Patients should safeguard medications. While the patient may not abusethe medication, family members may.• Monitor prescriptions. Keep careful track of the number of pills you prescribe,and beware of warning signs of abuse, such as premature requestsfor refills or “lost prescriptions.” These usually indicate overuse of themedication.Pharmacotherapy Targeting Substance Dependencein Dually Diagnosed PopulationsAlthough pharmacotherapies aimed specifically at decreasing alcohol or druguse (e.g., naltrexone, disulfiram) can be efficacious in improving SUD outcomesin non-dually-diagnosed populations, the literature on the use of thesemedications in dually diagnosed populations is quite thin. Concerns thatdisulfiram may cause or exacerbate psychosis (Mueser, Noordsy, Fox, & Wolfe,2003) have contributed to a reluctance to prescribe it in patients with SPMI(Kingsbury & Salzman, 1990). While there have been no controlled studies ofdisulfiram in populations with alcohol dependence and SPMI, there have beena few published case reports (Brenner, Karper, & Krystal, 1994) and case series(Kofoed, Kania, Walsh, & Atkinson, 1986; Mueser et al., 2003) describing itstolerability and potential benefit for improving alcohol outcomes and hospitalizationrates for those who remain in treatment. Additionally, there is preliminaryevidence that naltrexone may improve drinking outcomes in patients withalcohol dependence and schizophrenia (Batki et al., 2002) or major depression(Salloum et al., 1998). The benefit or tolerability of naltrexone in patients withbipolar disorder and alcohol disorders is less clear, based on one case report(Sonne & Brady, 2000).INTEGRATION OF PSYCHOTHERAPY ANDPHARMACOTHERAPY FOR DUALLY DIAGNOSED PATIENTSIntegrated psychosocial treatments are increasingly accepted and provided topatients as more and varied evidence accrues regarding their benefits. However,there continue to be few trials that integrate novel psychosocial treatments

292 IV. SPECIAL POPULATIONSwith novel pharmacotherapies. Instead, most treatments either focus on newpharmacological or new psychosocial interventions. Despite this, more recentresearch has emphasized the importance of integrating pharmacological andpsychotherapeutic treatment options.FUTURE DIRECTIONSIn the approximately 20 years since researchers and clinicians in the mentalhealth and addictions fields first noted the high prevalence rate of comorbidityand poorer outcomes in dually diagnosed populations, important strides havebeen made in further understanding the epidemiology and sequelae of thesedisorders, as well as the critical need to develop specific treatments for thesepopulations. Significant progress has been made in developing new treatments,testing them with increasing methodological rigor, and developing optimaltreatment methods for these often poorly served patient populations. In thenext decade, we are hopeful that this continued research effort will translateinto improved treatment methods and outcomes in these patients.ACKNOWLEDGMENTSThis work was supported by Grant Nos. K02 DA00326 (Dr. Weiss), R01 DA015968(Drs. Busch and Weiss), U10 DA015831 (Drs. Busch, Weiss, and Najavits), and K02DA00400 (Dr. Najavits) from the National Institute on Drug Abuse.REFERENCESAdinoff, B. (1992). Long-term therapy with benzodiazepines despite alcohol dependencedisorder. Am J Addict, 1(4), 288–293.Aharonovich, E., Nguyen, H. T., & Nunes, E. V. (2001). Anger and depressive statesamong treatment-seeking drug abusers: Testing the psychopharmacological specificityhypothesis. Am J Addict, 10(4), 327–334.Albanese, M. J., Bartel, R. L., Bruno, R. F., Morgenbesser, M. W., & Schatzberg, A. F.(1994). Comparison of measures used to determine substance abuse in an inpatientpsychiatric population. Am J Psychiatry, 151(7), 1077–1078.Alcoholics Anonymous. (1984). The AA member: Medications and other drugs [Brochure].New York: Alcoholics Anonymous World Services.American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders(3rd ed., rev.). Washington, DC: Author.American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders(4th ed.). Washington, DC: Author.Ball, S. A. (1998). Manualized treatment for substance abusers with personality disorders:Dual focus schema therapy. Addict Behav, 23(6), 883–891.

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302 IV. SPECIAL POPULATIONSWeiss, R. D., Griffin, M. L., Greenfield, S. F., Najavits, L. M., Wyner, D., Soto, J. A., &Hennen, J. A. (2000). Group therapy for patients with bipolar disorder and substancedependence: Results of a pilot study. J Clin Psychiatry, 61, 361–367.Weiss, R. D., & Hufford, M. R. (1999). Substance abuse and suicide. In D. Jacobs (Ed.),Harvard Medical School guide to assessment and intervention in suicide (pp. 300–310).New York: Simon & Schuster.Weiss, R. D., Mirin, S. M., & Frances, R. J. (1992). The myth of the typical dual diagnosispatient. Hosp Community Psychiatry, 43, 107–108.Weiss, R. D., Najavits, L. M., & Greenfield, S. F. (1999). A relapse prevention groupfor patients with bipolar and substance use disorders. J Subst Abuse Treat, 16, 47–54.Weiss, R. D., Najavits, L. M., Greenfield, S. F., Soto, J. A., Shaw, S. R., & Wyner, D.(1988). Psychopathology in cocaine abusers: Changing trends. J Nerv Ment Dis,176, 719–725.Wilens, T. E. (2001, Fall). Does the medicating of ADHD increase or decrease the riskfor later substance abuse? An evaluation of the literature [Insert]. Am Assoc AddictPsychiatry News, pp. 1–4.Wilens, T. E., Biederman, J., Prince, J., Spencer, T. J., Faraone, S. V., Warburton, R., etal. (1996). Six-week, double-blind, placebo-controlled study of desipramine foradult attention deficit hyperactivity disorder. Am J Psychiatry, 153, 1147–1153.Wilens, T. E., Spencer, T. J., Biederman, J., Girard, K., Doyle, R., Prince, J., et al.(2002). A controlled clinical trial of bupropion for attention deficit hyperactivitydisorder in adults. Am J Psychiatry, 158, 282–288.Woodward, B., Fortgang, J., Sullivan-Trainor, M., Stojanov, H., & Mirin, S. M. (1991).Underdiagnosis of alcohol dependence in psychiatric inpatients. Am J Drug AlcoholAbuse, 17, 373–388.Ziedonis, D., Richardson, T., Lee, E., Petrakis, I., & Kosten, T. (1992). Adjunctivedesipramine in the treatment of cocaine abusing schizophrenics. PsychopharmacolBull, 28, 309–314.Ziedonis, D., & Trudeau, K. (1997). Motivation to quit using substances among individualswith schizophrenia: Implications for a motivation-based treatment model.Schizophr Bull, 23, 229–238.Ziedonis, D., Williams, J., Corrigan, P., & Smelsen, D. A. (2000). Management of substanceabuse in schizophrenia. Psychiatr Ann, 30, 67–75.Zimmet, S. V., Strous, R. D., Burgess, E. S., Kohnstamm, S., & Green, A. I. (2000).Effect of clozapine on substance use in patients with schizophrenia and schizoaffectivedisorder: A retrospective study. J Clin Psychopharmacol, 20, 94–98.

CHAPTER 13Pathological Gamblingand Other “Behavioral” AddictionsJON E. GRANTMARC N. POTENZASeveral disorders, particularly those formally categorized in the fourth edition ofthe Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) asimpulse control disorders (ICDs) not elsewhere classified, have been describedas “behavioral” addictions (American Psychiatric Association, 2000). TheICDs include pathological gambling (PG), kleptomania, intermittent explosivedisorder, trichotillomania, and pyromania, and diagnostic criteria for compulsivecomputer use, compulsive sexual behavior, and compulsive buying (CB)have been proposed. Although there exists some controversy regarding themost precise categorization of these disorders, mounting evidence supports phenomenological,clinical, epidemiological, and biological links between behavioraland drug addictions. As such, it seems increasingly important that individualsinvolved in the prevention and treatment of substance use disorders(SUDs) have a current understanding of ICDs and the potential for futureresearch findings to guide prevention and treatment efforts for addictions ingeneral.PG represents the most thoroughly investigated ICD; consequently, thischapter largely focuses on PG, the relationship of PG to SUDs, and currenttreatment options for PG. We will also review two other ICDs (kleptomaniaand CB) that, despite having been less studied than other psychiatric disorders,have been receiving increasing attention from clinicians and researchers.303

304 IV. SPECIAL POPULATIONSCORE FEATURES OF BEHAVIORAL AND DRUG ADDICTIONSBehavioral and drug addictions share common core qualities: (1) repetitive orcompulsive engagement in a behavior despite adverse consequences; (2) diminishedcontrol over the problematic behavior; (3) an appetitive urge or cravingstate prior to engagement in the problematic behavior; and (4) a hedonic qualityduring the performance of the problematic behavior. These features have ledto a description of ICDs as “addictions without the drug.”Clinical similarities between ICDs and SUDs are best reflected in the diagnosticcriteria for PG. Criteria for PG (Table 13.1) share common features withthose for SUDs (American Psychiatric Association, 2000), including aspects oftolerance, withdrawal, repeated unsuccessful attempts to cut back or stop, andimpairment in major areas of life functioning (Blanco, Moreyra, Nunes, Saiz-Ruiz, & Ibanez, 2001). Epidemiological data also support a relationship betweenPG and SUDs, with high rates of co-occurrence in each direction(Potenza, Fiellin, Heninger, Rounsaville, & Mazure, 2002). PhenomenologicalTABLE 13.1. Diagnostic Criteria for Pathological GamblingA. Persistent and recurrent maladaptive gambling behavior as indicated by five(or more) of the following:(1) is preoccupied with gambling (e.g., preoccupied with reliving pastgambling experiences, handicapping or planning the next venture, orthinking of ways to get money with which to gamble)(2) needs to gamble with increasing amounts of money in order toachieve the desired excitement(3) has repeated unsuccessful efforts to control, cut back, or stop gambling(4) is restless or irritable when attempting to cut down or stop gambling(5) gambles as a way of escaping from problems or of relieving adysphoric mood (e.g., feelings of helplessness, guilt, anxiety,depression)(6) after losing money gambling, often returns another day to get even(“chasing” one’s losses)(7) lies to family members, therapist, or others to conceal the extent ofinvolvement with gambling(8) has committed illegal acts such as forgery, fraud, theft, orembezzlement to finance gambling(9) has jeopardized or lost a significant relationship, job, or educational orcareer opportunity because of gambling(10) relies on others to provide money to relieve a desperate financialsituation caused by gamblingB. The gambling behavior is not better accounted for by a Manic EpisodeNote From American Psychiatric Association (2000, p. 674). Copyright 2000 by the AmericanPsychiatric Association. Reprinted by permission.

13. Pathological Gambling and Other “Behavioral” Addictions 305data further support a relationship between behavioral and drug addictions: Forexample, high rates of PG and SUDs have been reported during adolescenceand young adulthood (Chambers & Potenza, 2003); the telescoping phenomenon(reflecting the rapid rate of progression from initial to problematic behavioralengagement in women as compared with men) initially described foralcoholism has been applied to PG (Potenza et al., 2001); and similar typologiesto those defining groups with alcoholism have been proposed for PG(Lesieur, 2000; Potenza, Steinberg, McLaughlin, Rounsaville, & O’Malley,2000). Emerging biological data, such as those identifying common geneticcontributions to alcohol use and gambling disorders (Slutske et al., 2000) andcommon brain activity changes underlying gambling urges and cocaine cravings(Potenza et al., 2002), provide further support for a shared relationshipbetween PG and SUDs.OTHER MODELS FOR IMPULSE CONTROL DISORDERSAlthough much data from diverse sources support a close relationship betweenPG and SUDs, other non-mutually-exclusive proposed models for ICDs includecategorizations as obsessive–compulsive spectrum (Potenza & Hollander, 2002)and affective spectrum (McElroy et al., 1996) disorders. The range of medicationclasses (serotonin reuptake inhibitors [SRIs], mood stabilizers, opioidantagonists) investigated in the treatment of ICDs reflects the different categorizations.Conceptualization of ICDs within an obsessive–compulsive spectrum isbased on common features of repetitive thoughts and behaviors (Potenza &Hollander, 2002). Although clinical aspects, such as ritualistic behaviors,are shared between obsessive–compulsive disorder (OCD) and ICDs, otheraspects seem different (e.g., the ego-syntonic nature of gambling in PG andthe ego-dystonic nature of compulsions in OCD). Although some evidencesupport high rates of co-occurring OCD and ICDs (McElroy, Hudson, Pope,Keck, & Aizley, 1992), multiple studies do not report an association (Grant& Kim, 2001, 2002a; Potenza et al., 2002). Personality features of individualswith ICDs (impulsive, reward and sensation seeking) differ from those withOCD (harm avoidant) (Kim & Grant, 2001). Biological differences alsoexist; for example, whereas increased activity in corticobasal ganglionic–thalamic circuitry has been described during symptom provocation studies ofOCD, relatively decreased activity in these brain regions was observed in cueelicitation studies in PG (Potenza et al., 2003). Family history and large-scaleepidemiological studies have also not demonstrated associations between PGand OCD (Potenza et al., 2002). Thus, there is less evidence linking PG toOCD than to SUDs.

306 IV. SPECIAL POPULATIONSThe association of ICDs with mood disorders has led to their grouping asan affective spectrum disorder (McElroy et al., 1996). Many people withICDs report that the pleasurable yet problematic behaviors alleviate negativeemotional states. Because the behaviors are risky and self-destructive, thequestion has been raised whether ICDs reflect subclinical mania or cyclothymia.The elevated rates of co-occurrence between ICDs and depression,and bipolar disorder support their inclusion within an affective spectrum, asdo early reports of treatment response to SRIs, mood stabilizers, and electroconvulsivetherapy (McElroy, Hudson, Pope, Keck, &White, 1991; McElroyet al., 1996). However, as has been suggested with SUDs, depression in ICDsmay be distinct from primary or uncomplicated depression; for example,depression in ICDs may represent a response to shame and embarrassment(Grant & Kim, 2002a). In addition, rates of co-occurrence of ICDs and bipolardisorder may not be as high as initially thought (Grant & Kim, 2001,2002a), and the response to SRIs not as robust as initially anticipated(McElroy et al., 1991). Nonetheless, brain imaging studies have found commonregional brain activity differences distinguishing bipolar subjects fromcontrols, and PG subjects from controls, during a cognitive task involvingattention and response inhibition (Potenza et al., 2003). For these reasons,the relationship between ICDs and mood disorders requires clarification, particularlybecause appropriate classification has implications for treatmentdevelopment.EPIDEMIOLOGYArguably the best data on the prevalence of ICDs exist for PG. A recent metaanalysisof 120 published studies and a national prevalence study estimate thatthe lifetime prevalence of serious gambling (meeting DSM criteria for PG)among adults ranges from 0.9 to 1.6% (National Opinion Research Center,1999; Shaffer, Hall, Vander Bilt, 1999), with past-year rates for adults rangingfrom 0.6 to 1.1% (National Opinion Research Center, 1999; Shaffer & Hall,1996).Rates of problem gambling, a less severe form of disordered gambling thanPG, not presently defined in the DSM, have been estimated at an additional 3–5% of the general adult population. As with SUDs, higher rates of problemgambling and PG have been reported in males, particularly during adolescenceand young adulthood.Although the precise prevalence of kleptomania remains unknown, a preliminaryestimate of 0.6% has been reported (Goldman, 1991). Furthermore,there is emerging evidence that kleptomania may be more common thaninitially throught (Grant, Potenza, Levine, & Kim, in press). Estimates of the

13. Pathological Gambling and Other “Behavioral” Addictions 307lifetime prevalence of compulsive buying have ranged from 1.1 to 5.9%(Christenson et al., 1994; McElroy, Keck, Pope, Smith, & Strakowski, 1994).ETIOLOGYA growing body of literature implicates multiple neurotransmitter systems (e.g.,serotonergic, dopaminergic, noradrenergic, opioidergic), as well as familial andinherited factors, in the pathophysiology of ICDs (Potenza & Hollander, 2002).The most consistent findings involve the serotonin (5-hydroxyindole or 5-HT) system, believed to underlie impulse control (Potenza & Hollander, 2002).Evidence for serotonergic involvement in ICDs comes in part from studiesof platelet monoamine oxidase B (MAO-B) activity, which correlates withcerebrospinal fluid (CSF) levels of 5-hydroxyindoleacetic acid (5-HIAA, ametabolite of 5-HT) and is considered a peripheral marker of 5-HT function(Potenza & Hollander, 2002). Low CSF 5-HIAA levels have been found tocorrelate with high levels of impulsivity and sensation seeking (Potenza &Hollander, 2002). Pharmacological challenge studies that measure hormonalresponse after administration of serotonergic drugs also provide evidence for serotonergicdysfunction in ICDs (Potenza & Hollander, 2002).Dopaminergic systems influencing rewarding and reinforcing behaviorshave also been implicated in ICDs. “Reward deficiency syndrome,” a hypothesizedhypodopaminergic state involving multiple genes and environmentalstimuli that puts an individual at high risk for multiple addictive, impulsive,and compulsive behaviors, is one proposed mechanism (Blum et al., 2000).Alterations in dopaminergic pathways have been proposed as underlying theseeking of rewards (gambling, drugs) that trigger the release of dopamine andproduce feelings of pleasure (Blum et al., 2000).Noradrenergic systems, believed to underlie arousal, excitement, and sensationseeking, have been implicated in impulsive behaviors (Potenza & Hollander,2002). Anticipation of or engagement in seemingly impulsive behaviorscan activate the autonomic nervous system. Correlations between scores on theextroversion scale of the Eysenck Personality Questionnaire and markers ofnoradrenergic functioning (e.g., CSF or plasma 3-methoxy-4-hydroxyphenylglycol[MHPG] levels, urinary outputs of norepinephrine and its major metabolites)suggest a disturbance in central noradrenergic system functioning in PG(Roy, De Jong, & Linnoila, 1989).The mu opioid system is believed to underlie urge regulation through theprocessing of reward, pleasure, and pain, at least in part via modulation ofdopamine neurons in mesolimbic pathway through gamma-aminobutyric acid(GABA) interneurons (Potenza & Hollander, 2002). Opioidergic involvementin ICDs comes from studies of naltrexone, a mu opioid receptor antagonist with

308 IV. SPECIAL POPULATIONSefficacy in reducing the urges in ICDs (Grant & Kim, 2002b; Kim, Grant,Adson, & Shin, 2001).PATHOLOGICAL GAMBLINGClinical CharacteristicsPG shares many features with SUDS. Gambling usually begins in childhood oradolescence, with males tending to start at an earlier age (Chambers &Potenza, 2003; Grant & Kim, 2001). Higher rates of PG are observed in men,with a telescoping phenomenon observed in females (Potenza, Steinberg, et al.,2001). PG has been described as a chronic, relapsing condition (Potenza,Kosten, & Rounsaville, 2001). High rates of PG in adolescents and youngadults suggest a similar natural history to that observed with SUDs (Chambers& Potenza, 2003).Other gender-related differences in PG have been described. Female ascompared with male pathological gamblers tend to have problems with nonstrategicforms of gambling, such as slot machines and bingo, whereas men aremore likely than women to have problems with strategic forms, such as sportsand card gambling (Potenza, Steinberg, et al., 2001). As is the case of SUDSand specific substances, the extent to which problems with specific forms ofgambling might relate to prevention and treatment efforts requires furtherinvestigation. Both female and male gamblers report that advertisements are acommon trigger of their urges to gamble, although females are more likely toreport that feeling bored or lonely may also trigger their urges to gambling(Grant & Kim, 2001; Ladd & Petry, 2002).As with SUDs, financial and marital problems are common (Grant & Kim,2001) and often include illegal behaviors, such as stealing, embezzlement, andwriting bad checks (Grant & Kim, 2001; Potenza et al., 2000). Cognitive featureshave also been reported as common between PG and SUDs; for example,both groups have been found to have high rates of temporal discounting ofrewards and to perform disadvantageously on decision-making tasks (Bechara,2003).Co-Occurring DisordersStudies consistently find that patients with PG have high rates of lifetime mood(60–76%), anxiety (16–40%), and personality (87%) disorders, particularlyantisocial personality disorder (Black & Moyer, 1998; Crockford & el-Guebaly,1998). Elevated rates of CB, compulsive sexual behavior, and intermittentexplosive disorder have also been found (Black & Moyer, 1998).High rates of co-occurrence have been reported for SUDs (including nicotinedependence) and PG, with the highest odds ratios generally observed

13. Pathological Gambling and Other “Behavioral” Addictions 309between gambling and alcohol use disorders (Cunningham-Williams, Cottler,Compton, & Spitznagel, 1998; Welte, Barnes, Wieczorek, Tidwell, & Parker,2001). A Canadian epidemiological survey estimated that the relative risk foran alcohol use disorder is increased 3.8-fold when disordered gambling is present(Grant, Kushner, & Kim, 2002), and odds ratios ranging from 3.3 to23.1 have been reported between PG and alcohol abuse/dependence in U.S.population-based studies (Cunningham-Williams et al., 1998; Welte et al.,2001).TreatmentGiven the high rates of placebo response often observed in treatment trials ofPG, the treatment section focuses on findings from double-blind, placebocontrolledtrials (see Table 13.2).AntidepressantsSRIs are the most well-studied pharmacotherapy for PG. In a double-blindstudy with one subject, 125 mg/day of clomipramine resulted in significantimprovement. The patient sustained improvement for 28 weeks on a dose of175 mg/day (Grant, Kim, & Potenza, 2003). Fluvoxamine has demonstratedmixed results in two placebo-controlled, double-blind studies, with one 16-week crossover study supporting its efficacy at an average dose of 207 mg/day(Hollander et al., 2000), and a second 6-month parallel-arm study with highrates of dropout finding no significant difference in response to active or placebodrug (Blanco, Petkova, Ibanez, & Saiz-Ruiz, 2002).Paroxetine at doses between 20 and 60 mg/day (average end-of-study dose= 52 mg/day) has been shown in a short-term, parallel-arm, placebo-controlled,double-blind study to be well-tolerated and efficacious in the treatment of PG(Kim, Grant, Adson, Shin, & Zaninelli, 2002). However, a 16-week multicenterstudy of paroxetine did not find a statistically significant differencebetween active drug and placebo, perhaps in part due to the high placeboresponse rate (48% to placebo, 59% to active drug) (Grant, Kim, Potenza, etal., 2003). A similarly high placebo response rate was seen in a recent studyusing sertraline (Saiz-Ruiz et al., 2005).Opioid AntagonistsGiven their ability to modulate dopaminergic transmission in the mesolimbicpathway, mu opioid receptor antagonists have been investigated in the treatmentof PG. Initially, open-label treatment suggested the efficacy of naltrexone,an FDA-approved treatment for alcohol dependence, in reducing theintensity of urges to gamble, gambling thoughts, and gambling behavior when

TABLE 13.2. Double-Blind, Placebo-Controlled Pharmacotherapy Trials for Impulse Control DisordersDisorder Reference Treatment Duration Sample sizeMean dailydose (± SD) OutcomePathologicalgamblingHollander et al.(2000)Fluvoxamine(Luvox)Crossover 16weeks with a 1-week placebolead-in15 enrolled,10 completers195 mg(± 50)Fluvoxamine superior toplacebo on CGI and PG-YBOCSPathologicalgamblingPotenza &Hollander (2002)Olanzapine(Zyprexa)7 weeks 23 Video Pokergamblersenrolled,21 completers10 mg (± 0) No significant differencefound between olanzapineand placebo-treated groupsPathologicalgamblingKim et al. (2001) Naltrexone(ReVia)12 weeks with 1-week placebolead-in89 enrolled,45 completers188 mg (±96)Naltrexone groupsignificantly improvedcompared with placebo onCGI and G-SASPathologicalgamblingHollander et al.(2005)Lithiumcarbonate SR(Lithobid SR)10 weeks 40 bipolarspectrumpatientsenrolled,29 completers1,170 mg(± 221)Lithium group significantlyimproved compared withplacebo on CGI, PG-YBOCS, and CARS-MPathologicalgamblingBlanco et al.(2002)Fluvoxamine(Luvox)6 months 32 enrolled,13 completers200 mg Fluvoxamine not statisticallysignificant from placeboexcept in young males310

PathologicalgamblingPathologicalgamblingKim et al. (2002) Paroxetine(Paxil)Grant et al.(2003)Paroxetine(Paxil)8 weeks with 1-week placebolead-in53 enrolled,41completers16 weeks 76 enrolled,45 completers51.7 mg(± 13.1)50 mg(± 8.3)Paroxetine groupsignificantly improvedcompared to placebo on CGIParoxetine and placebogroups with comparableimprovement on all measuresPathologicalgamblingSaiz-Ruiz et al.(2005)Sertraline(Zoloft)6 months 66 enrolled,37 completers95 mg Sertraline and placebo groupswith comparableimprovement to CCPGQCompulsivebuyingBlack et al.(2000)Fluvoxamine(Luvox)9 weeks with 1-week placebolead-in23 enrolled,18 completers220 mg Fluvoxamine and placebogroups with comparableimprovement on YBOCS-SVand CGICompulsivebuyingNinan et al.(2000)Fluvoxamine(Luvox)13 weeks 37 enrolled,23 completers215 mg(± 76.5)Fluvoxamine and placebogroups with comparableimprovement on YBOCS-CB, CGI, and GAFCompulsivebuyingKoran et al.(2003)Citalopram(Celexa)7-week openlabelfollowed by9 weeksrandomized24 enrolled,15 randomized42.1 mg(± 15.3)Citalopram groupsignificantly improvedcompared to placebo onYBOCS-SV and CGINote. PG-YBOCS, Yale–Brown Obsessive Compulsive Scale Modified for Pathological Gambling; YBOCS-SV, Yale–Brown Obsessive Compulsive Scale—Shopping Version;YBOCS-CB, Yale–Brown Obsessive Compulsive Scale Modified for Compulsive Buying; CGI, Clinical Global Impression scale; G-SAS, Gambling Symptom AssessmentScale; GAF, Global Assessment of Functioning; CARS-M, Clinician-Administered Rating Scale for Mania; CCPGQ, Criteria for Control of Pathological GamblingQuestionnaire.311

312 IV. SPECIAL POPULATIONSreceiving high dose (range = 50–250 mg/day; mean dose of 157 mg/day)(Grant, Kim, & Potenza, 2003). A larger double-blind study using a meannaltrexone dose of 188 mg/day confirmed these earlier findings (Kim, Grant,Adson, & Shin, 2001). In particular, individuals reporting higher intensitygambling urges responded preferentially to treatment (Kim et al., 2001).Mood StabilizersA recent double-blind study found sustained-release lithium carbonate superiorto placebo in 29 bipolar-spectrum pathological gamblers over 10 weeks (Hollander,Pallanti, & Baldini-Rossi, 2005). Bipolar spectrum disorders weredefined as including DSM-IV diagnoses of bipolar II disorder, bipolar disordernot otherwise specified (NOS), and cyclothymia, and mood swings thatoccurred at times unrelated to gambling urges/behavior.Atypical AntipsychoticsAtypical antipsychotics have been explored as augmenting agents in the treatmentof nonpsychotic disorders and behaviors, including OCD. Olanzapine wasnot found to be superior to placebo in the treatment of video poker pathologicalgamblers (Potenza & Hollander, 2002). A case report described symptomimprovement following the initiation of olanzapine at 10 mg/day in the treatmentof a woman with PG and schizophrenia (Grant, Kim, & Potenza, 2003).Further systematic investigation of the potential of atypical antipsychotics, particularlyin treating individuals with co-occurring psychotic disorders and PG,seems indicated.PsychotherapyMultiple behavioral treatments have been investigated (Petry & Roll, 2001).Cognitive therapy focuses on changing the patient’s beliefs regarding perceivedcontrol over randomly determined events. Case reports have demonstrated successwith cognitive therapy (Petry & Roll, 2001), and further support is derivedfrom two randomized trials. In the first, individual cognitive therapy resulted inreduced gambling frequency and increased perceived self-control over gamblingwhen compared with a wait-list control group (Sylvain, Ladouceur, & Boisvert,1997). A second trial that included relapse prevention also produced improvementin gambling symptoms compared to a wait-list group (Ladouceur et al.,2001).Cognitive-behavioral therapy has also been used to treat pathologicalgambling, including one published randomized trial (Echeburua, Baez, &Fernandez-Montalvo, 1996). In this study, four groups were compared: (1) individualstimulus control and in vivo exposure with response prevention, (2) group

13. Pathological Gambling and Other “Behavioral” Addictions 313cognitive restructuring, (3) a combination of 1 and 2, and (4) a wait-list control.At 12 months, rates of abstinence or minimal gambling were higher in the individualtreatment (69%) compared with group cognitive restructuring (38%) andthe combined treatment (38%). An independent controlled trial, based on cognitivebehavioral therapies used in the treatment of SUDs and including relapseprevention strategies, is currently underway, with initial results suggesting theefficacy of manually driven cognitive-behavioral therapy (Petry & Roll, 2001).Brief interventions in the form of workbooks have also been studied. Onestudy assigned gamblers to a workbook alone (which included cognitivebehavioraland motivational enhancement techniques) or to the workbook inaddition to one clinician interview (Dickerson, Hinchy, & England, 1990).Both groups reported significant reductions in gambling at a 6-month followup.Similarly, a separate study assigned gamblers to a workbook, a workbookplus a telephone motivational enhancement intervention, or a wait list.Compared to gamblers using the workbook alone, those assigned to the motivationalintervention and workbook reduced gambling throughout a 2-yearfollow-up period (Hodgins, Currie, & el-Guebaly, 2001).Two studies have also tested aversion therapy and imaginal desensitizationin randomized designs. In the first study, both treatments resulted in improvementin a small sample of patients (McConaghy, Armstrong, Blaszczynski, &Allcock, 1983). In the second study, 120 pathological gamblers were randomlyassigned to aversion therapy, imaginal desensitization, in vivo desensitization, orimaginal relaxation. Participants receiving imaginal desensitization reportedbetter outcomes at 1-month and up to 9 years later (McConaghy, Blaszczynski,& Frankova, 1991).KLEPTOMANIAKleptomania (stealing madness) was formally designated a psychiatric disorderin DSM-III, and the core features include (1) a recurrent failure to resist animpulse to steal unneeded objects; (2) an increasing sense of tension beforecommitting the theft; (3) an experience of pleasure, gratification or release atthe time of committing the theft; and (4) stealing that is not performed out ofanger, vengeance, or due to psychosis (American Psychiatric Association,2000).Clinical CharacteristicsKleptomania usually appears first during late adolescence or early adulthood(Goldman, 1991). The course is generally chronic, with waxing and waning ofsymptoms. Women are twice as likely as men to suffer from kleptomania (Grant& Kim, 2002a).

314 IV. SPECIAL POPULATIONSLike individuals with SUDs, most with kleptomania try unsuccessfully tostop. In one study, all participants reported increased urges to steal when tryingto stop (Grant & Kim, 2002a). The diminished ability to stop often leads tofeelings of shame and guilt, reported in most (77.3%) subjects (Grant & Kim,2002a). Of married subjects, less than half had disclosed their behavior to theirspouses due to shame and guilt (Grant & Kim, 2002a).Although people with kleptomania often steal various items from multipleplaces, the majority steal from stores. In one study, 68.2% of patients reportedthat the value of stolen items had increased over time (Grant & Kim, 2002a), afinding suggestive of tolerance. Patients may keep, hoard, discard, give as gifts,or return stolen items (McElroy et al., 1991). Many (64–87%) have been apprehendedat some time due to their behavior (McElroy et al., 1991), and 15–23%report having been jailed (Grant & Kim, 2002a). Although the majority of thepatients who were apprehended reported that their urges to steal were diminishedafter the apprehension, their symptom remission generally lasted only fora few days or weeks (McElroy et al., 1991). Together, these findings demonstratea continued engagement in the problematic behavior despite adverseconsequences, a core feature of addiction.Co-Occurring Disorders and Family HistoryHigh rates of other psychiatric disorders have been found in patients with kleptomania.Rates of lifetime comorbid affective disorders range from 59% (Grant& Kim, 2002a) to 100% (McElroy et al., 1991). The rate of comorbid bipolardisorder has been reported as ranging from 9% (Grant & Kim, 2002a) to 60%(McElroy et al., 1991). Studies have also found high lifetime rates of comorbidanxiety disorders (60–80%; McElroy et al., 1991, 1992), ICDs (20–46%; Grant,2003), SUDs (23–50%; Grant & Kim, 2002a; McElroy et al., 1991), and eatingdisorders (60%; McElroy et al., 1991).Individuals with kleptomania are more likely to have a first-degree relativewith a psychiatric disorder compared to nonaffected controls (Grant, 2003), Inaddition, high rates of mood (20–35%) and substance use disorders (15–20%)have been observed in first-degree relatives of patients with kleptomania(McElroy et al., 1991).TreatmentPharmacotherapyOnly case reports, two small case series, and one open-label study of pharmacotherapyhave been performed for kleptomania. Given the high placebo responserates observed in the treatment of ICDs, findings from these studies should beinterpreted cautiously. Various medications have been studied in case reports or

13. Pathological Gambling and Other “Behavioral” Addictions 315case series, and several have been found effective: fluoxetine, nortriptyline,trazodone, clonazepam, valproate, lithium, fluvoxamine, paroxetine, and topiramate(Grant & Kim, 2002b; McElroy et al., 1991).The only formal trial of medication for kleptomania involved 10 subjectsin a 12-week, open-label study of naltrexone. A mean dose of 145 mg/dayresulted in a significant decline in the intensity of urges to steal, stealingthoughts, and stealing behavior (Grant & Kim, 2002b).PsychotherapyAlthough multiple types of psychotherapies have been described in the treatmentof kleptomania, no controlled trials exist in the literature. Treatmentsdescribed in case reports as demonstrating success include psychoanalytic,insight-oriented, and behavioral therapies (Goldman, 1991; McElroy et al.,1991). Because no controlled trials of therapy for kleptomania have been published,the efficacies of these interventions are difficult to evaluate.COMPULSIVE BUYINGOriginally termed “oniomania” by Kraeplin and Bleuler, CB has been describedfor over 100 years (Christenson et al., 1994). Although not specifically recognizedin the DSM-IV-TR, the following CB diagnostic criteria have been proposed:(1) maladaptive preoccupation with or engagement in buying (evidencedby frequent preoccupation with or irresistible impulses to buy, frequentbuying of items that are not needed or not affordable, or shopping for longerperiods of time than intended); (2) preoccupations or the buying lead to significantdistress or impairment; and (3) the buying does not occur exclusively duringhypomanic or manic episodes (McElroy et al., 1994).Clinical CharacteristicsAs with other ICDs and SUDs, the onset of CB appears to occur during lateadolescence or early adulthood, although the full disorder may take severalyears to develop (Christenson et al., 1994). Unlike most SUDs, CB shows afemale preponderance, ranging from 80–92% in clinical samples (Christensonet al., 1994; McElroy et al., 1994; Schlosser, Black, Repertinger, & Freet, 1994).CB is characterized by repetitive urges to shop that are most often unprovokedbut may be triggered by being in stores. These urges may worsen duringtimes of stress, emotional difficulties, or boredom. Urges are generally intrusive,and most patients attempt to resist them, although usually unsuccessfully.Buying often results in large debts, marital or family disruption, and legal consequences(Christenson et al., 1994). Although the behavior is pleasurable and

316 IV. SPECIAL POPULATIONSmomentarily relieves the urges to shop, guilt, shame, and embarrassment generallyfollow buying episodes.A positive interaction with salespeople is often described as a motivatingfactor in CB. The items bought vary considerably, and can include clothing,jewelry, books, and auto parts. Most items are not used or removed from thepackaging, and many are given away, returned, or hoarded (Christenson et al.,1994).Co-Occurring Disorders and Family HistoryRates of co-occurring mood disorders range from 28 to 95% (Christenson et al.,1994; McElroy et al., 1994; Schlosser et al., 1994), with the mood disorderoften preceding the compulsive buying by at least 1 year (Christenson et al.,1994). Lifetime histories of anxiety (41–80%), substance use (30–46%), eating(17–35%%), and impulse control (21–40%) disorders are fairly common(Christenson et al., 1994; McElroy et al., 1994; Schlosser et al., 1994). In addition,patients with CB frequently report first-degree relatives with SUDs(25%), mood disorders (20%), or CB (10%) (Black, Repertinger, Gaffney, &Gabel, 1998).TreatmentPharmacotherapyThe effectiveness of pharmacotherapies in treating CB is beginning to be systematicallyinvestigated (see Table 13.2). Case reports and open-label studieshave suggested that the following agents may be beneficial: nortriptyline,fluoxetine, buproprion, lithium, clomipramine, naltrexone, fluvoxamine, citalopram,and valproate (Black, Monahan, & Gabel, 1997; Koran, Bullock,Hartston, Elliott, & D’Andrea, 2002; McElroy et al., 1994).In the first of two double-blind fluvoxamine studies, 37 subjects weretreated for 13 weeks. Only 9 of 20 patients assigned to medication wereresponders (mean dose of 215 mg/day), and this rate did not differ significantlyfrom that in the placebo group (8 of 17 were responders) (Ninan et al., 2000).In the second double-blind study, Black, Gabel, Hansen, and Schlosser (2000)treated 23 patients for 9 weeks, following a 1-week placebo lead-in phase. Usinga mean dose of 200 mg/day, no differences in response rates were observedbetween the groups treated with active and placebo drug.A double-blind study using citalopram, however, suggests the efficacy ofselective SRIs in treating CB. Seven weeks of open-label treatment was followedby randomization of responders to medication or placebo for another 9weeks. Patients taking active citalopram demonstrated statistically significantdecreases in terms of the frequency of shopping, as well as the intensity of

13. Pathological Gambling and Other “Behavioral” Addictions 317thoughts and urges concerning shopping (Koran, Chuong, Bullock, & Smith,2003).PsychotherapyThere are no formal studies of psychotherapy for CB. Several case reports suggestthat possible effective psychotherapeutic interventions might includeexposure and response prevention, and supportive or insight-oriented psychotherapy(McElroy et al., 1994).CONCLUSIONSBehavioral addictions, such as the ICDs, have historically received relativelylittle attention from clinicians and researchers. As such, our understanding ofthe basic features of these disorders is relatively primitive. Future researchinvestigating ICDs and their relationship to SUDs holds significant promise inadvancing prevention and treatment strategies for addiction in general.REFERENCESAmerican Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders(4th ed., text rev.). Washington, DC: Author.Bechara, A. (2003). Risky business: emotion, decision-making, and addiction. J GamblStud, 19, 23–51.Black, D. W., Gabel, J., Hansen, J., & Schlosser, S. (2000). A double-blind comparisonof fluvoxamine versus placebo in the treatment of compulsive buying disorder.Ann Clin Psychiatry, 12, 205–211.Black, D. W., Monahan, P., & Gabel, J. (1997). Fluvoxamine in the treatment of compulsivebuying. J Clin Psychiatry, 58, 159–163.Black, D. W., & Moyer, T. M. (1998). Clinical features and psychiatric comorbidity ofsubjects with pathological gambling behavior. Psychiatr Serv, 49, 1434–1439.Black, D. W., Repertinger, S., Gaffney, G. R., & Gabel, J. (1998). Family history andpsychiatric comorbidity in persons with compulsive buying: Preliminary findings.Am J Psychiatry, 155, 960–963.Blanco, C., Moreyra, P., Nunes, E. V., Saiz-Ruiz, J., & Ibanez, A. (2001). Pathologicalgambling: Addiction or compulsion? Semin Clin Neuropsychiatry, 6, 167–176.Blanco, C., Petkova, E., Ibanez, A., & Saiz-Ruiz, J. (2002). A pilot placebo-controlledstudy of fluvoxamine for pathological gambling. Ann Clin Psychiatry, 14, 9–15.Blum, K., Braverman, E. R., Holder, J. M., Lubar, J. F., Monastra, V. J., Miller, D., et al.(2000). Reward deficiency syndrome: A biogenetic model for the diagnosis andtreatment of impulsive, addictive, and compulsive behaviors. J Psychoactive Drugs,32(Suppl 1), 1–68.

318 IV. SPECIAL POPULATIONSChambers, R. A., & Potenza, M. N. (2003). Neurodevelopment, impulsivity, and adolescentgambling. J Gambl Stud, 19, 53–84.Christenson, G. A., Faber, R. J., de Zwaan, M., Raymond, N. C., Specker, S. M., Ekern,M. D., et al. (1994). Compulsive buying: Descriptive characteristics and psychiatriccomorbidity. J Clin Psychiatry, 55, 5–11.Crockford, D. N., & el-Guebaly, N. (1998). Psychiatric comorbidity in pathologicalgambling: A critical review. Can J Psychiatry, 43, 43–50.Cunningham-Williams, R. M., Cottler, L. B., Compton W. M. III, & Spitznagel, E. L.(1998). Taking chances: Problem gamblers and mental health disorders—resultsfrom the St. Louis Epidemiologic Catchment Area study. Am J Public Health, 88,1093–1096.Dickerson, M., Hinchy, J., & England, L. S. (1990). Minimal treatments and problemgamblers: A preliminary investigation. J Gambl Stud, 6, 87–102.Echeburua, E., Baez, C., & Fernandez-Montalvo, J. (1996). Comparative effectivenessof three therapeutic modalities in psychological treatment of pathological gambling:Long term outcome. Behav and Cogn Psychother, 24, 51–72.Goldman, M. J. (1991). Kleptomania: Making sense of the nonsensical. Am J Psychiatry,148, 986–996.Grant, J. E. (2003). Family history and psychiatric comorbidity in persons with kleptomania.Compr Psychiatry, 44, 437–441.Grant, J. E., & Kim, S. W. (2001). Demographic and clinical features of 131 adultpathological gamblers. J Clin Psychiatry, 62, 957–962.Grant, J. E., & Kim, S. W. (2002a). Clinical characteristics and associated psychopathologyof 22 patients with kleptomania. Compr Psychiatry, 43, 378–384.Grant, J. E., & Kim, S. W. (2002b). Kleptomania: Emerging therapies target mood,impulsive behavior. Curr Psychiatry, 1, 45–49.Grant, J. E., Kim, S. W., & Potenza, M. N. (2003). Advances in the pharmacologicaltreatment of pathological gambling. J Gambl Stud, 19, 85–109.Grant, J. E., Kim, S. W., Potenza, M. N., Blanco, C., Ibanez, A., Stevens, L. C., et al.(2003). Paroxetine treatment of pathological gambling: A multi-center randomizedcontrolled trial. Int Clin Psychopharmacol, 18, 243–249.Grant, J. E., Kushner, M. G., & Kim, S. W. (2002). Pathological gambling and alcoholuse disorder. Alcohol Res Health, 26, 143–150.Grant, J. E., Potenza, M. N., Levine, L., & Kim, D. (in press). Prevalence of impulsecontrol disorders in adult psychiatric inpatients. Am J Psychiatry.Hodgins, D. C., Currie, S. R., & el-Guebaly, N. (2001). Motivational enhancement andself-help treatments for problem gambling. J Consult Clin Psychol, 69, 50–57.Hollander, E., DeCaria, C. M., Finkell, J. N., Begaz, T., Wong, C. M., & Cartwright, C.(2000). A randomized double-blind fluvoxamine/placebo crossover trial in pathologicalgambling. Biol Psychiatry, 47, 813–817.Hollander, E., Pallanti, S., & Baldini-Rossi, N. (2005). Does sustained-release lithiumreduce impulsive gambling and affective instability versus placebo in pathologicalgamblers with bipolar spectrum disorders? Am J Psychiatry, 162, 137–145.Kim, S. W., & Grant, J. E. (2001). Personality dimensions in pathological gambling disorderand obsessive–compulsive disorder. Psychiatry Res, 104, 205–212.Kim, S. W., Grant, J. E., Adson, D. E., & Shin, Y. C. (2001). Double-blind naltrexone

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Substance Abusein Minority PopulationsCHAPTER 14JOHN FRANKLINMARYLINN MARKARIANThis chapter highlights issues in the treatment of addictive disorders in AfricanAmericans, Hispanic Americans, Asian Americans, and Native Americans.Cultural competency of caregivers in treatment programs is vital but is oftenlacking (Westermeyer, 1995). Substantial knowledge gaps still exist in minoritysubstance abuse, and continued research in this area is needed. The growingethnic diversity of the United States makes the significance of these issues evengreater. According to the 2000 census, African Americans make up 12.2% ofthe population, Hispanics 11.8%, Asian Americans/Pacific Islanders 3.9%,Native Americans 0.7%, and whites 71.4% (U.S. Bureau of the Census, 2002).The fastest growing ethnic groups are Hispanics and Asian Americans. It is estimatedby the year 2060, the U.S. non-Hispanic white population will be aminority. This chapter reviews selected data on addictive disorders in minoritypopulations.Divisions along ethnic lines can be complicated by variations in country oforigin, religious and spiritual orientation, and political and economic conditions.These differences may influence the clinical presentation and therapeuticneeds of the patient. Other variables include socioeconomic status, educationallevel, occupational stability, dwelling situation, marital status, family of origin,and age.Thus, a middle-class African American woman with a college degree andstable employment, dwelling in a reasonably safe neighborhood, may share adaily world outlook toward the future more similar to that of a European Amer-321

322 IV. SPECIAL POPULATIONSican woman of a similar background than to a single, unemployed AfricanAmerican mother dwelling in an inner city. Their experiences within ethnicgroups can be vastly different. There are scant data about differences in biologicalvulnerability for substance abuse between ethnic groups (Berrettini &Persico, 1996; Chan, McBride, Thomasson, Ykenny, & Crabb, 1994; Goldmanet al., 1993), but new, yet unconfirmed biological findings are presented later inthis chapter. This chapter highlights socioeconomic issues in substance abusetreatment for minorities.Ethnic differences among women have received attention in the literature.In terms of alcohol, African American families produce more abstainers thando European and Hispanic American families. African American women mayexpress more conservative drinking norms (Herd, 1997). African Americanwomen have rates of heavy drinking comparable to European American rates;however, they report fewer social and personal problems related to drinking.African American women may be more insulated from alcohol-related socialproblems by their families, communities, and churches. A larger proportion ofAfrican American women, however, experience alcohol-related health problemsthan do European American cohorts (Herd, 1989). One study of AfricanAmerican and Native American pregnant women shows African Americanwomen using higher quantities of malt liquor (higher alcohol content) (Graves& Kaskutas, 2001). African American women exhibit higher rates of fetal alcoholsyndrome. These findings may be attributed to issues such as nutrition andaccess to health care. Concurrent illicit drug use may also be a contributing factor.In 1998, the percentage of African American women using illicit drugs duringthe preceding month, compared to European American cohorts, was 8.1versus 7.6% in whites (Substance Abuse and Mental Health Services Administration,2000). There are higher rates of cocaine use in African American andHispanic women compared to Asian or Hispanic women.Hispanic American women are more likely than European Americanwomen to abstain, though there is a one-sided convergence with increasingacculturation. For example, in one study, 75% of Mexican immigrant womenabstained from alcohol, whereas 38% of third-generation Mexican Americanwomen were abstainers (Gilbert, 1991). Younger American-born Hispanicwomen are more likely to report moderate to heavy drinking than their immigrantcohorts. Mexican American women who use substances suffer significantlyhigher lifetime rates of physical and sexual assault (Lown & Vega, 2001).A substantially higher percentage of Native American/Alaskan Native womendrink compared to whites, blacks, or Hispanics.African American women in treatment often have myriad needs: employment,child care, and treatment for victimization and psychiatric symptoms.Personal losses, such as death of loved ones, separation, and loss of child custody,have a profound impact on drug use in African American women (Roberts,1999). Women in substance abuse treatment are oversampled in terms of

14. Substance Abuse in Minority Populations 323sexual abuse. In a study of 1,272 randomly selected women in a jail predominantfor women of color, 8% had a comorbidity of severe mental disorder andsubstance abuse (Abram, Teplin, & McClelland, 2003). Life stress has beenfound to be a strong correlate of crack cocaine use in African American women(Boyd, Hill, Holmes, & Purnell, 1998), as is gang affiliation in women (Harper& Robinson, 1999). Child care has traditionally been a major obstacle to substanceabuse treatment, but especially for minorities, although this is notunique to ethnic minorities. Financial restriction is a fundamental barrier totreatment for women, with added hardship for more women belonging to ethnic/minoritygroups.Supportive networks are important to substance abuse recovery, irrespectiveof child care needs. A strong focus on the development of supports is indicatedin the treatment of addicted women. Isolation among addicted womenoccurs for multiple reasons, including feelings of shame, guilt, and depression,and minority women may experience a double stigma. Creative social networksshould be a strong focus of recovery for addicted minority women. It may benecessary to utilize extended family, as well as supports outside the family whoserve as positive maternal figures. Respect for family systems is especially importantin treating Hispanic women (Ruiz, Langrod, & Alksne, 1981).AFRICAN AMERICANSHeavy alcohol use by white men peaks in the 20s, then declines. Based on 1-month prevalence data, African American teens ages 12–17, compared towhite teens of similar age, drink heavily less often, 0.7% versus 3.4%. However,by the age of 26, heavy use of alcohol is similar, 7.8% in blacks versus 7.1% inwhites. Heavy use among black men is relatively low in the early years, peaks inmiddle age, then declines (Herd, 1990). One hypothesis of the etiology is thatissues of racism and limited opportunities become more evident as AfricanAmericans mature into adulthood. The factors involved in the later onset ofheavy alcohol use in African Americans and the subsequent rise in alcohol useneed further research.Diagnostic screening instruments for substance abuse in African Americanshave been shown to be valid (Duncan, Duncan, & Strycker, 2002). In alarge inpatient sample, African Americans were found to have later onset of usebut earlier onset of alcohol-related problems (Hesselbrock, Hesselbrock, Segal,Schuckit, & Bucholz, 2003). In addition, the prevalence of alcohol-relatedproblems in black men showed significant differences in psychosocial distresscompared to that of white men (Herd, 1994). The greatest differences betweenthe groups were found in scores for loss of control, symptomatic drinking, bingedrinking, health problems, and problems with friends and relatives. Blacks andwhites had similar drinking patterns, as measured by frequency and maximum

324 IV. SPECIAL POPULATIONSamounts consumed. Black men were significantly less permissive in attitudestoward alcohol use in particular situations, such as driving a car or spendingtime with small children in a parental role. Further analyses showed that thehigher rates of alcohol-related problems were not fully accounted for by socialand demographic differences between black and white men.An earlier study by Herd (1990), reporting on data from a 1984 nationalsurvey, showed similar findings of greater alcohol-related problems among blackmen than among white men in the past year. The exception was drunk driving,in which white men scored higher. Black men scored higher on symptoms ofphysical dependence and health problems. Here, the rates of frequent heavydrinking were lower, not higher, for black men. Limited financial resources andaccess to health care likely also contributed to the higher prevalence ofalcohol-related health problems in black men. African Americans may be athigher risk for hepatic damage and cirrhosis from drinking (Singh & Hoyert,2000; Stewart, 2002). Herd (1994) suggested that this finding may represent alonger duration of heavy use, as opposed to more discrete phases of heavy alcoholuse seen in some white men. The body, it is hypothesized, is less resilient toalcohol toxicity at older ages.Jones-Webb, Hsiao, and Hannan (1995) found that lower socioeconomicclass seems to have a more profound influence on alcohol-related problems forblack men than for white men, as did other researchers (Barr, Farrell, Barnes, &Welte, 1993; Herd, 1994; Jones, 1989). Black men of lower socioeconomic statusmay experience more overt forms of discrimination and may be more likelyto reside in communities in which there is more police surveillance. Groupnorms may be predictive of problematic alcohol use in African Americans(Jones-Webb, Snowden, Herd, Short, & Hannan, 1997). Greater ethnic identitymay be protective against problematic drinking (Herd & Grube, 1996).Lower neighborhood cohesion has been associated with adolescent drug andalcohol problems.Polymorphism of the ADH2*3 alcohol dehydrogenase metabolic enzymemay play a role in alcohol expectations in African Americans (Ehlers, Carr,Betancourt, & Montane-Jaime, 2003). Lower P3 amplitudes during eventrelatedpotentials have also been reported in alcoholic African Americans(Ehlers et al., 2003). The association of alcohol use and hypertension may beparticularly problematic in African American men (Russell, Cooper, Frone, &Peirce, 1999). The association between hypertension and illicit drug use hasalso been reported (Kim, Dennison, Hill, Bone, & Levine, 2000). Ziedonis,Rayford, Bryant, and Rounsaville (1994) have reported on differential rates oflifetime psychiatric comorbidity in black and white cocaine addicts, withwhites having significantly higher rates of lifetime depression, alcohol dependence,and attention deficit and conduct disorder. African Americans oftenexhibit significant general coping skills but fewer treatment resources comparedto whites (Conigliaro et al., 2000; Walton, Blow, & Booth, 2001). There is

14. Substance Abuse in Minority Populations 325some evidence that substance abuse in whites may be associated with greaterunderlying psychopathology, whereas African Americans may have greatersocial and environmental factors (Roberts, 1999). Early initiation of sexualactivity may be predictive of later substance abuse in African Americans(Stanton et al., 2002).Historically, a greater proportion of African Americans abstain from illicitdrug use than do whites. This difference is especially pronounced in the 12–25 agegroups. However, public databases such as the Client Data Acquisition Processand Drug Abuse Warning Network (DAWN) suggest that African Americansand Hispanics are overrepresented in categories of heroin and cocaine use. Sincethe 1980s, we have seen up-and-down patterns of perceived harm among highschool students. However, data still show a higher overall prevalence of illicitdrug use in blacks: 8.2% in blacks versus 6.1% in whites (Substance Abuse andMental Health Services Administration, 2000). Higher rates of marijuana andcocaine use account for the difference. In the 1998 National Household Surveyon Drug Abuse (NHSDA), African Americans had higher prevalence of marijuana(5 vs. 6.6%) and cocaine (0.7 vs. 1.3%) (Substance Abuse and MentalHealth Services Administration, 2000). The gap between white and black adolescents’marijuana use has disappeared. African Americans have higher rates ofmarijuana use by age 20 (Brown, Flory, Lynam, Leukefeld, & Clayton, 2004;Reardon & Buka, 2002). Also emerging from epidemiology studies is a somewhathigher concentration of heroin use among blacks as compared to whites. TheNHSDA (Substance Abuse and Mental Health Services Administration, 2000)shows that past-month use of any illicit drug is higher for whites between the agesof 12 and 25, and higher for African Americans age 26 and up. Asian/PacificIslanders show the lowest rates of past-month use across all age groups.As with alcohol, illicit drug use appears to take a greater toll on AfricanAmericans’ health, as measured by emergency department data. African Americansare overrepresented, as a percentage of the population, in emergencyroom (ER) visits. Whites represent 57.5% of ER visits compared to 21.4% byAfrican Americans (DAWN, 2004; National Institute on Drug Abuse, 2003).Although DAWN data are derived from large cities where African Americanpopulations are proportionally high, this is still an overrepresentation of ER visitsfor drug abuse. African Americans are more likely than whites to be treatedand released rather than hospitalized. The 1998 NHSDA showed cocaine is theprimary drug leading to the ER visits for African Americans. African Americansare also overrepresented in medical examiners’ morbidity data. Theyaccount for 30% of drug-related deaths, while making up 23% of the populationof the cities surveyed in DAWN. Cocaine is the most frequent cause of death,56.7%, followed by heroin and morphine. Much of the information about hardcore drug use comes from similar data derived from public facilities. These datamay seriously underestimate the number of persons who obtain alternativetreatment for medical and psychosocial problems.

326 IV. SPECIAL POPULATIONSLiterature reviewed by Brown, Alterman, Rutherford, Cacciola, and Zaballero(1993) suggest that correlates of heroin abuse may be educational impairment,poor employment history, history of legal problems, including incarceration,and possibly psychiatric problems. A national sample of by Kandel and Davies(1991) showed that early sexual intercourse was associated with elevated lifetimecocaine use among all ethnic groups; and that a correlate to cocaine usewas daily marijuana use (defined by use at least 20 times in the last 30 days).Low rates of condom use among cocaine, marijuana, and alcohol abusersmay be contributing to an HIV epidemic among African Americans (Kingree& Betz, 2003; Timpson, Williams, Bowen, & Keel, 2003). Cocaine use, in particular,may contribute to intracerebral bleeding, renal failure, chest pain, andmyocardial infarctions in African Americans (Oureshi et al., 2001). In addition,the severity of asthma exacerbation seems to be worse in African Americanurban settings (Rome, Lippmann, Dalsey, Taggart, & Pomerantz, 2000).Several groups are also studying strategies to decrease cigarette smoking in AfricanAmericans (Ahluwalia, Harris, Catley, Okuyemi, & Mayo, 2002; Benowitz,2002; Okuyemi, Ahluwalia, Richter, Mayo, & Resnicow, 2001).A coarse reading of this literature might imply that some intrinsic naturewithin the ethnic groups accounts for the differences. Lillie-Blanton, Anthony,and Schuster (1993) conducted a study in which they regrouped participantsaccording to neighborhood rather than race or ethnicity. They held constantsocial and environmental risk factors that likely influence the racial comparisonsand applied this design to the apparent differences in crack cocaine useamong whites, Hispanics, and African Americans. This interesting analysisrevealed that the odds ratios did not vary significantly among the ethnic groups.Being African American did not place individuals at higher risk for crack use.Though this analysis does not refute the epidemiological findings of the study,it does suggest that the apparent differences may be more a product of socialconditions, including availability of drugs, than are issues intrinsic to ethnicity.Drug trafficking, often concentrated in minority neighborhoods, is a risk factorfor use (Li, Feigelman, Stanton, Galbraith, & Huang, 1998).Among African American and European Americans, there may be differentmu receptor polymorphisms (Crowley et al., 2003). However, strong evidencehas yet established that these gene findings are associated with actualdrug use (Kranzler, Gelernter, O’Malley, Hernandez-Avila, & Kaufman, 1998).One report found no association between particular dopamine receptor allelesand cocaine dependence in African Americans (Gelernter, Kranzler, & Satel,1999). Negative findings have also been reported for the association betweenserotonin transporter polymorphisms and aggression in African Americancocaine dependence (Patkar et al., 2002).It is well-known that as a result of the “war on drugs” and other pressures,African Americans arrested for drug-related charges are overrepresented in pris-

14. Substance Abuse in Minority Populations 327ons and jails. Inequalities in sentencing factors may indicate subtle racism. Forexample, the differential sentencing for crack cocaine use, which is more prevalentin black communities, and powder cocaine has been a matter of nationaldebate.Access to treatment is still a problem for African Americans (Zule, Lam, &Wechsberg, 2003). Some argue that prevention and treatment of substanceabuse and HIV in African American communities must recognize and addressinstitutional racism, sociopolitical exploitation, patterns drug of distribution,limited employment opportunities, and historical African American copingstrategies (Adimora et al., 2001; Agar & Reisinger, 2002; Bowser & Bilal,2001). Increasing gainful employment is a particularly powerful intervention(Petry, 2003). Poverty in black neighborhoods compared to white neighborhoodsmay have a greater impact on alcohol-related problems. Many in theAfrican American community stress the issues of self-help and communityempowerment to combat divisive elements leading to drug and alcohol use. Asa result, network therapy may have a particular role in more distressed communities.In a large Veterans Administration residential study, African Americanshad similar rates of program participation to whites but tended to do better inaftercare programs with greater African American staff presence (Rosenheck &Seibyl, 1998). Another study, using data from the National CollaborativeStudy, found that social and peer relationship problems predicted 18.8% of thevariance for future substance use in an urban adolescent population (Friedman& Glassman, 2002). School dropout rates have been associated with injectiondrug use in African Americans; dropout rates should be targeted for intervention(Obot & Anthony, 2000; Obot, Hubbard, & Anthony, 1999).Problackness and awareness of racial oppression have been associated withnegative substance use attitudes (Gary & Berry, 1985). Strong ethnic identitymay protect against substance abuse and should be incorporated in treatmentprograms, especially for adolescents (Brook, Balka, Brook, Win, & Gursen,1998, Longshore, 1999). However, one study reported high levels of culturalidentity to be positively associated with heavy drug use (James, Kim, & Armijo,2000). Culturally sensitive interventions have been shown to enhance gettingpeople into treatment and improving outcomes (Dushay, Singer, Weeks,Rohena, & Gruber, 2001; Longshore, Grills, & Annon, 1999). There is noquestion that standard treatment approaches highlighted in the rest of thisbook can readily be applied to all ethnic groups. Standard cognitive-behavioraltreatments have been shown to be as effective for African Americans as forwhites (Milligan, Nich, & Carroll, 2004).Misdiagnosis of psychiatric comorbidities in African Americans can limittreatment effectiveness (Baker & Bell, 1999). There is an association betweensubstance abuse and suicide in black men but it may be less robust than that inwhite men (Garlow, 2002; Kaslow et al., 2000). The core features of loss of con-

328 IV. SPECIAL POPULATIONStrol and compulsivity that make a drug abuser or alcoholic are not dissimilarbetween ethnic groups. However, as we continue to tailor treatment to individuals,racial and cultural factors have to be addressed.Should programs in primarily African American communities be especiallydesigned to promote cultural sensitivity? In some sense this goes on naturally.The feel, look, and language of an Alcohol Anonymous (AA) meeting in anAfrican American community is different from that in a white self-help group.AA had its beginnings in the Oxford movement and was initially white andmiddle class. However, given that the church and spiritual dimensions of blacklife are an integral aspect of black culture, it is not surprising that AA has beensuccessfully transplanted to the black community. There have been attempts todevelop and describe culturally sensitive mental health facilities (Deitch &Solit, 1993; Rowe & Grills, 1993). These attempts often are trapped in a quagmireof definitions of culture, race, and what is crucial to a culturally relevantprogram. Culturally relevant programs might promote positive racial and culturalidentity, enhance self-esteem, increase self-determination, and appreciatetraditional African American values. Afrocentric values stress relationships,verbal fluidity, emotional expressiveness, and spirituality. A study of substanceabuse programs, using the National Drug Abuse Treatment System Survey, suggeststhat culturally competent treatment is holistic and emphasizes employment,spiritual strength, and physical health (Howard, 2003a). Programs thathire staff that mirror patients’ ethnic background may minimize racial bias. Inaddition, possessing knowledge of African American history and culture is acomponent of a culturally competent program (Howard, 2003b).Research questions related to primary hypotheses that especially addressethnic concerns are needed. There may be dimensions to an all-black treatmentprogram that go beyond variables currently thought to be important. Ethnicbiological differences, if any exist, of African Americans need further work. Differencesin health outcome and possibly medication responses need furtherconsideration. The issue of matching or nonmatching of therapist or patientalong racial and ethnic dimensions has been a subject of considerable discussionin mental health and has a role in the substance abuse field. Matching ofracial and cultural attributes between therapist and client may enhance empathyor in some cases result in therapist overidentification with the client.Empathy and respect of others’ cultural norms are an essential components toany discussion of cultural sensitivity.HISPANIC AMERICANSHispanics comprise a heterogeneous group, including Mexican Americans,Puerto Ricans, Cuban Americans, and others. As with other ethnic groups, agreater number of Hispanic men drink alcohol and use drugs than do Hispanic

14. Substance Abuse in Minority Populations 329women. Mexican American men are more likely to abstain than other Hispanicmen. However, they drink more heavily and report more alcohol-related problems.Puerto Rican men have the highest prevalence of illicit drug use, 10%versus 5% of Mexican Americans (Substance Abuse and Mental Health ServicesAdministration, 2000). White Hispanic men have high rates of cirrhosis,especially among Mexican Americans (Stinson, Grant, & Dufour, 2001). Selfreportedrates of drinking and driving are highest in Hispanics and whites(Caetano & Clark, 2000). In New York City, cocaine- and opiate-positiveurine analysis in victims of firearms deaths are highest in Latino men (Galea etal., 2003). Also, Latinos and African Americans have higher rate of overdosedeaths. Cuban men had fewer abstainers, a smaller proportion of heavy drinkers,and fewer alcohol-related problems. Drinking increases with education andincome for both sexes (Caetano, 1989).According to the 1995 NHSDA, for all age groups except 12–17 years,Hispanics had the fewest members in the “ever used any illicit drug” category ascompared to whites and African Americans. Data derived from the NHSDA(1996–1997) reported that Hispanics are more likely to binge drink and usedrugs more heavily. Caetano and Medina-Mora (1990) compared the drinkingpatterns of Mexican Americans and Mexicans living in Mexico. A more permissiveattitude about alcohol use was associated with acculturation. Alcoholuse increased with acculturation in both Mexican men and woman. However,Mexican Americans reported fewer alcohol-related problems than did Mexicanmen living in Mexico. For Mexican women born in the United States, abstentionrates steadily decreased and rates of infrequent drinking steadily increasedwith acculturation. This pattern is not seen in Mexican-born women living inthe United States (Caetano & Medina-Mora, 1990). Similarly, in SouthFlorida, U.S.-born Hispanic young adults have increased rates of substanceabuse and mental health problems compared to Hispanic immigrants. Inhalantuse is reported to be high among Hispanic youth in southwestern border states.Polymorphism of the alcohol dehydrogenase 2 gene and P450 2E1 has beenreported to contribute to development of alcoholism in Mexican Americanmen (Konishi et al., 2003).Among people of need, Hispanics and African Americans compared towhites have greater unmet need for alcohol and drug abuse treatment. Hispanicsreceive active treatment 22.4% of the time, and African American 25% ofthe time, versus whites at 37% (Wells, Klap, Koike, & Sherbourne, 2001). Languagecan be the most concrete barrier to adequate treatment for Hispanics incommunities without adequate Spanish-speaking facilities. However, culturalsensitivity is not guaranteed by just speaking the language. In the state of Massachusetts,Latinos are one-third less likely to enter residential treatment(Lundgren, Amodeo, Ferguson, & Davis, 2001). For example, Spanish-speakingmale staff must be able to treat female clients with respect and be sensitive tosexual, family, and child-rearing issues. A number of authors (e.g., Szapocznik

330 IV. SPECIAL POPULATIONS& Fein, 1995) identify family issues as being perhaps the most important componentof addiction treatment of the Hispanic client.Gfroerer and De La Rosa (1993) found that parents’ attitudes and use ofdrugs, licit or illicit, played an important role in the drug use behavior of 12- to17-year-old Hispanic youth. Parents need to be informed clearly and honestlyabout their influence. Also, the role of family should be well understood bytreatment staff. Each family member has a function within the family. If properlyeducated, the family members can each provide support, using their alreadyestablished role. Some of the traditional roles, according to Ruiz and colleagues(1981), are the elderly, esteemed for their wisdom, the father for his authority,the mother for her devotion, and the children for their future promise. Denialof alcoholism may be extensive in Hispanic fathers who drink only on theweekend and fulfill work obligations. Szapocznik and Fein (1995) included thecultural tradition of interdependence with extended family made up of uncles,aunts, cousins, and lifelong friends. Basically, the functional family does includeany person who has day-to-day contact with and a role in the family. The familyis an important resource and must be integrated into the treatment.ASIAN AMERICANSPeople of Asian heritage make up nearly 3.9% of the U.S. population accordingto U.S. Bureau of the Census (2002): Chinese Americans (the largest group,24%), Filipinos (20%), Asian Indians (12%), Koreans (12%), Japanese (12%),and Vietnamese (9%). Other countries of Asian immigration include Mongolia,Pakistan, Nepal, Bangladesh, Burma, Thailand, Cambodia, Malaysia,Singapore, and others. Many languages, cultures, and political systems arerepresented. Most of the world’s major religions are represented, includingBuddhism, Hinduism, Judaism, Christianity, and Islam. These religions havevarying views regarding alcohol use. Alcohol use is prohibited in the Moslemteachings. Hinduism and Buddhism suggest avoidance of alcohol and othermind-altering substances. The Judeo-Christian perspective is more lenient andincorporates alcohol use into some religious ceremonies. These views affect theway the society, the family, and the problem drinker deal with the concept andacceptance of alcoholism. Acceptance and availability of treatment for individualsalso have an impact.The well-described “flushing” reaction seen in some Asian people has beenlinked to variations of aldehyde dehydrogenase isoenzymes. The reaction occursbecause of a limited ability to degrade acetaldehyde to acetic acid. The toxicacetaldehyde is responsible for the flushing, headache, nausea, and other symptomsof alcohol use estimated to occur in 47–85% of Asians (National Instituteon Alcohol and Alcoholism, 2000). This was thought to explain the lower ratesof alcohol abuse among Asians. However, studies have shown that sociocultural

14. Substance Abuse in Minority Populations 331factors play a substantial role in alcohol use (Johnson & Nagoski, 1990;Newlin, 1989).Some major databases on alcoholism in ethnic minority populations donot include information on Asian Americans. The Epidemiologic CatchmentArea (ECA) study placed Asian Americans in the “other” category. Twonational studies do survey Asians as a specific category: DAWN and theNHSDA (Substance Abuse and Mental Health Administration, 2000). Thepercentage of past-month use among Asians/Pacific Islanders is 2.8%, the lowestamong the major ethnic groups. The 1-month prevalence for Native Hawaiiansand other Pacific Islanders is 6.2%, versus 2.7% for Asians. However, theKorean subgroup of Asians has a 6.9% prevalence rate, similar to that of AfricanAmericans. The available research literature is mostly community based orpertains to a specific subgroup within the Asian American community, such asstudents. Given these limitations, a number of studies show that there is significantvariation in drinking patterns among the different Asian groups. There issome evidence that rates of heavy drinking are higher for Filipino Americans(29%) and Japanese Americans (28.9%), followed by Korean Americans(25.8%) and Chinese Americans (14.2%) (Kitano & Chi, 1989). The breakdownby sex found heavy drinking in 11.7% of Japanese women, 3.5% of Filipinowomen, and 0.8% of Korean women, whereas Chinese women registerednear zero. In a large inpatient sample, Alaskan Native men and women had earlieronsets of alcohol dependence (Hesselbrock et al., 2003). Interestingly,there is a Japanese AA-like organization called the All Nippon Sobriety Association(Gomberg, 2003).Potential treatment problems in the Asian American community beginwith the lack of acceptance of alcoholism and drug addictions as treatable illnesses.Ja and Aoki (1993) write about the typical chain of events in the life ofan intact Asian family when substance abuse begins to appear. Often, substanceabuse problems are ignored or denied, with the hope that they will disappear.Also, the family will make efforts to conceal it from the community to avoidembarrassment and shame. Prevention or early treatment is unlikely in thisfamily and community dynamic. When denial is overwhelming, the familybreaks down and may resort to shaming and other attempts at punishment. Thefamily may also turn to extended family members and elders, basically movinggradually outward from nuclear family to external community. There is a deepsense of failure on the part of the family by the time members resort to outsideprofessional help. It is not uncommon at this point to have family memberscompletely turn over the alcoholic or addict and resist participation themselves.The client is often still in denial and resistant to treatment, until an alliancewith staff is facilitated.Treatment barriers begin with ignorance of the actual extent of drug andalcohol problems in the Asian American community. Asians are thought of bymany as model immigrants. The 1960s brought a large wave of educated, skilled

332 IV. SPECIAL POPULATIONSAsian professionals. Migration since the 1970s has resulted in people with lesseducation, and fewer language and work skills immigrating to the United States(Varma & Siris, 1996). Many of them entered as refugees from war-ravagedcountries. Poverty, overcrowded domiciles, discrimination, and other socialproblems are present in the lives of Asian Americans; however, documentationof these problems is sparse. This notion of “model” immigrant may be hurtingthe Asian American community from outside and within. It also lends itself tothe denial within the community and amplifies the elements of shame andembarrassment felt by the family.Better documentation of the extent of drug and alcohol abuse in the AsianAmerican population would, ideally, enhance the funding for culturally sensitiveeducation and treatment. Education at the community level is needed tofoster awareness and acceptance, and assist in prevention. Treatment programsthat target Asian Americans might consider the insular and private style of theAsian American family. Also essential is recognition of the dominance of thefamily and community over the psychological and social needs of the individual.Acceptance of these differences would decrease conflict between the familiesand treatment providers. This show of respect for their values might facilitatethe families’ participation in the treatment. A treatment goal for allindividuals should be reintegration back into their family and community, if atall possible.NATIVE AMERICANSMore than 200 Native American tribes have a differential use of illicit substances.Studies show that Native American/Alaskan Native youth have twicethe prevalence of cigarette, alcohol, marijuana, and cocaine use as that of Hispanics,blacks, or whites. Alcohol abuse is recognized as a significant problemamong Native Americans (Shalala, Trujillo, Nolan, & D’Angelo, 1996). TheCAGE questionnaire, however, has not been particularly useful among NativeAmericans (Saremi et al., 2001). Conduct disorder has been found to be a significantrisk factor for alcohol dependence in Navajo Indians (Kunitz et al.,1999). In the past, arrest rates secondary to alcohol use for Native Americanswere reported to be 12 times the national average (Stewart, 1964). In a MichiganMonitoring the Future study, Native American adolescents had the highestlevels of tobacco, alcohol, and illicit drug use (Wallace et al., 2002). NativeAmerican/Alaskan Native youth may also participate in more risky behaviors(Frank & Lester, 2002). Although the alcohol mortality rate for Native Americanswas three to four times the national average, evidence indicates that therehas been a decrease in mortality since 1969 (Burns, 1995). This drop seems tobe in concert with the doubling of alcohol treatment services by the Indian

14. Substance Abuse in Minority Populations 333Health Service in the 1980s. Primary case settings may be important for detectingsubstance use (Shore, Manson, & Buchwald, 2002).Illicit drug use among Native Americans is less clear, because the dataavailable are poor. Furthermore, the use of hallucinogens has an important rolein some Native American religious rituals. The heterogeneity of Native Americancultures is plainly evident and further discourages simplistic discussions ofIndian culture. The “firewater” myth states that alcohol introduced to NativeAmericans by white settlers produced exaggerated biological effects in such persons.Garcia-Andrade, Wall, and Ehlers (1997), however, found less subjectiveintoxication among nonalcoholic Mission Indian men with greater NativeAmerican heritage. The same researchers implicate alcohol expectancy andmetabolism rates as possible differential effects among members of this tribe(Garcia-Andrade et al., 1997; Wall, Garcia-Andrade, Thomasson, Cole, &Ehlers, 1996).Native Americans share a belief in the unity and sacredness of all nature.Individual or ethnic groups may be more or less familiar with their own culture.Confrontational approaches, successful in many Anglo programs, cause NativeAmericans to shy away. Risk factors for alcohol and drug use in Native Americansparallel many of the same issues of other disenfranchised groups. Attemptsat assimilation of Native American culture, in the context of isolation frommainstream opportunities, have contributed to further cultural stress. Therecent increase in Indian-owned casinos has offered monetary opportunities,but also the possibilities of increased gambling and substance abuse. The breakdownof Native American culture, a factor that allowed alcohol to take a foothold,has been reversing in recent years. Self-determination and a return to traditionalspiritual and healing beliefs have helped springboard alternativeindigenous models of alcohol and drug recovery.REFERENCESAbram, K. M., Teplin, L. A., & McClelland, G. M. (2003). Comorbidity of severe psychiatricdisorders and substance use disorders among women in jail. Am J Psychiatry,160(5), 1007–1010.Adimora, A. A., Schoenbach, V. J., Martinson, F. E., Donaldson, K. H., Fullilove, R. E.,& Aral, S. O. (2001). Social context of sexual relationships among rural AfricanAmericans. Sex Transm Dis, 28(2), 69–76.Agar, M., & Reisinger, H. S. (2002). A heroin epidemic at the intersection of histories:The 1960s epidemic among African Americans in Baltimore. Medical Anthropol,21(2), 115–156.Ahluwalia, J., Harris, K. J., Catley, D., Okuyemi, K. S., & Mayo, M. S. (2002).Sustained-release bupropion for smoking cessation in African Americans: A randomizedcontrolled trail. JAMA, 288(4), 468–474.

334 IV. SPECIAL POPULATIONSBaker, F. M., & Bell, C. C. (1999). Issues in the psychiatric treatment of African Americans.Psychiatr Serv, 50(3), 362–368.Barr, K. E. M., Farrell, M. P., Barnes, G. M., & Welte, J. W. (1993). Race, class andgender differences in substance abuse: Evidence of a middle-class/under-classpolarization among black males. Social Problems, 403, 314–327.Berrettini, W. H., & Persico, A. M. (1996). Dopamine D2 receptor gene polymorphismsand vulnerability to substance abuse in African Americans. Biol Psychiatry, 40,144–147.Bowser, B. P., & Bilal, R. (2001). Drug treatment effectiveness: African-American culturein recovery. J Psychoactive Drugs, 33(4), 391–402.Boyd, C., Guthrie, B., Pohl, J., Whitmarsh, J., & Henderson, D. (1998). African Americanwomen who smoke crack cocaine: Sexual trauma and the mother–daughterrelationship. J Psychoactive Drugs, 26(3), 243–247.Boyd, C. J., Hill, E., Holmes, C., & Purnell, R. (1998). Putting drug use in context: Lifelinesof African-American women who smoke crack. J Subst Abuse Treat, 15(3),235–249.Brook, J. S., Balka, E. B., Brook, D. W., Win, P. T., & Gursen, M. D. (1998). Drug useamong African Americans: Ethnic identity as a protective factor. Psychol Rep, 83(3Pt. 2), 1427–1446.Brown, L. S., Jr., Alterman, A. I., Rutherford, M. J., Cacciola, J. S., & Zaballero, A. R.(1993). Addiction Severity Index scores of four racial/ethnic and gender groups ofmethadone maintenance patients. J Subst Abuse, 5(3), 269–279.Brown, T. L., Flory, K., Lynam, D. R., Leukefeld, C., & Clayton, R. R. (2004). Comparingthe developmental trajectories of marijuana use of African-American andCaucasian adolescents: Patterns, antecedents, and consequences. Exp Clin Psychopharmacol,12(1), 47–56.Burns, T. R. (1995). How does IHS relate administratively to the high alcoholism mortalityrate? Am Indian Alsk Native Ment Health Res, 6(3), 31–45.Caetano, R. (1989). Drinking patterns and alcohol problems in a national sample ofU.S. Hispanics. In D. L. Spiegler, D. A. Tate, S. S. Aitken, & C. M. Christian(Eds.), Alcohol use among U.S. ethnic minorities: Proceedings of a conference on theepidemiology of alcohol use and abuse among ethnic minority groups (NIAAA ResearchMonograph No. 18, DHHS Publication No. ADM 89-1435, pp. 147–162). Washington,DC: U.S. Government Printing Office.Caetano, R., & Clark, C. L. (2000). Hispanics, blacks and whites driving under theinfluence of alcohol: Results from the 1995 National Alcohol Survey. Accid AnalPrev, 32(1), 57–64.Caetano, R., & Medina-Mora, M. E. (1990, June). Reasons and attitudes toward drinkingand abstaining: A comparison of Mexicans and Mexican-Americans. InEpidemiologic trends in drug use: Community epidemiology work group proceedings (pp.173–191). Rockville, MD: National Institute of Drug Abuse.Chan, R. J., McBride, A. W., Thomasson, H. R., Ykenney, A., & Crabb, D. W. (1994).Allele frequencies of the preproenkephalin A (PENK) gene CA repeat in Asians,African-Americans, and Caucasians: Lack of evidence for different allele frequenciesin alcoholics. Alcohol Clin Exp Res, 18(3), 533–535.Conigliaro, J., Maisto, S. A., McNeil, M., Kraemer, K., Kelley, M. E., Conigliaro, R., &O’Connor, M. (2000). Does race make a different among primary care patients

14. Substance Abuse in Minority Populations 335with alcohol problems who agree to enroll in a study of brief interventions? Am JAddict, 9(4), 321–330.Crowley, J. J., Oslin, D. W., Patkar, A. A., Gottheil, E., DeMaria, P. A. Jr., O’Brien, C.P., et al. (2003). A genetic association study of the mu opioid receptor and severeopioid dependence. Psychiatr Genet, 13(3), 169–173.Deitch, D., & Solit, R. (1993). International training for drug abuse treatment and theissue of cultural relevance. J Psychoactive Drugs, 25(1), 87–95.Drug Abuse Warning Network (DAWN). (2004). Mortality data from DAWN, 2002.(DAWN Series D-25, DHHS Publication No. [SMA] 04-3875). Rockville, MD.http://dawninfo.samhsa.gov/old_dawn/pubs_94_02/mepbus/default.aspDuncan, S. C., Duncan, T. E., & Strycker, L. A. (2002). A multilevel analysis of neighborhoodcontext and youth alcohol and drug problems. Prev Sci, 3(2), 125–133.Dushay, R. A., Singer, M., Weeks, M. R., Rohena, L., & Gruber, R. (20010. LoweringHIV risk among ethnic minority drug users: Comparing culturally targeted interventionto a standard intervention. Am J Drug Alcohol Abuse, 27(3), 501–524.Ehlers, C. L., Carr, L., Betancourt, M., & Montane-Jaime, K. (2003). Association of theADH2*3 allele with greater alcohol expectancies in African-American youngadults. J Stud Alcohol, 64(2), 176–181.Frank, M. L., & Lester, D. (2002). Self-destructive behaviors in American Indian andAlaska Native high school youth. Am Indian Alsk Native Ment Health Res, 10(3),24–32.Friedman, A. S., & Glassman, K. (2002). Family risk factors versus peer risk factors fordrug abuse: A longitudinal study of an African-American urban community sample.J Subst Abuse Treat, 18(3), 267–275.Galea, S., Ahern, J., Tardiff, K., Leon, A., Coffin, P. O., Derrk, K., & Vlahov, D.(2003). Racial/ethnic disparities in overdose mortality trends in New York City,1990–1998. J Urban Health, 80(2), 201–211.Garcia-Andrade, C., Wall, T. L., & Ehlers, C. L. (1997, July). The firewater myth andresponse to alcohol in mission Indians. Am J Psychiatry, 154(7), 983–988.Garlow, S. J. (2002). Age, gender and ethnicity differences in patterns of cocatin andethanol use preceding suicide. Am J Psychiatry, 159(4), 615–619.Gary, L., & Berry, G. (1985). Predicting attitudes toward substance use in a black community.Community Ment Health J, 21, 45–51.Gelernter, J., Kranzler, H., & Satel, S. L. (1999). No association between D 2dopaminereceptr (DRD2) alleles or haplotypes and cocaine dependence or severity ofcocaine dependence in European- and African-Americans. Biol Psychiatry, 45(3),340–345.Gfroerer, J., & De La Rosa, M. (1993). Protective and risk factors associated with druguse among Hispanic youth. J Addict Dis, 12(2), 87–107.Gilbert, M. J. (1991). Acculturation and changes in drinking patterns among Mexican-American women. Alcohol Health Res World, 15(3), 234–238.Goldman, D., Brown, G. L., Albaugh, B., Robin, R., Goodson, S. , Trunzo, M., et al.(1993). DRD2 dopamine receptor genotype, linkage disequilibrium, and alcoholismin American Indians and other populations. Alcohol Clin Exp Res, 17(2), 199–204.Gomberg, E. S. (2003). Treatment for alcohol-related problems: Special populations:Research opportunities. Recent Dev Alcohol, 16, 313–333.

336 IV. SPECIAL POPULATIONSGraves, K., & Kaskutas, L. A. (2001). Beverage choice among Native-American andAfrican-American urban women. Alcohol Clin Exp Res, 26(2), 218–222.Harper, G. W., & Robinson, W. L. (1999). Pathways to risk among inner-city African-American adolescent females: The influence of gang membership. Am J CommunityPsychol, 27(3), 383–404.Herd, D. (1989). The epidemiology of drinking patterns and alcohol-related problemsamong U.S. blacks. In D. Spiegler, D. Tate, D. S. Aitkens, & C. Christian (Eds.),Alcohol use among U. S. ethnic minorities (NIAAA Research Monograph No. 18,DHHS Publication No. ADM 89-1435, pp. 3–50). Washington, DC: U.S. GovernmentPrinting Office.Herd, D. (1990). Subgroup differences in drinking patterns among black and whitemen: Results from a national survey. J Stud Alcohol, 51(3), 221–232.Herd, D. (1994). Predicting drinking problems among black and white men: Resultsfrom a national survey. J Stud Alcohol, 55, 61–71.Herd, D. (1997). Sex ratios of drinking patterns and problems among blacks and whites:Results from a national survey. J Stud Alcohol, 58(1), 75–82.Hesselbrock, M. N., Hesselbrock, V. M., Segal, B., Schuckit, M. A., & Bucholz, K.(2003). Ethnicity and psychiatric comorbidity among alcohol-dependent personswho receive inpatient treatment: African Americans, Alaska Natives, Caucasiansand Hispanics. Alcohol Clin Exp Res, 27(8), 1368–1373.Howard, D. L. (2003a). Are the treatment goals of culturally competent outpatient substanceabuse treatment units congruent with their client profile? J Subst AbuseTreat, 24(2), 103–113.Howard, D. L. (2003b). Culturally competent treatment of African-American clientsamong a national sample of outpatient substance abuse treatment units. J SubstAbuse Treat, 24(2), 89–102.Ja, D., & Aoki, B. (1993). Substance abuse treatment: Cultural barriers in the Asian-American community. J Psychoactive Drugs, 25(1), 61–71.James, W. H., Kim, G. K., & Armijo, E. (2000). The influence of ethnic identity ondrug use among ethnic minority adolescents. J Drug Educ, 30(3), 265–280.Johnson, R. C., & Nagoski, C. T. (1990). Asians, Asian-Americans, and alcohol. J PsychoactiveDrugs, 22(1), 45–52.Jones, R. J. (1989). The socio-economic context of alcohol use and depression: Results from anational survey of black and white adults. Paper presented at the 15th annual KetilBruun Alcohol Epidemiology Symposium, Maastricht, The Netherlands.Jones-Webb, R., Hsiao, C., & Hannan, P. (1995). Relationships between socioeconomicstatus and drinking problems among black and white men. Alcohol Clin ExpRes, 19(3), 623–627.Jones-Webb, R., Snowden, L., Herd, D., Short, B., & Hannan, P. (19970. Alcoholrelatedproblems among black, Hispanic and white men: The contribution ofneighborhood poverty. J Study Alcohol, 58(5), 539–545.Kaslow, N., Thompson, M., Meadows, L., Chance, S., Puett, R., Hollins, L., et al.(2000). Risk factors for suicide attempts among African-American women. DepressAnxiety, 12(1), 13–20.Kim, M. T., Dennison, C. R., Hill, M. N., Bone, L. R., & Levine, D. M. (2000). Relationshipof alcohol and illicit drug use with high blood pressure care and controlamong urban hypertensive black men. Ethn Dis, 10(2), 175–183.

14. Substance Abuse in Minority Populations 337Kingree, J. B., & Betz, H. (2003). Risky sexual behavior in relation to marijuana andalcohol use among African-American, male adolescent detainees and their femalepartners. Drug Alcohol Depend, 72(2), 197–203.Kitano, H. H. L., & Chi, I. (1989). Asian Americans and alcohol: The Chinese, Japanese,Koreans, and Filipinos in Los Angeles. In D. Spiegler, D. Tate, S. Aitkens, &C. Christian (Eds.), Alcohol use among U.S. ethnic minorities (NIAAA ResearchMonograph No. 18, DHHS Publication No. ADM 89-1435, pp. 373–382). Washington,DC: U.S. Government Printing Office.Konishi, T., Calvillo, M., Leng, A. S., Feng, J., Lee, T., Lee, H., et al. (2003). TheADH3*2 and CYP2E1 c2 alleles increase the risk of alcoholism in Mexican-American men. Exp Mol Pathol, 74(2), 183–189.Kranzler, H. R., Gelernter, J., O’Malley, S., Hernandez-Avila, C. A., & Kaufman, D.(1998). Association of alcohol or other drug dependence with alleles of the muopioid receptor gene (OPRM1). Alcohol Clin Exp Res, 22(6), 1356–1359.Kunitz, S. J., Gabriel, K. R., Levy, J. E., Henderson, E., Lampert, K., McCloskey, J., et al.(1999). Alcohol dependence and conduct disorder among Navajo Indians. J StudAlcohol, 60(2), 159–167.Li, X., Feigelman, S., Stanton, B., Galbraith, J., & Huang, W. (1998). Drug traffickingand drug use among urban African-American adolescents: A casual analysis. JAdolesc Health, 23(5), 280–288.Lillie-Blanton, M., Anthony, J., & Schuster, C. R. (1993). Probing the meaning ofracial/ethnic group comparisons in crack cocaine smoking. JAMA, 296(8), 993–997.Longshore, D. (1999). Help-seeking by African-American drug users: A prospectiveanalysis. Addict Behav, 24(5), 683–686.Longshore, D., Grills, C., & Annon, K. (1999). Effects of a culturally congruent interventionon cognitive factors related to drug-use recovery. Subst Use Misuse, 34(9),1223–1241.Lown, A. E., & Vega, W. A. (2001). Alcohol abuse and dependence among Mexican-American women who report violence. Alcohol Clin Exp Res, 25(10), 1479–1486.Lundgren, L. M., Amodeo, M., Ferguson, F., & Davis, K. (2001). Racial and ethnic differencesin drug treatment entry of injection drug users in Massachusetts. J SubstAbuse Treat, 21, 145–153.Milligan, C. O., Nich, C., & Carroll, K. M. (2004). Ethnic differences in substanceabuse treatment retention, compliance, and outcome from two clinical trials.Psychiatr Serv, 55(2), 167–173.National Institute on Alcohol Abuse and Alcoholism. (2000, June). 10th Special Reportto the U.S. Congress on Alcohol and Health. Rockville, MD: Author.Newlin, D. B. (1989). The skin-flushing response: Autonomic, self-report and conditionedresponses to repeated administrations of alcohol in Asian men. J AbnormPsychol, 98, 421–425.Obot, I. S., & Anthony, J. C. (2000). School dropout and injecting drug use in anational sample of white, non-Hispanic American adults. J Drug Educ, 30(2), 145–155.Obot, I. S., Hubbard, S., & Anthony, J. C. (1999). Level of education and injectingdrug use among African Americans. Drug Alcohol Depend, 55(1–2), 177–182.Okuyemi, K. S., Ahluwalia, J. S., Richter, K. P., Mayo, M. S., & Resnicow, K. (2001).

338 IV. SPECIAL POPULATIONSDifferences among African-American light, moderate and heavy smokers. NicotineTob Res, 3(1), 45–50.Patkar, A. A., Berrettini, W. H., Hoehe, M., Thornton, C. C., Gottheil, E., Hill, K., &Weinstein, S. P. (2002). Serotonin transporter polymorphisms and measures ofimpulsivity, aggression and sensation-seeking among African-American cocainedependentindividuals. Psychiatry Res, 110(2), 103–115.Petry, N. M. (2003). A comparison of African-American and non-Hispanic Caucasiancocaine-abusing outpatients. Drug Alcohol Depend, 69(1), 43–49.Qureshi, A. I., Mohammad, Y., Suri, M. F., Bramimah, J., Janardhan, V., Guterman, L.R., et al. (2001). Cocaine use and hypertension are major risk for intracerebralhemorrhage in young African Americans. Ethn Dis, 11(2), 311–319.Reardon, S. F., & Buka, S. L. (2002). Differences in onset and persistence of substanceabuse and dependence among whites, blacks and Hispanics. Public Health Rep,117(Suppl 1), S51–S59.Roberts, C. A. (1999). Drug use among inner-city African-American drug users: Theprocess of managing loss. Qual Health Res, 9(5), 620–638.Rome, L. A., Lippmann, M. L., Dalsey, W. C., Taggart, P., & Pomerantz, S. (2000).Prevalence of cocaine use and its impact on asthma exacerbation in an urban population.Chest, 117(5), 1324–1329.Rosenheck, R., & Seibyl, C. L. (1998). Participation and outcome in a residential treatmentand work therapy program for addictive disorders: The effects of race. Am JPsychiatry, 155(8), 1029–1034.Rowe, D., & Grills, C. (1993). African-centered drug treatment: An alternative conceptualparadigm for drug counseling with African-American clients. J PsychoactiveDrugs, 25(1), 21–33.Ruiz, P., Langrod, J., & Alksne, L. (1981). Rehabilitation of the Puerto Rican addict: Acultural perspective. Int J Addict, 16(5), 841–847.Russell, M., Cooper, M. L., Frone, M. R., & Peirce, R. S. (1999). A longitudinal study ofstress, alcohol and blood pressure in community-based samples of blacks and nonblacks.Alcohol Res Health, 23(4), 299–306.Saremi, A., Hanson, R. L., Williams, D. E., Roumain, J., Robin, R. W., Long, J. C., et al.(2001). Validity of the CAGE questionnaire in an American Indian population. JStud Alcohol, 62(3), 294–300.Shore, J., Manson, S. M., & Buchwald, D. (2002). Screening for alcohol abuse amongurban Native Americans in a primary care setting. Psychiatr Serv, 53, 757–760.Singh, G. K., & Hoyert, D. L. (2000). Social epidemiology of chronic liver disease andcirrhosis mortality in the United States, 1935–1997: Trends and differentials byethnicity, socioeconomic status and alcohol consumption. Hum Biol, 72(5), 801–820.Stanton, B., Li, X., Pack, R., Cottrell, L., Harris, C., & Burns, J. M. (2002). Longitudinalinfluence of perceptions of peer and parental factors on African-Americanadolescent risk involvement. J Urban Health, 79(4), 536–548.Stewart, O. (1964). Questions regarding American Indian criminality. Human Organ,23, 61–66.Stewart, S. H. (2002). Racial and ethnic differences in alcohol-associated aspartateaminotransferase and gamma-glutamyltransferase elevation. Arch Intern Med,162(19), 2236–2239.

14. Substance Abuse in Minority Populations 339Stinson, F. S., Grant, B. F., & Dufour, M. C. (2001). The critical dimension of ethnicityin liver cirrhosis mortality statistics. Alcohol Clin Exp Res, 25(8), 1181–1187.Substance Abuse and Mental Health Services Administration. (2000). National HouseholdSurvey on Drug Abuse: Population estimates (DHHS Publication No. BK0355).Washington, DC: U.S. Government Printing Office.Szapocznik, J., & Fein, S. (1995). Issues in preventing alcohol and other drug abuse amongHispanic/Latino families (CSAP Cultural Competence Series 2, DHHS PublicationNo. SMA 95-3034). Washington, DC: U.S. Government Printing Office.Timpson, S. C., Williams, M. L., Bowen, A. M., & Keel, K. B. (2003). Condom usebehaviors in HIV-infected African American crack cocaine users. Substance Abuse,24(4), 211–220.U.S. Bureau of the Census. (2002). Current population reports. Washington, DC: U.S.Government Printing Office.Varma, S., & Siris, S. (1996). Alcohol abuse in Asian Americans. Am J Addict, 5(2),136–143.Wall, T. L., Garcia-Andrade, C., Thomasson, H. R., Cole, M., & Ehlers, C. L. (1996).Alcohol elimination in Native American Mission Indians: An investigation ofinterindividual variation. Alcohol Clin Exp Res, 20(7), 1159–1164.Wallace, J. M., Jr., Bachman, J. G., O’Malley, P. M., Johnston, L. D., Schulenberg, J. E.,& Cooper, S. M. (2002). Tobacco, alcohol, and illict drug use: Racial and ethnicdifferences among U.S. high school seniors, 1976–2000. Public Health Rep,117(Suppl 1), S67–S75.Walton, M. A., Blow, F. C., & Booth, B. M. (2001). Diversity in relapse preventionneeds: Gender and race comparisons among substance abuse treatment patients.Am J Drug Alcohol Abuse, 27(2), 225–240.Wells, K., Klap, R., Koike, A., & Sherbourne, C. (2001). Ethnic disparities in unmetneed for alcoholism, drug abuse and mental health care. Am J Psychiatry, 158(12),2027–2032.Westermeyer, J. (1995). Cultural aspects of substance abuse and alcoholism: Assessmentand management. Psychiatr Clin North Am, 18(3), 589–605.Ziedonis, D., Rayford, B., Bryant, K. J., & Rounsaville, B. (1994). Psychiatric comorbidityin white and African-American cocaine addicts seeking substance abuse treatment.Hosp Community Psychiatry, 45(1), 43–49.Zule, W. A., Lam, W. K., & Wechsberg, W. M. (2003). Treatment readiness amongout-of-treatment African-American crack users. J Psychoactive Drugs, 35(4), 503–510.

CHAPTER 15Addictions in the WorkplaceAVRAM H. MACKJEFFREY P. KAHNRICHARD J. FRANCESClinicians are frequently asked to address addictions in the workplace, includingprevention, treatment, assessment of performance, benefit structure, disability,and risk management. Anyone involved with these topics must recognizeissues of importance to the organization, the individual, the public safety,and the relevant laws and ethics (Kahn & Langlieb, 2002). And, as in any situationin which the clinician is a third party, privacy, confidentiality, and otherethical considerations must be appropriately addressed. This chapter serves asan introduction to this complex task. We begin by exploring the problemsposed by substance use, abuse, and dependence in the workplace, the laws thatgovern the organizations roles, and the issues faced by psychiatrists involved inthese situations; we then describe aspects of management of the problems and,finally, address a number of specific occupations in which particular issues areimportant. Chapter 4 in this volume, on drug testing, covers its use in the workplaceand highlights these issues as related to sports and professional athletes.THE PROBLEM: EXTENT AND CAUSESThe use of illicit or addictive substances in the workplace can have devastatingeffects, including accidents, injuries, disability, lateness/absenteeism, theft,reduced performance, and reduced morale. By 1998, the societal cost of drugabuse was $143.4 billion, with lost productivity accounting for around $100 bil-340

15. Addictions in the Workplace 341lion of that amount (Office of National Drug Control Policy, 2001). It is projectedthat the cost to business of alcohol abuse is $185 billion, with lost productivityaccounting for 70% of that amount (National Institute on AlcoholAbuse and Alcoholism, 2001). Beyond lost productivity, however, are othercosts, including liability for workplace accidents due to intoxication or the associationwith violence (see Chapter 16 on forensic addiction psychiatry, thisvolume). The Substance Abuse and Mental Health Services Administration(SAMSHA) has published findings from recent National Household Survey onDrug Abuse (NHSDA) studies on the extent of use and institutional policies(Office of Applied Studies, 1999). Since any type of worker at any level of hierarchycan cause an accident or be violent, it is important to consider every caseindividually and to take each case seriously.The nature of the use, abuse, and dependence of both alcohol and illicitsubstances in the workplace is generally similar to that out of the workplace.Many different substances are used by individuals with many different psychologicalbackgrounds and in different places in the organizational hierarchy,before, during, or after business hours. Individuals who use or abuse certainperformance-enhancing substances include military pilots, musicians, artists,and athletes. A 1997 study of workplace alcohol use on a national level foundthat 7.6% of full-time employees were heavy drinkers (five or more drinks on 5or more days in the month prior to the survey) and a third of those also wereusing illicit drugs (Office of Applied Studies, 1999).Why should the leadership of an organization care about occupational substanceuse? In addition to compassion, quality of productivity, and quality ofwork environment, there are many other compelling reasons why attentionshould be given to the matter: the potential for worker’s compensation claims,the potential for violence, and legal liability. A significant relationship betweenuse of alcohol and the likelihood of a claim of injury was demonstrated inone prospective study of municipal railways operators (Raglans et al., 2002).Both violence and sexual harassment in the workplace are associated with substanceabuse. Besides prevention of loss and liability, various legal foundationsguide the way in which organization leaders seek and manage workers with substanceuse disorders (SUDs). The 1970 Occupational Safety and Health Act,the 1988 Drug-Free Workplace Act, the 1990 Americans with Disabilities Act(Westreich, 2002), and the Family and Medical Leave Act all established legalguidelines for addressing and treating substance use at the workplace. On theother hand, the Contract with America Advancement Act of 1996 removedaddictions from coverage under Social Security. It is always advisable to ask anattorney to provide the applicable statutes before providing an opinion. Furthermore,since drug–alcohol testing has been frequently challenged, all organizationsshould seek specific guidance on current and local standards for enforcementof testing.

342 IV. SPECIAL POPULATIONSOrganizational Contributions to Substance MisuseFrom the organization’s perspective, the paramount issue is how or why substanceuse has transgressed into the workplace. The consultant’s function is toaddress the areas upon which to focus, including organizational permissiveness,work stress, culture and attitude, and the worker’s preemployment understandingof tolerated behavior.PermissivenessEach workplace has its own personality, and its own view of substance use.Some are militantly antidrug, while others are relatively laissez-faire. Whentop leadership may be impaired or in denial, the whole organization may beaffected. Fads, outbreaks, and epidemics of drug use in organizations can alsooccur.Culture and AttitudeThis includes both the culture created by the organizational setup and the unofficialpractices of those in the organization (e.g., chewing tobacco among baseballplayers). In terms of institutional structure, one study compared the organizationof two groups of employees in the United States: one organized in atypical manner, the other based on Japanese principles. The latter group hadfewer problems (Ames, Grube, & Moore, 2000).Work StressA lack of specificity has impeded the creation of workplace stress reduction programsthat would diminish the putative stress–addiction relationship (Roman& Blum, 2002). Studies that have measured “burnout” have failed to link“burnout” with alcohol abuse or use. However, alcohol use has been associatedwith less-specific measures of occupational stress (Crum, Muntaner, Waton, &Anthony, 1995).Diagnosis, Case Findings, and RecognitionAn important role for the organization and for the consultant is detecting casesof substance abuse in the work setting. This function must be handled withfinesse on many levels, including, among others, the company structure, reporting,confidentiality rules, and the requirement of periodical medical evaluations.The first opportunity to identify problem substance use is before the individualbecomes an employee: the preemployment screen. Human resources/

15. Addictions in the Workplace 343benefits officers should be trained to recognize the importance of physical, historical,or social signals of misuse, and this should, with a low threshold of suspicion,lead to further inquiry, including, for example, direct questioning, professionalevaluation, or request for records of prior treatment.Once the individual is an employee, sources include physical findings (e.g.,stench of cannabis, bottles of alcohol, change in work performance, reportsfrom others; ideally, confidential or anonymously), violence or legal problems,or the development of associated medical problems. The extent to which thedependent or abusing worker spends most of his or her time thinking about(obtaining, concealing, using) the drug leaves less time for work or anythingelse. Many addicts in the workplace are able to conceal their drug use for years!Supervisors should be trained to spot problems, and workers should also be providededucation for self-diagnosis.A tenet of addiction is continued use despite adverse consequences. Denialof a problem is a challenge, and confrontation is often part of the intervention.The first steps to recovery are recognition of a problem and agreeing to a needfor help. The addict is unwilling (earlier in the course of addiction) or unable(in the later stages) to stop use. Sadly, the employer who says “Get help oryou’re fired” often has more leverage than family or friends.Loss of control is an important criterion for addiction, and one of the moreconfusing aspects for employers to comprehend. Over time, untreated drug useprogresses from social and recreational use to more problematic heavy use, andfinally to out-of-control addiction. In order to understand the loss of control,addiction must be presented to third parties as a progressive, not static, illness.Of course, denial of this progression is characteristic: It is difficult to accept theeventual loss of control. The addict at first minimizes the damage, then blamesothers as justification for continued abuse, which may be followed by rationalizinghis or her behavior.In this progression, the first step toward successful treatment of alcohol ordrug addiction in the workplace is the direct confrontation of denial. Theemployer or partners often have more leverage and more emotional neutralitythan a family member. The supervisor does not make a diagnosis but does recommendan evaluation by a professional. The substance abuser is usuallyunwilling to seek help on his or her own, and must be made to see the adverseconsequences of not stopping drug use (e.g., loss of job, divorce). The employeeis given the choice of treatment or termination, and the usual result is a referralto an Employee Assistance Program (EAP).Diagnosing Specific Substances in the WorkplaceIt is important to remember that each drug may have a different course in theworkplace, and relapse depends very much on the drug being used.

344 IV. SPECIAL POPULATIONSStimulants and CocaineDependence or abuse of stimulants and cocaine is difficult to detect in theworkplace; they produce no odor and no hangovers. Users are often workerswho were once industrious but now have difficulty concentrating and stayingalert. Physical signs of cocaine or stimulant abuse do become apparent. Frequentunexplained absences, lateness, inability to sit still, and excessive trips tothe restroom, along with paranoia, irritability, and hypomanic symptoms,should lead the employer to suspect stimulant, especially cocaine, abuse.Crashing, depression, and abuse of sedatives are also signs.MarijuanaThe marijuana-dependent individual who smokes daily will have deficits invocational, social, and psychological functioning. Common findings includeinability to concentrate, difficulty with judgement and fine motor coordination,memory impairment, and social withdrawal. Lethargy, depression, and aloss of goal-directed behavior are common. In the workplace, the results can bedangerous to the individual user, coworkers, and the general public, dependingon the occupation of the user.Opiates and OpioidsBoth legal and illicit opiates and opioids are major problems in the workplace.The heroin addict is frequently absent and late. He or she is prone to accidentsbecause of heroin intoxication (lethargy, somnolence, difficulty concentrating,impaired motor coordination and judgment) or withdrawal. Injuries resulting indisability and theft or embezzlement to support the dependence are common.The abuse of legally prescribed opiates has increasingly been portrayed in thelay press. Regular use of these substances leads to a high level of tolerance andto a withdrawal syndrome identical to that of heroin. Use of “hard drugs,” suchas heroin or opiates, has stigmatized many individuals in the past. For thosewho are motivated to quit, compassion and support in the workplace can makea big difference in successful abstinence from this class of substance, and personsmaintained on methadone or buprenorphine are frequently able to workwell.Sedatives/HypnoticsAs is the case with the prescription opioids, employees become adept at concealingtheir dependence on these medications. Intoxication can be dangerousif the employee is required to drive, operate equipment, or perform complex

15. Addictions in the Workplace 345tasks. Cases of acute stress disorder and posttraumatic stress disorder (PTSD)drastically increased on Wall Street after the September 11, 2001, terroristattacks. Disasters, terrorism, and war pose additional workplace stress, and concomitantincreases in abuse of these substances will likely occur with them.TREATMENT AND INTERVENTIONSAddiction psychiatrists may be called upon for preemployment screening,fitness-for-work evaluations, crisis situations, case management, treatment, orto review organizational policy regarding substances. Before any contact with apatient, the addiction psychiatrist working in the occupational setting musthave a clear sense of his or her duty. Interactions between a clinician/consultantand an employee/patient are complicated by the various roles inherent inthe setup. At the least, the patient must be made aware of policy regarding confidentialityand the physician’s dual agency. One SAMHSA-sponsored groupdemonstrated the utility of such an approach when enacted by an EAP(Lapham, McMillan, & Gregory, 2003).Preemployment ScreeningPreemployment screening to identify various potential problems, including substanceabuse, may produce referrals for evaluation. In addition, it is helpful toeducate employers about how to screen and when to refer. Those who performthese screens need to have a low threshold for referral. Important informationcan be gleaned from reference letters, a history of arrests, the admission of medicalproblems, or the applicant’s physical appearance. Special attention shouldbe paid not only to use but also to use in the workplace.Once all the information has been gathered, the question is what to dowith it. There are two important questions for the consultant: (1) Is the behaviora treatable condition, and (2) has it affected occupational function in thepast? With these questions in mind, the psychiatrist may come to a recommendation,especially when considering the type of work being sought. It would befoolhardy to reject every single potential employee simply because he or she hasmisused a substance. Hiring talented persons in stable recovery makes goodbusiness sense.Problem OrganizationsFor the organization that has sought the consultant’s advice, there is an assumptionthat change is sought: that a problem has been identified. The consultantmust gather a bird’s-eye view of the organization, from the demographics of the

346 IV. SPECIAL POPULATIONSemployer to the proximity of the work location to areas high in drug trafficking.One should even determine the type of beverages served at company functions.There may be a need to discuss perceptions of permissiveness and of the actualwritten or unwritten consequences of legal or illicit substance use during workhours.Is some cases an organization may choose to become a “drug-free workplace.”The implications of this go beyond psychiatric consultation and requirelegal advice. The Drug Enforcement Agency (2004) has provided a guidelinefor implementing this standard.Random Drug TestingPreemployment and periodic mandatory, random urine testing for illicit drugshas become a controversial topic in recent years. The main argument in favorof mandatory urine testing is deterrence of illicit drug use, both at work and athome. Random testing is mandated by federal regulations for the transportationindustry, for example. Those who are opposed to mandatory urine testing saythat it is a violation of constitutional rights to privacy. And even with safeguards,concerns are also raised about reporting errors and potential breaches ofconfidentiality. An employee’s right to privacy must be balanced with society’sbest interests. As mentioned earlier, any testing program needs to be developedin concert with legal consultation.The third party must be reminded that urine tests do not distinguish druguse from drug abuse or dependence. This can only be done with a comprehensivemedical and psychiatric history, and physical examination. At best, laboratorytests are adjunctive and provide diagnostic confirmation. It is accepted inthe treatment community that urine testing is a useful adjunct in the treatmentof the drug-dependent individual, but not all drug users are abusers.Nonrandom TestingThere are a number of situations in which testing is done on a nonrandombasis, including when there is reasonable suspicion, after an accident or violence,or as a part of a posttreatment follow-up. Employees seem to favor testsfollowing accidents (Howland, Mangione, Lee, Bell, & Levine, 1996).Brief InterventionsAfter an assessment has been made, brief interventions are sometimes the requisitenext step. It can be immensely helpful to have the individual’s family be apart of the intervention. The family is the mediator between the individual andhis or her culture, and the family environment is where attitudes toward drugsare first learned.

The Employee Assistance Program Model15. Addictions in the Workplace 347When available, it is ideal to place the employee’s “case” within the EAP. Theoverall approach of the EAP is to identify and treat the drug-abusing employeeand to help the employee maintain his or her career and productivity, ratherthan to fire him or her. EAPs provide both primary and secondary prevention.They make job-based evaluations and referrals, and some also provide substanceabuse treatment, thus increasing job retention and lowering complications.EAPs are valuable for workers in that they provide a nonthreatening place toobtain alcohol and drug abuse information and counseling, as well as early diagnosisand treatment. In some companies, up to 40% of the employees use EAPs;approximately 17% of these are for substance abuse. Approximately 30,000EAP programs exist in the United States. They have been in decline recently asmanaged care has grown. Employers are generally in favor of the EAP system,since they feel that, in the long run, it is more cost-effective to treat employeesthan to fire them and retrain new ones. Seeing recovering alcoholics and drugabusers return to work happier and more productive is also helpful for companymorale. Insurance companies are generally in favor of EAPs, since successfulsubstance abuse treatment has been shown to reduce overall medical costs.Company EAPs vary in demeanor, from stern to forgiving, and also from amoral to a medical model (which most EAPs encourage).By definition, EAPs are in a difficult position. They are the advocate ofthe employee, yet at the same time must protect the interests of the employer.And although patient confidentially must be preserved in all types ofmental health treatment, in order for the EAP to be effective, there must besome degree of communication with the employee’s supervisor, union, or personneloffice. It is important that the guidelines for communication of thistype be clear at the very beginning of treatment. In most programs, theemployer communicates with the EAP regarding job performance, and theEAP provides the employer with periodic progress reports, without divulgingconfidential information. The “success rate” of the EAP has been cited to be70% (Blum, Martin, & Roman, 1992), although outcome measures requirefurther refinement.More often than not, participation is voluntary, though for some employeesreferral is an alternative to a job action. It is best for the EAP to beproactive about its roles (Lapham et al., 2003). Education about the EAP isessential, and a clearly written policy indicating that drug use will not be toleratedis helpful as well. EAPs can also train both employees and supervisors.Supervisors should be trained to (1) understand their role in implementation ofthe policy, (2) observe and document job performance problems, (3) confrontemployees who are unsatisfactory in job performance, (4) understand the effectsof substances in the workplace, and (5) know how to refer employees with suspectedproblems to the EAP or other mental health professional. Employees

348 IV. SPECIAL POPULATIONSshould be taught the dangers of alcohol and drug abuse to themselves and theirfamilies; the negative effects of substances on job performance, health, andsafety; company policy and consequences of violating it; the functions of theEAP; drug testing policy and confidentiality; and the ways in which they canget help.There are important limitations to EAPs. First, many executives, upperlevel managers, and company presidents do not seek treatment for substanceabuse through their EAPs. They often prefer off-site treatment programs or cliniciansfor the following reasons: (1) Their substance abuse may involve anillicit drug rather than alcohol; (2) company morale would suffer if it becameknown, for example, that the CEO was a cocaine addict; and (3) it is difficult tobe treated by someone they employ. Second, the EAP focus on substance abusecan lead to referral to broadly trained clinicians, and less careful attention toother emotional and psychiatric problems. Many of these patients benefit fromconsultation with an addiction psychiatrist.SPECIAL POPULATIONSEach of the many special work populations may differ in terms of types of drugsused, reasons for use (e.g., boredom, exhilaration, etc.), and potential consequences.AthletesAthletes are usually young adults whose jobs involve stardom, celebrations, disappointments,access to illicit drugs, large amounts of cash, great physical exertion,and great physiological reserve. Sometimes the athlete may be trying tomake the grade in any way possible, or may be little-noticed. Drug misuse maybe for enhancement of performance, recreation, pleasure, or self-medication ofpain.A vast number of substances are used by athletes to improve their performance.Many have been discovered and regulated (or banned), many moreexist now, and others will surface in the future. These substances are regulatedmostly because they affect fair competition or may endanger the user; this sortof use, often diagnosed as other substance use disorder, includes steroids, nutritionalsupplements, or stimulants or opioids.Athletes use all kinds of addictive substances recreationally, includingcocaine, marijuana, and tobacco. The use of smokeless tobacco is endemicamong baseball players (including college and high school players) (Colborn,Cummings, & Michaelek, 1989). Coaches and those concerned about playersmust be able to make recommendations for treatment regardless of “who” theplayer is.

Executives and Other VIPs15. Addictions in the Workplace 349Some special considerations exist for dealing with substance-abusing executivesand leaders, because their impact on other people magnifies the effects of theirproblems. Moreover, they are often insulated from help by virtue of their positionand may feel pressure to appear professional and authoritative. Some executiveshave always dealt with emotional distress by covering it over, perhapsthrough self-medication with drugs or alcohol. Similarly, others have relied onthe socially lubricating effects of alcohol, or on the short-term performanceenhancement of cocaine for their success. Leaders with addictions feel furtherimpelled to avoid advice and help, and can end up feeling quite “lonely at thetop.” Being at the top of the heap can enable substance use. Executives canmake their own schedule in a way that allows for substance use. Some feel thatordinary rules do not apply to them—a feeling that is further compounded bythe physical and psychological effects of substance abuse. Among VIPs such asmedia celebrities, the acquired narcissism that accompanies a successful careercan lead to greater difficulty in reaching out for or accepting help.Employees often feel helpless and demoralized when faced with a distressedand possibly substance-abusing boss. Under these circumstances, employees(and other executives) commonly protect the impaired executive. This caninclude doing his or her work, ignoring inappropriate instructions, covering upmistakes, and helping to keep the secret. This is sometimes rationalized as “TheDevil you know is better than the Devil you don’t know.”As a result, management, human resources, and occupational medicinepersonnel need to be alert to signs of possible substance abuse. This includesvisible distress or intoxication, impaired judgment or performance, decreasedinterpersonal skills, unexplained absences, and more. An ombudsman programoffers a discrete and protected channel for employee concerns, as can a confidentialoccupational medicine department. If a problem is noticed at work, theexecutive needs to be approached by senior management, human resources,occupational medicine personnel, or an ombudsman. The approach should bediscrete and focus on genuine business performance concerns. Occasionally, itis appropriate to involve family members in the process.It is important that any clinical treatment not treat the executive as a VIP.To do so often results in attempts by the patient to control the treatment, minimizeproblems, avoid comprehensive psychiatric and medical evaluation andtreatment, or avoid Alcoholics Anonymous (AA) or similar programs.Health Care WorkersHealth care workers (HCWs), a diverse group that includes, for example, academicphysicians, floor nurses, and laboratory technicians, share a niche in aworkplace that combines high stress and sometimes access to addictive sub-

350 IV. SPECIAL POPULATIONSstances, or to the hardware needed for their use (e.g., syringes, alcohol swabs).It may be no surprise that they often use substances to cope. This area hasreceived a fair amount of research attention. For physicians, all 50 states havesystems for physician health.Occupational stresses in the health care setting may contribute to substancemisuse. One study that viewed the 2002 Washington-area sniper shootingsas terrorism found that among employees of a local hospital, with highexposure to trauma, the perception of safety was inversely proportional to therisk of alcohol misuse. Conversely, the use of alcohol was a risk factor for acutestress disorder (odds ratio = 5.1) (Greiger, Fullerton, Ursano, & Reeves, 2003).Abuse is widespread among both nurses and physicians. Using an anonymoussurvey, Trinkoff and Storr found (1998) that 32% of nurses admitted touse of substances. For physicians, alcohol use may be common: One study suggesteda 12% rate of abuse (Moore, Mead, & Pearson, 1990). Physicians may beamong the most resistant to seek help for a real problem (Aach et al., 1992).Physicians also have a high risk factor for addiction. Actually, adults who havegrown up in families with addiction have a tendency to choose health care professions.Physicians have higher access to pharmaceutical drugs but are lessinclined to use street drugs. In the New York State Physicians’ Health Program,88% of the participants used alcohol or prescription drugs, and only 12% usedmarihuana or cocaine. Additional risk factors for SUDs in physicians have beenpostulated to be “pharmacological optimism,” intellectual strength, strong will,love of challenges, instrumental use of medications, and a daily need for denial(Mansky, 1999).As in other professions, there may be a need to tailor treatments for thisgroup. New research has demonstrated that prevention aimed at HCWs can besuccessful (Lapham, Chang, & Gregory, 2000). Confidentiality is a major concernin the care of HCWs, and many centers are especially adept at caring forHCWs (e.g., Talbott Recovery Program). Physicians may gain help throughtwo mutual-help groups, caduceus groups and International Doctors in AlcoholicsAnonymous, which supplement mainstream 12-step programs.High-Responsibility Workers: Air Traffic Controllers,Machine Operators, Drivers, and PilotsOne of the most difficult issues with regard to working with this population is inconsidering when and where to speak up about the dangers posed by theworker, especially when the consultant has a dual agency. While a therapeuticalliance is central to treatment, an important role of the addiction psychiatristis to confront denial and to protect the public (Leeman, Cohen, & Parkas,2001) whether the setting is occupational or private. Notwithstanding the narrownessof the Tarasoff duties, the therapist should remind the patient of thelegal liabilities that result from the risky behavior. One should consider referral

15. Addictions in the Workplace 351to another caretaker if the patient refuses to bring his or her dangerous behaviorto a halt.The American Society for Addiction Medicine guidelines (2000) recognizethat reporting substance abuse is necessary when there is an “immediatethreat to public safety,” which might be construed to be anytime a person drivesunder the influence of alcohol.For the worker with people’s lives in his or her hands, there may be no“safe” level of blood alcohol. One study performed in the United Kingdomdemonstrated that despite a lack of sense of sleepiness following a lunch withalcohol, drivers driving at the typical “circadian dip” who were at half the legalalcohol limit nonetheless performed worse on driving and evidenced electroencephalographic(EEG) evidence of alteration (Horne, Reyner, & Barrett,2003). Alcohol certainly increased preexisting sleepiness in this experimentaldesign. One study demonstrated that substance abuse of all drug classes ishigher than expected among construction workers (Hersh, McPherson, &Cook, 2002).Both governmental and commercial aviation systems have been keenlyaware of the problem of alcohol and flying for some time. It is an environment“unforgiving” of mistakes. Little research has been conducted on the issue andpolicies designed to stop use (Cook, 1997). Actually, it is in the unregulated,general aviation sphere that most accidents occur today.Of course, both alcohol and nicotine are legal drugs. There are no guidelinesregarding nicotine at all. Changes in regulations about use of tobacco mayhave potentially created a situation in which pilots may go through nicotinewithdrawal during flight (Giannakoulas, Katramados, Melas, Diamantopoulos,& Chimonas, 2003).Individuals with Access to Weapons: Police and the MilitaryAkin to HCWs, police and military workers may be at high risk of causing harmwhen intoxicated, in that they have access to lethal weapons such as firearms.There are countless anecdotes about suicides and murders done by policemenwhile intoxicated. The full impact on veterans of the war on terrorism andthose who have fought in Afghanistan and Iraq is not clear and will emergeover the years to come. Those who learn to kill during war may be more proneto substance use, violence, and posttraumatic stress disorder, with signs of theseapparent in the workplace.During the Vietnam War, a large number of American servicemen andwomen were abusers of drugs, ranging from heroin to marijuana. This phenomenonwas partially explained by the prevailing culture, availability of drugs inthe war theater, antipathy for the war, and stresses of the war experience.Strangely, the addiction to heroin did not generally continue once the usersreturned to the United States, which reinforced the concept that addiction can

352 IV. SPECIAL POPULATIONSbe halted. Since that period, the U.S. military has been highly attentive to drugabuse among its ranks.Performance-enhancing drugs may be more prevalent in the armed forcesthan recreational drugs. There is anecdotal evidence that military pilots areincreasingly being asked to use sedatives for sleep and stimulants during theperiod of their missions. Unfortunately, soldiers leaving the military get littlehelp with the transition to civil life.We advocate that supervisors have an extremely low threshold for addressingsuch problems when they arise. Any institutionalized tendency to minimizesuch dangers should be addressed as well. Amnesty programs or anonymousreporting may help. Military medical services often are organized to care forlarge numbers of individuals, and some bases have begun programs for surveillanceof individuals who are at risk, or who demonstrate “drug-seeking behaviors”(Lewis & Gaule, 1999). Unfortunately, the military does not providemuch treatment for drug abusers and tends to process them out of the military.CONCLUSIONThe practice of addiction psychiatry in occupational settings can be complex,but it also may produce important assistance to organizations. Ideally, furtherresearch will be publicized and made more generalized.REFERENCESAach, R. D., Girard, D. E., Humphrey, H., McCue, J. D., Reuben, D. B., Smith, J. W., etal. (1992). Alcohol and other substance abuse and impairment among physiciansin residency training. Ann Int Med, 116, 245–254.American Society of Addiction Medicine. (2000). Public policy statement on reportingof patient information related to fitness for driving or other potentially dangerousactivities. J Addict Dis, 19, 125–127.Ames, G. M., Grube, J. W., & Moore, R. S. (2000). Social control and workplace drinkingnorms: a comparison of two drinking cultures. J Stud Alcohol, 61, 203–219.Blum, T. C., Martin, J. K., & Roman, P. M. (1992). A research note of EAP prevalence,components, and utilization. J Employee Assist Res, 1, 209–229.Colborn, J. W., Cummings, K. M., & Michaelek, A. M. (1989). Correlates of adolescent’suse of smokeless tobacco. Health Ed Q, 16, 91–100.Cook, C. C. H. (1997). Alcohol policy and aviation safety. Addiction, 97, 793–804.Crum, R., Muntaner, C., Waton, W., & Anthony, J. (1995). Occupational stress andthe risk of alcohol abuse and dependence. Alcohol Clin Exp Res, 19, 647–655.Drug Enforcement Agency. (2004). Guidelines for a drug-free workforce. Retrieved onJuly 11, 2004, from www.usdoj.gov/dea/demand/dfmanual/index.htmlGiannakoulas, G., Katramados, A., Melas, N., Diamantopoulos, I., & Chimonas, E.

15. Addictions in the Workplace 353(2003). Acute effects of nicotine withdrawal syndrome in pilots during flight.Aviat Space Environ Med, 74, 247–251.Greiger, T. A., Fullerton, C. S., Ursano, R. J., & Reeves, J. J. (2003). Acute stress disorder,alcohol use, and perception of safety among hospital staff after the sniperattacks. Psychiatr Serv, 54, 1383–1387.Hersh, R. K., McPherson, T. L., & Cook, R. F. (2002). Substance use in the constructionindustry: A comparison of assessment methods. Subst Use Misuse, 37, 1331–1358.Horne, J. A., Reyner, L. A., & Barrett, P. R. (2003). Driving impairment due to sleepinessis exacerbated by low alcohol intake. Occup Environ Med, 60, 689–692.Howland, J., Mangione, T. W., Lee, M., Bell, N., & Levine, S. (1996). Employee attitudestoward work-site alcohol testing. J Occup Environ Med, 38, 1041–1046.Kahn, J., & Langlieb, A. (2002). Mental health and productivity in the workplace. SanFrancisco: Jossey-Bass.Lapham, S., Chang, G., & Gregory, C. (2000). Substance abuse intervention for healthcare workers: A preliminary report. J Behav Health Serv Res, 27, 131–143.Lapham, S. C., McMillan, G., & Gregory, C. (2003). Impact of an alcohol misuse interventionfor health care workers: 2. Employee Assistance Programme utilization, onthe job injuries, job loss, and health services utilization. Alcohol Alcohol, 38, 183–188.Leeman, C. P., Cohen, M. A., & Parkas, V. (2001). Should a psychiatrist report a busdrivers’ alcohol and drug abuse?: An ethical dilemma. Gen Hosp Psychiatry, 23,333–336.Lewis, P., & Gaule, D. (1999). Dealing with drug-seeking patients: The Tripler ArmyMedical Center experience. Milif Med, 164, 838–840.Mansky, P. A. (1999). Issues in the recovery of physicians from addictive illnesses.Psychiatr Q, 70, 107–122.Moore, R. D., Mead, L., & Pearson, T. A. (1990). Youthful precursors of alcohol abusein physicians. Am J Med, 88, 332–336.National Institute on Alcohol Abuse and Alcoholism. (2001, January). Alcohol Alert 51.Retrieved on December 20, 2004, from www.niaaa.nih.gov/publications/aa51.htmOffice of Applied Studies. (1999). Worker drug use and workplace policies and programs:results from the 1994 and 1997 NHSDA (SAMHSA). Rockville, MD: Author.Office of National Drug Control Policy. (2001). The economic costs of drug abuse in theUnited States, 1992–1998 (Publication No. NCJ-190636). Washington, DC: ExecutiveOffice of the President.Raglans, D., Krause, N., Greiner, B. A., Holman, B. L., Fisher, J. M., & Cunradi, C. B.(2002). Alcohol consumption and incidence of workers’ compensation claims: A5-year prospective study of urban transit operators. Alcohol Clin Exp Res, 26, 1388–1394.Roman, P. M., & Blum, T. C. (2002). The workplace and alcohol problem prevention.Alcohol Res Health, 26, 49–47.Trinkoff, A. M., & Storr, C. L. (1998). Substance use among nurses: Differences amongspecialties. Am J Public Health, 88, 581–555.Westreich, L. (2002). Americans and the Americans with Disabilities Act. J Am AcadPsychiatry Law, 30, 355–363.

CHAPTER 16Addiction and the LawAVRAM H. MACKRICHARD J. FRANCESSHELDON I. MILLERLegal problems, from violence to accidents to crime, frequently accompany useof substances of abuse and vice versa. Clinicians who deal with addictedpatients need a grasp of many forensic psychiatry issues in order to practice withskill and communicate effectively in legal settings. This chapter covers a widerange of issues relative to addiction and the law, including issues in criminaljustice system (e.g., not guilty by reason of insanity [NGRI], treatment forparolees or probationers, pleas for sentence reduction, advice to Drug Courts)or other settings, and civil matters such as inpatient and outpatient commitment,child custody, competence, and confidentiality.It is likely that the addiction psychiatrist will have interactions with thelegal system. A significant portion of the growing number of incarceratedAmericans suffers from addictions. Conversely, around 20% of patients withaddictions have sociopathy and major problems with the law, including offensessuch as driving while intoxicated (DWI), drug possession, and prescriptionforgery. Addiction work among this population may involve clinical care orexpert testimony. In each scenario, knowledge of the interface between addictionpsychiatry and the law is very important. This chapter is geared for thegeneral psychiatrist or the addiction psychiatrist who needs guidance in consultingas an expert in the intersection of substances and the law, which simultaneouslycan be interesting, rewarding, anxiety provoking, and hazardous.354

16. Addiction and the Law 355PSYCHIATRY AND THE LAWAny psychiatrist may, willingly or not, become involved in legal issues. Theuninitiated must become familiar with general knowledge on the law and psychiatry(Group for the Advancement of Psychiatry, 1991; Gutheil, 1998;Rosner, 2003). Some universals should be stated. First, in the United States,“local rules” matter. Every jurisdiction has its own laws, rules, case law, andadministrative regulations under which medicine and psychiatry are practiced,and these should be reviewed by the psychiatrist before addressing the facts.Second, in the United States, administrative, criminal, and civil cases areset in an adversarial system in which one side is pitted against the other. Theadversarial system can create situations in which the expert is attacked by theopposing side, and such attacks have gone as far as complaints to professional orethical boards, but experts very rarely have been accused of perjury (Binder,2002). Thus, maintaining a professional stance is vital. The forensic expert isalways better served in the position of friend to the Court (as is the case in DrugCourts), rather than to one of the parties.Third, it is important to be aware that there is an opprobrium against “junkscience.” The psychiatrist who serves as an expert witness under oath should beprepared for his or her ideas to be questioned, perhaps in great detail and incomparison with the general knowledge of the field. Until recently, the Federalstandard was that created by the Frye case, otherwise known as the “generalacceptance test,” but Daubert v. Merrell Dow and subsequent cases established anew precedent with which experts should be familiar (Gutheil & Stein, 2000)in order to be ethical and effective.ADDICTION AND THE LAWThere are areas of psychiatry and addiction testimony that are contested, evenif clinically valid and important. Therefore, some guidance into what is saidabout addictions and substances in court may be useful.“Addiction”: A Courtroom Definition“Addiction” is a powerful word, and it should not be misused. Its meaning carriesbiological, behavioral, and social connotations. Among physicians, it hasbeen interchangeable with “substance dependence,” and this has been linked todemonstrable alterations in neural activity. However, the medical communityalso has come to consider food, gambling, and sex as “addictions,” and attorneys,clients, and some doctors may wish to apply the suffix “-ism” to anybehavior they wish to portray as compulsive or uncontrollable. There has beena backlash to the expanding application of this word and, so far, courts have

356 IV. SPECIAL POPULATIONSobjected to this expansion; so one should exercise caution in using the term“addiction” when discussing behaviors rather than substances of abuse.Basics of DiagnosisIn forensic situations, it is essential to utilize diagnostic terms that are acceptedby all parties. The legal sphere is not the setting to further academic theories.The addiction psychiatrist must be vigilant about new theories and their prematureapplication, and should inform his or her side of the need to be criticalof the assertions of the other side’s expert. Notwithstanding current scientifictheories, the current classification of mental disorders, the Diagnostic and StatisticalManual of Mental Disorders (DSM-IV-TR; American Psychiatric Association,2000a) is the standard. On the other hand, DSM-IV-TR has an “imperfectfit” with the needs of courts: For example, the court often asks the expertfor predictions on the future, or degree of dangerousness, neither of which has aDSM category. In addition, courts and attorneys frequently misunderstandDSM-IV-TR substance use disorder (SUD) diagnoses, which should be clarified.AssessmentThere is no such thing as a “complete psychiatric assessment.” All forensic psychiatryassessments must be done with a particular focus and a question inmind. The forensic assessment of a subject for whom substances of abuse arepresent needs to include a thorough review of all history, including medical,psychiatric, and social function (we discuss correctional setting assessmentbelow). It is acceptable to utilize standardized instruments, especially insofar asthese may provide normalized data with which to make comparisons. Collateralsources of data are essential. Laboratory studies may be important, dependingon the time setting. Sinha and Easton (1999) have provided a guide for a“Forensic Substance Abuse Evaluation.”ADDICTION AND CRIMINAL LAWCriminality, Violence, and Substance AbuseThe various substances of abuse all seem to be associated with aggression or violenceduring intoxication or withdrawal (Hoaken & Stewart, 2003), or witheffects on personality when used chronically.Among the substances, alcohol has been most scrutinized: Independentof crime and incarceration, the relationship between alcohol and aggression(including suicide) has been well documented (Graham et al., 1998) in bothepidemiological (Murdoch, Pihl, & Ross, 1990) and “laboratory” (controlled

16. Addiction and the Law 357environment) studies (Bushman & Cooper, 1990). The findings of the EpidemiologicCatchment Area (ECA) Study indicated that those who met criteriafor antisocial personality disorder were 21 times as likely to developabuse or dependence on alcohol at some point in their lives (Moeller &Dougherty, 2001). There is a relationship between violence and other substancesas well, including nicotine and cannabis. The basis of these relationshipsis unknown, although theories abound from biological, environmental,to social causes.In terms of the relationship between substance use and crime, the link iswell documented. Seventy percent of those arrested for violent offenses testpositive for substances (Sinha & Easton, 1999). The MacArthur study foundviolence to be greatest among mentally ill persons using substances (Monahan& MacArthur Violence Risk Assessment Study, 2001). In this vein, some havesuggested that the decline in violent crimes in the United States in the 1990swas related to changes in the use of alcohol and other drugs (Greenfield &Henneberg, 2001). There is an association between severity of abuse and frequencyof criminal acts, especially as abuse becomes dependence.Associations between certain types of violence and substances also havebeen studied: Male-to-female domestic violence is associated with substanceuse. There is evidence suggesting that alcohol precedes or accompanies maritalviolence, especially among men (Leonard & Quigley, 1999), and especially duringpregnancy. Studies have shown that there is an increased risk of child abuseand child neglect when substances are used (Schuck & Widom, 2003). Finally,substances commonly are used by perpetrators of sexual assault. In perhaps 50%of all cases, the perpetrator has used alcohol.Accidents and injuries are clear consequences of substance use. Clinicianswho treat addicted persons may sense a need to report use in order to preventsuch events, especially for those whose personal or professional activities mayplace others at great risk. This is not guided by Tarasoff considerations, inwhich there are intended targets (Felthous, 1993). Our advice is to seek out thelaws in one’s own state and Federal law. Clinicians may need to make difficultchoices and should at least feel free to contact the interested professional orregulatory bodies. Seeking clarification from a judge may be helpful as well,when there is a wish to report in questionable cases (see Chapter 15 on workplaceaddictions, this volume).Substances in the CourtroomIn the Anglo-American adversarial criminal justice system, the basic goal ofcriminal proceedings is to establish responsibility for the illegal event. A majortenet of responsibility is the intention of the actor. A criminal convictionrequires the proof of mens rea or, “intent” to do the evil act, and it is around thisconcept that almost all debate and reasoning about substances hinge.

358 IV. SPECIAL POPULATIONSOver time, case law and statutes have almost completely eviscerated intoxicationas a defense against responsibility, but substances and their effects stillhave a place in criminal proceedings in terms of the mitigation of responsibility,when substance use treatment is mandated as an alternative to incarceration, orwhen the long-term medical or psychiatric effects of substances interfere with thedefendant’s ability to proceed. This section reviews these areas. The “irresistibleimpulse” defense, an antiquated and little-used argument, asserts that an impulseto commit the offense could not be resisted by the offender.There are few situations in which responsibility cannot be assigned to thecriminal offender. These include insanity, involuntary intoxication, and beingotherwise incompetent (such as being a minor). Voluntary intoxication itself isnot an excuse; nor has it been over the past 500 years of Anglo-American law,but it may alter the punishment (Slovenko, 1995). When “specific intent” isrequired to be convicted of a particular charge (e.g., murder rather than manslaughterfor a homicide), voluntary intoxication has been successfully used as adefense—that the perpetrator could not have had the specific intent as requiredby law. In some states, when accidents occur while a person is intoxicated, thepresence or absence of mens rea when the substance is first ingested must beassessed when determining intent (Wagenaar & Toomey, 2002).In general, intoxication can be exculpatory when it occurs via trickery orunder duress, in the case of previously unknown susceptibility to an atypicalreaction or side effect to a substance or medication. This is described by Myersand Vondruska (1998). In this sort of defense, mens rea is negated. However, insome jurisdictions, there are specific guidelines and limitations for an acceptableinvoluntary intoxication defense (Downs & Billick, 2000).“Strict liability crimes” are those in which mens rea is not required for aconviction. These include driving while intoxicated or driving under the influence(DWI or DUI). In a number of states, maximum sentences are mandated ifdeath results from a driver who was DWI yet there was only a minimal impactfrom the substance. “Settled insanity” is a situation in which long-term use,which is different from an acute intoxication or toxic psychosis, leads to achronic injury (Slovenko, 1995).Diminished capacity, a partial defense allowed in some jurisdictions, isused to reduce the integrity of the mens rea partial defense in cases in which specificintent is required. If the defense is able to prove the lack of specific intent,then guilt could be found for a lesser/other crime that does not have suchrequirement. This is contrary to the NGRI defense. According to the diminishedcapacity defense, due to intoxication, whether voluntary or not, the personcould not deliberate. The expert must check with the attorney as to whichcharge is a specific intent crime and what rules apply in which jurisdictions. Forexample, a person suffering from delirium tremens may strike out at a healthcare worker he perceives to be a bear coming toward him. Genetic factorsshould, perhaps, be taken into account in a wise and just sentencing.

16. Addiction and the Law 359“Blackouts” are real phenomena that can occur in the occasional user, aswell as in the chronic abuser or the alcohol-dependent person. They can leadto a person being unable to account for hours or days of his or her life. Duringa blackout, the individual may not be perceived by observers to have anyimpairment of cognitive or intellectual ability. This does not mean that committedacts were not intended. State-dependent memory may also occur, withreturn of some learning during intoxication. In some cases in which criminalor civil offenses have been alleged, the defendant who is an abuser of drugs oralcohol may state that he or she is not able to comment upon the act becausehe or she was in a state of “blackout.” The actor’s apparent lack of impairmentduring the actions leads to very different accounts of the action.ADDICTION AND CIVIL MATTERSCivil matters are often encumbered by addictions. The topics of civil law rangefrom family matters (e.g., divorce, custody) to administrative proceedings (e.g.,medical or pilot’s license proceedings), to personal injury, to negligence to willsand estates. As in criminal proceedings, the psychiatrist may be asked to placethe substance use in the context of the past behavior or to make predictionsabout future behavior. We discuss a number of frequently visited topics. Issuesrelating to the workplace and the Americans with Disabilities Act (ADA) arediscussed in Chapter 15, this volume.Family and Matrimonial LawIn disputes over divorce, custody, guardianship, adoption, or child safety, thesubstance use of any involved party is commonly at issue. The expert is oftenasked to comment upon the substance use of parents and effects on the child,with recommendations for custody, visitation, and treatment as a pretense forrights. The presence of an SUD does not mean lack of fitness, but it can be afactor. The fiercely adversarial nature of these proceedings often impedes theformation of a valid picture.Personal InjuryWhen an individual who is injured sues another party for damages, the defendantmight allege that the plaintiff was intoxicated at the time. Either sidemight need an addiction psychiatrist to assist or rebuff the claim of intoxicationand long-term addiction. Injured parties may also blame the party that providesthe substance of abuse. Many cases have exposed the liability of bars, bartenders,and parents of minors (Wagenaar, 2001).

360 IV. SPECIAL POPULATIONSDisabilityClaims for disability insurance (whether through the state or a private organization)may be based on a claim of addiction. Each case is decided on its ownmerits, but addiction psychiatrists are naturally the experts of choice. If the casegoes to court, the expert would seem essential. Complex management of addictionsin pain cases requires expertise to sort out whether or not return to work isindicated or possible.Other areas in which an addiction psychiatrist may have special expertiseinclude malpractice cases, either when a patient alleged that a physician made apatient become addicted, or when the physician was impaired by substances.Since workplace actions frequently lead to legal consequences, the addictionpsychiatrist is frequently involved in consultation regarding the workplace(Chapter 15, this volume). Sexual harassment cases may be brought in eithercriminal or civil settings and addictions may be raised as in issue in such cases aswell.ADDICTION AND CORRECTIONAL PSYCHIATRYThe nationwide decline in crime has been associated with a rise in the numberof incarcerated Americans, and a great proportion of these individuals haveactive SUDs or are dually diagnosed. It is important for a psychiatrist to reviewthe issues of correctional psychiatry, so that he or she may be prepared to adviseon screening, treatment, and recommendations for release. Basic guidelineshave been delineated for correctional facilities both by the American PsychiatricAssociation Manuscript (American Psychiatric Association, 2000b) and theNational Commission on Correctional Health Care (2003).There are three very different incarceration settings: lockup (upon arrest),jail (following arraignment, during trial, prior to sentencing, or in sentences ofup to 1 year), and prison (postsentencing more than 1 year). Psychiatric issuesdiffer greatly among these settings (Weinstein, Kim, Mack, Malavade, &Saraiya, in press). SUDs present different pictures in each setting.Correctional Center EpidemiologySubstance use and SUDs are essentially epidemic among the incarcerated.Peters, Greenbaum, Edens, Carter, and Ortiz (1998) found that 74% of inmatesin the U.S. criminal justice system have a lifetime DSM-IV SUD. Abram andTeplin (1991) found that a large majority of male jail detainees with severemental disorders had a co-occurring SUD at some point in their lifetime. Morethan half who had current severe psychiatric disorders had a co-occurring SUDor had used a substance at the time of arrest. These prevalence rates were signif-

16. Addiction and the Law 361icantly higher than rates in the general population, and were also higher thanrates found in patient populations (Abram & Teplin, 1991). Among womenjail detainees in Cook County, 72% with a current severe mental disorder hada co-occurring SUD at some point in their lifetime (Abram, Teplin, &McClelland, 2003). These rates were higher than those found among women inthe general population and among male jail detainees. Likewise, the rates of cooccurringmental disorders are elevated among the incarcerated. Peters andHills estimated in 1993 that between 3 and 11% of all inmates have both substanceuse and psychiatric diagnoses. This is a population that requires solidassessment for the misuse of substances.Benefits of Addressing the ProblemThe first stage of benefit is in terms of reduction of the aggression of intoxication.Finding and treating intoxication and withdrawal also reduce the potentialfor morbidity and mortality associated with intoxication (e.g., cocaine) orwithdrawal (e.g., alcohol). Proper recognition of SUDs can lead to long-termbenefits for the institution: When individuals receive treatment for addiction,research has shown that focused, rehabilitation-oriented treatment canlead to favorable outcomes following incarceration (Gendreau, 1996; Knight,Simpson, & Hiller, 1999), and moreso if aftercare is provided (Griffith, Hiller,Knight, & Simpson, 1999). A number of measures from a process evaluation ofa therapeutic community program suggest that the presence of a therapeuticcommunity within a prison is associated with significant advantages for managementof the institution, including lower rates of infractions, reduced absenteeismamong correctional staff, and virtually no illicit drug use among inmates.Over the longer term, the offender and society benefit, because there is areduced likelihood of eventual recidivism.Case FindingsClearly the cases are present and should be found, but how can they, or shouldthey, be found? This is an area of enormous interest with few answers. Fromlockups to jails to prisons, the potential types of misuse differ; therefore, so doesthe value of particular screening approaches and treatment plan choices. Aresource for those interacting with juveniles should be available as well(McClelland, Teplin, & Abram, 2004).New Arrest or SurrenderWhen an individual enters custody directly from the outside world, any of thedrugs of abuse may be present. This “intake” is a most critical time, when thestaff must be most careful to look for intoxication, overdose, or active with-

362 IV. SPECIAL POPULATIONSdrawal from any substance, but especially alcohol, benzodiazepines, or othersedatives. It is common for those who are surrendering to have had a “last hit”before entering incarceration. For long-term users who are not actively intoxicatedor in withdrawal, the opportunity to be referred to rehabilitation programscan be missed. Medical screening at intake can likewise be of greatimportance, because it alone may produce evidence of an SUD. Conversely, ahistory of an SUD prompts further, specialized medical assessment. These individualsare at high risk for infectious diseases such as human immunodeficiencyvirus (HIV) and the viral hepatidities, especially hepatitis C (Baillargeon et al.,2003).Screening instruments and other manner of case finding need to be appropriatefor the setting. In general, searching for SUDs among the incarcerated isdifficult because of a high degree of antisocial personality style, which includesdenial and sometimes the wish not to attend to one’s addiction. For this reason,the authority must use instruments or simple assumptions to lead to the case.Instruments such as the Michigan Alcoholism Screening Test (MAST) and theCAGE Questionnaire are helpful in the assessment of alcohol use in the primarycare setting but have not been specifically assessed for use among prisoners.It is likely that the single best means of finding cases is through face-to-faceclinical evaluations with nonaggressive interviewing styles. Additionally, findingson physical examinations, such as spider angiomata, needle tracks, nasalseptum injuries, or autonomic arousal may trigger suspicion. Testing of bodyfluids or hair is seen as costly and inefficient, since it basically serves to confirmeither use in the past days or at some point in the past 3 months. Nonetheless,urine, blood, and hair testing, which all have high rates of sensitivity and specificityfor cannabis, opiates, benzodiazepines, and alcohol, can help (see Chapter4, this volume). Screening for SUDs must also be geared to detect comorbidpsychiatric conditions, which are common among the addicted incarceratedpopulation.Long-Term IncarcerationFor those who remain in custody for months or years, another approach isneeded. In this setting, there is the opportunity for treatment and possibly rehabilitation.On the other hand, drugs and alcohol also make their way to prisoners.Authorities and clinicians must be ready to address both issues.There is great variation in the available resources given to long-term treatmentof addictions among the incarcerated. Unfortunately, many prison systemsdo not address addiction in long-term inmates. Or in some systems, addictionis addressed only in the last months of incarceration. On the other hand,other systems have ongoing Alcoholics Anonymous (AA) meetings, education,and group, and even individual, psychotherapies.

16. Addiction and the Law 363Dispositions after PrisonAddiction psychiatrists may work with parole boards to mandate treatment.There may be times when the psychiatrist is asked to comment to a paroleboard about an inmate who is addicted in prison or beforehand. On discharge,both inmates with SUDs and those with SUDs comorbid with psychiatric conditionsare at high risk of relapse, which may affect criminality as well. OneScottish study found that of the increased deaths after release, many were intravenousdrug users, especially those with HIV (Bird & Hutchinson, 2003). Someparole boards mandate treatment either using their own authority or by referringparolees to the mandated treatment programs (see below). Such requirementshave been accepted in the case of sex offenders but have not been successfullyutilized for addictions to this point.When asked by a court to suggest a treatment plan for the addictedoffender, it is best to offer multiple modes of treatment and surveillance. Considerresidential, groups, day treatment, medication management, and others.The period of treatment should be a minimum of 1 year. Random screens arebest done twice weekly. Attendance at required activities should be required.The clinician should reevaluate the individual on some regular basis.ALTERNATIVES AND ADJUNCTS TO, AND DIVERSIONS FROM,THE INCARCERATION/JUSTICE SYSTEMFor those with SUDs who have been or will likely become dangerous to themselvesor others, various states, counties, and federal government agencies havebeen developing ways in which to intervene. This includes “diversion” programs(such as drug courts), as well as mandated treatment laws. These institutionsmay protect the public from violence or accidents, and they may reduceexpenditure on incarceration.“Diversion” refers to institutions, practices, and laws that divert criminaloffenders who have a mental disorder or an SUD out of the standard criminaljustice system and into alternatives. There are moral and economic rationalesfor diversion, which may occur at any stage of the justice process, from arrest tosentencing. A review of the many programs can be found in a volume by theCouncil of State Governments (2002).Drug courts, one type of diversion, are special courts given the responsibilityto handle cases involving substance-abusing offenders through comprehensivesupervision, drug testing, treatment services, and immediate sanctions and incentives.These courts mandate treatment, seem to have low recidivism rates, andlead to education, cost savings, and drug-free babies. They have been shown tohave good outcomes, to save money, and to reduce criminal recidivism.

364 IV. SPECIAL POPULATIONSStates have created laws that can be used to force those with either mentaldisorders or SUDs into treatment plans. Thomsen Hall and Appelbaum (2002)have commented on the valid legal basis for this approach. In Robinson v. California,the U.S. Supreme Court ruled in 1961 that “a state might establish aprogram of compulsory treatment for those addicted to narcotics. Such a programmight require periods of involuntary confinement and penal sanctionsmight be imposed for failure to comply with established treatment procedures.”As of 1997, 31 states and the District of Columbia had statutes specificallyallowing involuntary treatment or commitment for dependent individuals. Thiscan be inpatient or outpatient treatment, or partial hospitalization. The criteriaand processes for commitment vary by state but usually require a judicial hearingin which the individual’s or the community’s safety is seen to be endangeredby the refusal of the patient to be in treatment. The use of monitored disulfiramadministration has been shown to increase compliance (Brewer, 1993).CONCLUSIONIn 1939, Penrose accurately predicted an inverse relationship between the numberof individuals in a society who are psychiatrically hospitalized and those withpsychiatric disorders who are incarcerated. For patients released from state,municipal, Veterans Administration, and private hospitals, homelessness, comorbidaddiction, and incarceration have resulted. In this era of continued hospitaldeinstitutionalization and increased incarceration, psychiatrists are increasinglyessential in forensic, legal, and correctional settings. This will be true so longas long-term institutions for the mentally ill are absent and community resourcesare inadequate; the next-best alternative will be the implementation and expansionof procedures and practices of diversion from the justice system. Clinicianscould have the greatest impact on helping addicted and mentally ill offenders andreducing their placement in the justice system by advocating for effective diversionprograms that not only promote proper medical care and maintain libertyrights but also protect the public. Clinicians need also to know how best to usecoercion wisely and compassionately as a means to confront denial, engagepatients in treatment, and liberate them from the ravages and confinement oftheir addiction. Working with these addicted patients, who suffer more than mostof humanity, can be personally interesting and rewarding.REFERENCESAbram, K. M., & Teplin, L. A. (1991). Co-occurring disorders among mentally ill jaildetainees: implications for public policy. Am Psychol, 46, 1036–1045.Abram, K. M., Teplin, L. A., & McClelland, G. M. (2003). Comorbidity of severe psy-

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366 IV. SPECIAL POPULATIONSMcClelland, G. M., Teplin, L. A., & Abram, K. M. (2004). Detection and prevalenceof substance use among juvenile detainees. Office of Juvenile Justice and DelinquencyPrevention Bulletin. Retrieved July 10, 2004, from www.ojjdp.ncjrs.org/publications/PubAbstract.asp?pubi=11680Moeller, F. G., & Dougherty, D. M. (2001). Antisocial personality disorder, alcohol,and aggression. Alcohol Res Health, 25, 5–11.Monahan, J., & MacArthur Violence Risk Assessment Study. (2001). Rethinking riskassessment: The MacArthur study of mental disorder and violence. Oxford, UK:Oxford University Press.Murdoch, D., Pihl, R. O., & Ross, D. (1990). Alcohol and crimes of violence: Presentissues. Int J Addict, 25, 1065–1081.Myers, W. C., & Vondruska, M. A. (1998). Murder, minors, selective serotoninreuptake inhibitors, and the involuntary intoxication defense. J Am Acad PsychiatryLaw, 26, 487–496.National Commission on Correctional Health Care. (2003). Standards for health servicesin prisons. Chicago: Author.Penrose, L. (1939). Mental disease and crime: Outline of a comparative study of Europeanstatistics. Br J Med Psychol, 18, 1–15.Peters, R. H., Greenbaum, P. E., Edens, J. F., Carter, C. R., & Ortiz, M. M. (1998).Prevalence of DSM-IV substance abuse and dependence disorders among prisoninmates. Am J Drug Alcohol Abuse, 24, 573–587.Peters, R. H., & Hills, H. A. (1993). Inmates with co-occurring substance abuse andmental health disorders. In H. J. Steadman & J. J. Cocozza (Eds.), Mental illness inAmerica’s prisons (pp. 159–212). Seattle, WA: National Coalition for the MentallyIll in the Criminal Justice System.Rosner, R. (Ed.). (2003). Textbook of forensic psychiatry (2nd ed.). New York: OxfordUniversity Press.Schuck, A. M., & Widom, C. S. (2003). Childhood victimization and alcohol symptomsin women: an examination of protective factors. J Stud Alcohol, 64(2), 247–256.Sinha, R., & Easton, C. (1999). Substance abuse and criminality. J Am Acad PsychiatryLaw, 27, 513–526.Slovenko, R. (1995). Psychiatry and criminal culpability. New York: Wiley.Thomsen Hall, K., & Appelbaum, P. (2002). The origins of commitment for substanceabuse in the U.S. J Am Acad Psychiatry Law, 30, 33–45.Wagenaar, A. C. (2001). Liability of commercial and social hosts for alcohol-relatedinjuries: A national survey of accountability norms and judgments. Public Opin Q,65, 344–368.Wagenaar, A. C., & Toomey, T. L. (2002). Effects of minimum drinking age laws:Review and analyses of the literature from 1960 to 2000. J Stud Alcohol Suppl,63(Suppl 14), 206–225.Weinstein, H., Kim, D., Mack A., Malavade, K., & Saraiya, A. (in press). Correctionalpsychiatry. In C. Scott (Ed.), The clinical handbook of correctional psychiatry. Washington,DC: American Psychiatric Press.

CHAPTER 17Pain and AddictionRUSSELL K. PORTENOYDAVID LUSSIERKENNETH L. KIRSHSTEVEN D. PASSIKThe complex issues at the interface between pain management and chemicaldependence have received increasing attention during the past decade. Themost intense focus from the clinical perspective has been on the evolving rolefor opioid therapy. In an interesting paradox, specialists in addiction usuallyfocus on the role of these drugs as a major cause of abuse, whereas pain specialistsfocus on their role as essential medications for pain and suffering. Althougheach discipline, of course, is aware of the problems addressed by the other, theantithetical nature of these perspectives historically has supported a lack ofcommunication between these two groups.Given the extraordinary prevalence and interactions between pain andchemical dependence, this lack of communication must be challenged. Bothchronic pain and substance abuse are highly prevalent problems. Numerous surveys,both domestic and international, have recorded a prevalence rate forchronic pain that is as high as 40% (Verhaak, Kerssens, Dekker, Sorbi, &Bensing, 1998). Suveys of substance abuse in the United States have indicatedthat 6–10% of the population regularly use illicit drugs, and approximately 33%have sampled one of these drugs at least once (Colliver & Kopstein, 1991;Groerer & Brodsky, 1992; Regier et al., 1984). It is inevitable that cliniciansencounter patients with pain who abuse drugs, and the need to address issuesthat relate to both pain and drug abuse occurs commonly.367

368 IV. SPECIAL POPULATIONSThe expanding role of opioid therapy in the treatment of chronic painlends particular urgency to the need for an accurate and dispassionate appraisalof the benefits and risks associated with pain control and chemical dependence.Medical perceptions surrounding opioid therapy have cycled dramatically duringthe past century (Musto, 1999; Rock, 1977). A more liberal approach toprescribing began during the latter part of the 20th century with worldwideendorsement of opioid therapy for cancer pain. This spurred a more gradualacceptance of the view that opioid therapy may be appropriate for larger numbersof patients with chronic pain. During the past 10 years, this acceptance hasadvanced throughout the community of pain specialists, driven by favorableexperiences with these drugs, incontrovertible evidence of widespread undertreatmentof pain, and the reduced stigmatization of opioid drugs. From thisperspective, opioid use was encouraged, with relatively little focus on thepotential risks associated with abuse, addiction, and diversion. Indeed, for somepractitioners, the myth of inevitable addiction was replaced by another myth,based on the misapprehension that chronic pain patients are somehow “immune”to the problems of misuse, abuse, addiction, or diversion (Friedman,1990).Pain specialists now have begun to realize that the issues related to chemicaldependence are central to the safe and effective use of opioids as analgesicsfor chronic pain. The emphasis is now on a balanced perspective, in whichpotential therapeutic benefits are weighed against this risk. With a balancedperspective, the divide between professionals in addiction medicine and painmedicine is narrowing, and a new level of discourse may enhance the ability ofeach discipline to comprehend clinical phenomena and formulate questions forresearch.DEFINITIONS AND PHENOMENOLOGYRedefining Abuse and AddictionBoth clinical practice and research depend on a valid nomenclature for thephenomena associated with drug abuse and addiction. Unfortunately, this terminologyhas been problematic historically, and clarification is a necessary firststep in advancing the understanding of the relationship between pain andchemical dependence.ToleranceTolerance is a pharmacological property defined by the need for increasingdoses of a drug to maintain effects (Dole, 1972; Martin & Jasinski, 1969). Itimplies that exposure to the drug itself is the “driving force” for the physiologi-

17. Pain and Addiction 369cal changes that result in declining effects. It may involve one drug effect, anycombination of effects, or all effects simultaneously.Although tolerance is commonly regarded to be a problematic occurrenceduring opioid therapy, this characterization only applies to analgesic or otherpotentially positive drug effects. Tolerance to adverse effects, such as respiratorydepression, nausea, and sedation, typically occurs rapidly and is a favorableoutcome. By opening the “therapeutic window,” this type of tolerance improvesthe risk:benefit ratio and allows dose titration in a manner that optimizes benefit.In contrast, tolerance to analgesia is not favorable and can potentially leadto several adverse outcomes. Clinicians and patients alike commonly expressconcerns that tolerance will compromise analgesic therapy by necessitatingprogressively higher, and ultimately unsustainable, doses. Equally important,the drug-induced decline in the reinforcing effects of these drugs could, in thesubpopulation predisposed to addiction, impel dose escalation in an effort toregain these effects, thereby potentially contributing to the development of thecompulsive drug use (Wikler, 1980; American Psychiatric Association, 2000).The concern about declining analgesic effects has not been borne out duringan extensive clinical experience with the long-term administration ofopioid drugs for the treatment of chronic pain (Nghiemphu & Portenoy, 2000;Portenoy, 1994). Most patients with chronic pain achieve an opioid dose associatedwith a favorable balance between analgesia and side effects, and remainat this dose for prolonged periods. When the need for dose escalation occurs,there are usually findings consistent with worsening pain (such as progression ofa pain-producing lesion), and tolerance cannot be said to be the “driving force”for dose escalation. Interestingly, addicts who receive methadone for maintenancetherapy also appear largely unaffected by the development of toleranceto the blocking actions of this drug.Moreover, a strongly reinforcing effect (a “high”) is distinctly uncommonwhen opioids are administered for pain in the nonaddicted population. Thedevelopment of tolerance to these effects is now viewed as neither necessarynor sufficient for the development of addiction.Physical DependencePhysical dependence is defined solely by the occurrence of an abstinence syndromefollowing abrupt dose reduction or administration of an antagonist(Dole, 1972; Martin & Jasinski, 1969; Redmond & Krystal, 1984). The doseand duration of treatment required to produce clinically significant physicaldependence in humans varies remarkably, and it is prudent to assume that thepotential for withdrawal exists after an opioid has been administered repeatedlyfor only a few days.

370 IV. SPECIAL POPULATIONSThere continues to be confusion about the differences between physicaldependence and addiction. Physical dependence, like tolerance, has been suggestedto be a component of addiction (American Psychiatic Association,2000); specifically, the desire to avoid withdrawal has been postulated to createbehavioral contingencies that reinforce drug-seeking behavior (Wikler, 1980).Although this phenomenon may be important in the subpopulation of individualspredisposed to addiction, it has no relevance for the vast majority ofpatients who receive opioid therapy for the treatment of acute or chronic pain.Physical dependence does not preclude the uncomplicated discontinuationof opioids during multidisciplinary pain management of nonmalignant pain(Halpern & Robinson, 1985), and opioid therapy is routinely stopped withoutdifficulty in the cancer patients whose pain disappears following effectiveantineoplastic therapy.In the clinical setting, therefore, the capacity to experience abstinenceshould never be labeled “addiction.” Unless abstinence is intentionally or unintentionallyinduced by discontinuation of therapy or administration of anantagonist (including a partial agonist like buprenorphine or an agonist–antagonist opioid), the phenomenon of physical dependence is subclinical andnot an issue in practice.Abuse and AddictionThe definitions of abuse and addiction are complex when potentially abusabledrugs are prescribed for specific medical indications (Kirsh, Whitcomb,Donaghy, & Passik, 2002). In the nomenclature of the American PsychiatricAssociation (2000), substance abuse refers to a maladaptive pattern of drug useassociated with some manifest harm to the user or others. A less restrictive definitioncharacterizes drug abuse as any use outside of socially accepted norms(Rinaldi, Steindler, Wilford, & Goodwin, 1998). Although the latter definitionraises concerns about cultural sensitivity in labeling abuse, it can be appliedmore easily to misuse of prescribed analgesics and therefore has greater utility inthe clinical setting. For the clinician, the use of any illicit drug, the maladaptiveuse of alcohol, and the use of prescribed drugs in a manner not intended bythe clinician all may be perceived as abuse. If a prescribed regimen is inappropriatelyused in a manner that is not persistent or extreme, however, the term“misuse” is sometimes applied.The American Psychiatric Association (2000) uses the term “substancedependence” to refer to addiction and defines this disorder as a maladaptivepattern of drug use associated with harm and, most importantly, characterizedby compulsive drug use. Although this definition can be applied broadly to painpatients, it has been criticized because of specific criteria that include toleranceand physical dependence. Other definitions of addiction developed by specialistsin addiction medicine (American Psychiatric Association, 2000; Rinaldi et

17. Pain and Addiction 371al., 1988; Wikler, 1980; World Health Organization, 1969) have been similarlycriticized.In an effort to bridge the gap between pain specialists and addiction specialists,a working group jointly created by the American Society of AddictionMedicine, the American Pain Society, and the American Academy of PainMedicine has developed a definition that has now been endorsed by all threeprofessional societies:Addiction is a primary, chronic, neurobiologic disease, with genetic, psychosocial,and environmental factors. . . . It is characterized by behaviors that include one ormore of the following: impaired control over drug use, compulsive use, continueduse despite harm, and craving. (Savage et al., 2003, p. 662)This definition is a useful starting point for clinicians and future investigators.Studies are needed to characterize each of the criteria empiricallyand to define the predictive validity of the various behaviors subsumed byeach.Aberrant Drug-Related Behaviorsand Their Differential DiagnosisThe diagnosis of addiction is based on the observation of a drug-related phenomenologythat meets defined criteria. In the clinical setting, where opioids orother potentially abusable drugs are prescribed for legitimate medical purposes,a broad range of aberrant drug-related behaviors occurs, from those that are relativelymild and limited (e.g., use of a prescribed dose to self-medicate a problemnot intended by the clinician, such as insomnia) to those that are profound(e.g., injection of an oral formulation). On the basis of clinical experience,these drug-related behaviors have been divided into those that are more or lessegregious and likely to predict addiction (Table 17.1).The observation that aberrant drug-related behavior varies in severity andmay or may not meet criteria for the diagnosis of addiction suggests that drugrelatedphenomenology in the clinical setting has a differential diagnosis(Table 17.2). Recognition of these potential disorders, which are not mutuallyexclusive, should guide a careful, ongoing assessment, the goal of which is toestablish the nature of the problem for the purpose of treatment planning(Passik, Kirsh, & Portenoy, 2002; Passik & Portenoy, 1998).The concept of “pseudoaddiction” is included in the differential diagnosisof aberrant drug-related behaviors and is particularly challenging when patientshave both pain and comorbid substance use disorders. “Pseudoaddiction” refersto the occurrence of problematic behavior related to desperation associatedwith unrelieved pain. Paradoxically, the behaviors disappear if access to analgesicmedication is increased. Originally described in the cancer population

372 IV. SPECIAL POPULATIONSTABLE 17.1. Aberrant Drug-Related BehaviorsBehaviors more suggestive of an addiction disorder• Selling prescription drugs• Prescription forgery• Stealing or “borrowing” drugs from others• Injecting oral formulations• Obtaining prescription drugs from nonmedical sources• Obtaining drugs from multiple medical sources without informing or despiteprohibition• Concurrent abuse of alcohol or illicit drugs• Multiple episodes of self-escalation of dose, despite warnings not to do so• Multiple episodes of prescription “loss”• Evidence of functional deterioration unexplained by the pain or other comorbidity• Repeated resistance to changes in therapy despite clear evidence of adverse effectsBehaviors less suggestive of an addiction disorder• Aggressive complaining about the need for more drug• Drug hoarding during periods of reduced symptoms• Requesting specific drugs• Openly acquiring similar drugs from other medical sources• Occasional unsanctioned dose escalation• Unapproved use of the drug to treat another symptom• Reporting psychic effects not intended by the clinician• Resistance to a change in therapy associated with “tolerable” adverse effects• Expression of family concerns(Weissman & Haddox, 1989), the term is now commonly applied to patientswith any type of chronic pain.Patients with addiction also may develop an increase in drug seeking thatis driven by uncontrolled pain. In some cases, this behavior reflects both addictionand pseudoaddiction. If the patient is receiving a prescribed opioid forpain, the diagnosis may only be clarified if medical access to the drug isincreased in a structured plan. Should drug-seeking behavior continue in thiscontext, the likelihood that pseudoaddiction predominates is less.TABLE 17.2. Differential Diagnosis of Aberrant Drug-Related Behavior• Addiction• Pseudoaddiction• Psychiatric disorders• Axis I disorders (e.g., depression, anxiety, somatoform)• Axis II disorders (e.g., borderline personality, sociopathic personality)• Encephalopathy (confusion in dose and interval of prescription)• Criminal intent

17. Pain and Addiction 373Impulsive drug use also may be unrelated to both addiction and pseudoaddiction.Instead, it may reflect the existence of another psychiatric disorder.For example, patients with borderline personality disorder may exhibit aberrantdrug taking to express fear and anger, or to improve chronic boredom. Similarly,some patients use opioids to self-medicate symptoms of anxiety or depression,insomnia, or problems of adjustment.Other causes of problematic drug-related behaviors occur uncommonly inthe clinical setting. Occasionally, drugs are misused because of a confusionalstate. This problem is exemplified by the repetitive use of a hypnotic at night,particularly in the elderly. Rarely, patients engage in criminal behavior, divertingcontrolled prescription drugs for profit.Categories of Substance AbusersThe challenge of pain assessment and management in the population with substanceabuse presumably varies with many specific characteristics. For example,patients with a history of addiction presumably pose greater concerns as a groupthan those whose involvement with drugs never reached this level. Similarly, itis likely that patients with a remote history of drug abuse or addiction have agreater potential for responsible drug use than those who are actively abusing(Fultz, 1975; Gonzales & Coyle, 1992; Macaluso, Weinberg, & Foley, 1988).These observations may influence the assessment of risk during therapy andthereby guide therapeutic decision. Studies are badly needed to confirm andclarify the nature of these impressions given their relevance to practice.Patients who are receiving opioid agonist therapy for opioid addiction,either methadone or buprenorphine maintenance, represent another importantsubgroup. A recent survey indicated that 37% of methadone patients experiencechronic severe pain, and 65% report interference by pain with functioning(sleep, affect, physical activity, and social relationships) (Rosenblum et al.,2003). Two-thirds of those with chronic severe pain had been prescribed anopioid analgesic during the 3 months prior to the survey.Like those patients who have a remote history of substance abuse, thosewho are receiving a substitution therapy and have a well-established recoveryprobably can control a therapeutic opioid regimen, as long as it is carefullymonitored and structured. Indeed, it is likely that undertreatment of chronicpain, which may relate to clinician bias, reluctance of patients to seek care, orreduced effectiveness of standard therapy because of opioid tolerance, is agreater risk in this population than the occurrence of iatrogenic relapse. Studiesare needed, however, to evaluate the risks and benefits of opioid treatment inthis population and the barriers to effective therapy.The treatment of pain in patients with active drug abuse is particularlychallenging. Pain management in this population is complicated by the druguse itself, the adverse physical and psychosocial consequences that result, and

374 IV. SPECIAL POPULATIONScommon medical and psychiatric comorbidities. The degree of psychopathologymay be severe enough that a useful therapeutic alliance is impossible, and boththe veracity of the complaints and adherence to prescribed therapies becomemajor problems. Some patients cannot be treated with any potentially abusabledrug.Careful assessment is again critical to appropriate management. The typesof drugs abused, the extent of the consequences, and the comorbidities must beclarified. An understanding of the past psychiatric condition of the patient canprovide a context for therapeutic decisions. For example, sociopathy is relativelycommon among a subset of addicts (Hill, Haertzen, & Davis, 1962; Hill,Haertzen, & Glaser, 1960), and information about the occurrence of sociopathicbehaviors prior to the diagnosis of chronic pain can inform the decisionto treat with potentially abusable drugs. Straightforward questioning about illegalpractices may yield surprisingly frank answers, from which an assessment ofthese behaviors can be made.Categories of Patients with PainPatients with pain can be categorized in several clinically meaningful ways.Some distinctions are particularly relevant to the selection of treatmentapproaches.Most patients who require opioid therapy present with acute monophasicpain that may accompany trauma or a procedure and is expected to be selflimited.When severe, the short-term administration of an opioid drug is widelyconsidered to be medically appropriate treatment. Surveys suggest that thesepain syndromes are often undertreated (Edwards, 1990; Perry & Heidrich,1982).Recurrent acute pains also are extremely prevalent. They include commonpainful disorders, such as headache and dysmenorrhea, and many diseases associatedwith periodic flares, including sickle-cell anemia, inflammatory boweldisease, and some arthritides or musculoskeletal disorders. The preferred treatmentof these recurrent pains varies with the diagnosis and severity. The use ofopioid therapy is conventional practice for some, such as the pain of sickle-cellanemia. The decision to implement a trial should be based on an assessment ofpain characteristics and risks, rather than on diagnosis alone.A third category is chronic pain associated with cancer or other progressivemedical disease. Opioid therapy is considered to be the major therapeuticapproach for patients with moderate or severe cancer pain (American PainSociety, 2003; Portenoy & Lesage, 1999), and pain associated with advancedmedical illness of other types, including pain due to AIDS.The role of opioid therapy in chronic pain syndromes of other types is lesswell accepted (see below). These syndromes include numerous disorders associatedwith nonprogressive organic lesions, such as osteoarthritis and various

17. Pain and Addiction 375nerve injuries. They also include many syndromes defined solely by the patternof pain and associated symptoms, including chronic daily headache syndrome,fibromyalgia, chronic pelvic pain of unknown origin, and many cases of backand neck pain. A small subgroup has pain and disability that is perceived by theclinician to be primarily related to psychopathology. These patients are characterizedin psychiatric parlance as having a somatoform disorder (American PsychiatricAssociation, 2000), usually a pain disorder. More generically, the term“chronic pain syndrome” is often applied, denoting a chronic pain associatedwith a high level of disability and psychiatric comorbidity. Finally, somepatients with chronic pain have no identifiable medical or psychiatric syndrome;these pains are best termed “idiopathic” (Arner & Myerson, 1988).PAIN ASSESSMENT AND MANAGEMENTThe skills required to treat pain in any patient population include the ability toperform a comprehensive assessment and select a treatment strategy based onthe diagnostic formulation. If drug therapy is used for pain, competent managementdepends on the ability to implement state-of-the-art prescribing principles.For opioid pharmacotherapy, the latter skills must be accompanied by thecapacity to perform an assessment of the risks associated with misuse, abuse,addiction and diversion, and the ability to manage these risks over time. Theseskills are particularly needed in the population of chronic pain patients with ahistory of substance abuse.Pain AssessmentChronic pain is a complex, multidimensional phenomenon. It is commonly associatedwith other symptoms and disturbances in function. It is best conceptualizedas a chronic illness that can be managed but seldom cured. The goals of therapyusually relate to comfort, functional restoration, and improved quality of life.Given this complexity, comprehensive pain assessment requires historytaking that focuses on the pain complaint, its consequences, prior treatments,relevant comorbidities, and other elements in a routine history. The characteristicsof the pain include intensity, temporal features, location, quality, and provokingor relieving factors. Intensity should be measured, usually with a verbalrating scale (e.g., “mild,” “moderate,” “severe”) or a numerical scale (e.g., “0–10”). The selection of the specific metric is less important than its regular applicationover time. Pain quality is assessed by eliciting verbal descriptors, such as“sharp,” “burning,” “lancinating,” or “dull.” The temporal pattern includesonset, course (progressive, stable, or fluctuating) and daily pattern.The history also must characterize the impact of the pain and specificallyquery both physical and psychosocial functioning. The objective is to under-

376 IV. SPECIAL POPULATIONSstand the role of the pain in the patient’s life. Depending on the patient, thismay require a discussion about work, social engagements, intimate relationships,interactions with health care providers, or other experiences.The history of prior treatments for the pain should illuminate both prescribedand nonprescribed therapies. If prescribed drugs have been used, it isimportant to review the doses and durations of therapy, and to determinewhether the lack of effectiveness was related to side effects.Relevant comorbidities should be explored in both the physical andpsychosocial domains. The psychosocial history should seek information onpremorbid psychiatric disease, work and education history, current psychologicalstate (particularly anxiety and depression), and premorbid interpersonalproblems. A history of substance use is essential and should include informationabout the prior and present use of both licit (e.g., alcohol, tobacco, over-thecounterand prescription drugs) and illicit drugs.In patients with a known history of substance abuse, the interviewer mustgather detailed information on the specific pattern of addictive behaviors (e.g.,drugs, routes, frequency of administration, means of acquisition, means offinancing). The perceived relationship between these behaviors and the painshould be clarified.History, physical examination, and results of diagnostic studies provide thedata for a meaningful interpretation of the pain. This interpretation can beviewed from several perspectives. First, an etiology for the pain should be characterized,if possible. This etiology, which is usually reflects some structuralpathology, may be a target for primary treatment.Second, the data may allow labeling of the pain by syndrome. Syndromeidentification can be very useful in guiding the selection of the appropriatemanagement plan and indicating prognosis. Appropriate diagnosis of specificpain syndromes is facilitated by the taxonomy of pain developed by the InternationalAssociation for the Study of Pain (Merskey & Bogduk, 1994).Third, the information should permit inferences to be drawn about thepredominating pathophysiology. Most broadly, pain can be classified as havinga pathogenesis that is organic, psychogenic (e.g., somatoform disorder), mixed,or unclassifiable (idiopathic pain). Pain with a predominating organic contributioncan be described as either nociceptive or neuropathic (American PsychiatricAssociation, 2000; Arner & Myerson, 1988; Portenoy, Payne, & Jacobsen,1999). Although this is a gross simplification of complex biological processes, ithas clinical utility and is widely employed. Nociceptive pain is perceived to beconsistent with the degree of evident tissue injury, and is therefore conceptualizedas being related to the ongoing activation of pain-sensitive primary afferentneurons. Subtypes include somatic pain (related to injured somatic structures,such as bone and joint) and visceral pain (related to injury to visceral structures).Neuropathic pain results from aberrant somatosensory processing in thecentral or peripheral nervous system and is disproportionate to the extent of

17. Pain and Addiction 377evident tissue injury. There are numerous well-defined syndromes, includingpostherpetic neuralgia, painful neuropathy, poststroke pain, phantom limbpain, and complex regional pain syndrome (reflex sympathetic dystrophy andcausalgia).The distinction between nociceptive and neuropathic pain has clinical relevance.If a pain is nociceptive and the underlying etiology can be eliminated,or isolated from the central nervous system, long-term analgesia is expected.The profound analgesia associated with joint replacement illustrates this observation.In contrast, the diagnosis of a neuropathic pain suggests the use of medicationsthat appear relatively specific for pains of this type (see below).Management of Chronic PainThe pain assessment guides the selection of therapies. For the patient withchronic pain, particularly pain associated with disability, a multimodality strategytargeted to both pain and disability may be preferable. There are numerousTABLE 17.3. Therapeutic Strategies for Pain Management1. Primary therapies directed against the underlying etiology2. Primary analgesic therapies• Pharmacological approachesExamples: Nonopioid analgesicsAdjuvant anaglesicsOpioid analgesics• Rehabilitative approachesExamples: Physical/occupational therapyOrthoses/prostheses• Psychological approachesExamples: Cognitive-behavioral therapy• Anesthesiological approachesExamples: Neural blockadeNeuraxial infusion• Neurostimulatory approachesExamples: Transcutaneous electrical nerve stimulationDorsal column stimulation• Surgical approachesExamples: Cordotomy• Complementary and alternative medicine approachesExamples: AcupunctureMassageNeutraceuticals• Lifestyle changesExamples:Weight lossExercise

378 IV. SPECIAL POPULATIONSapproaches that may be combined in such a strategy (Table 17.3). If primarytherapy against an identified etiology is possible, and appropriate, this should beconsidered as symptomatic treatments are offered.Analgesic PharmacotherapyDrugs used to treat chronic pain can be divided in three categories: nonopioidanalgesics (acetaminophen and the nonsteroidal anti-inflammatorydrugs [NSAIDs]), adjuvant analgesics, and the opioids. Opioid pharmacotherapyis most relevant for the current discussion.OPIOID ANALGESICSPain specialists now consider long-term opioid therapy to be a major element inthe approach to chronic pain, and specialists in pain medicine and in addictionmedicine have begun to discuss the role of this approach in patients with historiesof drug abuse or addiction. During the past few years, there has been a dramaticincrease in the willingness of primary care physicians to consider longtermtreatment for selected patients. As a result, overall access to these drugshas risen substantially. Concurrently, indicators of abuse and diversion havealso tracked upward. Warnings raised by regulators and law enforcement havebegun to increase concerns on the part of prescribers about the possibility ofinvestigation and even sanction for prescribing opioids. This concern has beena constant in the United States for many decades and has been viewed by painspecialists as a significant barrier to appropriate opioid use.The call for a more balanced approach to the role of opioid drugs derivesfrom this present tension. Whether from the larger perspective of society orhealth care, or the microperspective of the individual clinician, the appropriateparadigm now emphasizes the need for a more nuanced perspective. This perspectiveaccepts the legitimate role of opioid therapy in the management ofappropriate patients with chronic pain (and the likelihood that prescribingneeds to be increased to address the problem of undertreated pain) and concurrentlyrecognizes the need to minimize the risk of adverse outcomes associatedwith chemical dependence. This paradigm now forms the foundation for themanagement principles that guide opioid therapy (Table 17.4).Patient Selection. It is no longer appropriate to peremptorily reject the useof opioid drugs solely on the basis of pain syndrome or the psychiatric conditionof the patient. Given the existing data and a large clinical experience, the mostreasonable posture is to consider a trial of opioid therapy for any patient withchronic or frequently recurrent pain of moderate to severe intensity, and thento base the decision to proceed or not on the responses to the following questions:

17. Pain and Addiction 379TABLE 17.4. Proposed Guidelines for the Management of Long-Term Opioid Therapy1. Chronic opioid therapy should be considered for any patient with chronic or frequently recurrentpain of moderate to severe intensity, based on the responses to the following questions: (a) What isconventional practice for pain of this type? (b) Are opioids likely to work well? (c) Is the patient atrelatively increased risk of side effects by virtue of medical comorbidities or their treatments? (d)Are there other available therapies that might be considered in lieu of an opioid trial, for whichthere is evidence of the same or better efficacy at no greater risk? (e) Is the patient likely to manageopioid therapy responsibly? (f) Does this patient have a pain problem for which opioid therapy couldbe administered given the clinician’s knowledge and skills; if not, could the patient be managedwith the help of a consultant, or should referral be considered?2. A single clinician should take primary responsibility for treatment. Treatment must be preceded by acomprehensive assessment that includes a detailed evaluation of current and past drug use. Pastmedical records should be obtained, and if needed, other health care providers, family, and pharmaciesshould be contacted to assess prior drug-taking behavior.3. Patients should give informed consent before the start of therapy and the consent discussion shouldbe documented in the medical record. This discussion should cover the issue of addiction, potentialfor cognitive impairment and other side effects, and the goals of the therapy.4. Based on the assessment, clarify expectations regarding risk of problematic drug-related behavior andstructure a treatment approach based on the level of risk. The approach may or may not incorporateactions such as very frequent visits, urine drug screening, required treatment by a mental health careprovider or addiction medicine specialist, requirement to participate in ongoing addiction treatment,a written agreement stipulating expectations and consequences for problematic behavior, a requirementto use one pharmacy and do pill counts at visits, treatment with only long-acting drugs, andother strategies. None of these approaches are needed for some patients; others require very tightcontrols to enhance monitoring and assist the patient in maintaining responsible use.5. After drug selection, doses should be given on an around-the-clock basis if the pain is continuous;several weeks should be agreed upon as the period of initial dose titration, and although improvementin function should be continually stressed, meaningful partial analgesia should be accepted asthe appropriate goal of therapy.6. Failure to achieve at least partial analgesia at relatively low initial doses in the patient with no substantialprior exposure raises questions about the potential treatability of the pain syndrome withopioids; such an occurrence should lead to reassessment of the pain syndrome.7. Emphasis should be given to attempts to capitalize on improved analgesia by gains in physical andsocial function. Opioid therapy should be considered complementary to other analgesic and rehabilitativeapproaches.8. Exacerbations of pain may occur and, following a careful assessment, the clinician may decide toincrease the stable dose. This change in therapy should be stated clearly for the patient and documentedin the medical record. If repeated dose escalation is needed to maintain pain control, theclinician should reevaluate the pain syndrome and the patient.9. Ongoing monitoring of a range of outcomes is essential. At each contact, assessment should specificallyaddress (a) comfort (degree of analgesia; self-report instruments may be helpful but should notbe required); (b) opioid-related side effects; (c) functional status (physical and psychosocial); (d)existence of aberrant drug-related behaviors.10. Initially, most patients must be seen and assessed at least monthly. If therapy is uneventful and consistentlybeneficial, monitoring can become less frequent. If, however, monitoring reveals problematicdrug-related behavior, this should initiate an evaluation intended to interpret the phenomenon.Treatment for a new diagnosis (e.g., addiction) may be needed, as well as a new strategy for theanalgesic drugs. In some cases, tapering and discontinuation of opioid therapy will be necessary.Other patients may appropriately continue therapy within a revised structure for monitoring therapy(see item 4). Consideration should be given to consultation with an addiction medicine specialist.11. Documentation is essential, and the medical record should specifically address comfort, side effects,functional status, and the occurrence of aberrant behaviors repeatedly during the course of therapy.

380 IV. SPECIAL POPULATIONS1. What is conventional practice for pain of this type?2. Are there other available therapies that might be considered in lieu ofan opioid trial, for which there is a reasonable likelihood of the same orbetter efficacy at no greater risk?3. Is the patient at relatively increased risk of side effects by virtue of medicalcomorbidities or their treatments?4. Is the patient likely to manage opioid therapy responsibly?5. Is a trial of opioid therapy in this patient appropriate given the clinician’sknowledge and skills; if not, could the patient be managed withthe help of a consultant, or should referral be considered?These questions apply to all patients, irrespective of drug use history. Theyimply that there is no population for whom opioids are absolutely contraindicated,but that concerns such as the ability to control drug use are central in thedecision-making process.Principles of Prescribing. Guidelines for the selection and administration ofopioid drugs derive from knowledge of opioid pharmacology and clinical experience(American Pain Society, 2003; Portenoy & Lesage, 1999; World HealthOrganization, 1996) and follow a few key principles.1. Issues in drug selection. Opioids can be classified as pure agonistsand agonist–antagonist drugs (Table 17.5). In contrast to the pure agonists,the agonist–antagonist opioids, including the mixed agonist–antagonists (e.g.,pentazocine, nalbuphine, butorphanol, dezocine) and the partial agonists (e.g.,buprenorphine), are characterized clinically by a ceiling effect for analgesia, thecapacity to precipitate an abstinence syndrome in patients who are physicallydependent on pure agonists, and a lesser degree of “liking” by those with thedisease of addiction (Houde, 1979; Hoskin & Hanks, 1991). Some (pentazocineand butorphanol) have an incidence of psychomimetic effects substantiallygreater than that of the agonist drugs.With the exception of buprenorphine, which now is also used as agonisttherapy for opioid addiction, the agonist–antagonist drugs are not generallyconsidered for chronic pain management. Although these drugs appear to haveless abuse potential than the pure agonists and therefore might be selected forlonger term use in patients with drug abuse histories, no specific data supportthe comparative safety and efficacy of this approach, and most pain specialistsemploy pure agonist drugs even with these patients. Because of the risk of precipitatingan abstinence syndrome, agonist–antagonists should not be administeredto patients who have developed physical dependence to opioids.In the United States, the most common approach to the treatment ofmoderate pain involves the administration of a product combining a nonopioidanalgesic (acetaminophen, aspirin, or ibuprofen) and an opioid (hydrocodone,

17. Pain and Addiction 381codeine, oxycodone, or propoxyphene). If the maximum daily dose of thenonopioid analgesic is reached without providing adequate pain relief, thepatient is considered for a trial of a single entity pure agonist drug. Tramadol isa centrally acting analgesic with a mechanism that is partially opioid and also iscommonly tried for moderate pain.Pure agonist drugs commonly employed for severe pain include morphine,hydromorphone, oxycodone, fentanyl (transdermal formulation), levorphanol,oxymorphone (rectal formulation and oral formulation in development), andmethadone. Some clinicians use meperidine in this setting, but this generallyshould be avoided because of potential toxicity (dysphoria, tremulousness,hyperreflexia, and seizures) related to the accumulation of a metabolite(normeperidine), especially in renally impaired patients (Kaiko et al., 1983).The modified-release, long-acting drugs now are usually favored for thetreatment of chronic pain. These include several morphine formulations, transdermalfentanyl, and an oxycodone formulation. Other modified release drugs,such as oxymorphone, hydromorphone, and buprenorphine, will most likely beavailable soon. Methadone is long acting by virtue of its half-life; it, too, isoften considered in this setting (see below).There is great individual variation in the response to the different pureagonist drugs, an observation that has justified the use of sequential opioid trialsto identify the most favorable drug. This practice is generally known as opioid“rotation” (de Stoutz, Bruera, & Suarez-Almazor, 1995). Initial drug selection isusually influenced by prior experience with opioids, cost, and the preferences ofthe patient. Morphine has active metabolites that accumulate in patients withrenal insufficiency (Peterson, Randall, & Paterson, 1990; Sjogren, 1997) andmay be less preferred when renal function is expected to vary. On the basis ofextensive clinical observation, transdermal fentanyl may be preferred whenopioids are expected to cause severe constipation or other gastrointestinal toxicities.Despite the media awareness of oxycodone abuse, there is no substantiveevidence that this drug possesses characteristics that increase its risk relative toothers. Nonetheless, if street value is an issue that influences drug selection,drugs that raise concern now include oxycodone, hydrocodone, and hydromorphone.Methadone is gaining in popularity as a drug for long-term opioid therapyfor pain. It is relatively inexpensive, has no active metabolites, and may possesshigh potency when substituted for another pure mu agonist drug. The lattereffect may be related to the d-isomer of the commercially available racemicmixture, which is an antagonist at the N-methyl-D-aspartate (NMDA) receptor(Bruera & Neumann, 1999). Studies of NMDA antagonists suggest that thiseffect may be associated with an independent analgesic potential, and the abilityto partially reverse opioid tolerance (Davis & Inturrisi, 1999).Enthusiasm for the expanded use of methadone as an analgesic is temperedby several characteristics. Despite its long half-life, and contrary to its daily

TABLE 17.5. Opioid AsnalgesicsEquianalgesic Half-lifedoses a (hours)Peak effect(hours)Duration ofeffect (hours) CommentssPure agonists (morphine-like)Morphine 10 i.m. 2–3 0.5–1 3–6 Standard comparior for opioids.20–60 p.o. b 2–3 1.5–2 4–7 Multiple routes available.Controlled-release morphine 20–60 p.o. b 2–3 3–4 8–12Sustained-release morphine 20–60 p.o. b 2–3 4–6 24Hydromorphone 1.5 i.m. 2–3 0.5–1 3–4 Multiple routes available.7.5 p.o. 2–3 1–2 3–4Oxycodone 20–30 p.o. 2–3 1 3–6 Combined with aspirin or acetaminophen for moderate pain;available orally without coanalgesic for severe pain.Controlled-release oxycodone 20–30 2–3 3–4 8–12Oxymorphone 1 i.m. — 0.5–1 3–6 No oral formulation.10 p.r. — 1.5–3 4–6Meperidine 75 i.m. 2–3 0.5–1 3–4 More CNS excitation than with other opioids. Not300 p.o. 2–3 1–2 3–6preferred for chronic pain due to potential toxicity.Heroin 5 i.m. 0.5 0.5–1 4–5 Analgesic action due to metabolites, predominantly inmorphine; not available in United States.Levorphanol 2 i.m. 12–15 0.5–1 3–6 Long half-life; accumulation occurs after starting or4 p.o.increasing dose.Methadone 10 i.m. 12– >150 0.5–1.5 4–8 Risk of delayed toxicity due to accumulation; useful to start20 p.o.to start dosing on p.r.n. basis, with close monitoring.Codeine 130 i.m. 2–3 1.5–2 3–6 Usually combined with nonopioid.200 p.o.382

Propoxyphene hydrocholorideor napsylate— 12 1.5–2 3–6 Toxic metabolite accumulates with overdose but notsignificant at doses used clinically; often combined withnonopioid.Hydrocodone — 2–4 0.5–1 3–4 Only available combined with acetaminophen.Dihydrocodeine 2–4 0.5–1 3–4 Only available combined with acetaminophen or aspirin.Partial agonistsBuprenorphine 0.4 i.m. 2–5 0.5–1 4–6 Can produce withrawal in opioid-dependent patients; has0.8 s.l. 2–3 5–6ceiling for analgesia; s.l. tablet not available in UnitedStates.Mixed agonist–antagonistsPentazocine 60 i.m. 2–3 0.5–1 3–6 Produces withdrawal in opioid-dependent patients; oral180 p.o. 2–3 1–2 3–6formulation combined with naloxone or nonopioid in theUnited States; ceiling doses and side-effect profile limitsrole in chronic pain.Nalbuphine 10 i.m. 4–6 0.5–1 3–6 Same as pentazocine.No oral formulation.Not preferred for chronic pain.Butorphanol 2 i.m. 2–3 0.5–1 3–4 Same as nalbuphine.Dezocine 10 i.m. c 1.2–7.4 0.5–1 3–4 Same as nalbuphine.Note. p.o., orally; i.m., intramuscularly; p.r., rectally; p.r.n., as needed; s.l., sublingually; CNS, central nervous system.aDose that provides analgesia equivalent to 10 mg i.m. morphine. These ratios are useful guides when switching drugs or routes of administration. When switching drugs, reducethe equianalgesic dose of the new drug by 25–50% to account for incomplete cross-tolerance. The major exception to this is methadone, which appears to manifest a greaterdegree of incomplete cross-tolerance than other opioids; when switching to methadone, reduce the equianalgesic dose by 75–90%.bExtensive survey data suggest that the relative potency of i.m.:p.o. morphine of 1:6 changes to 1:2–3 with chronic dosing.cApproximate equianalgesic dose suggested from meta-analysis of available comparative studies.383

384 IV. SPECIAL POPULATIONSadministration in the treatment of opioid addiction, the use of methadone as ananalgesic requires multiple doses per day. The long and variable half-life, whichranges from 12 hours to more than 150 hours (Plummer, Gourlay, Cherry, &Cousins, 1988), increases the risk of accumulation during dose titration.Patients who are predisposed to adverse effects due to advanced age or majororgan failure require particularly careful monitoring (for a period of more than 1week) when the dose of methadone is increased. There also have been recentconcerns about the potential for methadone to cause a prolonged QT syndrome,and thereby predispose to serious cardiac arrhythmias (Kornick et al.,2003). The data are yet limited, and studies are underway to evaluate this further.2. Issues in the selection of a route. The oral and transdermal routes are preferredfor chronic opioid therapy due to their simplicity and acceptability.Chronic parenteral administration, either continuous subcutaneous infusion orcontinuous intravenous infusion through an indwelling venous access device, isusually considered in selected patients with advanced medical illness. Neuraxialinfusion via the epidural or subarachnoid route has achieved a high level ofsophistication and is available in developed countries for a small subgroup ofchronic pain patients, typically those with intolerable side effects from systemicdrugs (Plummer et al., 1991; Smith et al., 2002). The utility of this approach islikely to increase as studies establish the effectiveness of drug combinations andnew drugs are approved specifically for intraspinal use.Alternative routes have also been developed to deliver short-acting opioidsfor the treatment of breakthrough pain. Oral transmucosal fentanyl citrateis now available and has an onset of effect substantially faster than orallyadministered drugs (Fine, Marcus, Just De Boer, & Van der Oord, 1991). Othersystems, including iontophoretic transdermal, buccal, and intrapulmonary drugdelivery, are in development.3. Issues in dosing. The most important step in optimizing opioid therapy isindividualization of the dose through a process of dose titration. It is usuallymore effective to prevent the recurrence of pain than to abort it, and fixedscheduledosing is preferred when treating continuous or frequently recurrentpain. “As needed” dosing may be useful during the initiation of therapy and ismost commonly employed when a short-acting “rescue” opioid is combinedwith a long-acting drug to treat acute exacerbations of pain (breakthroughpain) (Portenoy et al., 1999). Although the addition of a rescue opioid is conventionalpractice in the management of cancer pain, it should be viewed as anoption that may or may not be appropriate in any specific case. The use of rescuemedication may be particularly problematic in those with a history ofaddictive disease, whose potential for abuse or relapse may be greater withaccess to a short-acting opioid.Once an opioid and route of administration are selected, the dose shouldbe increased until adequate analgesia occurs or intolerable and unmanageable

17. Pain and Addiction 385adverse effects supervene. The opioid responsiveness of a specific pain syndromecan only be ascertained by dose escalation to limiting adverse effects.The opioid dose is immaterial as long as the patient attains a favorable balancebetween analgesia and adverse effects.Although doses typically stabilize for prolonged periods during long-termmanagement, dose escalation is usually required at intervals to maintain analgesia.In patients with progressive medical illness, this dose escalation is usuallyexplained by a worsening of the pain-producing organic lesion (Nghiemphu &Portenoy, 2000; Portenoy, 1994). As observed previously, experience withlong-term management of pain suggests that tolerance is rarely the “drivingforce” for dose escalation in the clinical setting.Relative potencies have been determined for most pure agonist drugs insingle-dose analgesic assays (Table 17.5). Using potency ratios, equianalgesicdose tables have been created that provide guidance when switching drugs orroutes of administration (Indelicato & Portenoy, 2002). Due to incompletecross-tolerance between opioids, which may result in a potency greater thananticipated for the newly initiated drug, a change from one drug to anothershould always be accompanied by a 25–50% reduction in the calculatedequianalgesic dose. The exceptions to this include methadone, which should bereduced by 75–90% when initiated after treatment with another pure agonistdrug, and transdermal fentanyl, which should be started at the dose indicated inthe package insert (dose reduction already has been built in to these recommendations).The extent to which the equianalgesic dose is reduced by a safetyfactor can be adjusted up or down depending on the clinical condition of thepatient, specifically the severity of the pain, the existence of opioid-related sideeffects, and the severity of medical comorbidities.4. Side effect management. The management of side effects is an essentialpart of opioid therapy. By adequately treating side effects, it is often possible totitrate the opioid to a higher dose and thereby increase the responsiveness ofthe pain. Although respiratory depression fosters the greatest concern, toleranceto this adverse effect develops rapidly, and it is very uncommon if theopioid is titrated according to the accepted dosing guidelines. Constipation isthe most frequent side effect encountered with chronic opioid therapy. Patientsotherwise predisposed to constipation by virtue of advanced age or medicalcomorbidity should be considered for a prophylactic bowel regimen whenopioid therapy is initiated. Although somnolence and mental clouding is frequentat the start of opioid treatment, these effects usually subside in a few days.In the absence of other medical problems, long-term opioid therapy should beaccompanied by clear thinking; the capacity to drive or otherwise function at ahigh level should be considered goals of the treatment. Occasionally, the analgesicresponse is satisfactory but therapy is persistently compromised by somnolenceor mental clouding. One option in this setting, which generally isaccepted by pain specialists, is coadministration of a psychostimulant (such

386 IV. SPECIAL POPULATIONSas methylphenidate, modafinil, or dextroamphetamine) (Bruera, Fainsinger,MacEachern, & Hanson, 1992). Given the potential for stimulant abuse andnew side effects, the use of such a drug requires careful assessment of risks versusbenefits, and appropriate monitoring if treatment is initiated. Nausea or othergastrointestinal symptoms, such as anorexia or bloating, occur commonly earlyin therapy and are usually managed with a antiemetic. Because the experienceof side effects with one opioid does not predict the occurrence of the samesymptoms with another one, opioid rotation is always an option for the treatmentof a challenging side effect.5. Risk assessment and management. Extensive experience in the managementof cancer pain has suggested that long-term opioid therapy of an olderpopulation with no prior history of substance abuse is rarely associated with denovo development of abuse or addiction. Similarly, very large surveys ofpatients who receive opioids to treat acute pain indicate that this therapy has avery low risk of precipitating addiction. These reassuring experiences, however,do not mean that the long-term administration of opioids to all populationscarries a low risk of abuse, addiction, or diversion. Indeed, given the base ratesof addiction in the population at large, the reality that neither the prevalencenor the pattern of aberrant drug-related behaviors during pain therapy areknown, and the experience of pain specialists who commonly encounter drugabuse in the referred population they treat, it is prudent to perform an assessmentof risk in all patients. Based on this assessment, treatment can be structuredin a way that facilitates monitoring and assists the patient who needs helpin controlling drug use.The most consistent predictor of misuse and abuse during opioid therapyappears to be a history of substance abuse. Surveys have begun to identify otherpredictors and develop validated methods for categorizing risk (Adams et al.,2004; Chabal, Erjavec, Jacobson, Mariano, & Chaney, 1997; Coambs & Jarry,1996; Compton, Darakjian, & Mitto, 1998; Friedman, Li, & Mehrotra, 2003).There is presently no single, well-accepted measure or risk profile. In additionto a history of drug abuse, factors that may raise a “red flag” include a report bythe patient about concern related to control of the medication, a family historyof drug abuse, a personal or family history of significant psychiatric disease,problematic behaviors with other prescribed drugs, a criminal record, and frequentautomobile accidents.Based on this assessment, the clinician should categorize the patient bydegree of perceived risk. Proactive strategies for prescribing should be applied insome combination for those whose risk is perceived to be relatively high (Table17.4). These strategies may include a written agreement defining the parametersof acceptable behavior; urine drug screening; frequent visits; various rulesconcerning pill counts, concurrent treatment for addiction or other psychiatricdisease, and response to lost prescriptions; no use of short-acting drugs; and similarapproaches. For the person who is perceived to be at relatively limited risk,

17. Pain and Addiction 387these strategies may be limited (e.g., frequent visits only until the relationship isestablished). For those perceived to be at high risk, such as the addict onlyrecently in a recovery program, all of the strategies can be required.These strategies should be explained to the patient as the foundationneeded by the clinician to act in the patient’s best interest. They are not punitiveand should not undermine the therapeutic alliance. Indeed, experiencesuggests that the patient with addiction and pain often will correctly perceivein this effort that the clinician is willing to undertake a relatively laborintensiveapproach in an effort to provide pain relief.During treatment, monitoring for aberrant drug-related behavior should beundertaken as a routine, similar to the conventional monitoring of efficacy(analgesia), side effects, and potential benefits on function (Table 17.4). Insome cases, this monitoring may appropriately be limited to the history; in others,the patient must be required to permit contacts between the clinician andothers, such as family, other physicians, a sponsor, or a pharmacist. The occurrenceof aberrant drug-related behavior should initiate reevaluation, so thatappropriate interpretation of the behavior is possible (discussed earlier). If thedecision is made to continue prescribing, the structure of therapy usually shouldbe altered to impose additional controls. These enhance the ability to monitorin the future and may assist the fragile patient in maintaining responsible druguse.OTHER ANALGESIC DRUGSAcetaminophen and the NSAIDs. The analgesia provided by nonopioidanalgesics is characterized by a ceiling effect, which usually limits the use ofthese drugs to pain that is usually moderate in severity. In the absence of relativecontraindications, however, it is reasonable to undertake trials of thesedrugs in all types of pain. Based on clinical observations, they are least likely tobe helpful in neuropathic pain and are most clearly indicated in pain associatedwith inflammatory diseases (e.g., rheumatoid arthritis).Acetaminophen possesses analgesic properties similar to aspirin but isbetter tolerated and lacks the adverse effects of NSAIDs. The main concernassociated with its use is the hepatotoxicity encountered with overdose. Theusual maximum daily dose is 4,000 mg. In those with liver disease (e.g., hepatitisC) or chronic alcoholism (Zimmerman & Maddrey, 1995), the risk ofhepatotoxicity is greater, and acetaminophen should be used in far lower doses,or avoided altogether.NSAIDs comprise an extremely diverse group of drugs (Table 17.6), all ofwhich inhibit the enzyme cyclo-oxygenase (COX), thereby reducing the synthesisof prostaglandins. Cyclo-oxygenase is produced in at least two isoforms,COX-1 and COX-2. The “constitutive” isoform COX-1 is involved in physio-

388 IV. SPECIAL POPULATIONSTABLE 17.6. Nonsteroidal Anti-Inflammatory DrugsChemical ClassDrugRecommendedstarting dose(mg/day orally) aRecommendedmaximum dose(mg/day orally)Nonselective COX inhibitorsSalicylates Aspirin 2,600 6,000Diflunisal 1,000 × 1 1,500Choline magnesium 1,500 × 1, then 1,000 4,000trisalicylateSalsalate 1,500 × 1, then 1,000 4,000Propionic acids Ibuprofen 1,600 4,200Naproxen 500 1,500Naproxen sodium 550 1,375Fenoprofen 800 3,200Ketoprofen 100 300Flurbiprofen 100 300Oxaprozin 600 1,800Acetic acids Indomethacin 75 200Tolmetin 600 2,000Sulindac 300 400Diclofenac 75 200Ketorolac 40 40Ketorolac (i.m.) 30 (loading) 60Etodolac 600 1,200Oxicams Piroxicam 20 40Meloxicam 7.5 15Naphthylalkanones Nabumetone 1,000 2,000Fenamates Mefenamic acid 500 × 1 1,000Meclofenamic acid 150 400Pyrazoles Phenylbutazone 300 400Selective COX-2 inhibitorsCelecoxib 200 400Valdecoxib 20 40a In elderly persons on multiple drugs or those with renal insufficiency, starting dose should be one-halfto two-thirds of the recommended starting dose.

17. Pain and Addiction 389logical processes, whereas the “inducible” COX-2 is mostly produced as part ofthe inflammatory cascade. A higher selectivity for the COX-2 isozyme is thereforedesirable in order to achieve higher analgesic and anti-inflammatory activitieswith fewer adverse effects. The various NSAIDs vary in their COX-2 selectivity.Commercially available drugs with high COX-2 selectivity comprisecelecoxib and valdecoxib; at a relatively low dose, meloxicam is also highlyselective. The appropriate positioning of the COX-2 selective drugs is still controversial;they are most clearly appropriate in patients who have not toleratedthe nonselective COX-1/COX-2 inhibitors and those at increased risk of gastrointestinalcomplications.The potential for toxicity during NSAID therapy influences the decisionto initiate therapy, the selection of drug, and the approach to dosing and monitoring.The most important toxicities are gastrointestinal, renal, and cardiovascular.Approximately 10% of patients treated with a nonselective COX-1/COX-2 NSAID experience clinically important gastrointestinal toxicity, and gastricor duodenal ulcers occur in about 2% (Loeb, Ahlquist, & Talley, 1992). Therisk of gastrointestinal toxicity is increased with advanced age (older than 60years old), higher NSAID dose, concomitant administration of a corticosteroid,a history of ulcer disease or previous gastrointestinal complication fromNSAIDs, and possibly by heavy alcohol or cigarette consumption (Hernandez-Diaz & Rodriguez, 2000; Loeb et al., 1992). The risk of ulcer can be reduced butnot eliminated (Mamdani et al., 2002) by use of the selective COX-2 inhibitorsor by concurrent administration of gastroprotective therapy, including a protonpump inhibitor (e.g., omeprazole), misoprostol (a prostaglandin analogue), or aH2 blocker (La Corte, Caselli, Castellino, Bajocchi, & Trotta, 1999).Renal function depends on both COX-1 and COX-2 isoforms; consequently,any NSAID can cause serious renal toxicity, including acute renal failureand hyperkalemia. NSAIDs should be used with caution in those with renaldisease, and all patients should have regular monitoring of renal function. Thenonselective COX-1/COX-2 NSAIDs can cause a bleeding diathesis by interferingwith platelet activity; this potential toxicity does not occur with theCOX-2 selective agents. Symptomatic coronary artery disease during treatmentwith the selective COX-2 drug, rofecoxib, recently led to the withdrawal of thisdrug from the U.S. market. At the present time, this problem is not believed tobe a class effect. Patients at risk for atherothrombotic disease who are treatedwith a COX-2 selective drug should also receive aspirin therapy.Adjuvant Analgesics. Adjuvant analgesics are drug that have primary indicationsother than pain but can be analgesic in some pain conditions (Lussier &Portenoy, 2003). This category is extremely diverse, representing numerousdrugs in many classes (Table 17.7). Some of these drugs have analgesic propertiesin several pain syndromes and are therefore referred as “multipurpose

390 IV. SPECIAL POPULATIONSTABLE 17.7 Adjuvant AnalgesicsIndication Drug class ExamplesMultipurposeanalgesicsAdjuvants forneuropathicpainAdjuvants formusculoskeletalpainAdjuvants forcancer painAntidepressantsTricyclic antidepressantsSSRIsSNRIOthersAlpha 2 -adrenergic agonistsCorticosteroidsAnticonvulsantsLocal anestheticsN-Methyl-D-aspartate blockersSympatholyticsTopical agentsMiscellaneous”Muscle relaxants”BenzodiazepinesFor bone painFor bowel obstructionAmitriptyline, doxepin,nortriptyline, desipramineParoxetine, citalopramVenlafaxine, duloxetineBupropion, trazodone, maprotilineClonidine, tizanidineDexamethasone, prednisoneGabapentin, lamotrigine, pregabalinoxcarbazepine, topiramate,levetiracetam, zonisamide,carbamazepine, phenytoin, valproateLidocaine, mexiletineKetamine, dextromethorphan,amantadinePrazosin, phentolamine,phenoxybenzamine, beta blockersLocal anesthetics, capsaicin,NSAIDsBaclofen, calcitoninOrphenadrine, carisoprodol,methocarbamol, chlorzoxazone,cyclobenzaprine, metaxaloneDiazepamBiphosphonates, calcitoninScopolamine, octreotide,corticosteroidsNote. SSRI, selective serotonin reuptake inhibitor; NSRI, norepinephrine–serotonin reuptake inhibitor.adjuvant analgesics.” These include antidepressants (tricyclics, selective serotoninor serotonin and norepinephrine reuptake inhibitors, bupropion), corticosteroids(mainly dexamethasone), and alpha-2-receptor agonists (clonidine,tizanidine). Other adjuvant analgesics are indicated only for specific painsyndromes. Anticonvulsants (e.g., gabapentin, topiramate, levetiracetam, lamotrigine),local anesthetics (e.g., intravenous or topical lidocaine, oral mexiletine),and NMDA receptor antagonists (ketamine, dextromethorphan, amantadine)are used in neuropathic pain.

Other Analgesic Approaches17. Pain and Addiction 391Although the range and effectiveness of the pharmacological therapies for painoffer extraordinary opportunities for the patient with chronic pain, pharmacotherapyshould not be considered a uniform first-line approach for pain. Theassessment of the patient should allow a thoughtful positioning of drug treatmentoverall, and opioid treatment specifically, in relation to the large numberof nonpharmacological treatments now available. Some patients are reasonablecandidates for drug therapy alone; others should receive drugs only as part of amultimodality strategy, and still others should not be offered pharmacotherapybecause the risk:benefit ratio for other treatments is better. These decisionsoften evolve over time and require ongoing evaluation of outcomes. By gaininginsight into the available approaches for pain, clinicians can make reasoneddecisions about the selection of patients for treatment and referral when appropriate.CONCLUSIONIssues at the interface between pain and chemical dependence are complex andclinically relevant. In a striking paradox, concern about abuse and addictioncontributes to undertreatment at the same time that a tendency to prescribeabusable drugs, without addressing the risk of abuse and addiction, may be contributingto bad therapeutic outcomes. Clinicians would be best served by gainingthe skills to assess pain comprehensively, learning about the range ofapproaches available to treat pain in diverse populations, and approaching theproblem of opioid therapy from the perspective of balance. At the level ofpatient care, a balanced perspective implies that clinicians acquire both theskills to optimize the principles of prescribing and the skills necessary to performrisk assessment and management. The goals are to relieve pain andimprove quality of life, while minimizing the risk of all adverse outcomes.REFERENCESAdams, L. L., Gatchelm, R. J., Robinson, R. C., Polatin, P., Gajraj, N., Deschner, M., &Noe, C. (2004). Development of a self-report screening instrument for assessingpotential opioid medication misuse in chronic pain patients. J Pain Symptom Manage,27(5), 440–459.American Pain Society. (2003). Principles of analgesic use in the treatment of acute pain andcancer pain. Glenview, IL: Author.American Psychiatric Association. (2000). Diagnostic and statistical manual for mental disorders(4th ed., text rev.). Washington, DC: Author.

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CHAPTER 18Alcoholism and Substance Abusein Older AdultsSHELDON ZIMBERGPeople over 65 years of age are the fastest growing population in the UnitedStates. The U.S. Public Health Service’s Healthy People 2000 initiative notedthat 13% of the population is 65 years of age or older. It was noted that alcoholismand substance abuse are substantial problems in the general population,including elderly people (Menninger, 2002).Although there have been substantial increases in services for youngeralcoholics and substance abusers, including detoxification facilities, outpatientclinics, and inpatient rehabilitation over the years, few specialized programs forelderly people have been developed. Clinical experience has shown thatbecause of increased resistance to acknowledge an alcohol or substance useproblem and lack of emphasis in existing treatment programs on the life issuesthey experience, few elderly are willing to go to existing treatment facilities(Barrick & Conners, 2002). A substantial number of senior citizens have alcoholproblems, in the range of 10–15%. Illicit drug use among the elderly is rare,but prescription drug misuse and abuse is substantial (Reid & Anderson, 1997;Zimberg, 1995).In addition to patient resistance, among health care workers, there is a lowindex of suspicion about these conditions in elderly patients and negative attitudes,such as “Why bother to treat an older person? The alcohol is all that heor she has left.” This attitude can be considered a form of ageism. It is particularlyunfortunate, since elderly patients can be diagnosed and effectivelytreated, if the stresses of aging are recognized and dealt with in an “aging- specific”treatment approach utilized by myself and others to treat this population396

18. Alcoholism and Substance Abuse in Older Adults 397(Zimberg, 1996). The availability of treatment services is further complicatedby the lack of knowledge of addictive disorders among primary care physiciansand geriatric specialists, and the reciprocal lack of knowledge of aging-relatedproblems among addiction specialists.In this chapter, I discuss the prevalence of alcoholism and prescriptiondrug abuse among elderly persons, diagnostic approaches, and therapy directedat the maladaptations to aging that often lead to alcohol and prescription drugmisuse. In addition, I present a section on the recognition and treatment ofelderly alcoholics admitted to general hospitals, since so many such patients areoften not diagnosed and not treated or are inappropriately treated.PREVALENCE OF ALCOHOLISM AND PRESCRIPTION DRUGMISUSE IN ELDERLY PEOPLEPrevalence studies of alcoholism in elderly people in the community have beenreported in the range from 4 to 20% (Atkinson, Ganzini, & Bernstein, 1992;Bridgewater, Leigh, James, & Potter, 1987; Cahalan, Cisin, & Crossley, 1969).A study in the Washington Heights area in Manhattan indicated an alcoholismrate of 105/1000 residents among elderly widowers (Bailey, Haberman, &Alksne, 1965). The researchers asked questions about problems associated withdrinking rather than quantity–frequency questions, which often give unreliableinformation. The elderly widowers had the highest rates of alcohol problemsfound. Another community-based study of United Automobile Workers in Baltimorefound that 10% of men and 20% of women over age 60 were heavyescape drinkers and considered to be alcoholics (Siassi, Crocetti, & Spiro,1973).In studies in primary care settings, outpatient treatment, medical and psychiatricinpatient treatment, and emergency rooms, elderly patients show ratesof alcoholism in the 15 to 20% range (Adams, Barry, & Fleming, 1996; Adams,Magruder-Habid, Trued, & Broome, 1992; Adams, Zhung, Barhoriak, & Rimm,1993; McCusker, Cherubin, & Zimberg, 1971; Moore, 1972; Zimberg, 1969). Aparticularly significant study of hospital admissions under Medicare showedthat elderly patients with alcoholism or alcohol-related medical conditionswere admitted at a rate of 48 per 10,000 population, similar to the rates ofadmission for myocardial infarction for this age group (Adams et al., 1993).As indicated previously, illicit drug use of heroin, cocaine, marijuana, andother substances is relatively rare. The major concern, however, is with prescriptionand over-the-counter drug misuse and abuse. Many elderly individualsare on multiple prescription drugs, at times supplemented by over-the-counteranalgesics, antihistamines, laxatives, cold preparations, and sedatives. Thesemultiple drugs can produce side effects through interactions and can causeproblems for elderly people who are using and abusing alcohol. Confusion with

398 IV. SPECIAL POPULATIONSdrug effects, complicated by drug–drug interactions, is a major part of the problemin diagnosing alcohol dependence or abuse in elderly people (Schuckit,1979).The class of drugs most subject to misuse and abuse is the benzodiazapines.These drugs are prescribed for anxiety and depression; however, their liabilityto tolerance and dependence creates problems for patients, and demands areoften made on the prescribing physicians to give more. These drugs also causecognitive impairments and confusion that suggest dementia. It is particularlyproblematic when benzodiazepines are also used with alcohol, and by thosewith alcohol problems. Such a combination of benzodiazepines and alcohol useis common and often complicates treatment of the alcohol problem. Benzodiazepinesrepresent the most widely used psychiatric prescription drugs amongelderly patients in primary care and psychiatric settings, and can cause problemsby leading to organicity, drug interactions, and addiction. Their use, with theliabilities indicated, creates more problems than they solve and is particularlyinappropriate when other drugs, such as selective serotonin reuptake inhibitors,have been found to be safe and effective in geriatric patients with anxiety anddepression (Kennedy, 2000; Rigler, 2000; Zimberg, 1995), and their use is preferableto benzodiazepines in most cases.TYPOLOGY AND DIAGNOSIS OF ELDERLY ALCOHOLICSTypologyWork done more than two decades ago by Simon, Epstein, and Reynolds(1968) and Gaitz and Baer (1971) found distinctions between elderly alcoholics,with and without organic mental syndromes, and also typed an early- versuslate-onset typology. These authors suggested that the patients with significantorganic deficits did poorly in treatment and died at an earlier age. Simon andcolleagues also noted that in the psychiatric inpatient population of elderly personsthey studied, 23% had alcohol problems; 16% became alcoholic before age60, and 7% after age 60. Rosin and Glatt (1971) had similar findings andshowed that the early-onset group had personality characteristics similar toyounger alcoholics, whereas the late-onset group developed drinking problemsin reaction to bereavement, depression, retirement, loneliness, and physical illness.They suggested that late-onset alcoholism was related to the stresses ofaging.In my work with elderly alcoholics (Zimberg, 1974), I found this typologyto exist in the elderly patients I encountered in mental health clinics, homecare programs, nursing homes, senior citizen centers, and inpatient medical servicesin general hospitals. It was also noted that the early-onset group experiencedserious stresses of aging, and that reaction to these stresses perpetuateddrinking problems as the group aged (Schonfeld & Dupree, 1991).

18. Alcoholism and Substance Abuse in Older Adults 399There have been suggestions that people tend to drink less as they getolder, that alcoholism is a self-limiting disease, and that as people age, the alcoholproblems “burns out” (Drew, 1968). Those experiencing serious stresses ofaging may continue problematic drinking as a maladaptation to the stresses ofaging. With further study of the elderly alcoholic population, I noted a subgroupof early-onset alcoholics who had had alcoholism treatment when theywere younger and had experienced remissions, but relapsed as they got older.This group, also described by Carruth, Williams, Mysak, and Boudreau (1975),can be considered an early-onset group with late-onset relapse.DiagnosisPart of the resistance to developing programs for elderly alcoholics has been thedifficulties in making a diagnosis. There is often confusion regarding patientswith dementia, drug–drug interactions, greater denial by patients and family,and less acute medical problems associated with alcoholism. Graham (1986)noted that there are fewer social, legal, occupational, and interpersonal consequencesof alcoholism, because the elderly persons are often not working, livealone, and consume lesser quantities of alcohol, so that there is less alcoholdependence and withdrawal.In recent years, there have been advances in the diagnosis of alcohol problemsin the elderly population. A geriatric version of the Michigan AlcoholismScreening Test was developed (Blow et al., 1992). This 24-question screeninginstrument is reported to have good sensitivity and specificity. It can be usefulas a screening instrument in large populations, but it is cumbersome to use in aclinical interview.A useful and more practical tool, the CAGE Questionnaire (Ewing, 1984),has been found useful in diagnosing alcohol problems in general alcoholic populationsand also in the aged (Reid & Anderson, 1997; Rigler, 2000). A “yes”answer to any one of the four questions indicates a suspected alcohol problem;two “yes” responses are a strong indicator of an alcohol problem. I have usedthe CAGE (Zimberg, 1996) and have found it useful, with questions 1 and 3most commonly being answered positively among elderly alcoholics.Laboratory testing can assist in the diagnosis of alcohol problems in elderlypersons and includes liver function tests and elevated values of the mean corpuscularvolume (MCV) and mean corpuscular hemoglobin (MCH), which are partof the complete blood count (CBC). A newer test of the level of carbohydratedeficienttransferrin may prove useful as well (DuPont, 1999). Although, theselaboratory tests are by no means diagnostic in younger alcoholics, a study ofelderly alcoholics indicated that 70% of the 200 patients studied had abnormalitiesin the MCV, MCH, and liver function tests (Hunt, Finlayson, Morse, &Davis, 1988). This represented a much higher percentage of these abnormalblood studies in elderly alcoholics than in younger alcoholics.

400 IV. SPECIAL POPULATIONSI (Zimberg, 1996) conducted a pilot study of identified elderly alcoholicson a medical service in a New York City hospital. Of the 15 patients interviewed,all answered “yes” to questions 1 and 3 of the CAGE. In addition, allhad abnormal MCV or MCH and/or abnormal liver function tests. Thus, thesepatients could be readily identified in a medical setting.The other area of concern regarding diagnosis of elderly alcoholics is thelack of diagnostic signs so common in younger alcoholics, as I indicated earlier.I developed a list of key questions that can be asked of patients and their families(Zimberg, 1995). These questions are listed in Table 18.1. As can be seen,the questions relate to behavioral, cognitive, social, and activities of daily livingthat can be seriously affected by excessive alcohol consumption in a elderlyindividual. The use of benzodiazepines is also commonly seen in such patients.An accident or a fall can be the precipitating event that brings the alcoholproblem to the attention of family members and, if serious enough, result inhospitalization (Surock & Shimkin, 1988).Therefore, the ability to diagnose an alcohol problem in an older person ispossible and relatively easy to accomplish. The use of the CAGE, laboratorytesting, and the use of the key questions with the patient and with family canfacilitate this diagnostic process. Since the evidence of a relatively high prevalenceof alcohol problems in the elderly has been established, it is necessary toincrease the index of suspicion among health care professionals, utilizing thediagnostic tools indicated to make the diagnosis and engage the patient intreatment or referral for treatment.The other diagnostic concern with the elderly alcoholics in looking forTABLE 18.1. Approach to Interview and Assessment1. Has there been any recent marked change in behavior or personality?2. Are there recurring episodes of memory loss and confusion?3. Has the person tended to become more socially isolated and stay at home most ofthe time?4. Has the person become more argumentative and resistant to offers of help?5. Has the person tended to neglect personal hygiene, not been eating regularly, andnot keep appointments, especially doctor’s appointments?6. Has the individual been neglecting his or her medical treatment regimen?7. Has the individual been neglecting to manage his or her income effectively?8. Has the individual been in trouble with the law?9. Has the individual caused problems with neighbors?10. Has the individual been subject to excessive falls or accidents?11. Does the individual frequently use benzodiazepines (Valium, Librium, Xanax, etc.)?12. Has drinking been associated with any of the above situations?

18. Alcoholism and Substance Abuse in Older Adults 401coexisting psychiatric disorders, particularly depression, cognitive impairment,and prescription drug misuse. I have found that at least 50% of the elderly alcoholicsI have treated are clinically depressed and in need of antidepressanttreatment (Zimberg, 1996).Engaging in TreatmentTREATMENTOnce the diagnosis of an alcohol problem has been made and problems associatedwith the stresses of aging and any coexisting psychiatric problems determined,the patient should be told about these problems, including an alcoholproblem. The other problems should be indicated along with the alcohol problemas requiring treatment. This contrasts the confrontation necessary with ayounger alcoholic, where often the alcohol problem is the major concern thatmust be dealt with first.Elderly individuals have greater denial of an alcohol problem, and dealingwith the alcohol problem in the context of stresses of aging is more readilyaccepted and often engenders a willingness to accept treatment. Labeling anelderly patient an “alcoholic” will often result in the patient refusing to engagein treatment.DetoxificationMost elderly people with alcohol problems do not consume large amounts ofalcohol that will result in withdrawal if the drinking stops. However, somepatients may require detoxification. The patient should have a medical evaluation,or his or her primary care physician should be contacted. If the patient isnot suffering from serious medical problems, outpatient detoxification is oftenpossible (Evans, Street, & Lynch, 1996). Benzodiazepines are the drugs ofchoice (Kraemer, Conigliaro, & Saitz, 1999; Saitz & O’Malley, 1997).I prescribe diazepam, 10–15 mg daily, with a reduction of half a tabletevery other day, while monitoring blood pressure and pulse. The patient shouldbe seen at least three or four times during this period of ambulatory detoxification.A long-acting benzodiazepine is preferred because of its built-in taperingeffect after the last dose.If the patient has serious medical problems, the detoxification should bedone in a hospital. Patients dependent on benzodiazepines, or a combination ofalcohol and benzodiazepines, should be detoxified in a hospital setting. Mostelderly people find it more acceptable to be detoxified on a general medical servicerather than a specialized inpatient detoxification unit, and will often refuseto be admitted to such a unit.

402 IV. SPECIAL POPULATIONSAlcohol-Specific Approach to TreatmentThe treatment approach commonly used to treat alcohol-dependent individualsinvolves confronting them with the diagnosis and suggesting treatmentleading to abstinence. Detoxification is used, if indicated, and the treatmentcontract is established with the patient. This treatment is directed at the alcoholproblem, with cognitive therapy that involves relapse prevention and supportivetherapy to establish a positive relationship with the patient. Referral toAlcoholics Anonymous (AA) is often made to encourage peer support and rolemodels of recovery (Zimberg, 1999b).Pharmacological treatment, such as disulfiram, can be used with very resistantpatients, particularly if taking the disulfiram is observed (Kranzler, 2000).The use of naltrexone to reduce craving for alcohol has been found useful(Weinrieb & O’Brien, 1997). Clearly, the emphasis of this alcohol-specificapproach is centered on the use of alcohol and developing more effective waysto function without alcohol.With elderly people, such an approach has not been successful in my experience,except for the subgroup of elderly alcoholics treated for their alcoholproblem in an alcohol-specific way during their younger years. The reason forthis lack of success, and therefore for the very few elderly patients in treatmentat traditional alcohol programs, is that the stresses of aging are the major factorsleading to alcohol problems in older people. The inability to adapt the alcoholspecificapproach to the needs of the elderly has perpetuated the gap betweenthe awareness of the problem and the availability of effective treatment (Graham,1986; Schonfeld & Dupree, 1991).Aging-Specific Approach to TreatmentThe aging-specific approach involves identifying an alcohol problem amongother problems associated with aging: loneliness, retirement, deterioratinghealth, loss of loved ones, cognitive impairments, and depression. Depression isalso a condition in the elderly that is often underdiagnosed (Zimberg, 1996).Some early clinical literature on treating elderly alcoholics emphasized thestresses of aging, pointing the way toward a more effective treatment approach.An article by Droller (1964) reported on seven elderly alcoholic patients. Thisfamily physician visited elderly alcoholics at home. He found that in additionto medical and supportive treatment, primarily social treatment was most beneficialand reduced or eliminated the alcohol problem.Rosin and Glatt (1971), who treated 103 elderly alcoholics, found thatenvironmental manipulation, medical services, day hospital treatment, andhome visiting by staff or good neighbors were the most beneficial services. Hereagain, the therapeutic efforts that were directed at the stresses of aging provedthe most effective.

18. Alcoholism and Substance Abuse in Older Adults 403In more recent years, Kofoed, Tolson, Atkinson, Toth, and Turner (1987)found that aging-specific treatment was more effective than mainstreamingpatients in standard alcoholism treatment in an outpatient setting. Anotherstudy that compared an elder-specific approach to traditional alcoholism treatmentin an inpatient unit found that the elder-specific approach produced 2.1times more abstinence and was slightly less costly (Kashner, Rudell, Ogden,Guggenheim, & Karson, 1992). Other studies have found that aging-specificapproaches are more effective than treating elderly alcoholic in mixed-agegroups (Liberto, Oslin, & Ruskin, 1992; Rigler, 2000; Schonfeld & Dupree,1999). Taken together with my experience treating elderly alcoholics in differentsettings, this suggests that an aging-specific approach that deals with boththe stresses of aging and the alcohol can be more effective than the traditionalalcohol-specific approach in engaging patients in treatment and producingbetter outcomes.Patients should have a complete physical examination, including laboratorytests and a psychiatric evaluation. If detoxification is needed, the approachdescribed earlier for outpatient or inpatient should be utilized.The ideal approach is to use group therapy when possible. However, thisgroup approach should not be insight-oriented or deal with alcohol use as themajor problem. It can be a mixed group of elderly persons with a variety of socialand psychological problems, and organic mental disorders and physical disorders,not just alcoholism. Patients with alcoholism should be told they have an alcoholproblem, along with the other problems that they may be experiencing, and thattheir problems relate to difficulties in adjusting to their current situation.The group should meet at least once a week for 90 minutes. Some socializationtime and having cookies, coffee, and tea should be available prior to theformal group session. The approach utilized by the group leader should be supportiveand directed at problem solving, utilizing various group member’s experienceswith similar problems in their lives. Drinking should be one of the problemareas discussed. Members of the group should be encouraged to discuss theirown problems and give advise to other group members. This self-help and helpothers approach leads to members’ elevated self-esteem and helps them overcomefeeling of helplessness and despair. The reality is that most elderly personshave achieved experiences and wisdom during their lives that should be recognized,and they should be encouraged to utilize these assets. Our society, withrapid technological advances and quick obsolescence, often relegates elderlypeople to the sidelines of life. Encouraging utilization of their life experiencescan be a very therapeutic and counter the many of stresses of aging exhibited bythe patients.In addition to the socialization period, formal group sessions, outings, andtrips can be planned. Patients should be actively involved in deciding where togo and participate in the planning of trips. The more independence thepatients can show, the greater the therapeutic value.

404 IV. SPECIAL POPULATIONSStaffing of the group program should include a group leader who is knowledgeableabout alcoholism and geriatrics, ideally a psychiatrist, a nurse, or socialworker, or an alcoholism counselor helping patients with practical problems,such as economic and housing needs, and relationships to friends, relatives, andneighbors. Helping a patient make doctor appointments and attend to otherneeds should be continued until the patient is able to accomplish theses activitieson his or her own (Zimberg, 1995).The most important goal of the aging-specific approach to treatment ofalcoholism is not necessarily producing abstinence. This fact creates resistanceamong the clinicians used to the alcohol-specific approach, where abstinence isthe goal of treatment. The aging-specific approach is not designed as a harmreduction technique either. The paradox of the aging-specific approach directedmainly at the psychosocial stresses of aging is that it often results inabstinence achieved early in treatment and is more easily maintained, with few,if any, relapses to drinking. Abstinence is encouraged and occurs in the contextof reduction of the maladaptations to aging, the treatment of coexistingdepression, and improved self-esteem, with more opportunities to feel worthwhile.Current experiences support the findings of the early clinicians workingwith elderly alcoholics in the 1960s and 1970s that psychosocial treatments arebetter for alcohol problems that are caused or exacerbated by the psychosocialstresses of aging. This observation can be applied equally well to both earlyonsetand late-onset elderly alcoholics. Both groups respond to the agingspecificapproach (Zimberg, 1974).Pharmacological TreatmentPharmacological treatment of alcohol withdrawal in elderly persons involvesuse of tapering doses of long-acting benzodiazepines, as indicated earlier. I havefound that the use of benzodiazepines can be safe and effective. Ambulatorydetoxification can be carried out in those elderly alcoholics who do not haveserious cardiovascular disease, or other serious medical or neurological problems.A physical examination is necessary prior to starting an outpatient detoxification.Patients should not be maintained on benzodiazepines because of thedrug’s dependence liability, adverse cognitive effects, and the availability ofother, safer drugs to treat anxiety.Depression is a common problem among elderly alcoholics. The use ofselective serotonin reuptake inhibitor drugs, such as sertraline, or tricyclics,such as nortriptyline, has been found effective in treating depression in theelderly (Kennedy, 2000). The elderly alcoholic patient should not be activelydrinking and should be alcohol-free for 2–3 weeks to determine whether theobserved depression is alcohol induced. If alcohol is not a cause, starting onantidepressant medication can be very effective in helping patients maintain

18. Alcoholism and Substance Abuse in Older Adults 405abstinence, motivating them to increase their activities and get involved instimulating and worthwhile efforts that will enhance their self-esteem. Both thedepression and the alcohol use are thus effectively treated.In some cases of elderly alcoholics who appear severely depressed, it maybe possible to establish a differential diagnosis in a shorter period of time thanthe 2–3 weeks indicated. A dual-diagnosis typology has been developed, with aquestionnaire that can determine whether the depression is alcohol-induced orindependent of alcohol use (Zimberg, 1999a).The questions involve determining the presence of depression during periodsof sobriety, whether depression occurs after the onset of drinking, but not atother times, and whether there is a previous history of depression. This informationcan lead to a determination of coexisting depression and the start ofantidepressant medication sooner. The patient should be alcohol-free at thetime the antidepressant medication is started.Disulfiram has been available for the treatment of alcoholics for 50 years.Its value in controlled studies has been found to be equivocal. However, studiesusing disulfiram with observed administration or under the supervision ofemployee assistance programs, or with patients on probation or on parole, hasbeen found useful (Brewer, Meyers, & Johnsen, 2000). The conventional wisdomregarding the use of disulfiram in elderly alcoholics has been that the drugis too dangerous to use. However, in my experience, in elderly alcoholics whohave proved resistant to other treatment efforts and are not suffering from significantcardiovascular or liver disease, and who do not have serious cognitiveimpairment, the smaller dose of disulfinam (125 mg/day) given under supervisionhas been safe and effective.The long-acting opiate antagonist naltrexone has been found to be effectivein reducing craving and alcohol use in the alcohol-dependent patient(Weinrieb & O’Brien, 1997). A study of naltrexone in elderly alcoholics hasshown a similar beneficial effect (Oslin, Liberto, O’Brien, Krois, & Norbeck,1997). I have used this drug at a dose of 50 mg/day and have given patients acard to warn about the use of opiates for pain. In patients who have intensecraving and have not responded to the psychosocial treatment of the stresses ofaging, naltrexone can be safely used.Another drug that decreases craving, acamprosate, functions as a modulatorof glutamate in the central nervous system (Zornoza, Cano, Polache, &Granero, 2003). It has been used extensively in Europe and received Food andDrug Administration (FDA) approval for this indication in mid-2004. No studieson the elderly have been done. If effective, this may be an additional pharmacologicaltreatment (Whitworth et al., 1996).It should be noted that most elderly alcoholics respond to the agingspecificapproach, often with the use of antidepressants. For the minority ofpatients who are treatment-resistant, usually the early-onset type, the pharmacologicaloptions discussed should be considered.

406 IV. SPECIAL POPULATIONSLocation of TreatmentThe group approach I have described has been generally very effective. Thiscan be provided wherever elderly alcoholics are found in psychiatric clinics,inpatient alcoholism programs, geriatric clinics, and senior citizen centers ornursing homes. The approach can also be provided individually in primary carephysicians’ or psychiatrists’ offices. I provide the aging-specific approach individuallyin my office, with generally high recovery rates.The essence of the aging-specific approach includes determining whetherthere is an alcohol problem, what stresses of aging are affecting the patient, thepresence of coexisting depression or other psychiatric conditions, and relationshipto families and friends. Many elderly patients look forward to the visit tothe doctor’s office, and this interest can be utilized to engage patients in treatingnot only the alcohol problem but also other problems that they may beexperiencing.ELDERLY ALCOHOLICS IN GENERAL HOSPITALSElderly alcoholics can be found in significant numbers in general hospitals(Adams et al., 1993 Gerke, Hapke, Rumpf, & John, 1997; Moore et al., 1989).They are usually more frequently found on medical–surgical services ratherthan in inpatient detoxification or psychiatric units.The presence of elderly alcoholics in relatively large numbers presents aparticular challenge to consultation–liaison psychiatrists and addiction psychiatristsworking in general hospitals. Diagnostic approaches indicated for elderlyalcoholics can be readily applied in a general hospital setting. A studythat compared readiness to deal with alcohol problems in alcohol-dependentpatients in the general hospital and such patients in the general populationfound that the general hospital patients seemed more willing to engage in treatment(Rumpf, Hapke, Meyer, & John, 1999). However, my experience withidentifying and referring elderly alcoholics for treatment after discharge, byusing alcohol nurse coordinators, resulted in very few successful referrals. Thisfailure resulted in part because of the lack of an aging-specific program at thishospital’s alcoholism clinic and the fact that the patients were referred to a clinicianat the alcoholism clinic who was anonymous as far as the patients wereconcerned. They also resisted going to an alcoholism clinic. In contrast, in myexperience, patients seen at the general hospital by me and referred to myselffor outpatient care accepted the referral and followed up treatment.To be able to engage elderly alcoholics in the general hospital, treatmentprograms must be available to meet their needs. First, there should be a highindex of suspicion of alcohol problems among elderly persons admitted to generalhospitals. Administering the CAGE and reviewing blood studies should be

18. Alcoholism and Substance Abuse in Older Adults 407part of an alcohol screening effort. Information from relatives, friends neighbors,and home attendants, if possible, should be obtained. A staff memberinvolved in an aging- specific treatment program should see the patient in thehospital and have the patient referred to him- or herself at the treatment site.A particularly egregious situation exists for alcoholic patients in some generalhospitals, particularly patients admitted to the surgical services. Undiagnosedalcoholic elderly patients admitted with an acute surgical emergency, suchas a hip fracture, are operated on promptly, and on the first postoperative day maydevelop acute alcohol withdrawal that produces serious morbidity and, in somecases, death. I have observed such instances frequently. There are no data todetermine how frequent such a complication occurs, but it is a preventable one!Part of every evaluation for emergency surgical and medical admissions ofthe elderly should be screening for alcoholism, as indicated, not simply askingwhether the patient drinks alcohol. If there is a suspicion of an alcohol problemuse of a benzodiazepine taper on admission or postoperatively should be instituted.The problem of using benzodiazepines in surgical patients is complicatedby a lingering belief among some physicians that ethanol, including intravenousethanol, should be used to treat or prevent alcohol withdrawal. A recentstudy documents this inappropriate use of ethanol, which can be particularlydangerous in elderly alcoholics (Rosenbaum & McCanty, 2002).The low index of suspicion of alcohol problems in the elderly and the useof ethanol for detoxification represent a problem in diagnosis and treatment,with potentially serious consequences. The need to educate the medical communityabout the diagnosis and treatment of elderly alcoholics is important,since diagnostic clues exist and effective treatment is possible.CONCLUSIONAlcoholism and prescription drug abuse in the elderly are common problems.They often are not diagnosed or treated. This chapter presents tools that can behelpful in the diagnosis of alcoholism in the elderly and suggests psychosocialtreatment based on an aging-specific approach as being most effective. Pharmacologicaltreatments, including benzodiazepines for detoxification, antidepressantsfor coexisting depression, disulfiram as a deterrent, and the anticravingdrugs naltrexone and acamprosate, were presented.The general hospital can be a place to identify, to provide detoxification,and to engage elderly patients in a friendly way. The morbidity and mortality ofalcohol withdrawal syndrome in patients admitted for medical and surgicalemergencies can be prevented if the alcohol screening is done early and benzodiazepinedetoxification is carried out soon after admission in patients likey togo into withdrawal.

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410 IV. SPECIAL POPULATIONSSurock, G. S., & Shimkin, E. E. (1988). Benzodiazepine sedatives and the risk of fallingin a community cohort. Arch Intern Med, 148, 2441–2445.Weinrieb, R. M., & O’Brien, C. P. (1997). Naltrexone in the treatment of alcoholism.Annu Rev Med, 48, 447–487.Whitworth, A. B., Fischer, F., Lesch, O. M., Nimmerrichter, A., Oberbauer, H., Platz,T., et. al. (1996). Comparison of acamprosate and placebo in long-term treatmentof alcohol dependence. Lancet, 347, 1438–1442.Zimberg, S. (1969). Outpatient geriatric psychiatry in an urban ghetto with nonprofessionalworkers. Am J Psychiatry, 125, 1697–1702.Zimberg, S. (1974). The two types of problem drinkers: Both can be managed. Geriatrics,29, 135–138.Zimberg, S. (1995). The elderly. In A. M. Washton (Ed.), Psychotherapy and substanceabuse: A practitioner’s handbook (pp. 413–427). New York: Guilford Press.Zimberg, S. (1996). Treating alcoholism: An age-specific intervention that works forolder patients. Geriatrics, 51, 45–49.Zimberg, S. (1999a). A dual diagnosis typology to improve diagnosis and treatment ofdual disorder patients. J Psychoactive Drugs, 31, 47–51.Zimberg, S. (1999b). Individual psychotherapy: Alcohol. In M. Galanter & H. D.Kleber (Eds.), Textbook of substance abuse treatment (2nd ed., pp. 335–342). Washington,DC: American Psychiatric Press.Zornoza, T., Cano, M. J., Polache, A., & Granero, L. (2003). Pharmacology ofacamprosate: An overview. CNS Drug Rev, 9, 359–374.

CHAPTER 19HIV/AIDS and Substance Use DisordersCHERYL ANN KENNEDYJAMES M. HILLSTEVEN J. SCHLEIFERSince its appearance in 1981, the human immunodeficiency virus/acquiredimmune deficiency syndrome (HIV/AIDS) pandemic has been the focus ofglobal attention and remains a serious public health threat throughout theworld. By the end of 2004, over 40 million people worldwide, including 2.5 millionchildren under age 15, were living with HIV/AIDS, mostly in Africa andAsia (UNAIDS, 2004). Showing a decrease from prior years, 22% of the 43,171new cases of HIV/AIDS reported in the United States in 2003 had injectiondrug use (IDU) as the major risk factor for transmission. The majority of thosewith HIV/AIDS in the United States are minorities: African Americans andLatinos (Centers for Disease Control and Prevention, 2003). Among noninjectingdrug users (NIDUs) there are clear links between substance abuse andhigh-risk behaviors in both men and women, especially those who use crackcocaine (Astemborski, Vhalov, Warren, Solomon, & Nelson, 1994; De Souza,Diaz, Sutmoller, & Bastos, 2002; Edlin et al., 1994). Use of mind-altering substances,such as alcohol, other sedatives, stimulants, and club drugs, plays anincreasing, albeit less direct, role in HIV risk and disease progression. Impairedstates induced by alcohol and other drugs can influence sexual behavior andlead to risky, unsafe sexual practices that increase risk of HIV exposure (Kennedyet al., 1993; National Institute of Drug Abuse, 2002). HIV infectionamong IDUs has been reported in nearly 180 countries worldwide and presentsthe risk of spreading to 40 more. Once the virus has been introduced into alocal community of IDUs, spread is ordinarily rapid. Drug-using populations are411

412 IV. SPECIAL POPULATIONSfueling the epidemic around the world. There is increasing evidence that theseindividuals are at higher risk for accelerated and more severe neurocognitivedysfunction compared to non-drug-using HIV-infected populations (Nath etal., 2002).NEUROPSYCHIATRIC COMPLICATIONS OF AIDSEarly in the HIV epidemic, the extent to which neuropsychiatric complicationsoccurred in patients was not appreciated. It is now widely understood that cognitive,affective, and behavioral symptoms may often be manifestations of HIVinfection in the central nervous system (CNS). These symptoms are the initialmanifestation of AIDS in 7–20% of patients, with the frequency increasing asthe disease progresses (Reger, Welsh, Razani, Martin, & Boone, 2002). Neurologicalinvolvement may range from subtle changes to severe global impairment.HIV-associated dementia (also referred to as HIV-associated motor complex,HIV encephalopathy, or AIDS–dementia complex) has been described asprogressive and is the most common of the neurological manifestations of HIVinfection (Bouwman et al., 1998). It is currently estimated that up to one-thirdof the adults and more than one-half of the children with HIV will eventuallydevelop a dementing disease, and that HIV is the leading cause of dementia inpeople less than 60 years of age (Janssen, Nwanyanwu, Selik, & Stehr-Green,1992; Koutsilieri, Scheller, Sopper, ter Meulen, & Riederer, 2002). Whenworking with substance users with HIV, clinical expertise is essential for accuratediagnosis and optimal management of the neurological and neuropsychiatriccomplications. The symptom overlap between the neurological effects ofdrug use and HIV-associated illnesses presents an important clinical challenge.Early detection of HIV-associated dementia is based on careful trackingof mental status and cognitive changes. A recent meta-analysis of 41 neuropsychologicalstudies of HIV disease revealed that motor functioning, executiveskills, and information-processing speed were the functions showing the greatestdecline as disease progressed (Reger et al., 2002). Differentiating these CNSeffects of HIV from those related to drug and alcohol is difficult, in that there isneurological deficit overlap. Abnormal findings on measures of dexterity, sensoryprocessing, attention, concentration, language, verbal and nonverbal memory,abstraction, and problem solving have been demonstrated with chronic alcohol,cocaine, opiate, and polysubstance abuse (Ling, Compton, Rawson, & Wesson,1996). In addition to the actual drug used and chronicity of use, age at use (Klisz &Parsons, 1977), history of impairment preceding use, gender (Fabian, Parsons, &Sheldon, 1985; Glenn & Parsons, 1992), and educational level (Grant & Reed,1985) may further mediate neuropsychological findings. These factors have led tosome controversy as to the increased risk of developing dementia in HIV patientswith comorbid substance abuse disorders (SUDs). Some investigators (Bouwman

19. HIV/AIDS and Substance Use Disorders 413et al., 1998) have reported that substance users with HIV are at a higher risk fordementia than are individuals with other risk behaviors, but this finding has beennot found by others (Qureshi, Hanson, Jones, & Janssen, 1998; DeRonchi et al.,2002). Although the results of these studies vary, it is generally accepted that neuropsychologicalimpairments associated with substance use can vary from mild tosevere, and may be stabilized or reversed by abstinence (Selby & Azrin, 1998). Inthe AIDS patient, the impairment is progressive and, by the terminal phase of thedisease, severe. It is critical that physicians treating substance users who developAIDS be alert, because these patients may suffer from both drug- and infectionrelatedcognitive impairment. It is also important for physicians to consider thediagnosis of HIV in all substance users with cognitive impairment. They must beaware that timing of the effects of HIV on cognition is variable and not fullyunderstood.The clinical significance of the seroconversion and asymptomatic phasesare debatable, but the physician caring for people in high-risk groups shouldknow of possible CNS effects to increase the likelihood of early detection.Headaches and photophobia may be frequent in the seroconversion-relatedmononucleosis-like syndrome associated with HIV (Tindall & Cooper, 1991).Although this early syndrome is apparently common, it is frequently indistinguishablefrom other viral infections and may not be recognized. The virus canbe detected in cerebrospinal fluid shortly after infection and it has been assertedthat cognitive changes could begin during the asymptomatic phase of infectionthat usually lasts a decade or more (Bornstein et al., 1991; Lunn et al., 1991).There has been controversy over the possibility that cognitive decline canoccur before the onset of other medical symptoms. After controlling for substanceabuse, psychiatric history, use of psychoactive medications, and neurologicalproblems, HIV-positive asymptomatic patients show little difference incognitive functioning when compared with controls (Damos, John, Parker, &Levine, 1997). It is now generally accepted that caution should be exercised inassigning cognitive deficits to asymptomatic HIV-positive patients, but giventhe erratic health care utilization of substance users, which is a potential barrierto early HIV detection and intervention, professionals working with this groupshould have a low threshold for considering neurological and cognitive symptomsas possible complications of undiagnosed HIV.Early detection and monitoring of cognitive changes are critical, becausethese symptoms may be reversed and possibly prevented with antiretroviraltherapy (ART; Moore, Keruly, Gallant, & Chaisson, 1998; Price et al., 1999;Sacktor & McArthur, 1997). The impact of ART has added support to thehypothesis that, in most cases, HIV-associated dementia is the result of theeffect of the virus on the CNS rather than that of a secondary opportunisticinfection or process. Many believe that this effect is achieved by indirect mechanisms,since productive infection within the CNS is confined predominantlyto macrophages and microglia (Kolson, Lavi, Gonzalez, & Scarano, 1998;

414 IV. SPECIAL POPULATIONSLipton & Gendelman, 1995; Price, 1995). After infection with HIV, CNSmacrophages and microglia may be activated and induced to produce variousproinflammatory cytokines that may contribute to neuronal dysfunction ordeath (Glass, Fedor, Wesselingh, & McArthur, 1995; Portegies, 1995). Regardlessof the intermediary steps involved in the link of the HIV to CNS functioning,if brain infection is involved in the pathogenesis of HIV-associated dementia,ART may be critical to prevention and treatment.Recently there has been increased focus on mechanisms underlying neurodegenerationin patients with combined HIV and substance use. Althoughstudies assessing neuropsychological functioning in HIV-infected asymptomaticsubstance users have failed to offer consistent evidence of cognitive deficits,neuropathological studies comparing HIV-infected substance users to nonusershave shown a marked severity of HIV encephalitis in substance users (Bell,Brettle, & Chiswick, 1998), with significant loss of dopaminergic neurons inthe substantia nigra (Reyes, Faraldi, Senseng, Flowers, & Fariello, 1991). Sincemost drugs of abuse have dopaminergic activation properties, recent work inthis area has focused on the possibility that drugs of abuse may destabilize thedopaminergic system and result in a synergistic neurotoxicity when combinedwith HIV (Nath et al., 2002). This work adds further support for the importanceof achieving abstinence or limiting drug intake in HIV-infected patients.Although most HIV-associated dementia is from the effect of the virus onthe CNS, it has long been recognized that such cognitive changes can alsoresult from other mechanisms, including opportunistic infections (Price, Sidits,& Brew, 1991), HIV-related CNS neoplasms (DeAngelis, 1991; Remick et al.,1990; Shapshak et al., 1991), CNS effects of systemic illness (Holtzman, Kaku,& So, 1989), and CNS effects of antivirals and other medications used to treatrelated infections. Mass lesions and infectious processes in the CNS, includingCryptococcus neoformans, toxoplasmosis, cytomegalovirus, and lymphoma, arethought to account for approximately 30% of the CNS complications of AIDS(Navia, Jordon, & Price, 1986). Neuroimaging procedures, cerebrospinal fluidexams, serological titers, toxic screens, and stereotaxic biopsy techniques arehelpful in evaluating AIDS patients with CNS dysfunction and are useful inestablishing whether such potentially reversible conditions are involved withany cognitive decline. Accurate diagnosis of such underlying conditions is thefirst step in managing AIDS patients with CNS dysfunction.If HIV-associated dementia is established, antiretroviral drugs shouldbe considered, because they have reportedly lessened some cognitive losses.Psychotropics should be considered for specific symptom management. Giventhe sensitivity to psychotropic side effects in patients with CNS compromise,such treatments should be started with low doses and carefully monitored.Finally, supportive and insight-oriented psychotherapy with neuropsychoeducationmay assist the patient and significant others with coping and adaptation.

19. HIV/AIDS and Substance Use Disorders 415SUBSTANCE USE AND RISK OF HIV INFECTIONA variety of exposure and host factors influence seroconversion and diseaseprogression. These may include altered baseline host immune capacity and viralload in the seropositive person. The presence of host-concurrent infections,most notably viral (Herpes simplex, cytomegalovirus, the hepatitides) and bacterialinfections in the bloodstream (endocarditis, others), may contribute toaltered immunity. In the case of skin or mucosal ulcerations or inflammationfrom repeated injection sites or sexually transmitted diseases, breaches canafford easy entry of microorganisms. Clearly, some practices in drug use and sexualbehavior carry more risk than others for disease transmission. In general,infections have increased prevalence in substance-using populations, and sincesubstance users often do not restrict their use to a single drug, some risk effectsmay be synergistic.Heroin use by injection is a key element in the progression of the HIV epidemic.IDUs, as well as other substance abusers, have further increased risk dueto social and sexual contact with other high-risk individuals. Use of otheragents contributes substantially to behavioral risk through disinhibiting effectson the primary modes of transmission: sexual contact and injecting druguse (Booth, Kwiatkowski, & Chitwood, 2000; Woods et al., 1996). Stall,McKusick, Wiley, Coates, and Ostrow (1986) found that homosexual men withhigh-risk sexual behaviors were at least twice as likely to use drugs during sexualencounters as men considered at low risk for HIV exposure. Stimulant users,particularly, crack cocaine smokers and injecting stimulant users (cocaine,amphetamine), incur considerable risk for HIV. Cocaine injectors inject morefrequently to maintain a quickly decaying “high.” As with other disinhibitingdrugs, users are apt to engage in risky sexual behavior fueled by these drugs’stimulant properties. Consistent with an earlier report, Seidman, Sterk-Elifson,and Aral (1994), in a national study of 27,000 current drug users, found thatsexual risk behaviors for HIV transmission were significantly higher in crackcocaine smokers and crack-smoking IDUs than in nonsmoking IDUs, and thatthe alarmingly low rate of condom use (< 20%) was additionally associatedwith concurrent alcohol use (Booth et al., 2000). Female substance abusersare at particular risk for transmission through sexual risk behaviors (Booth,Koester, & Pinto, 1995), which include turning to commercial sex work as aprimary means of support. The use of crack cocaine is a strong predictor of riskysexual behaviors among women (Hoffman, Klein, Eber, & Crosby, 2000). Alcoholabuse has been increasingly recognized as a major cofactor in HIV transmissionrisk. Higher alcohol consumption in homosexual and bisexual men hasbeen associated with increased HIV seroconversion (Penkower et al., 1991)and NIDU ambulatory alcoholics had higher than expected HIV seroprevalencerates associated with more risky sexual behaviors (Avins et al., 1994).

416 IV. SPECIAL POPULATIONSCo-abuse of cocaine and alcohol has been associated with the highest risk(Wang, Collins, Kohler, DiClemente, & Wingood, 2000). The widespread useof alcohol and other drugs among adolescents presents a significant threatto adolescent health, associated with motor vehicle accidents, homicides,and suicides, as well as medical, psychological, and social morbidity (Singh,Kochaneck, & MacDorman, 1996). The use of alcohol and other drugs significantlyincreases adolescent risk behaviors for HIV transmission (Boyer & Ellen,1994; Rotheram-Borus, Rosario, Reid, & Koopman, 1995). Cases of AIDS andrates of HIV infection are rapidly rising among adolescents, particularly inthose from risk groups not easily accessed (Kennedy & Eckholdt, 1997;Mofenson, & Flynn, 2000).OpioidsIn addition to the exceptionally high risk of HIV transmission in opiate abuserswho inject and share needles, compromised immune function as a resultof exposure to opiates may add to risk of infection and disease progression.Brown, Stimmel, Taub, Kochwa, and Rosenfield (1974) and others(Govitaprong, Suttitum, Kotchabhakdi, & Uneklabh, 1998) found reducedlymphocyte stimulation in response to various mitogens in heroin addicts,suggesting a possible impairment in cell-mediated immunity. Addicts alsohave a significant reduction in numbers of T-cells when compared withnonaddicts (McDonough et al., 1980). A review of the literature defining theconnection between AIDS and opiate use concluded that numerous aspectsof the drug culture may have differential, even offsetting effects in terms ofthe potential to regulate either HIV-1 expression or host-regulation responses(Donahue & Vlahov, 1998).Opioids may incur considerable risk to some users; opiate addicts whoenter methadone treatment are significantly less likely to become HIV infectedin the first place (Metzger et al., 1993). In experimental studies of immunity,opiates have been found to have a variety of effects that are primarilyimmunosuppressive (McCarthy, Wetzela, Slikera, Eisenstein, & Rogers, 2001).There is evidence that chronic exposure to morphine may reduce HIV replication,while withdrawal, mediated by the stress effects, may lead to acuteimmunosuppression and disease exacerbation (Donahoe & Vlahov, 1998). Forthose already HIV-infected, consistent participation in methadone maintenancetreatment was associated with high probability and consistency of use ofART (Sambamoorthi, Warner, Crystal, & Walkup, 2000). More recent availabilityof oral outpatient opiate detoxification agents, buprenorphine and thebuprenorphine–naloxone combination, opens up new modalities to assist physiciansand patients in achieving drug-free or less harmful drug-using states (Linget al., 1998; O’Connor et al., 1998).

19. HIV/AIDS and Substance Use Disorders 417AlcoholAlcoholics, many of whom use multiple drugs, are at increased risk of exposureto HIV through high-risk behavior. Alcohol use is increasing worldwide, particularlyin countries in transition and throughout the developing world, whereit is contributing to an increasing number of health and social problems(Monteiro, 2001). Homosexual and bisexual men who drank high volumes ofalcohol had increased HIV seroconversion rates (Penkower et al., 1991).Nearly 20 years of studies have linked alcohol with high-risk behavior ofall types, including sexual behavior (Stall et al., 1986; Baldwin, Maxwell,Fenaughty, Trotter, & Stevens, 2000). In a study of alcohol treatment centers,non-IDUs had higher than expected seroprevalence for HIV that was associatedwith a high prevalence of risky sexual behaviors (Avins et al., 1994). In alarge study of sexually transmitted disease clinic attendees, alcohol was frequentlyused and was associated with other risk factors for HIV infection(Zenilman et al., 1994). Studies of alcohol abusers have described a range ofimmune alterations (Arria, Tarter, & Van Theil, 1991; Cook, 1998). Sincealcoholism and medical morbidity often coexist, it is difficult to distinguishimmune alterations associated with alcoholism per se from those associatedwith alcohol-related morbidity, such as liver disease or other comorbid medicalconditions. Acute exposure to alcohol has demonstrable immune effects, andchronic alcohol abusers, who may have adapted to ethanol effects, showimmune alterations of modest scope, unless they have developed secondaryliver disease or other comorbid medical conditions (Cook, 1998; Schleifer,Keller, Shiflett, Benton, & Eckholdt, 1999). The immune effects that havebeen observed in alcoholics, many of which may relate to the secondary complications,include suppressed natural killer cell activity (NKCA) (Irwin et al.,1990; Ochshorn-Andelson et al., 1994; Ristow, Starkey, & Hass, 1982), shiftsin CD4+ and CD8+ lymphocyte subsets, suggesting abnormal activation(Cook, 1998), and altered monocytic and phagocytic activity (Cook, 1998;Schleifer et al., 1999). Studies from our laboratory found that, compared withchronic alcoholics with no evidence of medical compromise, those with onlyminor such changes showed decreased CD45RA+ (inducer–suppressor/naive)cells, decreased HLA-DR+ (activated) T-cells, and an increased proportion ofcirculating CD56+ natural killer (NK) cells (Schleifer, Benton, Keller, &Dhaibar, 2002). Improvement of CD4+ cell count has been demonstrated aftercessation of alcohol use in some HIV-positive alcoholics (Pol, Artru, Thepot,Berthelot, & Nalpas, 1996).Important in assessing the role of substances of abuse, and especially alcohol,in immune change, is the role of comorbid depressive disorders. Irwin andcolleagues (1990) found decreased NKCA in patients with alcoholism that wasexacerbated significantly in patients with both alcoholism and major depres-

418 IV. SPECIAL POPULATIONSsion. We have found that comorbid major depression may account for many ofthe immune changes found in alcoholics (Schleifer, Keller, & Czaja, 2003). Itshould also be noted that exposure to alcohol and other drugs may influencethe symptomatic and pathological course of HIV-associated CNS disturbanceeither through additive effects on CNS function (Fein, Biggins, & MacKay,1995) or neurotoxic interactions with the viral effects (Tabakoff, 1994). Alcoholconsumption remains a risk factor for medication adherence and can modifyliver metabolism, both of which could lead to drug-resistant virus (Kresinaet al., 2002). Other researchers have found alcohol consumption prevalent intheir HIV-positive, drug-using population, and have found that it significantlynegatively impacts immunological and viral response to ART (Miguez, Shor-Posner, Morales, Rodriguez, & Burbano, 2003).MarijuanaThe contribution of cannabinoid use to human disease remains unclear and is asubject of considerable debate. A large study in California suggested that mortalityrates in the general population are not increased by marijuana use;however, marijuana use was associated with increased mortality in personswith HIV disease (Sidney, Beck, Tekawa, Quesenberry, & Friedman, 1997).Whether these reflect direct effects on the disease process or lifestyle differencesassociated with marijuana use remains to be determined (Klein, Newton,Snella, & Friedman, 2001; Sidney et al., 1997). Both the clinical and theexperimental data remain unclear as to whether marijuana use contributes negativelyto the course of HIV disease. Correspondingly, it is unclear whethercannabinoids are useful adjuncts to the management of AIDS-related symptomsand syndromes, such as the AIDS-wasting syndrome, nausea, vomiting,anorexia, and glaucoma.StimulantsStimulant users, particularly crack cocaine smokers or injecting stimulant users(cocaine, amphetamine) incur considerable risk for HIV. There is little definitiveevidence of cocaine effects on T-cell function (MacGregor, 1988). In contrast,a few studies have associated both cocaine and amphetamines withincreased NK activity (Swerdlow et al., 1991; Van Dyke, Stesin, Jones,Chuntharapai, & Seaman, 1986). Considering the prevalence of cocaine andother stimulant use, and its role as a behavioral risk factor for HIV transmission,the effects of cocaine use and withdrawal require further investigation. Onestudy reported only limited effects of cocaine withdrawal on immune-relatedmarkers in pregnant women (Johnson, Knisely, Christmas, Schnoll, & Ruddy,1996). Finally, the role of the most ubiquitous substance of abuse, tobacco, cannotbe underestimated. Tobacco exposure has pervasive effects on health,

19. HIV/AIDS and Substance Use Disorders 419including reported effects on the course of HIV, and has been associatedwith leukocytosis, shifts in T-cell subsets, decreased NKCA, and mitogenresponse; some studies also suggest immune activation under certain conditions(McAllister-Sistilli et al., 1998).Behavior–Immune InteractionsOther factors that are present in alcoholics and drug users may further compromisethe immune system and increase the risk for poor outcomes in HIV disease.Malnutrition is an important immunosuppressive factor influencing variouscomponents of the immune system (Chedid, 1995; MacGregor, 1988).Immune effects associated with life stress, poor coping mechanisms, and depression,which are highly prevalent in alcoholics and other substance abusers(Schuckit & Bogard, 1986), may further exacerbate AIDS risk and disease progressionin these populations. Depressive symptoms have been linked withincreased risk for mortality in HIV (Mayne, Vittinghoff, Chesney, Barrett, &Coates, 1996). Evans and colleagues (1995) have shown that the stress of HIV,even if asymptomatic, may adversely affect the immune system. In one study,psychological distress was independently associated with shorter time to AIDSamong HIV-infected IDUs, especially among those with the lowest CD4+counts (Golub et al., 2003).So-called “club drugs,” including 3,4-methylenedioxymethamphetamine(MDMA, Ecstasy), an amphetamine analogue with stimulant properties, andgamma-hydroxybutyrate (GHB), an analogue of gamma-aminobutyric acidwith sedative properties, have become increasingly popular, and their use iswidespread. These drugs are often used at all-night dance parties or “raves,”clubs, and bars. Other drugs in this group include flunitrazepam (Rohypnol—or“Roofies,” a long-acting, potent benzodiazepine not marketed in the UnitedStates), ketamine, methamphetamine, and hallucinogenics. The sedatives inthe group, GHB and Rohypnol, have become known as “date-rape” drugs. Allof these drugs enhance the risk of unsafe, novel, or repeated sexual behaviorsthat increase the risk of acquiring HIV and other sexually transmitted infections.In one ART adherence study of current and former drug users, the strongestpredictor of poor adherence and lack of viral suppression was activecocaine use. Depressive symptoms and the tendency to use alcohol and drugs tocope with stress were also predictive of nonadherence (Arsten et al., 2002). Alongitudinal study of HIV-positive drug and alcohol users found strong temporalassociation of ART adherence and viral suppression when users switched tononuse (Lucas, Gebo, Chaisson, & Moore, 2002). Interventions to treat affectivedisorders in substance users may have both medical and psychosocial benefits.Recent studies have begun to systematically investigate the links amongimmunologically relevant psychosocial predictors, psychosocial interventions,

420 IV. SPECIAL POPULATIONSand the course of disease. Attention to a wider range of immune measures otherthan CD4+ cells alone and more extensive psychosocial assessments havefound associations between specific stressors and depression and the course ofHIV (Burack et al., 1993; Cole, Kemeny, Taylor, Visscher, & Fahey, 1996;Evans et al., 1995; Goodkin et al., 1994).AIDS IN DRUG ADDICTION TREATMENTVigorous behavioral change strategies are required in the treatment of alcoholand drug abuse in those infected with or at risk for HIV infection. AIDS education,prevention, and behavioral training should be a regular and ongoing componentof drug treatment. Evaluators must use recognized general treatmentprinciples, such as those in the “Practice Guideline for Treatment of Patientswith Substance Use Disorders” (American Psychiatric Association, 1995) andwidely accepted placement criteria (American Society of Addiction Medicine,2003). Drug addiction is a chronic, relapsing disease and may require ongoingor repeated treatments. In one 12-year study, 29% of drug injectors remainedpersistent injectors and had the highest mortality rates (Galai, Safaeian,Vlahov, Bolotin, & Celentano, 2003). Overall care of those with HIV is likelyto be improved by integration of case management, medical, and substanceabuse treatment (Knowlton et al., 2001).BASIC COMPONENTS OF HIV/AIDS PREVENTION/TREATMENT IN DRUG ABUSE TREATMENT SETTINGSEffective management of these cases requires a multidisciplinary team that canimplement an individualized treatment plan structured to succeed within theconstraints of available resources and motivational forces:• Assessment of HIV risk behavior with frequent reassessments• Complete physical examination• Psychiatric assessment and indicated treatment• HIV testing• Safe sex training for all. This includes explicit discussion of proper use ofbarrier methods and techniques (latex condoms, gloves, and dentaldams), and stressing the importance of using barrier methods for all penetrativesexual practices or when body fluids are transmitted or exchanged(Centers for Disease Control and Prevention, 1993).Active alcohol and drug abusers encountered in any health care settingsshould be offered appropriate referrals and encouraged to enter treatment. Cul-

19. HIV/AIDS and Substance Use Disorders 421tural competency presents the primary hurdle in altering risk behaviors, particularlysince community-based outreach programs have proved to be the mosteffective (Kwiatowski, Booth, & Lloyd, 2000). For the users who cannot or willnot enter treatment, specific counseling methods can be employed to communicateeffective harm reduction techniques. IDUs must learn the hazards ofneedle sharing and, for those who do not stop injecting, emphasis must beplaced on use of a new, sterile needle for each injection to prevent blood-borneinfections. Methods of needle decontamination, such as flushing with bleach,can reduce some exposure risk, but are not as safe as using a sterile, unused needlefor each injection (Gostin, Lazzarini, Jones, & Flaherty, 1997).Counseling for noninjecting substance abusers is no less important—especially when sex partners may be IDUs (see “Prevention and Public Health”).Alcoholics, especially females and stimulant users, should be specifically targetedfor counseling on sexual practices during intoxicated states. Commercialsex work, often found linked with drug use to support habits (Edlin et al., 1994)or bartering sex to obtain drugs, further adds to risk by introducing multiplepartners (Catania et al., 1992, 1995) and circumstances where safe sex practicesare unlikely to be easily maintained.HIV TESTING: CLINICAL CONSIDERATIONSThe Centers for Disease Control and Prevention (CDC) has suggested since1988 that all patients admitted to substance abuse treatment programs bescreened for the presence of the HIV antibody. Screening and treatment forHIV infection are often linked to substance abuse programs. Literature on thebehavioral impact of HIV testing is mixed. For some who are HIV positive,testing and notification are catalysts for needle use risk reduction among IDUsin treatment (Casadonte, Des Jarlais, Friedman, & Rotrose, 1990) or otherforms of behavioral change (Cleary et al., 1991). Comprehensive counselingmust accompany testing. For some individuals, either a positive or negativeHIV test can be a powerful motivating factor for continued treatment for theaddictive disorder (Perry, Fishman, Jacobsberg, Young, & Frances, 1991).Health professionals can help facilitate positive motivation by stressing thebeneficial effects that drug abstinence and other healthy lifestyle changes canhave on the course of HIV infection, particularly in the context of effectiveART regimens. Watkins, Metzger, Woody, and McLellan (1993) found thatknowledge of HIV status was an important determinate of condom use amongIDUs.Information on HIV status can aid physicians in evaluating patients withnonspecific medical, neurological, and psychiatric symptoms and assist in theprompt recognition and treatment of infection (Stimmel, 1988). CD4+ lymphocytecounts and lymphocyte subsets, and viral load and viral resistance testingcan be used to stage treatment protocols for antiretroviral medications. In

422 IV. SPECIAL POPULATIONSthe immune compromised, some opportunistic infections can be preventedwith pharmacotherapy; others can be prevented through environmental manipulations(e.g., avoidance of undercooked or contaminated food or water).The CDC (1997, 2001) has extensive recommendations on the use ofART in HIV-positive pregnant or nursing women to reduce mother-to-infanttransmission (MIT). In the United States, the number of reported MITacquiredAIDS cases fell 43% from 1992 to 1996, likely because of providingzidovudine (AZT) to HIV-infected mothers, better guidelines for prenatal HIVcounseling and testing, and changes in obstetrical management (Centers forDisease Control and Prevention, 1997; Wilfert, 1999). Management of theHIV-positive pregnant woman who is undergoing treatment for an SUD is bestdone with a specialty team or in a specially designed program (Lindberg, 1996).HIV Testing: Guidelines for CounselingPretest Counseling• Get written informed consent.• Assess knowledge, attitude, and past experience with HIV/AIDS andHIV testing.• Assess individual risk factors.• Determine substance use (what, how, where, with whom, how muchand how often?).• Determine sexual behaviors, barrier use (condoms, gloves, dentaldams).• Explain antibody test in clear, easy-to-understand language.• Assess degree of risk.• Inform of the risk status.• Counsel on specific, effective means of reducing future risk behavior.Posttest Counseling: Positive Result• Anticipate emotional and behavioral responses to a positive test result.• Evaluate social support systems and coping strategies.• Advise of treatment options and available services.• Make referrals.• Medical evaluation.• Psychiatric evaluation: acute reaction, risk for suicide, past or currentdepression, other mental disorder, positive family history for mentaldisorder.• Provide opportunity to ask questions, respond to the results.• Provide information about symptoms associated with altered immunityand the effects of alcohol and drugs on the immune system (Stimmel,1988).

19. HIV/AIDS and Substance Use Disorders 423Reactions run the gamut and many immediately react as if they had animminently terminal condition. Delayed emotional reactions are common aswell. There are reports of knowledge of positive HIV status having severeadverse psychological effects, including suicidal behavior (Glass, 1988). Hospitalizedpatients may be especially vulnerable to suicidal ideation and intent(Alfonso et al., 1994).Posttest Counseling: Negative Result• Emphasize test limitations.• Emphasize the need for continued HIV precautions.• Emphasize the need for retesting.• Preemptively address erroneous conclusions about negative tests inhigh-risk individuals.• Have a low threshold for specialized referral to mental health services,especially for individuals from groups that have endured multiple andongoing losses to the AIDS epidemic or from particularly marginalizedgroups.Residential treatment programs should make information about HIV availableand provide a variety of support mechanisms for those affected, includingaccess to medical and mental health services. Ethical issues raised by HIV testingare not readily resolved. For example, if an individual is found to be HIVantibody positive, is there a duty to warn the sexual partner(s)? How will thesesorts of issues affect the therapeutic relationship? Because public health regulationsregarding these matters vary from state to state, practitioners must consultlocal public health requirements and guidelines.Clinical Assessment and ManagementThe many physical and emotional effects of AIDS complicate the contemporaneoustreatment of chemical dependence. The presence of those with AIDS indrug treatment units elicits complex feelings in staff and others if their status isknown. Issues of death and dying may dominate, and patients may express feelingsof hopelessness and question the value or practicality of abstinence fromdrug and alcohol use. Issues of medical regimen compliance and drug adherenceversus control become critical features in treatment. Arrangements for aftercareand placement of patients with AIDS following inpatient detoxification or residentialdrug treatment may be difficult.Combined diagnoses complicate treatment. Retention may be a problem:In one study, those with HIV who were receiving ambulatory psychiatric treatmentwere more likely to drop out of treatment if they drank or used drugs(Kennedy, Skurnick, & Lintott, 1994). The patient’s family and significant

424 IV. SPECIAL POPULATIONSothers who could be instrumental in motivating drug-addicted individuals fortreatment may, in the face of HIV, overlook or be reluctant to confront thesubstance abuse problem. Physicians and other health workers may minimize anindividual’s addiction in light of overwhelming physical illness. Those withlong-term addictions and multiple disabilities may be marginalized and mayhave long been estranged from families or other support mechanisms. Manyhave alienated health care providers by inconsistent compliance and subsequentcrisis use of the system, when life-threatening infections or overdosesoccur.It is important not to focus on substance abuse issues alone to the point ofexcluding AIDS-related psychological needs. Anxiety and depression, complicatedat times by cognitive impairment, frequently accompany HIV/AIDS. Asnoted, suicidal ideation is common. These symptoms need frequent reevaluationthrough treatment. Patients overwhelmed by illness, grief, and a senseof loss require a supportive, insight-oriented, and psychodynamically soundapproach. Depressive symptoms have been associated with increased mortalityfrom HIV infection (Mayne et al., 1996) and underscore the need for psychiatricservices for this population. Consultation–liaison psychiatrists may be particularlyvaluable in the care of patients with HIV and addiction, regardless ofsetting. A working knowledge of current therapies and scientific advances forHIV infection is important. Psychiatrists are in a unique position to assist thoseliving with or dying of HIV/AIDS to receive the type and level of care desired(Kennedy & Hill, 1997). Disclosure to others about lifestyle, risk behaviors,seropositivity, or complicated needs for care may be very difficult. Significantothers may benefit from referral to AIDS support resources. Women may havespecial issues and suffer more psychological distress than men (Kennedy,Skurnick, Foley, & Louria, 1995). Nonjudgmental attitudes that convey a truesense of willingness to help have a better chance of building successful rapportwith patients and may achieve a higher level of adherence to medical recommendationsand lifestyle changes.Patients do best with coordinated care at centers where there are specializedservices, integrated care management, and a track record with HIV. A psychiatristor therapist may be in a pivotal position to help coordinate and promotecooperation among the various caregivers. Pitfalls for mental healthprofessionals, addictions counselors, and other staff include countertransferenceissues linked to fear of contagion, addictophobia, racism, fear of homosexuality,denial of helplessness, and need for professional omnipotence. Mechanismssuch as displacement and reaction formation can result in failure to maintainappropriate empathic distance from the patients. Therapists need to be alert tothe how the overwhelming emotional issues may impact, strain, and push traditionalboundries observed in psychotherapy. The therapist must avoid becomingoverwhelmed by what he or she feels the patient is experiencing. Taking amoralistic attitude toward the patient’s drug use and sexual behaviors will

19. HIV/AIDS and Substance Use Disorders 425undermine treatment. Therapists must confront their own feelings and attitudestoward drug addiction, homosexuality, and AIDS.Legal IssuesIssues of confidentiality arise when treating individuals with drug addiction andHIV infection. Federal law protects the confidentiality of patient records forthose persons under treatment for drug abuse. This includes drug-abusingpatients who have AIDS. (There is, however, no general federal confidentialityprotection for medical records of AIDS patients not being treated for drugabuse.) These federal regulations protect both oral and written communications(Pascal, 1987). The more recent Health Insurance Portability Assurance Act(2003) provides for the electronic transmission of health information and isconcerned with medical record privacy and the U.S. standards for the protectionand privacy of personal health information. In the acute delivery of healthcare, use of universal precautions obviates the need to identify specifically anyindividual as HIV positive. Disclosure to those outside the clinical setting ispermitted only with the patient’s written consent. Reporting of HIV status topublic health authorities may be required in some states and may be disclosedwithout patient consent to the extent required by law. In all other situations,disclosure without the patient’s consent must be obtained through a courtorder, based on a finding of good cause (Pascal, 1987). All employers should beaware of the provisions of the Americans with Disabilities Act.Once a health care provider has knowledge of a positive HIV test, he orshe is obligated to inform the individual. Failure to do so may make the providerliable for any harm that results to the individual or to his or her sexualpartners (Pascal, 1987). Because HIV is communicable and AIDS can be fatal,situations may arise in which the physician or therapist is aware of a dangerposed to a third party, such as a sexual partner. HIV-positive patients must becounseled on their responsibilities and encouraged to voluntarily self-report tothird parties who may be at risk for infection (Pascal, 1987). Some states havepartner notification programs or requirements. If a substance abuse programconsiders it indicated to warn a third party concerning a patient’s HIV status,the patient’s consent or a court order must be obtained to comply with federalconfidentiality regulations. A policy of universal education for all patients,their spouses, significant others, and caregivers is often used and is consistentwith the consensus public health viewpoint that education, prevention, andvoluntary measures are the best approaches to stemming the AIDS epidemic,and that punitive approaches are counterproductive (Pascal, 1987).Single parents of minor children and, especially, pregnant women havespecial issues regarding custody and care should the mother or other primarycaregiver become disabled, incapacitated, or die. At the end stages of illness,patients may experience cognitive deficits; thus, issues of competency and

426 IV. SPECIAL POPULATIONSfuture planning should be addressed in a timely and appropriate manner. Again,consultation psychiatrists are in a unique position to assist patients who aregrappling with such difficult and serious matters. Many avenues and alternativescan be explored. Patients themselves prefer that physicians broach thesesubjects, and earlier rather than later (Kennedy & Hill, 1997).PREVENTION AND PUBLIC HEALTHPrevention is the strongest defense against spread of this blood-borne and sexuallytransmitted infection. Behavioral change studies indicate that some IDUsare attempting risk reduction, especially in needle sharing (Des Jarlais & Friedman,1987; Des Jarlais, Friedman, Choopanya, Varichseni, & Ward, 1992; Selwyn &Cox, 1985). There is evidence that IDUs can reduce their risk by alteringneedle-sharing behaviors. Attending a methadone-maintenance program promotesrisk reduction (Des Jarlais & Friedman, 1987). More recently, IDUs withAIDS knowledge reported that their consistent use of sterile new needlesdepended on availability (Des Jarlais et al., 1992; Gostin et al., 1997). Whensterile needles are unavailable, however, they use whatever is available. Needlesharing is common but not universal among IDUs. Sharing practices are influencedby many factors, including economics, regional drug norms, needle availability,length of habit, drug of choice (i.e., heroin, cocaine, or drug combinations),and others. A large national survey of the regulation of syringes andneedles concluded that deregulation of syringe sale and possession would reducethe morbidity and mortality associated with blood-borne infections, includingHIV, among IDUs, their sexual partners, and their children (Gostin et al.,1997). Regulations vary throughout the United States, but despite a U.S. GeneralAccounting Office (1993) report and numerous other government taskforce recommendations pointing out that new infections in IDUs plateau whereneedle exchanges have been tried, widespread support or federal backing forsuch strategies has been lacking. International studies show that needle exchangecoupled with other risk-reduction education and available treatmentslots has been successful (Des Jarlais et al., 1992). One evaluation of an experimentalU.S. needle exchange program showed that it was quickly adopted byIDUs, and an increase in injection and use did not occur (Watters, Estilo,Clark, & Lorvick, 1994). Lurie and Drucker (1997) estimated that from 4,000to 10,000 HIV infections in the United States, which cost between $250,000and $500,000 each, and untold amounts of human misery might have been preventedby needle exchange programs.Prevention strategies to reduce the risk of exposure to contaminated needlesinclude cessation of injection drug use, cessation of needle sharing, andimplementation of harm reduction methods, methadone maintenance, outpatientdetoxification, and drug-free treatment programs and needle exchange

19. HIV/AIDS and Substance Use Disorders 427programs. Male IDUs are especially important for the spread of HIV into thegeneral population. Murphy (1988) found that male IDUs reported a greaterpercentage of non-IDU heterosexual contacts than did female IDUs. Similarfindings were reported by Des Jarlais and colleagues (1987). In contrast, femaleIDUs may be at particular risk for being exposed to HIV as a result of heterosexualbehaviors and needle sharing. Des Jarlais and colleagues reported thatfemale IDUs were more likely than male IDUs to have sexual contacts thatwere also IDUs and tended to be needle sharers. Women who shared needleshad twice as many IDU sexual partners as those who did not, whereas themajority of sexual partners of male needle sharers were not themselves needlesharers. Kennedy and colleagues (1993) found that high-risk women (thosewith HIV-positive male partners) were more likely to insist on condom use forsex if they were employed. Skurnick, Abrams, Kennedy, Valentin, and Cordell(1998) also found that heterosexual couples who practiced safe sex at a studyentry were less likely to relapse into unsafe behaviors in 6 months if the femalewas employed. Unsafe sexual practices, most notably anal sex, are implicated insexual transmission of HIV within heterosexual couples (Skurnick et al., 1998).CONCLUSIONIDUs and other drug users are primary sources of HIV transmission to otheradults and to children in the general population. Health care providers have amajor responsibility to provide education, promote prevention, and providetreatment to this group. HIV counseling, testing, referral to drug treatment, andmental health and health services must be readily available. Those drug userswho are unable to abstain from injecting may benefit from therapeutic educationalstrategies about risk reduction. Public health measures may have to beaddressed through policy change. Counselors involved in the treatment of drugaddictedindividuals must explicitly discuss issues of safe sex and condom usage,as well as openly discuss the effects of drug use and intoxication on sexualbehavior and HIV risk. Furthermore, knowledge of medical, mental health, andsocial services resources is required for those caring for addicted individuals.Professionals should be aware of the wide range of presenting signs and symptomsof HIV infection, as well as treatment choice options and difficult, end-oflifedecisions regarding care, treatments and legal issues, including estate planningand care of minor children.The extraordinary rates of HIV infection among substance users suggestthat these individuals will occupy an increasing proportion of health careresources, particularly as the disease is stretched into a chronic, ongoing state asthose who are infected live longer. Numerous behavioral epidemiological studieshave shown that both injection-related risk factors (years of injecting drugs,type of drug injected, direct and indirect sharing of injection paraphernalia)

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CHAPTER 20Addictive Disorders in WomenSHEILA B. BLUMEMONICA L. ZILBERMANWhy write a chapter on women? Alcoholism and other addictions have traditionallybeen considered problems of men. The classical studies that haveshaped our understanding of the nature and course of these diseases, fromJellinek’s (1952) research on phases of alcoholism to Vaillant’s (1995) 45-yearlongitudinal study of alcohol abuse in an inner-city and college cohort, limitthemselves to male subjects. The earliest screening tools were developed formen. (The first version of the Michigan Alcohol Screening Test contained aquestion about the subject’s wife, which only later was changed to “spouse.”)Treatment methods and programs were also initially designed for male patients,and it was not unusual for women suffering from addictive disorders to behoused on general psychiatric wards, while men were in special units. Maleorientedtreatment models, like the so-called boot camps for addicts in thecriminal justice system, were “adapted” for women simply by subjecting them tothe same program, including masculine clothing and haircuts. Early studies thatincluded information about women often failed to analyze or report these data(Blume, 1980). Although there has been improvement, gender bias in addictionresearch remained evident in the 1990s (Brett, Graham, & Smythe, 1995).In spite of these limitations, a growing body of research has identifiedmale–female differences in the way addictions develop and in treatment needs.This chapter summarizes some of the more clinically relevant features of addictivedisorders in women. A number of recent reviews are available (Blume &Zilberman, 2004; Center on Addiction and Substance Abuse, 1996; Graham &Schultz, 1998; Zilberman & Blume, 2004), as are several federal publications on437

438 IV. SPECIAL POPULATIONSthe treatment of women (Substance Abuse and Mental Health ServicesAdministration, 2001a; U.S. Department of Health and Human Services, 1993,1994).EPIDEMIOLOGYIn general, men are more likely to report any use of psychoactive substances,including alcohol and nicotine. However, changes in use differ by gender. Forexample, over the last 30 years, the proportion of U.S. men who smoke hasfallen at a much greater rate than the corresponding decrease among women, sothat the difference is progressively smaller (27 vs. 23%). Among adolescentsages 12–17, girls already outnumber boys in rates of tobacco use (14 vs. 13%).Furthermore, while reduction in the rate of smoking has been detected amongboys, the same is not true for girls (Substance Abuse and Mental Health ServicesAdministration, 2001b).Table 20.1 summarizes data on rates of substance use disorders. These rateswere estimated for noninstitutionalized U.S. adults, ages 15–54, from a diagnosticinterview based on criteria according to the revised third edition of Diagnosticand Statistical Manual of Mental Disorders (DSM-III-R; American PsychiatricAssociation, 1987), administered to more than 8,000 subjects in the early1990s as part of the National Comorbidity Survey (Warner, Kessler, Hughes,Anthony, & Nelson, 1995). The overall higher prevalence in men masks subgroupgender differences. Women ages 45–54 reported a higher lifetime prevalenceof drug dependence (other than alcohol or nicotine) than did men (3.8%compared to 2.1% for men), whereas the 12-month prevalence is similarbetween the sexes at this age (0.8% for women, 0.6% for men). This findingTABLE 20.1. Relative Prevalence of Addictive Disordersin the United States, Ages 15–54Disorder Males (%) Females (5) Male:female ratioLifetime abuse/dependenceAny substance 35.4 17.9 2.0:1Alcohol 32.6 14.62 2.2:1Other drug a 14.6 9.4 1.6:112-month abuse/dependenceAny substance 16.1 6.6 2.4:1Alcohol 14.1 5.3 2.7:1Other drug a 5.1 2.2 2.3:1Note. Date from the National Comorbidity Study (Warner et al., 1995).a Excludes nicotine; includes nonmedical use of prescription psychotropics.

20. Addictive Disorders in Women 439reflects the higher prevalence of prescription drug dependence in women,whereas men have higher rates of dependence on illicit drugs.Among young people, ages 15–24, the male rate of 12-month drug dependence(4.5%) is about twice the female rate (2.1%). However, among youngpeople who have used a drug within the past 12 months, the rates are almostequal (males 13.6%, females 10.6%).Demographic risk factors for alcohol problems in women have been foundto be age-dependent in a large general population sample. Women ages 21–34years reported the highest problem rates. Among them, those who were nevermarried, childless, and not employed (“roleless”) were at highest risk. Forwomen ages 35–49, those who were divorced or separated, had children not livingwith them, and were unemployed (“lost role”), and for women ages 50–64,those who were married, had children not living with them, and were not workingoutside the home (“role entrapment”) had the highest problem rates. Thelast group is reminiscent of the so-called “empty nest” syndrome describedamong older women (Blume & Zilberman, 2004).A prominent risk factor for both alcohol and other drug abuse/dependencein women is a history of physical and/or sexual abuse (Center on Addiction andSubstance Abuse, 1996; Simpson & Miller, 2002). In data derived from theEpidemiologic Catchment Area (ECA) study in the early 1980s, it was foundthat the lifetime prevalence of alcohol abuse/dependence increased threefoldand that of other drug abuse/dependence increased fourfold in women whoreported a history of sexual assault (Blume & Zilberman, 2004).Several researchers documented the influence of male “significant others”on the substance use patterns of women (e.g., Amaro & Hardy-Fanta, 1995).Men are likely to introduce women to the use of drugs and to supply drugs totheir female partners.Rates of both alcohol and other drug abuse/dependence are thought to beparticularly high among lesbian women (McKirnan & Peterson, 1989) andwomen in the criminal justice system (Center on Addiction and SubstanceAbuse, 1996). Among women convicted of homicide, rates of alcohol abuse/dependence were increased nearly fiftyfold above rates in the general population(Eronen, 1995). Among Jewish Americans who voluntarily participated intwo studies, an overrepresentation of women compared to men was found (Vex& Blume, 2001).PharmacologyPHYSIOLOGICAL FACTORSEarly research on the pharmacology of alcohol and other drugs was performedon male subjects and thought to apply to both sexes. More recently, however, ithas been found that given equal doses of alcohol (even if corrected for body

440 IV. SPECIAL POPULATIONSweight), women reach higher blood alcohol levels than men. This fact is partlyrelated to alcohol’s distribution in total body water, because women have agreater proportion of fat and less body water than do men. In addition, menhave higher levels of the enzyme alcohol dehydrogenase (ADH) in the gastricmucosa, leading to increased metabolism in the stomach (first-pass metabolism)and less absorption into the male bloodstream. Other differences includegreater variability in blood alcohol concentrations, faster alcohol metabolism,and reduced acute tolerance to alcohol in women compared to men, leading tomore intense and less predictable reactions to alcohol consumption in womenthan in men (Blume & Zilberman, 2004).Gender differences in the pharmacology of other drugs are less well studied.The differences in body composition noted previously produce longer halflivesin lipid-soluble drugs such as diazepam and oxazepam in women. Intranasalcocaine administration produces higher subjective effects accompanied byhigher plasma levels in men compared to women. Variations in women´splasma levels according to menstrual cycle phases have also been reported(Zilberman & Blume, 2004).Health EffectsChronic heavy alcohol use has been linked to many serious medical complicationsin both sexes (National Institute on Alcohol Abuse and Alcoholism,2000). However, many of these complications develop more rapidly in women,with a lower level of alcohol intake. Included are hepatic steatosis and cirrhosis,hypertension, anemia, malnutrition, gastrointestinal hemorrhage, peptic ulcer,and both peripheral myopathy and cardiomyopathy. Both human immunodeficiencyvirus (HIV) infection and other sexually transmitted diseases are linkedto substance use disorders in women (Center on Addiction and SubstanceAbuse, 1996). Seventy percent of currently HIV-infected women acquired thevirus either through injection drug use or during sexual relations with a druginjectingpartner, compared to less than half of HIV-infected men. Addictedwomen, particularly those dependent on crack cocaine or heroin, often becomeinfected by exchanging sex for drugs or by engaging in prostitution to obtainmoney for drugs.Alcohol and other drug use is closely linked to smoking in women. Mortalityfor lung cancer in U.S. women surpassed breast cancer mortality in 1986 tobecome the leading cause of cancer death. The risks for coronary artery disease,obstructive lung disease, peptic ulcer, and early menopause, as well as cancersof the mouth, larynx, esophagus, stomach, bladder, and cervix are increasedin female smokers (Zilberman & Blume, 2004), as is the risk for breast cancerin female drinkers (National Institute on Alcohol Abuse and Alcoholism,2000).

Effects on Reproductive Functioning20. Addictive Disorders in Women 441Whereas single doses of alcohol have little effect on sex hormone levels inwomen, chronic heavy drinking leads to inhibition of ovulation, infertility, anda variety of reproductive and sexual dysfunctions (Blume & Zilberman, 2004).Consumption of alcohol by women suppresses both sexual arousal andorgasmic function in a dose–response fashion. The physiological reality is contraryto the widely held cultural belief that alcohol is an aphrodisiac for women(Blume, 1991). This belief often leads alcoholic women to expect that theyneed alcohol to perform and enjoy the sexual act, in spite of their alcoholrelatedsexual problems. The clinician can help such women by explaining thattheir drinking has depressed rather than enhanced their sexual responsiveness,and that in the presence of a loving relationship, they will find sex more enjoyablein recovery than they did while drinking (Gavaler, Rizzo, & Rossaro,1993).Cocaine and amphetamines are widely believed by their users to be sexualstimulants, whereas chronic use is often associated with loss of sexual desire andinhibited orgasm. In addition, cocaine use has been associated with menstrualalterations, galactorrhea, infertility, hyperprolactinemia, and increased levels ofluteinizing hormones in women (Mendelson, Sholar, Siegel, & Mello, 2001).Heroin use has been reported to suppress both ovulation and sexual desire, ashas abuse of sedative drugs (Zilberman & Blume, 2004).Fetal Alcohol and Drug EffectsFetal alcohol syndrome (FAS), a combination of birth defects producing lifelongdisability, is currently estimated to affect about 1–3 infants for every 1,000live births in the United States. FAS is thus among the three most frequentbirth defects resulting in mental retardation, with a prevalence similar to Downsyndrome and spina bifida. A diagnosis of FAS is based on the co-occurrence ofpre- and postnatal growth deficiency, structural facial abnormalities, and centralnervous system dysfunctions, including poor coordination, mental retardation,and/or behavioral dyscontrol. In addition, a wide variety of other birthdefects affecting vision, hearing, and other body systems are often seen in thesechildren. Although the full FAS syndrome is seen almost exclusively in the offspringof alcoholic women who drink heavily (an average of six or more drinksper day) during pregnancy, women who drink at lower levels are at risk for fetalalcohol effects such as miscarriage, low birthweight, birth defects, and behavioralabnormalities (Warren et al., 2001). The prevalence of fetal alcoholeffects is thought to be many times greater than that of FAS.Fetal damage is also associated with other drug use and abuse (Singer et al.,2002). Cigarette smoking during pregnancy is implicated as an important factor

442 IV. SPECIAL POPULATIONSin miscarriage, low birthweight, and sudden infant death syndrome. Unfortunately,many young women believe that cocaine facilitates a quick and lesspainful delivery, whereas it actually produces obstetric complications that causedamage to the newborn, as well as birth defects secondary to its deleteriouseffects on fetal circulation. Pregnant heroin addicts are customarily treated withmethadone as a maintenance drug rather than detoxification to abstinence, as asafer regimen for the fetus. With good prenatal care, such patients can bebrought to term and experience normal deliveries. However, their infantsrequire treatment for neonatal opiate withdrawal (U.S. Department of Healthand Human Services, 1993).Whether or not birth defects occur, untreated substance abuse/dependencein a new mother will interfere with maternal–infant bonding, parenting,and family life. Thus, pregnancy is a critical time for case findingand intervention. Among the approximately 4 million pregnancies in theUnited States annually, approximately 12% of women smoke (Ibrahim, Floyd,Merritt, & De Couble, 2000), 23% use alcoholic beverages, and 4.4% useother substances (Substance Abuse and Mental Health Services Administration,2002).GENETIC INFLUENCESA great deal of research has been devoted to the effort to differentiate geneticfrom environmental factors in the etiology of alcoholism, as well as other drugdependencies. Almost all implicate a combination of nature and nurture(Kendler, Walters, & Neale, 1995). Of interest here is that some studies showdifferent patterns of alcoholism heredity for men and women (Prescott, Aggen,& Kendler, 1999).Studies of possible genetic markers in children of alcoholics have largelybeen confined to males, or to a small number of women. Daughters of alcoholicparents have also been found to have more positive and pleasant mood reactionsto a single dose of alprazolam, suggesting that they may be at greater riskfor abuse of this drug. Regarding the heritability of drug use disorders, there isindication that genetic influences are stronger for males than for females, whileenvironmental factors are more evident in females than in males (Blume &Zilberman, 2004; Zilberman & Blume, 2004).In addition, some research suggests that there is a genetic link betweenalcoholism in male relatives and major depressive disease in women, in a combinationof genetic and environmental causation (Cadoret et al., 1996). Astudy in female twin pairs suggests separate heredity but common environmentalrisk factors for comorbid alcoholism and major depression in women(Kendler, Heath, Neale, Kessler, & Eaves, 1993).

20. Addictive Disorders in Women 443PSYCHOLOGICAL FACTORSThe role of psychological factors in the etiology of substance use disorders hasbeen a subject of uncertainty for many years. Long-term longitudinal studies ofmale alcoholics have found that psychiatric disorders and symptoms are morelikely to be the result of alcoholism than to have been predisposing factors(Vaillant, 1995). However, the lack of similar studies in women leaves thequestion open. The strong association between childhood physical and sexualabuse and later addictive disease in women, alluded to in the section “Epidemiology,”suggests mediation through psychological symptoms such as low selfesteem,depression, shame, guilt, and feelings of sexual inadequacy. One of thefew longitudinal studies that did include women, a 27-year follow-up of a collegedrinking study, looked at risk factors for later drinking problems. These factorswere different for males and females. Although women who had alcoholrelatedproblems in college had a higher prevalence of later problems than didtheir female classmates, the women at highest risk for problems later in lifewere those who reported in college that they drank to relieve shyness, to feelgay, to get along better on dates, and to get high. This pattern suggests psychologicaldependence as a risk factor for women (Blume & Zilberman, 2004).Another approach to the study of psychological factors is to examine genderdifferences in the patterns of comorbid psychiatric disorders in identifiedalcoholics and other drug addicts. Both in general population studies and inclinical populations, female alcoholics and addicts have higher rates of comorbidpsychiatric disorders in general, and higher rates of depressive and anxietydisorders in particular, compared to males (Zilberman, Tavares, Blume, & el-Guebaly, 2003). In fact, the only comorbid diagnoses found more frequently inaddicted males are residual attention deficit disorder, antisocial personality disorder,and pathological gambling (Lesieur, Blume, & Zoppa, 1986). Eating disorders(Walfish, Stenmark, Sarco, Shealy, & Krone, 1992) and posttraumaticstress disorder (commonly related in women to sexual abuse) (Kessler, Sonnega,Bromet, Hughes, & Nelson, 1995) are seen frequently in women with addictions.Of particular interest from the point of view of etiology is the questionconcerning which disorders occur first (primary) and which develop subsequently(secondary). As mentioned earlier, Vaillant (1995) found that alcoholismwas usually primary in men. However, in the general population ECAstudy, it was found that among adults with lifetime diagnoses of both alcoholabuse/dependence and major depression, depression was primary in 66% of thewomen compared to only 22% of men. Likewise, in an inpatient alcoholismtreatment population, it was found that depression was primary in 66% of thewomen with comorbid major depression compared to 41% of men. Similar findingswere reported for alcoholic research volunteers (Roy et al., 1991) and dual-

444 IV. SPECIAL POPULATIONSdiagnosed adolescents. Longitudinal survey evidence in women also tends tosupport a relationship between earlier reports of depression and later increasesin alcohol use or chronicity of alcohol problems. Interestingly, alcohol use attime 1 in these longitudinal studies in women also predicted later depression(Blume & Zilberman, 2004). Similar findings have been reported in a longitudinalstudy of adolescents (Brook, Brook, Zhang, Cohen, & Whiteman, 2002).Taken together, the previous discussion suggests some link between primarydepression and secondary alcoholism in women. Because alcohol is not aneffective antidepressant (Vaillant, 1995), the link is probably not simple selfmedication.Further research is needed to elucidate this relationship. However,the relationship highlights the need to take careful psychiatric histories in allwomen suffering from addictive disorders, with special emphasis on the temporaldevelopment of comorbid disorders. Patients whose depression precededtheir addiction or occurred during a prolonged period of abstinence are likely tohave a primary depressive disorder requiring specific treatment, whereas depressionsecondary to addiction is more likely to improve spontaneously with recoveryfrom the addiction. In addition, patients with primary depression should bewarned about the possibility of recurrence and carefully educated to recognizeearly symptoms of a recurrent major depressive episode. Vigorous treatment ofsuch an episode during remission of the patient’s addiction can avoid alcohol/drug relapse and promote further progress in the patient’s recovery.SOCIOCULTURAL FACTORSAs pointed out in the section “Genetic Influences,” environmental factors areparticularly important in the etiology of addictive disorders in women. Socioculturalinfluences include general cultural and subcultural norms for alcohol,tobacco, and other drug use; culturally based attitudes and beliefs about suchuse (including popular media stereotypes of users and abusers); peer pressure;prescription practices; laws regulating availability and use; and the economicsof supply, demand, price, and disposable income. In all societies that allow alcoholand/or drug use, these norms, attitudes, stereotypes, peer pressures, and evenlaws (dating as far back as the Code of Hammurabi in 2000 B.C.E.) differ formales and females.Social attitudes act as a double-edged sword for women. On the one hand,the expectation that women will drink lower quantities of alcoholic beveragesand drink less frequently is protective (Blume & Zilberman, 2004). On theother hand, the intense stigma linked to stereotypes of alcoholic and addictedwomen creates serious problems for women who drink and/or use other drugs(Blume, 1991). Behavior tolerated in men is considered scandalous for women.Compare the expression “drunk as a lord” with its feminine equivalent, “drunk

20. Addictive Disorders in Women 445as a lady.” In addition, the drinking/drugging woman is considered promiscuous.Society believes, contrary to fact, that alcohol is a sexual stimulant for women,so that a woman under the influence who says “no” really means “yes.”Although a general population survey of nearly 1,000 women failed to find evidencethat women who drink become less particular in their choice of sexualpartner, even if drinking heavily, women’s drinking is a frequent rationalizationfor sexual assault, including date rape (Blume, 1991). In a study of beliefs aboutrape, young adults considered a rapist who is intoxicated less responsible for thecrime, whereas they considered a victim who has been drinking more to blame.It is not surprising, then, that alcoholic women are much more likely to be victimsof violent crime, including rape, than are matched controls. These womenare also more likely to report spousal violence than are control women. Society’sview of alcohol/drug-abusing women is one of moral and sexual degradation,making them acceptable targets for sexual aggression (Blume, 1991).Another result of this stigma is denial on the personal, family, and societallevels. A woman in the early stage of alcohol/drug dependence, accepting thecultural stereotype, denies that she may have a problem (“I’m not like that!”).Families also deny that the difficulty with their mother, daughter, sister, or wifecould be alcoholism or addiction (“She’s not like that!”). Physicians and otherhealth professionals often fail to diagnose alcoholism in patients who do notresemble social stereotypes. Alcoholic patients least likely to be correctly identifiedin a large general hospital study were those with higher incomes and educationallevels, those with private insurance, and those who were female(Blume & Zilberman, 2004).As the disease progresses in the addicted woman, intense guilt and shameoften drive the sufferer into hiding, so that the alcoholic woman is far morelikely to drink alone than is the alcoholic man. If she lives alone or is a singleparent with small children, there may be no significant others in her social networkable to recognize her problem and intervene. Although alcoholic womenfrequently seek medical help for a variety of complaints ranging from infertility,depression, anxiety, or insomnia to hypertension and peptic ulcer, their guilt,shame, and denial require that the interviewing professional screen actively foralcohol/drug problems. Undetected alcohol/drug use disorders can lead to inappropriatesymptomatic treatment, with the danger of adding dependence onprescription sedatives, analgesics, or tranquilizers to the patient’s problems.Failure in diagnosis in women of childbearing age may lead to the appearance ofpreventable birth defects in their offspring. Finally, delay in diagnosis allowsthe development of late-stage physical, psychological, and social complications,making eventual treatment more costly, more difficult, and less successful. Earlydiagnosis and adequate treatment of substance use disorders in women is also animportant component in the prevention of teen pregnancy, acquired immunedeficiency syndrome, hepatitis, suicide, and other negative outcomes.

446 IV. SPECIAL POPULATIONSCLINICAL FEATURES OF ADDICTIVE DISORDERSIN WOMENTable 20.2 summarizes the more important features that have been described inthe literature as differentiating addictive disorders in women from their occurrencein men. In general, alcoholic women are less likely to report “acting out”behaviors such as breaking the law, problems with the criminal justice system,or feeling “out of control.” Women more commonly report problems withhealth and family, and psychological symptoms such as depression and low selfesteem.Because of the differences in self-identified problems and clinical manifestations,investigators developed several screening tools designed specially toidentify alcoholism in women. These include the T-ACE (Sokol, Martier, &Ager, 1989), TWEAK (Russell, Martier, & Sokol, 1994), SWAG (Spak &Hallstrom, 1996) and Health Questionnaire (Blume & Russell, 1993). Laboratorytesting has also been found helpful in screening for alcoholism in women.In a cohort of 100 early-stage alcoholic women, it was found that a screeningcriterion of either an elevated gamma-glutamyl transferase (GGT) or anincreased mean corpuscular volume (MCV) correctly identified two-thirds ofthe women. The same two laboratory tests were found useful in screening anobstetric population and predicting birth defects (Blume & Zilberman, 2004).Although the clinical presentation of any individual patient depends on acombination of physical, psychological, and social factors, sex differences insymptoms and problems are themselves subject to social and cultural influences.Thus, sex differences may be expected to change over time as society itselfchanges.Mortality rates for alcoholic women are high compared to both the generalpopulation of women and alcoholic men (Klatsky, Armstrong, & Friedman,TABLE 20.2. Features of Addictive Disorders in Women, Compared to Men• Start substance use later (A).• Disease progresses more rapidly (A, C).• Drink significantly less than males (A, C, O).• “Significant other” more likely to be substance abuser (A, C, O).• Higher rates of comorbid psychiatric disorders (A, C).• Higher rates of comorbid prescription drug dependence (A).• More likely to make suicide attempts (A).• More likely to have a history of physical and sexual abuse (A, C, O).• More often date the onset of pathological alcohol/drug use to a specific stressful event(A, C).• More likely to report previous psychiatric treatment (A).• Higher mortality rate (A).Note. See Blume and Zilberman (2004); White, Brady, and Sonne (1996); Lewis, Bucholz, Spitznagel,and Shayka (1996); and Griffin, Weiss, and Mirin (1989). A, reported for alcoholism; C, reported forcocaine; O, reported for other drugs.

20. Addictive Disorders in Women 4471992). In a longitudinal study of 5,000 treated alcoholics, the mortality rate formen was three times the expected rate, whereas for women it was 5.2 times thecomparable rate in the general public (Lindberg & Agren, 1988).TREATMENT OF ADDICTIVE DISORDERS IN WOMENAlthough utilization of treatment resources for alcoholism has increased duringrecent years, women remain underrepresented in treatment. When women dolook for help, they are more likely to use mental health services and other facilitiesnot specific to addiction (Weisner & Schmidt, 1992). The reasons for this,including social stigma, denial, and the frequent failure to diagnose women,have been mentioned. In addition, however, the most common current, organizedcase-finding methods (e.g., drinking driver programs, drug courts, andemployee assistance programs) are primarily useful for identifying male alcoholics/addicts.Appropriate settings for identifying women in need of treatmentwould be medical settings of all kinds (including mental health facilities) andfamily counseling services. Unfortunately, organized screening in health facilitiesis the exception rather than the rule, and women identified in these settingsare usually in late stages of addiction.Research on the effectiveness of treatment for women has employed a widevariety of methods (Ashley, Marsden, & Brady, 2003). In general, adult womenand men treated together in the same specialized addiction programs doabout equally well (Vannicelli, 1986). A recent study reported that althoughproblem-drinking women started off more symptomatic than men, they actuallydid better than men at the 8-year follow-up in different interventions. Particularly,women seem to benefit from maintained Alcoholics Anonymous (AA)attendance (Timko, Moos, Finney, & Connell, 2002). Studies of specialwomen´s programming have shown positive effects, although few have employedrandom assignment techniques. Research supports the value of addingchild care, mother–child residential programming, all-female counselinggroups, and supplemental women-focused educational sessions (e.g., sexual andreproductive counseling, assertiveness, parenting, and communication skillstraining) (Ashley et al., 2003). Comprehensive programming, combining severalof these specific components, is also effective. Whether women-only programsare superior to mixed programs is still not well established. The only publishedrandom-assignment study found a superior outcome in a 2-year follow-upof 100 alcoholic women randomly assigned to a specialized women’s clinic comparedto 100 assigned to a mixed-sex treatment (Dahlgren & Willander, 1989).A women-only self-help program, Women for Sobriety, is thriving in someparts of the country (Kaskutas, 1996), while the number of women utilizing AAis also growing, and women-only AA groups are available in some areas. Basedon what is known about the characteristics of addicted women, Table 20.3 sum-

448 IV. SPECIAL POPULATIONSTABLE 20.3. Special Considerations in Women’s Treatment• Psychiatric assessment for comorbid disorders; date of onset for each(primary/secondary).• Attention to past history and present risk of physical and sexual assault.• Assessment of prescription drug abuse/dependence.• Comprehensive physical examination for physical complications andcomorbid disorders.• Need for access to health care (including obstetric care).• Psychoeducation to include information on substance use in pregnancy.• Child-care services for women in treatment.• Parenting education and assistance.• Evaluation and treatment of significant others and children.• Positive female role models (among treatment staff; self-help).• Attention to guilt, shame, and self-esteem issues.• Assessment and treatment of sexual dysfunction.• Attention to the effects of sexism in the previous experience of thepatient (e.g., underemployment, lack of opportunity, and rigid sex roles).• Avoidance of iatrogenic drug dependence.• Special attention to the needs of minority women, lesbian women, andthose in the criminal justice system.marizes the special emphases that have been found helpful in treating thesewomen. For pregnant women, the provision of prenatal care, along withwomen-centered programming, has been shown to improve both treatmentretention and birth outcomes (Ashley et al., 2003).The good news is that specific program components for women can beadded to existing programs, and staff sensitivity can be improved by training.The bad news is that, in a large survey, only 19% of addiction programsreported providing special programming for pregnant or postpartum women,and only 28% offered women´s programming at all (Office of Applied Studies,2000). We can and must do better.PREVENTIONEffective primary prevention of alcohol, tobacco, and other drug dependence inwomen has received little research attention, with the exception of specificpublic education campaigns to prevent FAS. Such efforts have proven moreeffective in persuading light and moderate drinkers to abstain during pregnancythan in persuading the heaviest alcohol consumers. Thus, screening in medicaland obstetric practice remains essential.In designing educational approaches in the schools and for the generalpublic, it is important to remember the double-edged sword quality of societal

20. Addictive Disorders in Women 449attitudes. The goal of reducing the social stigma attached to the female addictmust be balanced against that of preserving the cultural expectation thatwomen will practice abstinence or moderation. Straightforward informationshould be provided about women’s sensitivity to alcohol; principles for the safeuse of prescribed psychoactive drugs; the health effects of tobacco, alcohol, andother drugs particular to women (e.g., breast cancer, birth defects, and obstetriccomplications); the dangers of using substances to “medicate” feelings of inadequacyor sexual problems; and the special risks of women from alcoholic families.These general education efforts are particularly important, because thealcoholic beverage industry has targeted women as a “growth market,” linkingdrinking in their advertisements with youth, beauty, sexual attractiveness, andsuccess. Such advertising sends messages that can alter the cultural norms thatprotect women. Likewise, cigarette advertising aimed at women stressing slimnessand “liberation” (e.g., the slogan “You’ve come a long way baby”) tends tomake smoking more socially acceptable for women and adolescent girls.Because smoking is more strongly associated with the use of illegal drugs in girlsthan boys (Center on Addiction and Substance Abuse, 1996), smoking amongadolescent girls should be a priority prevention target.In addition to general population efforts, specific alcohol/drug preventiontechniques should be aimed at high-risk groups such as adolescent and adultdaughters of alcoholics/addicts, victims of physical and sexual abuse, womenentering new social groups with different drinking customs (e.g., college freshmenand women entering the military), women undergoing stressful life transitions(e.g., divorce, widowhood, childbirth, and reentry into the labor force),and women acting as caretaker for a chronically ill relative. Such risk groupscan be helped to develop self-esteem and coping skills that do not involve substanceuse.Laws and their applications also exert an important influence on substanceuse disorders in women. Recently, the resources of the criminal justice systemhave been used to initiate prosecution of women who use alcohol and otherdrugs during pregnancy. Such women have been charged with “prenatal childabuse” or “delivery of controlled substances to a minor” (via the umbilicalcord). Although many cases have been thrown out of court, and many convictionshave been reversed on appeal, the result of these policies has been lessoften prevention of substance use than deterring pregnant substance users fromseeking either prenatal or addiction treatment (Harris & Paltrow, 2003).In summarizing this overview of use and abuse of psychoactive substancesby girls and women in the United States, it is clear that our society has strongfeelings about such use but has not translated those feelings into an adequateinvestment in prevention, treatment, and research. Let us hope that a renewedfocus on the problems of women will stimulate medical and social policymakersto rethink the priority devoted to this issue.

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20. Addictive Disorders in Women 451Harris, L. H., & Paltrow, L. (2003). MSJAMA: The status of pregnant women andfetuses in US criminal law. JAMA, 289(13), 1697–1699.Ibrahim, S. H., Floyd, R. L., Merritt, R. K., & De Couble, P. (2000). Trends inpregnancy-related smoking rates in the United States 1987–1996. JAMA, 283(3),361–366.Jellinek, E. M. (1952). Phases of alcohol addiction. Q J Stud Alcohol, 13, 673–684.Kaskutas, L. A. (1996). Pathways to self-help among women for sobriety. Am J DrugAlcohol Abuse, 22(2), 259–280.Kendler, K. S., Heath, A. C., Neale, M. C., Kessler, R. C., & Eaves, L. J. (1993). Alcoholismand major depression in women: A twin study of the causes of comorbidity.Arch Gen Psychiatry, 50(9), 690–698.Kendler, K. S., Walters, M. S., & Neale, M. C. (1995). The structure of the genetic andenvironmental risk factors for six major psychiatric disorders in women. Arch GenPsychiatry, 52, 374–383.Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Posttraumaticstress disorder in the national comorbidity survey. Arch Gen Psychiatry,52(12), 1048–1060.Klatsky, A. L., Armstrong, M. A., & Friedman, G. D. (1992). Alcohol and mortality.Ann Intern Med, 117, 646–654.Lesieur, H. R., Blume, S. B., & Zoppa, R. M. (1986). Alcoholism, drug abuse, and gambling.Alcohol Clin Exp Res, 10(1), 33–38.Lewis, C. E., Bucholz, K. K., Spitznagel, E., & Shayka, J. J. (1996). Effects of gender andcomorbidity on problem drinking in a community sample. Alcohol Clin Exp Res,20(3), 466–476.Lindberg, S., & Agren G. (1988). Mortality among male and female hospitalized alcoholicsin Stockholm 1962–1983. Br J Addict, 83, 1193–1200.McKirnan, D. J., & Peterson, P. L. (1989). Alcohol and drug use among homosexualmen and women: Epidemiology and population characteristics. Addict Behav, 14,545–553.Mendelson, J. H., Sholar, M. B., Siegel, A. J., & Mello, N. K. (2001). Effects of cocaineon luteinizing hormone in women during the follicular and luteal phases of themenstrual cycle and in men. J Pharmacol Exp Ther, 296, 972–979.National Institute on Alcohol Abuse and Alcoholism. (2000). Tenth special report to theU.S. Congress on alcohol and health (NIH Publication No. 00-1583, pp. 197–338).Washington, DC: U.S. Department of Health and Human Services.Office of Applied Studies. (2000). Uniform Facility Data Set (DHHS Publication No.[SMA] 00-3463). Rockville, MD: Substance Abuse and Mental Health ServicesAdministration.Prescott, C. A., Aggen, S. H., & Kendler, K. S. (1999). Sex differences in the sources ofgenetic liability to alcohol abuse and dependence in a population-based sample ofU.S. twins. Alcohol Clin Exp Res, 23, 1136–1144.Roy, A., DeJong, J., Lamparski, D., Adinoff, B., George, T., Moore, V., et al. (1991).Mental disorders among alcoholics. Arch Gen Psychiatry, 48, 423–427.Russell, M., Martier, S. S., & Sokol, R. J. (1994). Screening for pregnancy risk-drinking:Tweaking the tests. Alcohol Clin Exp Res, 18, 1156–1161.Simpson, T. L., & Miller, W. R. (2002). Concomitance between childhood sexual

452 IV. SPECIAL POPULATIONSand physical abuse and substance use problems: A review. Clin Psychol Rev, 22, 27–77.Singer, L. T., Arendt, R., Minnes, S., Farkas, K., Salvator, A., Kirchner, H. L., &Kliegman, R. (2002). Cognitive and motor outcomes of cocaine-exposed infants.JAMA, 287, 1952–1960.Sokol, R. J., Martier, S. S., & Ager, J. W. (1989). The T-ACE questions: Practical prenataldetection of risk-drinking. Am J Obstet Gynecol, 160, 863–870.Spak, F., & Hallstrom, T. (1996). Screening for alcohol dependence and abuse inwomen: Description, validation, and psychometric properties of a new screeninginstrument, SWAG, in a population study. Alcohol Clin Exp Res, 20(4), 723–731.Substance Abuse and Mental Health Services Administration. (2001a). Benefits of residentialsubstance abuse treatment for pregnant and parenting women: Highlights from astudy of 50 demonstration programs of the Center for Substance Abuse Treatment.Rockville, MD: U.S. Department of Health and Human Services.Substance Abuse and Mental Health Services Administration. (2001b). Summary offindings from the 2000 National Household Survey on Drug Abuse (Office of AppliedStudies, NHSDA Series H-13, DHHS Publication No. [SMA] 01-3549). Rockville,MD: U.S. Department of Health and Human Services.Substance Abuse and Mental Health Services Administration. (2002). National HouseholdSurvey on Drug Abuse Survey Report 5/17/02. Retrieved April 10, 2003, fromwww.samhsa.gov/oas/2k2/preg/preg.htmTimko, C., Moos, R. H., Finney, J. W., & Connell, E. G. (2002). Gender differencesin help-utilization and the 8-year course of alcohol abuse. Addiction, 97(7), 877–889.U.S. Department of Health and Human Services. (1993). Pregnant, substance-usingwomen (DHSS Publication No. [SMA] 93-1998). Rockville, MD: Author.U.S. Department of Health and Human Services. (1994). Practical approaches in thetreatment of women who abuse alcohol and other drugs (DHSS Publication No.[SMA] 94-3006). Rockville, MD: Author.Vaillant, G. E. (1995). The natural history of alcoholism revisited. Cambridge, MA: HarvardUniversity Press.Vannicelli, M. (1986). Treatment considerations. In Women and alcohol: Health-relatedissues (Research Monograph No. 16, Publication No. ADM 86-1139, pp. 130–153). Washington, DC: U.S. Department of Health and Human Services.Vex, S. L., & Blume, S. B. (2001). The JACS Study I: Characteristics of a population ofchemically dependent Jewish men and women. J Addict Dis, 20(4), 71–89.Walfish, S., Stenmark, D. E., Sarco, D., Shealy, J. S., & Krone, A. M. (1992). Incidenceof bulimia in substance misusing women in residential treatment. Int J Addict,27(4), 425–433.Warner, L. A., Kessler, R. C., Hughes, M., Anthony, J. C., & Nelson, C. B. (1995).Prevalence and correlates of drug use and dependence in the United States. ArchGen Psychiatry, 52(3), 219–228.Warren, K. R., Calhoun, F. J., May, P. A., Viljoen, D. L., Li, T. K., Tanaka, H., et al.(2001). Fetal alcohol syndrome: An international perspective. Alcohol Clin ExpRes, 25, 202S–206S.

20. Addictive Disorders in Women 453Weisner, C., & Schmidt, L. (1992). Gender disparities in treatment for alcohol problems.JAMA, 268(14), 1872–1876.White, K. A., Brady, K. T., & Sonne, S. (1996). Gender differences in patterns ofcocaine use. Am J Addict, 5(3), 259–261.Zilberman, M. L., & Blume, S. B. (2004). Drugs and women. In J. Lowinson, P. Ruiz, R.B. Millman, & J. G. Langrodet (Eds.), Substance abuse: A comprehensive textbook(4th ed., pp. 1064–1079). Philadelphia: Lippincott/Williams & Wilkins.Zilberman, M. L., Tavares, H., Blume, S. B., & el-Guebaly, N. (2003). Substance usedisorders: Sex differences in psychiatric comorbidities. Can J Psychiatry, 48(1), 5–15.

PART VTREATMENTS FOR ADDICTIONS

Individual PsychodynamicPsychotherapyCHAPTER 21LANCE M. DODESEDWARD J. KHANTZIANIndividual psychotherapy is widely used in treatment of addicts, though it isperhaps still underappreciated in comparison with group modalities, includingself-help groups. Many addicts benefit from a combination of simultaneousindividual and group treatments, and some require the individual psychotherapyto be able to remain with other treatments (Khantzian, 1986). Furthermore,a significant number cannot, or choose not to, make use of other treatment andcan only be treated successfully with individual psychotherapy. This chapterrearticulates and extends ideas that we and others have developed previously,based on our understanding and treatment experience with addicted individualsover many years (Dodes, 1984, 1988, 1990, 1996, 2002, 2003; Dodes &Khantzian, 1991; Flores, 2004; Kaufman, 1994; Khantzian, 1980, 1986, 1995,1999a, 1999b, 2001, 2003; Khantzian, Dodes, & Brehm, 2005; Walant, 1995).The rationale for individual psychotherapy with addicts arises from anunderstanding of the psychological factors that contribute to addiction. Contemporarypsychodynamic formulations stress the role of conflict, the objectmeaning of alcohol or drugs, deficits and dysfunctions in ego functioning, andnarcissistic deficits as important factors in reliance on substances (Dodes &Khantzian, 1991). These deficits and dysfunctions result in self-regulationdisturbances involving affects, self-esteem maintenance, and the capacity forself-care and self–other relations. These areas of psychological vulnerability ordysfunction contribute significantly to addictions and are targeted in psychotherapy(Khantzian, 1986, 1995, 1999b, 2001).457

458 V. TREATMENTS FOR ADDICTIONSAlthough we believe that there are indications for referring addicts to psychotherapy,often patients themselves begin the treatment of their addictionwith psychotherapy (perhaps particularly those who are more psychologicallyoriented). Others start individual psychotherapy after first seeking treatmentthrough self-help groups or a more educationally based treatment program, suchas that offered in many inpatient settings and outpatient clinics. In either case,via exploring their emotional issues, patients begin to understand not only theirown psychology but also the place of substance abuse in their emotional lives.This understanding not only addresses the reasons for their continued problemseven when chemical free but also, by placing the substance problem in the contextof their emotional lives, provides a strong internal basis for avoidingrelapse.Another route into individual psychotherapy for addicted patients is viarepeated treatment failures in other, less introspective settings. Some of thesepatients repeatedly relapse, despite clear and conscious motivation to abstain,because they are unaware of the internal, largely unconscious factors that leadthem to resume substance use. Failing to recognize the role of unconscious processescauses patients to attribute their behavior to lack of willpower, whichcontributes further to their self-devaluation. Learning about themselves in individualpsychotherapy thus contributes not only to a more stable chemical-freestate and to overall general improvement in emotional function but also todiminished shame concerning their addiction.Many addicts may also successfully pursue individual psychotherapy inconjunction with other treatment (e.g., Alcoholics Anonymous [AA], NarcoticsAnonymous [NA], or a professionally led group therapy). In such cases,the individual work aims for the usual goals of insight and emotional growth,while the other modalities focus on supporting the patient’s chemical-free state.A number of studies substantiate the value of individual psychotherapywith addicts. Woody and colleagues (1983) noted that in seven investigationswith methadone-treated patients, where patients were randomly assigned topsychotherapy or a different treatment (most often drug counseling), five of thestudies showed better outcome in the psychotherapy group. Woody’s own groupalso found that patients who received psychotherapy and drug counseling hadbetter results than did patients who received drug counseling alone, when measuredin terms of number of areas of improvement, less use of illicit opiates, andlower doses of methadone required. This group (Woody, McLellan, Luborsky,& O’Brien, 1986) noted further that the patients with the most disturbedglobal psychiatric ratings benefited particularly from psychotherapy, as comparedwith drug counseling. A number of investigators documented early a highcorrelation between psychiatric disorders, especially depression, and addiction(Khantzian & Treece, 1985; Rounsaville, Weissman, Kleber, & Wilber, 1982).These findings have been substantiated in a more recent series of clinicaland epidemiological studies (Carroll & Rounsaville, 1992; Halikas, Crosby,

21. Individual Psychodynamic Psychotherapy 459Pearson, Nugent, & Carlson, 1994; Kessler et al., 1997; Kleinman, Miller, &Millman, 1990; Penick et al., 1994; Regier et al., 1990; Rounsaville et al., 1991;Schuckit & Hesselbrock, 1994; Schuckit, Irwin, & Brown, 1990; Wilens,Biederman, Spencer, & Frances, 1994).Brown (1985) found that 45% of a group of abstinent alcoholics inAA sought psychotherapy, and more than 90% of them found it helpful.Rounsaville, Gawin, and Kleber (1985) also reported positive results in a preliminarystudy treating outpatient cocaine abusers with a modified interpersonalpsychotherapy along with medication trials. Woody and colleagues(1986) reported that when psychotherapists were integrated in the treatmentteam, the entire staff reduced their stress as a result of the successful managementof the most psychiatrically troubled patients. More recently, Woody,McLellan, Luborsky, and O’Brien (1995) validated the benefit of psychotherapyin community programs. In contrast, Carroll and colleagues (1994), as wellas Kang and colleagues (1991), reported less benefit from psychotherapy inambulatory cocaine abusers. In the latter studies, the authors underscored theimportance of the severity of illness, stages of recovery, and level of care.Finally, when psychotherapy was added to paraprofessional drug counseling inan inpatient setting (Rogalski, 1984), patients improved in compliance withtreatment as measured in decreased number of discharges against medicaladvice, disciplinary discharges, or unauthorized absences.In addition to these studies that statistically examined effects of psychotherapy,a significant psychodynamic literature reports on the treatability ofaddicted patients with psychodynamic or psychoanalytically oriented psychotherapy(Brown, 1985; Dodes, 1984, 1988, 1990, 1996, 2002, 2003; Flores,2004; Johnson, 1992; Kaufman, 1994; Khantzian, 1986, 1999a, 1999b, 2001;Krystal, 1982; Krystal & Raskin, 1970; Silber, 1974; Treece & Khantzian, 1986;Walant, 1995; Woody, Luborsky, McLellan, & O’Brien, 1989; Wurmser, 1974).The experience of treating addicted individuals in psychodynamic therapy hasalso provided our best information about the psychology of addiction, which inturn serves as the theoretical basis for technical approaches to the therapy ofthese patients.Indications for psychodynamic psychotherapy depend on the patient’scapacity to benefit, as well as on his or her motivation. Addicted individualswho are able to achieve and maintain sobriety with substance abuse counselingand/or self-help groups, and who are unaware of conflict, anxiety, depression, orother symptoms, are unlikely to seek psychotherapy. Addicted patients who areable to develop a therapeutic alliance, who have the capacity to be at leastmoderately introspective, and who have emotional suffering are candidates forpsychotherapy as much as are nonaddicts with similar characteristics. Some ofthese patients use psychotherapy to help them to achieve abstinence; others useit to help them maintain abstinence, and both groups can also use their therapyto help their overall emotional health once they achieve abstinence.

460 V. TREATMENTS FOR ADDICTIONSPSYCHODYNAMIC BASIS FOR PSYCHOTHERAPYOF ADDICTED PATIENTSThere have been a number of major contributions to understanding the psychologyof the addictions, particularly over the past 25 years (Khantzian et al.,2005). The most frequently described function of substance use is the managementof intolerable or overwhelming affects. The idea that certain substancesare preferentially chosen on the basis of their specific ability to address (ameliorate,express) certain affective states is termed the “self-medication hypothesis”(Khantzian, 1985b, 1997). Various authors described connections between certainaffects and the use of alcohol or particular drugs, for example, use of narcoticsto manage rage or loneliness, and use of cocaine and other stimulants tomanage depression, boredom, and emptiness, or to provide a sense of grandeur(Khantzian, 1985b; Milkman & Frosch, 1973; Wurmser, 1974). In a more generalway, Krystal and Raskin (1970) spoke of a “defective stimulus barrier” inaddicts, causing them to be susceptible to flooding with intolerable affectivestates that are traumatic. They described a normal process of affective developmentin which affects are differentiated, desomatized, and verbalized, andpointed to defects in this development in (some) addicted individuals. Thesedefects leave some addicts with the inability to use affects as signals, a criticalcapacity for managing them. Without this signal capacity, drugs may be used toward off affective flooding. Others have noted the quality of addicts’ relatednessto their alcohol or drugs as akin to human object relationships. The chemicalbecomes a substitute for a longed-for or needed figure—one that has omnipotentproperties or is completely controllable and available (Krystal & Raskin,1970; Wieder & Kaplan, 1969; Wurmser, 1974).Related to these views are observations about the narcissistic pathology ofaddicts. Wurmser (1974) described a “narcissistic crisis” in addicts. He notedthat for some addicts, collapse of a grandiose self or of an idealized object providesthe impetus for substance use in an effort to resolve feelings of narcissisticfrustration, shame, and rage. Kohut (1971) also referred to the narcissistic functionof alcohol or drugs in addiction as a replacement for defective psychologicalstructure, particularly that arising from an inadequate idealized self-object.From another perspective, Khantzian (1978, 1995, 1999b) and Khantzianand Mack (1983) described defective self-care functions in addicts—the groupof ego functions involved with anticipation of danger, appropriate modulatedresponse to protect oneself, and sufficient positive self-esteem to care aboutoneself. These defective self-care functions may be seen in many substanceabusers who characteristically place themselves in danger or fail to protect theirhealth and well-being. In turn, this problem may be related to inadequateattention to the protection of the child by his or her parent, resulting in thefailure to internalize self-care functions.

21. Individual Psychodynamic Psychotherapy 461In addition to this ego deficit psychology, several investigators describeda generally defective capacity to be aware of affective states in certainaddicts. Some addicts appear to be “alexithymic,” that is, unable to name ordescribe emotions in words. Krystal (1982) described substance use in some ofthese patients as a search for an external agent to soothe them, associatedwith their lack of sense of ability to soothe themselves. McDougall (1984)described patients whose use of words and ideas is without affective meaning,and who use alcohol or drugs to disperse emotional arousal and thus avoidaffective flooding. Although the final appearance of this affective intolerancehas the quality of an ego deficit, its underlying basis is understood to be adefensive avoidance of intolerable feelings. Krystal (1982) described thisdefense as arising secondary to psychological trauma in either childhood oradult life.Khantzian (1999a) wrote about the preverbal origins of distress foundamong some substance abusers. He described a case in which early experiencethat remained out of conscious awareness created a nameless pain that recurredin response to a current stimulus (a film), leading to an alcoholic relapse. Ofequal importance, when the early experience of abandonment again recurred inthe setting of a group therapy, it could be clearly interpreted, understood, andborne rather than managed through substance abuse. Along similar lines,Walant (1995) stressed infantile origins of problems with interpersonal contactand interdependence that could predispose to addictive adaptations. Alongsimilar lines, more recently, Flores (2004) has elaborated on addictions as anattachment disorder for some patients.Finally, addiction may play a central role in seeking restoration of innercontrol of one’s affective state (Dodes, 1990, 1996, 2002). This need for controlin addicts involves a narcissistic vulnerability to being traumatized by the experienceof helplessness or powerlessness. The use of substances is seen as a way tocorrect the experience of helplessness; that is, by taking an action (using alcoholor drugs) that can alter their internal affective state, addicts may reassertthe power to control their inner experience, undoing and reversing the feelingof powerlessness. Because a sense of control of inner experience is a centralaspect of narcissism, the intense aggressive drive to achieve this control when itis felt to be threatened may appropriately be considered narcissistic rage.According to this view, narcissistic rage arising from feelings of powerlessnessgives addiction its most defining characteristics, namely, its insistent, compulsive,unrelenting quality and its relative unresponsiveness to realistic factors.This also offers an explanation for why, like narcissistic rage in general, theaddictive drive may well overwhelm other aspects of the personality (Dodes,1990).More recently, Dodes (1996) expanded this view to place addictions withinthe category of those psychological problems currently and historically

462 V. TREATMENTS FOR ADDICTIONSknown as compulsions. He pointed out that although addictions and compulsionsare clearly similar to each other in their “compulsive” quality, they havealways, incorrectly, been seen as fundamentally different, namely, because compulsionsare experienced as ego-dystonic—as things one feels compelled to doalthough one does not consciously wish to do them, whereas addictions havebeen experienced as ego-syntonic—as things one does because one consciouslywants to do them. However, addictions commonly move from being egosyntonicto ego-dystonic as people wish to stop their behavior, and compulsionsoften shift from being ego-dystonic to ego-syntonic as people make a virtue oftheir compelled behavior. Another false distinction has been that compulsionsare viewed as compromise formations between a forbidden wish and an opposing(superego) force. But addictions have been viewed as the result of either anego function (e.g., self-medication) or a deficit in ego function (e.g., self-caredeficiencies), rather than being centrally viewed as compromises. However, inhis formulation of addiction (an action driven to correct helplessness and toexpress the narcissistic rage engendered by this helplessness), Dodes describedan inherent compromise formation. This compromise is expressed in the defensivedisplacement of the reassertion of power and the expression of rage to theaddictive behavior. For instance, Dodes described a man who had an alcoholicbinge after he was unable to fire his son from his company, despite the fact theson had embezzled a large amount of money. This man felt it was morally wrongto fire his son, even though he felt a strong impetus to do so, and as a consequence,he rendered himself helpless. This was intolerable, but since he couldnot allow himself to act directly (fire his son), he displaced the need to beempowered to his drinking, which therefore acquired a compulsive character.The addictive behavior, then, reflected a psychological compromise betweendoing what he was driven to do, and forbidding himself to do it. Dodes concludedthat, with no distinction based on ego-syntonicity or on the psychologyof the two diagnoses, addictions are fundamentally the same as compulsions.The important implication of this finding is that addictions should be seen astreatable in traditional psychodynamic psychotherapy as much as are compulsions,which have traditionally been understood to be amenable to a psychodynamicor psychoanalytic approach (Dodes, 1996, 2002, 2003).TECHNICAL ASPECTS OF PSYCHOTHERAPY WITH ADDICTSThere are a number of special considerations in the psychodynamic psychotherapyof addicted individuals (Dodes & Khantzian, 1991). From the formulationsdiscussed previously, it is clear that various meanings and roles of drugs or alcoholneed to be considered in understanding the patient. In addition, addicts arefrequently still abusing substances at the time they are first seen, which poses an

21. Individual Psychodynamic Psychotherapy 463immediate threat to their emotional and physical health, their relationships,and their overall capacity to function. This threat makes it necessary to addressthe question of abstinence from substance use first, when beginning treatment.The first step is diagnosing substance abuse or dependence and informingthe patient of the diagnosis, since the patient may fail to perceive the extent ofthe problem or may present with overt denial or minimization. The manner inwhich this is accomplished is also an important first step in establishing a positivetherapeutic relationship, a basic element for all subsequent phases of treatment.To make the diagnosis and have a basis for showing it clearly to thepatient, it is necessary to take a detailed history of the problems that have beencaused by the patient’s use of drugs or alcohol. In taking this history, it is usefulto inquire systematically about trouble in the areas of work, medical health,relationships with friends, relationships with family (adults and children), legalproblems, and intrapsychic problems (depression, shame, anxiety). It is oftenhelpful to ask specifically what the patient is like when he or she drinks or usesdrugs and the details of what happens at these times, as well as the effects thepatient seeks from substance use. This involves exploring both the “positive”and negative effects he or she experiences from the use of drugs or alcohol. Inthe first instance, it is often reassuring and alliance building to ask, “What doesthe drug do for you?” Inquiring in this way, the patient is more apt to feelunderstood and not judged. Both the patient and therapist are provided anopportunity to appreciate how drugs or alcohol become compelling, such asenabling social contact, or relieving anxiety, agitation, depression or rage. Onthe maladaptive side, does he or she become more belligerent, moody, withdrawn,or sad? Might the patient have had more or better relationships withfriends if she had never had a drink or a drug? Patients often deny trouble intheir marriages but when the matter is explored in detail will acknowledge thattheir spouses would prefer that they drink less or have asked them on more thanone occasion to cut down or stop. Upon reflection, they may recognize thattheir use of alcohol or drugs has silently become a source of chronic tension intheir relationships. Once the patient clarifies or even lists the areas of difficultiesthat are due to alcohol or drugs, it is often possible for him to acknowledgethe global impact of substance abuse on his life.Focusing on the diagnosis of alcoholism or other drug abuse is more than amerely cognitive process. The realization that she is out of control in this areaof life is a significant psychological step in itself. Brown (1985), in her workwith alcoholic patients, stresses loss of control as a core issue and focus of psychotherapy.It is a blow to the narcissistic potency of the patient; as such, itmay be usefully investigated, because it bears on the patient’s important feelingsand issues concerning powerlessness and mastery (Dodes, 1988). Mack (1981)felt that an alcoholic’s recognition of failure to be in control of his or her drinkingis a first step in the assumption of responsibility.

464 V. TREATMENTS FOR ADDICTIONSThrough all this early diagnostic and at times confrontational work, as intherapy in general, the therapist’s attitude must be exploratory without beingjudgmental. The patient’s denial or minimization is often closely connectedwith his shame, and throughout this initial evaluation the patient is simultaneouslyevaluating the therapist—in particular, the therapist’s attitude towardthe patient and his addictive problem. To put it another way, the patient isfaced with her own projections onto the therapist, and it is important that thetherapist not accede to the role of a harsh or punitive superego that might beinvisibly imposed.Transference manifestations may also arise from narcissistic deficits, leadingto idealizing and mirroring relationships or fearful, guarded positions againstbeing overcontrolled or overwhelmed. Common countertransference difficultieswith substance abusers revolve around frustration, anger, and guilt, aspatients’ failures to abstain challenge the therapeutic potency of the treatmentprofessional. These countertransference feelings may result in withdrawal, inappropriatelycritical attitudes, or overinvolvement (when therapists attempt toreverse their desire to withdraw). The severe nature of the risks facing addictsmakes the work with them both particularly challenging and rewarding. It isimportant for the therapist to be able to view both the overt behavior and theinner psychopathology of the addict with the same combination of objectivityand compassion that is brought to any patient.Developing a therapeutic alliance early in therapy is also made difficult bythe patient’s frequently ambivalent relationship toward abstention from drinkingor drug use at the same time that the therapist is appropriately concernedwith the patient’s achieving abstinence. It may be ineffective and even counterproductiveto be seen as requiring (vs. suggesting) something the patientdoes not consciously feel is in his best interest. Once the patient concurs withthe diagnosis, he or she has a necessary, though not always sufficient, basis foran alliance with the therapist to achieve abstinence. In fact, the psychologicalissues in abstention are complex.We (Dodes, 1984; Khantzian, 1980) have addressed issues in abstentionwith alcoholics. Patients’ achievement of abstinence hinges not only on theplace of substance use in their psychological equilibrium but also critically onthe alliance with, and transference to, the therapist. Many patients quicklyachieve abstinence upon beginning psychotherapy, in spite of the evidentimportance to them of their drugs or alcohol. But others may continue to usesubstances, although not in a way that is malignantly out of control or that createsan emergency. In a number of these cases, we have helped patients establishabstinence over time, psychotherapeutically. When the therapist focuseson the patient’s failure to perceive the danger to herself that is contained in thecontinued abuse, the therapist’s caring concern may be internalized by thepatient, providing a nucleus for the introjection of a healthy “self-care” function(Dodes, 1984). However, the patient’s ability to perceive the therapist in a

21. Individual Psychodynamic Psychotherapy 465benign way that may be internalized depends on absence or resolution of negativetransference feelings at the beginning of treatment.For some patients, early achievement of abstinence is possible because of agenuine therapeutic alliance with the therapist. In other cases, abstinence maybe achieved early on because of unconscious wishes to merge with, or be heldby, a therapist who is idealized, or because of a compliant identification withthe aggressor (Dodes, 1984). When the patient does not initially abstain, subsequentconfrontation may produce abstention, because the patient finally perceivesthe confrontation as a longed-for message of caring that was absent orinsufficient in his childhood (Khantzian & Mack, 1983, also described this kindof parental insufficiency in their discussion of the origin of self-care deficits).From a practical standpoint, the clinical choices involved must depend on theimmediate risks to the patient. If patients drink only intermittently and are ableto participate genuinely in the process of psychotherapy, we have found thatthe psychotherapy can continue. Indeed, the psychotherapy provides an opportunityto explore the issues in the continued drinking, including problems withself-care and the transference implications of the failure to abstain. However,when drinking becomes continually destructive, patients are generally unableto participate in the process, requiring early confrontation around the need tobe hospitalized or to interupt therapy. Over the course of an ongoing psychotherapy,the capacity for abstinence may vary, depending in part on shifts in thetherapeutic relationship (Dodes, 1984). We discuss the question of relapses inan abstinent patient later.Once the patient achieves abstinence, the therapy may broaden to exploreall areas of her psychological life, as in any psychotherapy. Some authors writingabout alcoholism, however, recommend a kind of staging of the therapy.Prochaska and Di Clemente (1985), based on a cognitive-behavioral paradigm,introduced the “stages of change” model to help individuals shift froma “precontemplative” stage (denial) to a “contemplative” (acknowledgment)stage, to initiate a process of engaging in treatment and preventing relapse. Notinconsistent with the psychodynamic approach, the first phase is directedtoward helping the patient develop an identity as an alcoholic (Brown, 1985)focusing on the drinking, on ways to stay sober, and on mourning the lossesincurred as a result of drinking (Bean-Bayog, 1985). Kaufman (1994) similarlystresses the importance of abstinence, stabilization, and relapse prevention andthen, in advanced recovery, the importance of addressing issues of intimacy andautonomy. In our experience, however, it is generally unnecessary and potentiallycounterproductive to attempt to direct the therapeutic process accordingto a preconceived agenda. As with any patient, imposing one’s own focus risksinterfering with the free evolution of the patient’s thoughts toward deeper andmore meaningful understanding of the issues. In our opinion, although someaddicts (like some patients in general) require a more supportive rather than anexploratory approach, or special approaches based on some of the dynamic fac-

466 V. TREATMENTS FOR ADDICTIONStors described earlier, this decision should be based on an individual assessmentof the patient’s psychology rather than on a generalization for all substanceabusers. The approach in treatment may, and should, vary according to thestage of treatment and the status of the patient’s abstinence.The idea of imposing structure in psychotherapy with addicts arises in partfrom concerns about the ability of such patients to tolerate the process of therapy.At the heart of this thought is the worry that exploring the importantissues in their lives will lead addicts to resume their substance abuse. Actually,the reverse is often the case: Patients who do not deal with the issues that troublethem may be at much greater risk of continued substance use or relapse.Nonetheless, there may be difficulties with pursuing psychotherapy. At times,therapists fail to attend appropriately to the life-threatening nature of continuedsubstance abuse (Bean-Bayog, 1985) or fail to make the diagnosis (Brown,1985), overlooking the ongoing deterioration of their patients’ lives. Alcoholicsmay also try to use therapy to aid their denial of their alcoholism.However, these concerns largely hinge on failures of the therapist and maybe avoided by a therapist who is attentive to these issues (Dodes, 1988, 1991).For instance, as described earlier, attention must be paid initially to the questionof abstinence (whether or not it can be achieved). Likewise, if a patientmisuses the treatment to rationalize continued drug or alcohol use, an appropriatelyresponsive therapist would recognize this misuse and bring it into thetreatment process to identify and deal with it. Addicts have a wide variety ofcharacterological structures, strengths, and weaknesses, and are in general ascapable of dealing with the issues and strong transference feelings that mayarise in a psychotherapy as patients with other presenting problems. Brown’s(1985) concern that a psychodynamic psychotherapy may distract the alcoholicpatient from his or her task of establishing an identity as an alcoholic may alsobe taken principally as a reminder to the therapist to attend to the patient’salcoholism rather than a contraindication to psychotherapy (Dodes, 1988).In fact, in the ongoing therapy of addicts, once the patient achieves abstinence,the therapist should always be alert to the meanings and purposes of thepatient’s substance use as these become clearer. Part of the advantage of psychotherapywith addicts is that it offers an ongoing opportunity for patients totake firmer control over their addiction, based on understanding and toleratingthe feelings and issues that contribute to it. The therapist’s continual attentivenessto improved understanding of the patient’s drug use also avoids the problemof distracting the patient from his or her addiction.Of course, any therapist can be fooled: Patients who deny, minimize, ordistort the facts about their substance use may render its diagnosis and treatmentimpossible for any therapist. This is a limitation to psychotherapy, as it isto other attempted interventions.Having considered early issues of abstinence and allowing the focus of thetherapy to broaden, we may now consider how the dynamics of addicts may

21. Individual Psychodynamic Psychotherapy 467necessitate a modification of approach. In the case of alexithymic patients,Krystal (1982) and Krystal and Raskin (1970) proposed a preparatory stage inwhich patients’ affects are identified and explained—with the goal of increasingego function, which includes improving the use of affects as signals andimproving affect tolerance. McDougall (1984) focused on the countertransferenceproblems produced with such patients. She described feelings of boredomand helplessness, with consequent emotional withdrawal by the therapist, andpointed to the need for the therapist to provide a consistent holding environmentthat may last for years before patients are able to acknowledge their emotions.She also offered an understanding of this process in terms of the patient’screating a “primitive communication that is intended, in a deeply unconsciousfashion, to make the analyst experience what the distressed and misunderstoodinfant had once felt” (p. 399).A contemporary psychodynamic understanding of addicted patients, however,does not usually suggest this sort of modification of approach but, rather, aneed to attend to one or another aspect of the meaning and role of the addictionfor a patient. For instance, for some patients it is particularly important toattend to the object-substitute meanings of alcohol or drugs. In some patients,narcissistic vulnerabilities are of paramount importance, for instance, the collapseof idealized objects, as described by Wurmser (1974), or the role of particularaffective states in precipitating substance use, mentioned by a number ofauthors. With some patients, self-care deficits, as described by Khantzian andMack (1983), are of great significance. From a different perspective, the activenature of addictive behavior in seizing control against an intolerable feeling ofhelplessness, as described by Dodes (1990), is often an important focus. In suchcases, it is important to address patients’ experiences of helplessness and powerlessnessas major factors in precipitating substance use.With patients whose affect management and self-care are seriously impaired(Khantzian, 1986, 1995), it is important for the therapist to be especiallyactive. Excessive passivity with such patients can be dangerous. It is necessaryin these cases to empathically draw the patients’ attention to ways in whichthey render themselves vulnerable as a result of their self-care deficits, and topoint out how these self-care deficits render them susceptible to addictivebehavior. With some patients, it is necessary to explore the details of currentlife situations to help them recognize their feelings and see that these feelingsmay serve as “guides to appropriate reactions and self-protective behaviorrather than signals for impulsive action and the obliteration of feelings withdrugs” (Khantzian, 1986, p. 217).Consistent with the need to maintain an active stance, the therapist mayat times need to serve as a “primary care” physician—especially at the start oftreatment, when he or she must often play multiple roles to ensure that thepatient receives appropriate care from a number of sources (Khantzian, 1985a,1988). This task may include decisions about (and active involvement in

468 V. TREATMENTS FOR ADDICTIONSarranging) hospitalization and detoxification, involvement with AA or NA,professionally led group treatments, or pharmacological treatment. However,such an active approach, although possibly life saving, may interfere with thelater development of a traditional psychotherapeutic relationship because ofthe transference and countertransference issues it induces, particularly in regardto the patient’s realistic gratitude. If this gratitude becomes a prominent interferingfactor, referral to another therapist for continued psychotherapy may berequired (Khantzian, 1985a).Just as with the initial attention to abstinence, therapy must focus onrelapses when they occur. Relapses (or the patient’s awareness that he feels agreater urge to use alcohol or drugs) provide an opportunity to learn about thefactors leading to substance use. Frequently patients are unaware of these factors;their lack of awareness contributes to their feelings of frustration and helplessness,and leaves them unprepared for further relapses. A careful, even microscopic,investigation of the feelings, relationships, and events that preceded therelapse are often revealing. Once these issues and affects are clarified, theyoften contribute to an understanding of the patient’s psychology in general,because they center on areas felt to be intolerable by the patient. Commonly,patients bring up their increased thinking about drugs or alcohol when there isan impending relapse. At other times, the therapist may infer an increased riskbased on what he or she knows of the patient’s history and emotional life. Conveyingthis perception to patients is one way to help them learn to attend totheir affects, thoughts, and behaviors, and utilize them as signals. Often, abstinentaddicts have dreams about alcohol or drugs that can indicate that somethingcurrent in their lives is reviving the association with substance use, warningof the risk of relapse.Finally, we should mention organicity. Some treatment providers viewaddicted patients as too impaired in brain functioning, as a result of drug oralcohol abuse (“wet brain”), to be able to utilize a dynamic psychotherapy untilafter a lengthy time of abstinence. Certainly some patients exhibit impairedmemory and capacity for skilled cognitive functions immediately after stoppingdrug or alcohol use. However, in our experience this limitation is frequentlymild or not significant for all but the most severely affected addicts (e.g., alcoholicswith hepatic failure and elevated blood ammonia levels). In fact, as regularlyobserved in inpatient treatment centers, patients can do significant workto understand themselves and the dynamic issues in their families and can alsoreturn to complex tasks within the span of a few weeks immediately followingdetoxification. The implication for psychotherapy is that it is rarely necessaryto wait an extended time to begin because of organic factors. Patients who aretruly impaired because their drug or alcohol use is so continuous that they arealways either high/drunk or withdrawing should not be in psychotherapy tobegin with, because they require hospitalization to break the pattern beforethey will be able to attend to the work of the treatment.

21. Individual Psychodynamic Psychotherapy 469PSYCHOTHERAPY AND SELF-HELP GROUPSRosen (1981) looked at role of therapy in helping patients to separate from theirattachment to AA, which he viewed as having elements of a symbiosis. He notedthe striking fact that AA, unlike psychoanalytically oriented psychotherapy, providesno mechanism for termination. He saw a critical aspect of the role of psychotherapyas helping to work out separation and termination from AA.Patients in a combined treatment of psychotherapy and a 12-step groupoften engage differently with each element; that is, patients may split theirtransference projections, expectations, and attachments, engaging the therapyand the self-help group at separate psychological levels (Dodes, 1988). Patients’attachment to AA may provide opportunity for needed internalization of selfcareand self-valuing, with AA serving as a valuing, idealized object (or transitionalobject); important elements of the narcissistic (idealizing and mirroring)transference may be assigned to AA. The degree to which the transference issplit in this way varies in different patients. It is critical for the therapist to beaware of this split, because a patient’s sobriety may hinge on an idealization ofAA or its “Higher Power” concept, and this sobriety may be lost if the idealizationis prematurely challenged (Dodes, 1988). Consequently, the therapist mayfirst have to help the patient to increase his tolerance of affects and “awaitinternalization of sufficient narcissistic potency” (Dodes, 1988, p. 289) beforetoo closely examining the defenses and functions of AA.In our opinion, the need for a nondynamic, supportive approach throughAA may lessen eventually either as a consequence of the patient’s growth,including internalization of a sense of adequate narcissistic potency, or as a consequenceof greater insight into the psychology of the addictive behavior. However,this does not always occur, leading to the need to attend AA meetingsindefinitely (Dodes, 1984). Other long-term AA members remain involvedbecause of social and interpersonal factors, or because of their interest in helpingothers, even though they may not require AA for sobriety.Dodes (1988) suggested that the fear of disrupting the idealizing transferenceto AA (and consequently losing the sobriety that is dependent on thistransference) underlies the fear of psychotherapy among some patients andtreatment providers. A careful therapist, however, will avoid this pitfall. Overall,the combination of psychodynamic psychotherapy and AA or NA is usefulfor many patients (Dodes, 1988; Khantzian, 1985a, 1988).The disease concept is closely linked with self-help groups and has traditionallybeen difficult to reconcile with psychoanalytically oriented psychotherapy.Mack (1981) noted that this concept led to “oversimplified physiologicalmodels and a territorial smugness . . . which . . . precludes a sophisticatedpsychodynamic understanding of the problems of the individual alcoholic” (p.129). The term “disease” itself has not been well or clearly defined, a factaddressed by Shaffer (1985). However, it is possible to integrate the disease

470 V. TREATMENTS FOR ADDICTIONSconcept with a traditional psychoanalytic psychotherapy (Dodes, 1988). In thefirst place, focusing on the addictive behavior specifically as an illness may beuseful, because it helps to avoid the kind of failure to address the problem thatsome have worried about with psychotherapy. Moreover, acknowledgment of adisease or diagnosis often arouses feelings about being unable to control oneselfthat may be quite important to explore (Dodes, 1988, 1990).In order to integrate a disease concept with a psychodynamic psychotherapy,Dodes (1988) suggested that the “disease” (e.g., alcoholism) be defined to thepatient as having two parts: the patient’s history of alcoholism, and the patient’sbeing at permanent risk of repeating this behavior in the future. This definitiondoes not impede psychological exploration of the meanings of the patient’s drinking.The risk of repetition of drinking that is so central to the disease idea may betroublesome for dynamic exploration only if it has the quality of something that isinexplicable in dynamic terms. However, this risk is actually the same as theregressive potential of any patient in psychotherapy. Addicts, like all other individualsin psychotherapy, never totally eliminate the potential of resuming oldpathological defenses and behaviors, and of regressing. Their risk of resuming substanceabuse is therefore just an example of this general rule.CONCLUSIONThis chapter has presented a description of individual psychodynamic psychotherapywith addicts, based on a contemporary psychoanalytical understandingof their vulnerabilities and disturbances. We emphasized disturbances in egofunction and narcissistic difficulties that affect addicts’ capacities to regulatetheir feeling life, self-esteem, and relationships. A major psychotherapeutic taskfor addicted patients is to bring into their awareness their emotional difficultiesand the way their problems predispose them to relapse into drug/alcohol useand dependence. We have reviewed implications for technique with regard tocharacteristic central issues for addicts and the need in certain cases for activeintervention. We explored strategies for establishing abstinence, including thevalue of working with self-help groups such as AA and NA. Finally, we haveemphasized a flexible approach with regard to the timing, sequencing, and integrationof psychotherapy in relation to other interventions and needs based onpatient characteristics and clinical considerations.REFERENCESBean-Bayog, M. (1985). Alcoholism treatment as an alternative to psychiatric hospitalization.Psychiatr Clin North Am, 8, 501–512.Brown, S. (1985). Treating the alcoholic: A developmental model of recovery. New York:Wiley.

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CHAPTER 22Cognitive TherapyJUDITH S. BECKBRUCE S. LIESELISA M. NAJAVITSKim is a 32-year-old woman with a complex history of substance abuse thatbegan when she was 13 years old. At various times, Kim has experimentedwith most illicit substances (including marijuana, heroin, LSD, Ecstasy,and cocaine) and she has been dependent on nicotine, alcohol, amphetamines,and barbiturates. She also suffers from chronic depression. She hasbeen treated intermittently for depression since age 15 and has cycled inand out of substance treatment programs since age 19. Kim has never beenmarried. She works as a night janitor at a fast-food restaurant.Currently, Kim smokes marijuana several times daily. She says, “Ismoke so much, I don’t even get high anymore.” She smokes to deal withfeelings of depression, emptiness, and loneliness. She views herself ashopeless but says she has no plans to kill herself, because she is afraid ofdying. She has gained over 50 pounds in the last few years, and she says shewants to “do nothing but sit around the house all day.”Kim meets criteria for avoidant personality disorder with dependentand borderline features. She describes constant boredom and isolation.Nonetheless, she refuses to take social or occupational risks, saying “If I putmyself out there, I’ll only get burned.” She has a history of numerous failedrelationships and jobs.Eventually Kim joins a self-help group for women with depression,where she admits to daily marijuana use. Another group member, Jenna,explains that she, too, was a heavy marijuana smoker at one time. Jennawarns Kim that she will only feel better when she quits smoking marijuana.474

22. Cognitive Therapy 475After listening, Kim feels motivated to stop but finds it impossible to quit.After only a few days of abstinence, she feels more depressed and anxious,so she picks up smoking again.For over a decade cognitive therapy has been refined to help people like Kimwho are addicted to a variety of substances, including alcohol, cocaine, opioids,marijuana, prescription medications, nicotine, and other psychoactive substances(A. T. Beck, Wright, Newman, & Liese, 1993; Carroll, 1998, 1999;Liese & Beck, 1997; Liese & Franz, 1996; Najavits, Liese, & Harned, 2004;Newman & Ratto, 1999). Cognitive therapy is also used for compulsive gambling,shopping, and sexual behaviors. Applications of cognitive therapy tosubstance-abusing adolescents (Fromme & Brown, 2000; Waldron, Slesnick,Brody, Turner, & Peterson, 2001), dual diagnosis patients (e.g., Barrowcloughet al., 2001; Najavits, 2002a; Weiss, Najavits, & Greenfield, 1999), olderpatients (Schonfeld et al., 2000), and other important subgroups are additionalrecent developments. Patients like Kim have taught us a great deal about thedevelopment, maintenance, and treatment of addictive behavior (Liese &Franz, 1996). Currently, cognitive-behavioral therapy (CBT) approaches tosubstance abuse are considered among the most empirically studied, welldefined,and widely used approaches (Carroll, 1999; Thase, 1997).The cognitive therapy of substance abuse is quite similar to cognitive therapyfor other psychological problems, including depression (A. T. Beck, Rush,Shaw, & Emery, 1979), anxiety (A. T. Beck & Emery, with Greenberg, 1985),and personality disorders (A. T. Beck, Freeman, & Associates, 1990; Young,1999). Each places emphasis on collaboration, case conceptualization, structure,patient education, and the application of standard cognitive-behavioraltechniques. In addition, when working with substance abuse patients, cognitivetherapists focus on the cognitive and behavioral sequences leading to substanceuse, management of cravings, avoidance of high-risk situations, case management,mood regulation (i.e., coping), and lifestyle change. The cognitive therapyof substance abuse is an integrative, collaborative endeavor. Patients areencouraged to seek adjunctive services (e.g., 12-step and other programs) toreinforce their progress in cognitive therapy.In cognitive therapy of substance abuse, thoughts are viewed as playing amajor role in addictive behavior (e.g., substance use), negative emotions (e.g.,anxiety and depression), and physiological responses (including some withdrawalsymptoms). Although strategies and interventions vary based on theindividual and particular substance, the basic conceptualization of the patientin cognitive terms remains constant (A. T. Beck et al., 1993; see Figure 22.1 forthe basic cognitive model of substance abuse).Cognitive therapists assess the development of their patients’ beliefs aboutthemselves, their early life experiences, exposure to substances, the developmentof substance-related beliefs, and their eventual reliance on substances

476 V. TREATMENTS FOR ADDICTIONSFIGURE 22.1. The cognitive model of substance abuse. From A. T. Beck, Wright,Newman, and Liese (1993, p. 47). Copyright 1993 by The Guilford Press. Adapted by permission.(Liese & Franz, 1996; see Figure 22.2). An important assumption is that substanceabuse is in large part learned and can be modified by changing cognitivebehavioralprocesses.Our model for cognitive therapy of substance abuse has been substantiallyinfluenced by other cognitive behaviorists. For example, Marlatt and colleagues(Dimeff & Marlatt, 1998; Marlatt & Gordon, 1985) presented an importantmodel of relapse prevention that has contributed greatly to our own work. Identifyinghigh-risk situations, understanding the decision chain leading to substanceuse, modifying substance users’ dysfunctional lifestyles, and learningfrom lapses to prevent full-fledged relapses are all integral to the relapse preventionmodel and the cognitive models of addiction.There are numerous CBT approaches for substance abuse (Najavits etal., 2004), and the past several years have seen a variety of major empiricalstudies on CBT for substance abuse (e.g., Crits-Christoph et al., 1999;Maude-Griffin et al., 1998; Project MATCH Research Group, 1997; Rawsonet al., 2002; Waldron et al., 2001). In this chapter, we focus primarily on thecognitive therapy model defined by Aaron T. Beck and colleagues. The cognitivetherapy model, or some of its various components, is often part ofother CBTs.We address four key topics: cognitive case conceptualization; principles oftreatment; treatment planning (including specific cognitive and behavioralinterventions); and comparison to some other major psychosocial treatmentsfor substance abuse. Our patient, Kim, is used as an example throughout.

22. Cognitive Therapy 477FIGURE 22.2. The cognitive developmental model of substance abuse. From Liese andFranz (1996, p. 482). Copyright 1996 by The Guilford Press. Reprinted by permission.THE COGNITIVE CONCEPTUALIZATION DIAGRAMCognitive therapy begins with a formulation of the case, using a standardizedform for structuring the case conceptualization (J. S. Beck, 1995). An exampleusing Kim’s current difficulties is provided in Figure 22.3. She holds fundamentalbeliefs that she is helpless and incompetent, bad, unlovable, and vulnerable.These beliefs originated in childhood and became stronger and stronger as timewent on. The next to last of eight children in a poor family, Kim was emotionallyneglected by a depressed, alcoholic mother. Her father was cold, distant,and uninterested in Kim. He abandoned the family when Kim was 7 and nevercontacted them again. Kim had few friends, felt rejected by her family, didpoorly in school, and dropped out when she was halfway through 11th grade.

478 V. TREATMENTS FOR ADDICTIONSFIGURE 22.3. Cognitive conceptualization diagram. From J. S. Beck (1995, p. 139). Copyright1995 by Judith S. Beck. Adapted by permission.Kim’s core beliefs of helplessness, badness, and vulnerability have causedher great pain, and over the years, she has developed rules (i.e., conditionalassumptions) for survival. One such conditional assumption is, “If I avoid challenges,I won’t have to face failure.” Thus, Kim uses a typical compensatorystrategy: She avoids applying for any but the most menial jobs. She then quitsthese jobs when small problems arise, believing she is helpless to solve problems.Likewise, she tries only halfheartedly in substance abuse treatment programsand drops out prematurely, believing she cannot abstain from substances.She also avoids conflicts with others, believing that she does not deserve to getwhat she wants.Kim’s core beliefs of badness and unlovability permeate virtually all of herrelationships. In addition to her conditional belief, “If I try to get what I wantfrom a relationship, I’ll fail” (which stems from a core belief of helplessness),

22. Cognitive Therapy 479she also believes, “If I assert myself or let others get too close, they’ll reject me,because nobody could possibly love me.” Therefore, she uses compensatorystrategies such as isolating herself, avoiding assertion, avoiding intimacy, and,perhaps most obvious, taking substances. Most of her social contacts are withother substance abusers who manipulate and take advantage of her.Kim also has a core belief that she is vulnerable, especially to negativeemotion. Her conditional assumption is, “If I start to feel bad, my emotions willget out of control and overwhelm me.” She avoids even mildly challenging situationsin which she predicts she will feel sad, rejected, or helpless. Avoidanceitself, however, often leads to boredom and frustration, which increases hersense of failure and helplessness.Kim discovered at an early age that she could feel better by drinking alcoholand taking substances. As a result, she failed to develop healthier copingstrategies (e.g., learning to tolerate bad moods, solving problems, asserting herself,or looking at situations more realistically). For much of her life, she hastried to cope with a combination of avoidance and substance use.The cognitive conceptualization diagram in Figure 22.3 demonstrates howKim’s thinking in specific situations leads to substance use. In situation 1, forexample, Kim thinks about going to work. She has a mental image of her supervisorlooking at her “with a mean face” and she thinks, “All he ever does is criticizeme. I’ll probably get fired soon.” This is an automatic thought, because itseems to pop into Kim’s mind spontaneously. Prior to receiving therapy, Kimhad little awareness of her automatic thoughts; she was much more aware of hersubsequent negative emotions. As a result, she felt helpless, and her behavioralresponse was to stay home and take substances.Why does Kim consistently have these thoughts of failure and helplessness?Kim’s negative core beliefs about herself influence every perception. Sheassumes she will fail, never thinking to question such beliefs about herself.Given this tendency, it is no surprise that Kim avoids challenges. She thinks itis just a matter of time until her failure becomes apparent.In situation 2 (see Figure 22.3), Kim considers whether to attend a partygiven by neighbors. Because of her core belief that she is unlovable, she automaticallythinks, “I won’t have a good time. I don’t fit in.” Accepting thesethoughts as true, she feels sad and chooses to stay home and get high. Whereasmany automatic thoughts have a grain of truth, they are usually distorted insome way. Had Kim evaluated her thoughts critically, she might have concludedthat she could not predict the future with certainty, that several neighborshad seemed pleasant in the past, and that the reason for the neighbors onthe street to have the party was to get to know one another better. Kim’s corebelief of unlovability once again leads her to accept negative thoughts as trueand to use her dysfunctional strategies of avoidance and substance use.In situation 3, Kim becomes aware of how bored and sad she feels. Shethinks, “I’ll never feel good. I hate feeling like this.” Her negative prediction

480 V. TREATMENTS FOR ADDICTIONSand intolerance of dysphoria are again linked to her core beliefs of helplessnessand vulnerability. Again, she copes with her anxiety by turning to substances.The cognitive conceptualization diagram can serve as an aid to identifyquickly the most central beliefs and dysfunctional strategies of substance abusers,to recognize how their beliefs influence their perceptions of current situations,and to explain why they respond emotionally and behaviorally in suchineffective ways. An important part of the cognitive approach is to helppatients begin to question the validity of their perceptions and the accuracy ofautomatic thoughts that lead to substance abuse.A first step in therapy is to help patients recognize that their negativeautomatic thoughts are not completely valid. When they test their thinkingand modify it to more closely resemble reality, they feel better. A later step is tohelp them use the same kind of evaluative process with their core beliefs, toguide them in understanding that such beliefs are ideas, not necessarily truths.Once they see themselves in a more realistic light, they begin to perceive situationsdifferently, feel better emotionally, and use more functional strategieslearned in therapy. When this occurs, they become less likely to “need” substancesfor mood regulation, because they have developed internal strategies forcoping.Cognitive therapy for substance abuse, therefore, aims to modify thoughtsassociated with substance use (both surface-level “automatic thoughts” anddeep-level “core beliefs”). The goal is to develop new behaviors to take theplace of dysfunctional ones. An additional focus, described later in this chapter,is practical problem solving and modifying the patient’s lifestyle to decrease thelikelihood of relapse. The modification of patients’ long-term negative beliefsabout the self is crucial to their ability to see alternative explanations for distressingevents, to use more functional coping strategies learned in therapy, andto create better lives.At some point, cognitive therapists may explore childhood issues thatrelate to patients’ core beliefs and addictive behavior. Such exploration helpsboth clinicians and patients understand how patients came to such rigid, global,and inaccurate negative ideas about themselves.Figure 22.4 reflects the basic cognitive model of substance abuse as appliedto Kim’s substance abuse behavior. It illustrates the cyclical nature of substanceabuse. Kim, like most substance abusers, believes that taking substances is anautomatic process, beyond her control. This diagram helps her identify thesequence of events leading to an incident of substance use and identifies potentialpoints of intervention in the future. In this example, Kim feels hopeless,because she predicts she will lose her job. As she searches for a way to cope withher dysphoria, a basic substance-related belief emerges (“If I feel bad, I shouldsmoke”) and she thinks, “I might as well use.” She then experiences cravingsand gives herself permission to use (“My life is crummy. I deserve to feel

481FIGURE 22.4. Cognitive model of substance abuse applied to case example.

482 V. TREATMENTS FOR ADDICTIONSbetter”); she hunts for her marijuana and smokes a joint. This typical sequenceof events takes place in seconds, and Kim initially believes it is automatic. Bybreaking it down into a series of steps, Kim can learn a variety of ways to interveneat each stage along the way.PRINCIPLES OF TREATMENTA cognitive therapist could use hundreds of interventions with any givenpatient at any given time. In this section, we discuss cognitive therapy principlesthat apply to all patients, using substance abuse examples.1. Cognitive therapy is based on a unique cognitive conceptualization ofeach patient.2. A strong therapeutic alliance is essential.3. Cognitive therapy is goal-oriented.4. The initial focus of therapy is on the present.5. Cognitive therapy is time-sensitive.6. Therapy sessions are structured, with active participation.7. Patients are taught to identify and respond to dysfunctional thoughts.8. Cognitive therapy emphasizes psychoeducation and relapse prevention.Principle 1: Cognitive Therapy Is Basedon a Unique Cognitive Conceptualization of Each PatientConceptualization of the case includes analysis of the current problematic situationsof substance abusers and their associated thoughts and reactions (emotional,behavioral, and physiological). Therapists and patients look for meaningsexpressed in patients’ automatic thoughts to identify their most basic,dysfunctional core beliefs about themselves, their world, and other people (e.g.,“I am weak,” “The world is a hostile place”).They also identify patterns of behavior that patients develop to cope withthese negative ideas. Such patterns might include taking substances, preying onpeople, and distancing from others. The connection between their core beliefsand compensatory strategies becomes clearer when therapists and patients identifythe conditional assumptions that drive patients’ behavior (e.g., “If I try todo anything difficult, I’ll probably fail because I’m so weak”).Therapists and patients look at patients’ developmental histories to understandhow they came to hold such strong, rigid, negative core beliefs. They alsoexplore how these beliefs might not be true today and, in some cases, were notcompletely true even in childhood. They look at patients’ enduring patterns ofinterpretation that have caused them to process information so negatively.

22. Cognitive Therapy 483Therapists also draw diagrams of scenarios in which patients take substances(Figure 22.4) to illustrate the cyclical process of substance use and themany opportunities to intervene and avert a relapse.Principle 2: A Strong Therapeutic Alliance Is EssentialSuccessful treatment relies on a caring, collaborative, respectful therapeuticrelationship. Effective therapists explain their therapeutic approach, encouragepatients to express skepticism, help them test the validity of their doubts, provideexplanations for their interventions, share their cognitive formulation tomake sure they have an accurate understanding of the patient, and consistentlyask for feedback.Therapists who are very collaborative typically find that they can establishsound therapeutic relationships with most substance abuse patients. However,even the most skilled therapists, who embody the essential characteristics ofwarmth, empathy, caring, and genuine regard, find it challenging to developgood relationships with occasional patients who are suspicious, manipulative,or avoidant. Therapists are encouraged to examine relationship problems withthe same careful cognitive exploration of session-related behavior as is done forall other behaviors. See Figure 22.5 for a cognitive conceptualization diagram ofmissed sessions and dropout.An effective therapist seeks to avoid activating patients’ core beliefsthrough his or her own behavior in therapy and helps patients test the validityof their ideas about the therapist. For example, Kim’s therapist asked for evidencewhen Kim said she believed the therapist was judging her as “bad” forhaving a substance abuse problem. Of course, effective therapists need to examinetheir own thoughts, feelings, and behaviors periodically to ensure that theyare not viewing their patients in a negative light. When therapists maintaintrue nonjudgmental attitudes, they can sincerely tell patients that they are notnegatively evaluating them. They can further explain that they view patients asusing substances to try to cope with the difficulties inherent in their lives.At times, a persistent problem in the therapeutic relationship arises from aclash of patient and therapist beliefs. Therapists are advised to do conceptualizationdiagrams of patients and of themselves to identify dysfunctional ideasthey may have about interacting with difficult people.For example, one substance abuse patient held the core belief, “If I showany weakness, others will hurt me,” and a related assumption, “If I listen to mytherapist, he’ll see me as weak.” As a result, the patient was very controlling inthe session, kept criticizing the therapist, and would not do any self-help assignmentssuggested by the therapist. The problem persisted, at least in part,because the therapist too had a broad assumption, “If people don’t listen to me,it means they don’t value me, and therefore don’t deserve my best effort.” The

484 V. TREATMENTS FOR ADDICTIONSFIGURE 22.5. Cognitive conceptualization of missed sessions and dropouts.therapist became irritated with the patient, expressing dissatisfaction throughbody language and tone of voice. The patient, already hypervigilant for possibleharm from others, perceived the therapist’s negative attitude and dropped outof therapy prematurely.Liese and Franz (1996) have identified common dysfunctional beliefs oftherapists that interfere with delivering therapy to substance abuse patients.Although many patients may minimize their substance use, confronting themin a harsh manner is likely to result in diminished therapeutic efficacy anddropping out.

22. Cognitive Therapy 485When patients report no substance use during the previous week, it isoften useful to inquire about times when they felt cravings. Thus, therapists canobtain relevant cognitive material to help patients continue effective responsesin the coming week.Because patients with substance problems have high dropout rates (Simpson,Joe, Rowan Szal, & Greener, 1997), it is essential to build a strong therapeuticrelationship. Liese and Beck (1997) describe how cognitive therapy skills canmaximize retention in treatment. Figure 22.5 presents their model for missedsessions and dropout.Therapists increase the alliance by emphasizing that they and the patientare on the same team, working toward long-term goals. The patient can learnthat therapy is not an adversarial relationship. The therapist and patient collaborativelymake most of the decisions about therapy. However, therapistsshould know that a common compensatory strategy of substance abuse patientsis avoidance (e.g., minimizing difficulties in abstaining from substances). It isimportant, therefore, to help patients recognize in a nonconfrontational mannerthat the advantages of avoidance are clearly outweighed by the disadvantages.Principle 3: Cognitive Therapy Is Goal-OrientedAt the first session and periodically thereafter, therapists ask patients to setgoals. They identify objectives in specific behavioral terms by asking, “Howwould you like to be different by the end of therapy?” It is important to givepatients feedback about their goals, because they sometimes harbor unrealisticexpectations. Therapists also help to identify short-term goals and propose waysthe patient can meet those goals.For example, Kim’s therapist helped her specify her goal of “being happy”in behavioral terms: getting a job she enjoyed, entering into a romantic relationship,getting along with her family, and staying abstinent. He helped herset smaller goals along the way. A first step in getting a new job was to improveher attendance at her current job, so she could get a good letter of reference.Therapists also question patients about the degree to which they reallywant to meet their goals. A helpful technique is the advantage–disadvantageanalysis (Figure 22.6), adapted from Marlatt and Gordon (1985). In this exercise,the therapist explores the benefits of achieving a goal, while also reframingthe disadvantages.For some patients, a goal of harm reduction is more acceptable and achievablethan complete abstinence (Fletcher, 2001; Marlatt, Tucker, Donovan, &Vuchinich, 1997). While abstinence is generally the safest goal, a decrease insubstance use is more desirable than early dropout from therapy, which canoccur if the therapist tries too early or too strongly to impose a total ban on allsubstances.

486 V. TREATMENTS FOR ADDICTIONSAdvantages of Abstinence1. Feel better aboutmyself.2. Feel more in control.3. Get to work on time.4. More likely to keep my job.5. Save money.6. Better for my health.7. Not get so criticized by my sister.8. Not hang around other “druggies” so much.9. Spend my time better.Disadvantages of Abstinence (with reframe)1. I may feel bored and anxious (BUT it’sonly temporary and it’s good to learn tostand bad feelings).2. I don’t know what to do with my time (BUTI can learn in therapy how to spend timebetter).3. I won’t be able to hang out with my“friends” (BUT I do want to meet new“nondruggie” friends).Advantages of Taking Drugs (with reframe)1. Escape from feeling bad (BUT it’s only atemporary escape and I don’t really solvemy problems).2. Have people to hang out with (BUT they’redruggies and I don’t really like them).3. It’s hard work to quit (BUT I’ll do it step-bystepwith my therapist).Disadvantages of Taking Drugs1. Seems to make me depressed.2. Costs money.3. Bad for my health.4. Makes me feel like I’m not in control of mylife.5. Makes me feel unmotivated.6. Hard to solve my real problems.7. May make me lose my job.8. Makes relationship with my sister worse.9. Stops me from going out and making newfriends.10. Makes me feel like I’m wasting time.11. Makes me feel stuck, like I’m not gettinganywhere.FIGURE 22.6. Advantages–disadvantages analysis.Principle 4: The Initial Focus of Therapy Is on the PresentTherapists initially emphasize current and specific problems that are distressingto the patient. When the patient has a comorbid diagnosis, it is important toaddress problems related to both. For example, Kim needed help in problemsolving about a critical supervisor at work and in learning alternate copingstrategies (instead of using substances) when she was distressed about a workproblem. She and her therapist discussed how to respond to the hurt she feltwhen the supervisor rebuked her for lateness, how to decrease her anger byrehearsing a coping statement addressing her activated core belief, how to useanger management techniques such as controlled breathing and time-out, andhow to talk to the supervisor in a reasonable manner.The therapist also helped Kim respond to automatic thoughts. Through acombination of Socratic questioning and modeling, Kim learned to change thethought, “I should tell my supervisor off,” with “He’s just trying to do his job; Iwant to keep this job; I can just say OK for now and stay calm.” Toward themiddle of therapy, the therapist and Kim began discussing her past as well—tosee how she developed her ideas about relationships, and how they related toher current difficulties.

22. Cognitive Therapy 487Principle 5: Cognitive Therapy Is Time-SensitiveThe course of therapy for substance abuse patients varies depending on theseverity of the substance use. Weekly or even twice-weekly sessions are recommendeduntil symptoms are significantly reduced. With effective treatment,patients stabilize their moods, learn more tools, and gain confidence in usingalternate coping strategies. At this point, therapist and patient may experimentwith decreasing sessions. For example, in a major study of cognitive therapy forcocaine dependence (Crits-Christoph et al., 1997), the frequency of sessionswent from once a week to once every 2 weeks, then to once every 3 or 4 weeks.After termination, an “open door” approach is helpful, in which patients areinvited to return to therapy if they are tempted to use substances again.Principle 6: Therapy Sessions Are Structured,with Active ParticipationTypically, therapists use a structured format, unless it interferes with the therapeuticalliance. Usually therapists first check the patient’s mood and recentamount and type of substance use (including, if possible, objective assessment ofthese). They explore the patient’s progress or worsening, and elicit the patient’sfeelings about coming to therapy that day. Next the therapist sets an agenda anddecides with the patient what problems to focus on in the session. Standard itemsinclude the successes and difficulties the patient experienced during the pastweek and upcoming situations that could lead to substance use or dropout.The therapist then makes a bridge from the previous session, asking thepatient to recall the important things they discussed. If the patient has difficultyremembering the content, they problem-solve to help the patient make betteruse of future sessions. Encouraging patients to take notes and review these duringthe week helps them integrate the lessons of therapy. Also, during this partof the session, the therapist reviews the therapy homework completed duringthe week. If therapists suspect that patients have reacted badly to a previous session,they may ask for feedback about the session.Next, they address specific topics of concern to the patient. As they discussthe first problem, they collect information about it, conceptualize how it arose,evaluate thoughts about it, modify relevant beliefs, and problem-solve asneeded. In the context of discussing the problem, the therapist teaches thepatient skills in various domains: interpersonal (e.g., assertiveness), mood management(e.g., relaxation, anger management), behavioral (e.g., alternatebehaviors when cravings start), and cognitive (e.g., worksheets on dysfunctionalcognitions).Homework is customized to the patient. Typically, it includes monitoringsubstance use and mood, responding to automatic thoughts and beliefs, practicingnew skills, and problem solving.

488 V. TREATMENTS FOR ADDICTIONSThroughout the session, the therapist summarizes the material the patienthas presented and checks comprehension by asking about the “main message.”At the end of the session, they summarize what occurred, checking that thepatient understands and is likely to do the homework. Finally, the therapist asksfor feedback. Skillful questioning of the patient’s honest reactions and nondefensiveproblem solving by the therapist promote progress and lessen dropout.Adhering to this structure has many benefits: The most important issuesare discussed; there is continuity between sessions; substance use is monitored;and problems are directly addressed. In addition, patients learn new skills andare more likely to use these in the coming week. The structure also ensures thatpatient and therapist understand the lessons of the session, and that the patientis given the opportunity to provide feedback, so therapy can be modified ifneeded.Principle 7: Patients Are Taught to Identifyand Respond to Dysfunctional ThoughtsThe therapist emphasizes the cognitive model at each session—that patients’thoughts influence how they react emotionally, physiologically, and behaviorally,and that by correcting their dysfunctional thinking, they can feel andbehave better. The therapist does not assume that automatic thoughts are distorted;instead, therapist and patient investigate whether a given thought isvalid. When thoughts are accurate (e.g., “I want a fix”), they either problemsolve(discuss ways to respond to the thought) or explore the validity of theconclusion the patient has drawn (e.g., “Wanting a fix shows I am weak”).When evaluating thoughts, the therapist primarily uses questioning rather thanpersuading the patient, and standard tools such as the Dysfunctional ThoughtRecord (J. S. Beck, 1995) are used when possible.Principle 8: Cognitive Therapy Emphasizes Psychoeducationand Relapse PreventionFrom the first session, the goal is to maximize patients’ learning. The therapistencourages patients to write down important points during the session or doesthe writing for them, if necessary. When patients are illiterate, the therapistuses ingenuity to create a system for helping them remember (e.g., audiotapingthe session, a brief summary of the session, or brainstorming whom the patientmight ask to read therapy notes).The therapist teaches patients how to best use the new strategies. The goalis to make the patient her own best “cognitive therapist.” For example, thetherapist teaches Kim how to identify her negative thoughts when she feelsupset, how to respond to these thoughts, how to examine her behaviors, how touse coping strategies when she has cravings, how to communicate effectively,

22. Cognitive Therapy 489how to avoid high-risk situations, and many more cognitive, behavioral, moodstabilizing,and general life skills.Prior to termination, relapse prevention is emphasized. The therapist andpatient review skills; predict difficulties; note early warning signs of relapse; anddiscuss how to limit a lapse from becoming a relapse. They agree on when thepatient needs to return to therapy, that is, if a lapse is imminent (instead of justafter it occurs). Finally, they develop a plan for patients to continue to work ontheir goals, preferably with the support of friends and family.TREATMENT PLANNINGThe first step in treatment planning is to complete a thorough diagnostic assessmentbased on the criteria of the Diagnostic and Statistical Manual of Mental Disorders(DSM-IV-TR; American Psychiatric Association, 2000). It is essential toevaluate comorbid Axis I and Axis II disorders, as well as medical complications.According to research (Kessler et al., 1996), many patients with substanceuse disorders have a co-occurring psychiatric disorder. The treatment planshould address both. For example, Kim’s therapist conceptualized that she wasmedicating her depression with marijuana. In addition to treating her substanceuse, the therapist focused on the depression itself, using standard cognitivetherapy strategies to reduce her depressive symptoms: activity scheduling,responding to negative cognitions (e.g., “I can’t do anything right”), and problemsolving (e.g., about work problems and loneliness), among others (see A. T.Beck et al., 1979; J. S. Beck, 1995). She was also referred to a psychiatrist for amedication consultation.Kim also had an Axis II diagnosis: avoidant personality disorder with dependentand borderline features. One important implication of any personalitydisorder is the strong likelihood that associated dysfunctional beliefs (e.g., “I amhelpless; I am bad”) might arise in the therapy session itself. Her therapistplanned treatment to avoid intense schema activation early in therapy thatmight have led to premature dropout. Adding elements from cognitive therapyfor personality disorders may be helpful for Axis II issues (Beck et al., 1990;Young, 1999).A second key step in treatment planning is to identify the patient’s motivationfor change. Prochaska, DiClemente, and Norcross (1992) describe fivestages of change: the precontemplation stage (in which patients are only minimally,if at all, distressed about their problems and have little motivation tochange), the contemplation stage (in which they have sufficient motivation toconsider their problems and think about change, although not necessarilyenough to take action), the preparation stage (in which they want help to makechanges but may not feel they know what to do), the action stage (in which

490 V. TREATMENTS FOR ADDICTIONSthey start to change their behavior), or the maintenance stage (in which theyare motivated to continue to change).Kim, for example, was at the contemplation stage when she entered therapy.Her therapist helped her identify the problems associated with her substanceuse, some of which she had avoided focusing on before therapy. Hertherapist also helped her do an advantages–disadvantages analysis of marijuanause (Figure 22.6). He helped her “reframe” or find a functional response to herdysfunctional ideas of not changing. These techniques helped move Kim fromthe contemplation to the preparation stage. Had her therapist started with atreatment plan that emphasized immediate change of substance use behaviors,it is likely that Kim would have resisted, tried only halfheartedly, or droppedout of therapy altogether.Part of every treatment plan involves socializing patients to the cognitivemodel, so that they begin to view their reactions as stemming from their (oftendistorted) perceptions of situations. Once her therapist taught her to ask herselfwhat was going through her mind just before she reached for a joint, Kim couldunderstand how her automatic thoughts influenced her emotional and behavioralreactions. Later, he taught her how to identify the more complex sequence(Figure 22.4) leading to substance use and helped her identify how she couldintervene at each stage.An essential element in treatment planning is evaluating the strength ofthe therapeutic alliance. Substance abuse patients often enter treatment withdysfunctional beliefs about therapy, such as the following:“My therapist may try to force me to do things I don’t like.”“This therapy may do more harm than good.”“He probably thinks he knows everything.”“She’ll think I’m a failure if I use again.”“I’m better off without therapy.”The treatment plan should include the identification and testing of thesedysfunctional beliefs. Otherwise, patients may drop out prematurely. A goodtreatment plan also specifies patients’ problems (or, positively framed, theirgoals) and the concrete steps needed to ameliorate them. Kim and her therapistdiscussed her work problems. They did a combination of problem solving andcorrecting distortions related to work themes, such as getting to work on time,boredom on the job, fear of criticism, and relating to coworkers. Eventually shesought a new job, when it became clear that the disadvantages of the job (lowpay and lack of stimulation) still outweighed the positive aspects. Her therapistencouraged her in the job search.The work problem was one of the first problems they tackled, because Kimwas motivated to work on it, it was closely connected to her marijuana use, andit seemed they might make improvements on it in a short period. Later in ther-

22. Cognitive Therapy 491apy, they addressed situations that were even more difficult: getting along withher family, meeting new friends, and developing broader interests.Her therapist continuously assessed Kim’s readiness to change her substanceabuse by measuring the strength of her beliefs. At the beginning of therapy,she believed that her marijuana use might contribute to her work problems,her social isolation, and her lack of motivation. However, she alsobelieved that nothing, including therapy, could help. After several weeks, shebegan to see things differently, especially when she recognized that some initialbehavioral activation and responding to automatic thoughts improved hermood. Now she was ready to explore how she came to use marijuana, to startmonitoring her substance use, to learn strategies to manage cravings, to avoidhigh-risk situations, to respond to substance-related beliefs, to join a self-helpgroup, and to make some lifestyle changes. These strategies are described next.Teaching Patients to Observe Substance Use SequencesKim’s therapist used a blank version of Figure 22.4, asking Kim to fill in theboxes after thinking about a recent episode of marijuana use. For the first time,it became clear to Kim that her behavior was at least somewhat voluntary. Previouslyshe had believed that her use was completely out of her control.The therapist reviewed how a typical activating stimulus gave rise to negativethoughts, which led to feelings of hopelessness. They discussed how shecould learn to intervene. First, she could respond to her negative thoughts toreduce her dysphoria. Even if that did not work, she could still respond to hersubstance-related beliefs. She could, for example, read a coping card they developedin session. Such a card might contain “what to do if I want to smoke.”These coping cards are not merely affirmations but jointly composed statementsthat the patient endorses in session. They might include the following:1. Go for a walk.2. Call a friend.3. Go out for coffee.4. Watch a movie.5. Read my Narcotics Anonymous book.If Kim’s automatic thoughts about substance use continued, she wouldhave another opportunity to respond. Upon experiencing cravings, she couldtell herself to ignore these sensations and distract herself. For example, shemight create a coping card that said:“If I feel cravings, they are just cravings. I don’t have to attend to them. They’llgo away. I can stand them. I’ve stood cravings in the past. I’ll be very glad in afew minutes that I ignored them. When I ignore them, I get stronger!”

492 V. TREATMENTS FOR ADDICTIONSIf she recognized her permission-giving beliefs, she could read another copingcard that might say:“Don’t reach for a joint. Wait 5 minutes. I am strong enough to wait. Inthe meantime, do what’s on my ‘to do’ list.”If she found herself focusing on strategies to get substances, she could tryanother waiting period or do other tasks outlined in therapy. A careful analysisof the substance-taking sequence, along with potential interventions, gave Kimhope that she could conquer this problem.Kim and her therapist developed the coping cards over several sessions.First they discussed what Kim wished she could tell herself at each stage. Beforewriting the cards, the therapist asked Kim how much she believed each statement.When the strength of her belief was less than 90–100%, they rewordedthe statement or discussed it further to increase its validity. They observed thatif Kim did not believe an idea strongly in the session, it was unlikely to work in“real life”; thus, they needed more compelling beliefs.Monitoring ProgressProgress is monitored in several ways. Most obvious is the patient’s report ofsubstance use, obtained at each session. Urine and Breathalyzer tests can alsomotivate a decrease in use and an increase in the validity of self-reports. Whenpatients do use, they are encouraged to see it not as an indication of failure, butrather as an opportunity to learn from the experience and to make future abstinencemore likely. A variety of self-report instruments exist for substanceabuse, such as the Timeline Followback (Sobell & Sobell, 1993). For substanceabuse instruments that can be downloaded directly from the Web, see theappendices at the end of this chapter. Reports from others, such as family membersor probation officers, may also be particularly important for patients withlow motivation or a history of lying about their use.When a patient has a comorbid Axis I or II disorder, progress is also measuredby instruments such as the Beck Depression Inventory (A. T. Beck &Steer, 1993b), the Beck Anxiety Inventory (A. T. Beck & Steer, 1993a), theBrief Symptom Inventory (Derogatis, 1992), and other instruments relevant toparticular symptoms. Improvements in scores provide an opportunity to reinforcepositive changes that patients have made in their thinking and behaviorin the past week. Worsening scores raise a red flag, and careful questioningabout recent events and perceptions often reveals agenda items to prevent theresumption of substance use in the coming week.It is also important to monitor how patients spend their time. Kim, forexample, made some changes early in therapy: less time watching televisionalone and fewer visits to substance-using friends. Had her therapist not been

22. Cognitive Therapy 493vigilant about checking weekly on these improvements, he might have missedsignificant backsliding many weeks later, which could have led to a relapse.Another aspect of monitoring is assessment of old, dysfunctional beliefsversus newer, more functional ideas. At each session, the therapist assessed howmuch Kim believed substance-related ideas such as “I can’t stand to feel bored”and “Smoking marijuana is the only way to feel better,” and how much shebelieved the new ideas they had developed, such as “My life will improve if Idon’t use” and “I can feel better by answering my negative thoughts and completingmy ‘to do’ list.” This monitoring helped the therapist intervene earlywhen Kim’s dysfunctional beliefs occasionally resurfaced strongly.Dealing with High-Risk SituationsMarlatt and Gordon (1985) observed that exposure to activating stimuli, ortriggers, makes substance use more likely. In high-risk situations, activatingstimuli trigger substance-related beliefs, leading to cravings. These stimuli areidiosyncratic; what triggers one patient may not trigger another.Triggers can be internal or external. Internal cues include negative moodstates such as depression, anxiety, loneliness, and boredom, or physical factorssuch as pain, hunger, or fatigue. Although many patients use substances to regulatenegative moods, many also use substances when they already feel good, to“celebrate” or to feel great.External cues occur outside the individual: people, places, or things relatedto substance use, such as relationship conflicts or seeing substance paraphernalia.In one study, Cummings, Gordon, and Marlatt (1980) found that 35% ofrelapses were precipitated by negative emotional states, 20% by social pressure,and 16% by interpersonal conflict.The therapist helps patients identify the high-risk situations in which theirsubstance-related beliefs and cravings occur. They are encouraged to avoidthese situations and are taught relationship skills to handle conflict and pressureto use. For example, they might rehearse how Kim could respond when afriend offers her a drink.Managing Cravings and UrgesPatients should learn both cognitive and behavioral techniques for managingcravings. Distraction is often helpful, and patients can devise a list of thingsthey can easily do (e.g., exercise, read, and talk on the telephone). Thoughtstopping can reduce urges. Snapping a rubber band and yelling “Stop!” whileenvisioning a stop sign helped Kim manage her craving. Grounding is anotherstrategy that aids distraction from cravings and intense negative emotions; onecan teach mental, physical, and soothing grounding methods (see Najavits,2002a, for a description and handouts).

494 V. TREATMENTS FOR ADDICTIONSThe therapist can help patients identify beliefs that encourage the use ofsubstances to deal with cravings, for example, “I can’t stand the craving”; “If Ihave cravings, I have to give in.” Socratic questioning, examining past experiencesof resisting craving, reflecting on the relative difficulty versus impossibilityof tolerating cravings, and other cognitive techniques can modify these dysfunctionalideas.Case Management and Lifestyle ChangeHelping patients solve their real-life problems is an essential part of cognitivetherapy. Patients who abuse substances often have complex medical, legal,employment, housing, and family difficulties. Therapists should refer patientsfor assistance when needed. Therefore, they need to be aware of communityresources and social services. Sometimes they can help identify people inpatients’ social network who can help them work through such practical problems.In some cases, however, it is necessary to help patients directly in sessionto take steps to improve their lives. Examining employment ads in the newspaper,for example, or completing forms (e.g., for public housing) with the patientis often an important part of treatment. For examples of case management forsubstance abuse, including dual diagnosis, see Drake and Noordsy (1994),Najavits (2002b), and Ridgely and Willenbring (1992).Some lifestyle change is usually necessary for substance abuse patients toeliminate substance use and to maintain progress. Often the therapist needs tohelp the patient repair important supportive relationships and develop newrelationships with people who do not use. Many substance abusers are deficientin relationship skills and need to learn these through discussion and role plays.Patients often have dysfunctional beliefs about relationships, and modificationof these beliefs is a necessary step in learning to relate well to others.Patients sometimes need help identifying how they can build a new,nonusing network of friends. The therapist can discuss contact with nonusers inthe patient’s environment, as well as encourage new activities to meet new people.Self-help groups can be a valuable adjunct to therapy—for meeting new,nonusing people, reinforcing functional beliefs, and building a healthier lifestyle.Therapists should be aware of self-help groups in their area and encouragepatients to attend. AA, NA, SMART Recovery, and Moderation Managementare a few examples of groups that can be of significant benefit to patients. Seethe appendices at the end of this chapter for websites and phone numbers.Therapists can help patients who are reluctant to attend self-help groups byeliciting their automatic thoughts and aiding them in responding to thesethoughts. Problem solving may be needed to help the patient choose groups oractivities, find transportation, and manage anxiety about new experiences.

22. Cognitive Therapy 495Reducing DropoutStudies have shown that approximately 30–60% of substance abuse patientsdrop out of therapy (Wierzbicki & Pekarik, 1993). Many factors account forthis high rate, including continued substance use; legal, medical, relationship,or psychological problems; practical problems (e.g., transportation, finances);dissatisfaction with therapy; and problems with the therapeutic alliance (Liese& Beck, 1997). Early in therapy, therapist and patient should predict potentialdifficulties that might interfere with regular attendance in therapy and eitherproblem-solve in advance or collaboratively develop a plan for contact (usuallyby phone) if the patient misses a session.Kim’s therapist, for example, helped her with problems such as changingher work schedule and transportation, which otherwise would have impededher attendance. Both straightforward problem solving and responding to negativethinking (“I’ll be too tired to come after work”; “It’s not worth taking twobuses”) were necessary to avoid missed sessions.To maximize regular attendance, the therapist needs to monitor thestrength of the therapeutic relationship at each session. Negative changes inpatients’ body language, voice, and degree of openness usually signal that dysfunctionalbeliefs (about themselves or therapy) have been activated. A list of50 common beliefs leading to missed sessions and dropout (Liese & Beck, 1997)is a valuable guide for therapists. Testing negative thoughts immediately canprevent a negative reaction that otherwise might have resulted in the patientmissing the next session. Kim had many such cognitions, especially early intherapy: “I’m not smart enough for this therapy”; “I can’t do this.” A therapistwho still suspects a patient may miss the next session may be able to turn thetide by phoning the patient the day before the session and demonstrating careand concern.Formulating an accurate cognitive conceptualization of the patient from thestart enables the therapist to plan interventions to avoid inadvertent activationof dysfunctional beliefs within and between sessions. Kim’s therapist, for example,recognized how overwhelmed Kim became when faced with even minor challenges.She therefore took care to explain concepts simply, to limit the amount ofmaterial each session, to check her understanding frequently, and to suggesthomework that she could do. Thus, she avoided undue activation of Kim’s beliefsof inadequacy and helped maintain her therapy attendance.COMPARISON WITH OTHER MODELSIt may be helpful to compare cognitive therapy for substance abuse with someother widely known approaches, specifically, motivational enhancement therapyand dialectical behavior therapy.

496 V. TREATMENTS FOR ADDICTIONSMotivational enhancement therapy (MET; Miller, Zweben, DiClemente,& Rychtarik, 1995) derives from several different theories, including clientcentered,cognitive-behavioral, and systems theories, and the social psychologyof persuasion. The treatment is guided by five principles: The therapist shouldexpress empathy, develop discrepancy between the patient’s goals and currentproblem behavior, avoid argumentation, roll with resistance rather than opposingit directly, and support self-efficacy by emphasizing personal responsibilityand the hope of change. Specific strategies include reflective listening, affirmation,open-ended questions, summarizing, and eliciting self-motivational statements(e.g., asking evocative questions, inquiring about pros and cons of behavior,and exploring goals). The therapist also addresses ambivalence that mayinterfere with motivation and uses assessment instruments that are presented tothe patient to increase motivation for change (e.g., alcohol/drug use, functionalanalysis of behavior, readiness to change, life problems, and biomedical impact).MET differs from cognitive therapy for substance abuse in several ways.First, MET is primarily designed as a process-oriented method to increase motivation.It was not designed to teach specific new skills or coping strategies(such as cognitive therapy skills of identifying dysfunctional cognitions, rehearsalof new responses to cognitions, identification of alternative copingstrategies, mood monitoring, social skills training, and lifestyle changes). Second,and likely because of the difference in goals, MET is typically muchshorter. For example, in Project MATCH, MET was four sessions. Indeed,MET is primarily thought of as a precursor to or combination with other therapiesfor substance abuse, including cognitive therapy (e.g., Barrowclough et al.,2001).Dialectical behavior therapy (DBT) by Linehan (1993) is a CBT designedfor borderline personality disorder (BPD). It comprises twice weekly group sessionsand weekly individual sessions, and as-needed phone coaching. DBTteaches a variety of skills, in part inspired by Eastern philosophy, includingmindfulness, distress tolerance, emotion regulation, interpersonal effectiveness,and self-management (Linehan, 1993). After positive outcomes with patientswith BPD, it was adapted for substance abuse patients with BPD in the late1990s (Dimeff, Rizvi, Brown, & Linehan, 2000; Linehan et al., 1999, 2002).The adaptation for substance abuse includes several new skills, including alternaterebellion, adaptive denial, burning bridges to drug use, and building a lifeworth living. DBT differs from cognitive therapy in several ways. First, cognitivetherapy for substance abuse was designed for a very broad spectrum of substanceabuse patients, whereas DBT focuses on patients with the dual diagnosisof BPD and substance abuse. Thus, some precepts that may be especially helpfulfor BPD may not apply to the typical substance abuse patient without BPD. Forexample, under the “four-session rule” in DBT, if a client misses four or moresessions, she loses access to the therapy. Also, a patient in DBT must agree to a

22. Cognitive Therapy 497lengthy course of treatment (e.g., two full rounds of the DBT skills modules,and sessions three times per week). In cognitive therapy, such imperatives arenot required. Second, and again, likely due to the nature of BPD, therapists usea team or community-of-therapists approach, and therapists are asked to beavailable after hours for phone coaching of clients. Cognitive therapy followsmore traditional therapist roles. Finally, whereas both DBT and cognitive therapyfocus on teaching new coping skills, the skills themselves differ to somedegree. For example, cognitive therapy focuses much more formally on changingcognitions through the use of structured tools for cognitive change such asthe Dysfunctional Thoughts Record.CONCLUSIONCognitive therapy can be an effective treatment for substance abuse patients. Itrequires accurate conceptualization of the patient, a sound treatment planbased on this case formulation, a strong therapeutic relationship, and specializedinterventions. Structuring the therapy session, problem solving of currentdifficulties, education about the sequence of substance use, planning for highrisksituations, monitoring of substance use, lifestyle change, and intensive casemanagement are important facets of treatment.Kim could easily have become an unemployed “revolving door” user and aburden to family, friends, and society. Cognitive therapy helped her to engagein therapy, work through dysfunctional beliefs about herself and the therapist,develop functional goals, learn new skills to solve problems, tolerate negativeemotion, persist when she felt hopeless, engage in alternative behaviors whenshe craved substances, and develop a healthier lifestyle. Hard work by both thetherapist and substance abuse patient can pay off handsomely.APPENDIX 22.1. SUBSTANCE ABUSE RECOVERY RESOURCES*Resource Website PhoneNational Drug Information, Treatment www.drughelp.org800-662-HELPand Referral LineNational Clearinghouse for Alcohol www.health.org 800-729-6686and Drug InformationAlcohol and Drug Healthline www.samsha.gov 800-821-4357Alcoholics Anonymouswww.alcoholicsanonymous.org800-637-6237Cocaine Anonymous www.ca.org 310-559-5833Narcotics Anonymous www.na.org 818-773-9999

498 V. TREATMENTS FOR ADDICTIONSResource Website PhoneMarijuana Anonymouswww.marijuanaanonymous.org800-766-6779Nicotine Anonymouswww.nicotineanonymous.org415-750-0328Smart Recovery www.smartrecovery.org 440-951-5357Secular Organization for Sobriety/ www.secularsobriety.org 323-666-4295Save Our SelvesHarm Reduction Coalition www.harmreduction.org 510-444-6969Moderation Management Network www.moderation.org 212-871-0974Women for Sobriety www.womenforsobriety.org 215-536-8026*From Najavits (2002a). Copyright 2002 by the Guilford Press. Adapted by permission.APPENDIX 22.2. SUBSTANCE ABUSE ASSESSMENT RESOURCES*Resource Website PhoneNational Institute on AlcoholAbuse and AlcoholismSubstance Abuse and MentalHealth Services AdministrationNational Institute on Drug AbuseFree screening online foralcoholismUniversity of New Mexico Centeron Alcoholism, Substance Abuse,and AddictionsTo locate substance abuse hometestkitswww.niaaa.nih.gov/publications —store.health.org andwww.samsha.gov (click“publications,” then “substanceabuse treatment resources”)www.nida.nih.gov (click“publications”)800-729-6686—www.alcoholscreening.org —casaa.unm.edu/inst/inst.htmlwww.thomasregister.com (enter“alcohol drug test” for list ofcompanies that provide home testkits for substance abuse)*From Najavits (2004). Copyright 2004 by The Guilford Press. Adapted by permission.—REFERENCESAmerican Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders(4th ed., text rev.). Washington, DC: Author.Barrowclough, C., Haddock, G., Tarrier, N., Lewis, S. W., Moring, J., O’Brien, R.,et al.. (2001). Randomized controlled trial of motivational interviewing, cognitive

22. Cognitive Therapy 499behavioral therapy, and family intervention for patients with comorbid schizophreniaand substance use disorders. Am J Psychiatry, 158, 1706–1713.Beck, A. T., Emery, G., with Greenberg, R. L. (1985). Anxiety disorders and phobias: Acognitive perspective. New York: Basic Books.Beck, A. T., Freeman, A., & Associates, (1990). Cognitive therapy of personality disorders.New York: Guilford Press.Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression.New York: Guilford Press.Beck, A. T., & Steer, R. A. (1993a). Beck Anxiety Inventory manual. San Antonio, TX:Psychological Corporation.Beck, A. T., & Steer, R. A. (1993b). Beck Depression Inventory manual. San Antonio,TX: Psychological Corporation.Beck, A. T., Wright, F. D., Newman, C. F., & Liese, B. S. (1993). Cognitive therapy ofsubstance abuse. New York: Guilford Press.Beck, J. S. (1995). Cognitive therapy: Basics and beyond. New York: Guilford Press.Carroll, K. (1998). A cognitive-behavioral approach: Treating cocaine addiction (NIH PublicationNo. 98-4308). Rockville, MD: National Institute on Drug Abuse.Carroll, K. M. (1999). Behavioral and cognitive behavioral treatments. In B. S.McCrady & E. E. Epstein (Eds.), Addictions: A comprehensive guidebook (pp. 250–267). New York: Oxford University Press.Crits-Christoph, P., Siqueland, L., Blaine, J., Frank, A., Luborsky, L., Onken, L. S., etal. (1997). The NIDA Cocaine Collaborative Treatment Study: Rationale andmethods. Arch Gen Psychiatry, 54, 721–726.Crits-Christoph, P., Siqueland, L., Blaine, J., Frank, A., Luborsky, L., Onken, L. S., etal. (1999). Psychosocial treatment for cocaine dependence: The National Instituteon Drug Abuse Collaborative Cocaine Treatment Study. Arch Gen Psychiatry, 56,493–502.Cummings, C., Gordon, J. R., & Marlatt, G. A. (1980). Relapse: Prevention and prediction.In W. R. Miller (Ed.), The addictive behaviors: Treatment of alcoholism, substanceabuse, smoking and obesity (pp. 291–321). Oxford, UK: Pergamon Press.Derogatis, L. R. (1992). Brief Symptom Inventory. Baltimore: Clinical PsychometricResearch, Inc.Dimeff, L., Rizvi, S. L., Brown, M., & Linehan, M. M. (2000). Dialectical behavioraltherapy for substance abuse: A pilot application to methamphetamine-dependentwomen with borderline personality disorder. Cognit Behav Pract, 7, 457–468.Dimeff, L. A., & Marlatt, G. A. (1998). Preventing relapse and maintaining change inaddictive behaviors. Clin Psychol: Sci Pract, 5, 513–525.Drake, R. E., & Noordsy, D. L. (1994). Case management for people with coexistingsevere mental disorder and substance use disorder. Psychiatr Ann, 24, 427–431.Fletcher, A. (2001). Sober for good: New solutions for drinking problems—advice from thosewho have succeeded. Boston: Houghton Mifflin.Fromme, K., & Brown, S. A. (2000). Empirically based prevention and treatmentapproaches for adolescent and young adult substance use. Cog Behav Pract, 7, 61–64.Kessler, R. C., Nelson, C. B., McGonagle, K. A., Edlund, M. J., Frank, R. G., & Leaf, P.J. (1996). The epidemiology of co-occurring addictive and mental disorders: Implicationsfor prevention and service utilization. Am J Orthopsychiatry, 66(1), 17–31.

500 V. TREATMENTS FOR ADDICTIONSLiese, B. S., & Beck, A. T. (1997). Back to basics: Fundamental cognitive therapy skillsfor keeping substance-dependent individuals in treatment. In L. S. Onken, J. D.Blaine, & J. J. Boren (Eds.), Beyond the therapeutic alliance: Keeping substancedependentindividuals in treatment (NIDA Research Monograph No. 165, DHHSPublication No. 97-4142, pp. 207–230). Washington, DC: U.S. GovernmentPrinting Office.Liese, B. S., & Franz, R. A. (1996). Treating substance use disorders with cognitivetherapy: Lessons learned and implications for the future. In P. Salkovskis (Ed.),Frontiers of cognitive therapy (pp. 470–508). New York: Guilford Press.Linehan, M. M. (1993). Skills training manual for treating borderline personality disorder.New York: Guilford Press.Linehan, M. M., Dimeff, L. A., Reynolds, S. K., Comtois, K. A., Welch, S. S., Heagerty,P., & Kivlahan, D. R. (2002). Dialectal behavioral therapy versus comprehensivevalidation therapy plus 12-step for the treatment of opioid dependent womenmeeting criteria for borderline personality disorder. Drug Alcohol Depend, 67, 13–26.Linehan, M. M., Schmidt, H., Dimeff, L. A., Craft, J. C., Kanter, J., & Comtois, K. A.(1999). Dialectical behavioral therapy for patients with borderline personality disorderand drug-dependence. Am J Addict, 8, 279–292.Marlatt, G. A., Tucker, J., Donovan, D., & Vuchinich, R. (1997). Help-seeking by substanceabusers: The role of harm reduction and behavioral-economic approachesto facilitate treatment entry and retention. In L. Onken & J. Blaine & J. Boren(Eds.), Beyond the therapeutic alliance: Keeping the drug-dependent individual in treatment(pp. 44–84). Rockville, MD: U.S. Department of Health and Human Services.Marlatt, G. A., & Gordon, J. R. (Eds.). (1985). Relapse prevention: Maintenance strategiesin the treatment of addictive behavior. New York: Guilford Press.Maude-Griffin, P. M., Hohenstein, J. M., Humfleet, G. L., Reilly, P. M., Tusel, D. J., &Hall, S. M. (1998). Superior efficacy of cognitive-behavioral therapy for urbancrack cocaine abusers: Main and matching effects. J Consult Clin Psychol, 66, 832–837.Miller, W. R., Zweben, A., DiClemente, C. C., & Rychtarik, R. G. (Eds.). (1995). Motivationalenhancement therapy manual (Vol. 2). Rockville, MD: U.S. Department ofHealth and Human Services.Najavits, L. M. (2002a). Seeking safety: A treatment manual for PTSD and substance abuse.New York: Guilford Press.Najavits, L. M. (2002b). A woman’s addiction workbook. Oakland, CA: New Harbinger.Najavits, L. M. (2004). Assessment of trauma, PTSD, and substance use disorder: Apractical guide. In J. P. Wilson & T. M. Keane (Eds.), Assessing psychological traumaand PTSD (2nd ed., pp. 466–491). New York: Guilford Press.Najavits, L. M., Liese, B. S., & Harned, M. (2004). Cognitive-behavioral therapy. In J.H. Lowinson, P. Ruiz, R. B. Millman, & J. G. Langrod (Eds.), Substance abuse: Acomprehensive textbook (4th ed., pp. 723–732). Baltimore: Williams & Wilkins.Newman, C. F., & Ratto, C. L. (1999). Cognitive therapy of substance abuse. In E. T.Dowd & L. Rugle (Eds.), Comparative treatments of substance abuse (Vol. 1, pp. 96–126). New York: Springer.

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CHAPTER 23Group Therapy, Self-Help Groups,and Network TherapyMARC GALANTERFRANCIS HAYDENRICARDO CASTAÑEDAHUGO FRANCOTreatment modalities that employ social networks, such as group therapy, selfhelpprograms, and adaptations of individual office-based psychotherapy (suchas network therapy, described below), are of particular importance in treatingalcoholism and drug abuse. Family therapy is described elsewhere in this volume(Chapter 24). One reason is that the addictions are characterized by massivedenial of illness, and rehabilitation must begin with a frank acknowledgmentof the nature of the patient’s addictive process. The consensual validationand influence necessary to achieve such pronounced attitude change are mosteffectively gained through group influence. Indeed, for this purpose, a fellowaddict carries the greatest amount of credibility. Another reason for employingsocial networks is that they provide an avenue for maintaining ties to thepatient beyond the traditional therapeutic relationship. Furthermore, therapistsare not in the position to confront, cajole, support, and express feeling in amanner that can influence the abuser to return to abstinence; a group of fellowaddicts or members of the patient’s family can do so quite directly.This chapter explores the impact of group treatment in a number of disparatesettings. We look at therapy groups directed specifically at the treatment ofaddiction, at 12-step programs such as Alcoholics Anonymous (AA), and NarcoticsAnonymous (NA), and at institution-based self-help for substance abusers.The role of the clinician varies considerably in relation to each of these502

23. Group Therapy, Self-Help Groups, and Network Therapy 503modalities; in each case, the mental health professional is provided with anunusual opportunity to step out of the traditional role of the psychodynamictherapist or the psychopharmacologist and examine the ways in which socialinfluence is wrought through the group setting.GROUP THERAPY FOR ALCOHOLISM AND DRUG ABUSEHow to Refer a Patient to Group TherapyAdequate matching of the treatment needs of an addicted individual with themost appropriate group therapy format is important. Psychotherapeutic groupsfor alcoholics, for example, generally fare better when all members are alcoholics,and the focus of the group is on the characteristic behaviors and consequencesof this problem. Usually each group includes from 5 to 12 memberswho meet one to three times a week. Criteria for exclusion include severesociopathy or lack of motivation for treatment, acute or poorly controlled psychoticdisorders, and the presence of transient or permanent severe cognitivedeficits. Those patients who, because of their dual problems—addiction andmental illness—cannot be integrated into single-problem group formats mustbe treated within specialized dual-diagnosis groups and treatment settings(Galanter, Castañeda, & Ferman, 1988; Minkoff & Drake, 1991). Vannicelli(1982) observed that often patients are eventually excluded from the addictiongroup if they are unable to commit themselves to working toward abstinence.Polyaddicted individuals frequently are better integrated within multifocusedgroups. While dependent and nonsociopathic individuals are more easilyengaged in interactional group models, individuals with sociopathic and othercharacter problems are better retained in coping skills groups (Cooney, Kadden,Litt, & Getter, 1991; Poldrugo & Forti, 1988).Group Treatment ModalitiesGroup treatment for alcoholism and other addictions was developed out of generaldisappointment with the results of individual therapy (Cooper, 1987).Table 23.1 presents brief descriptions of different group modalities for treatmentof addicted individuals.Leadership Style and Group AimsThe optimum style for a leader conducting a group for substance abusersappears to be one in which the focus is group- rather than leader-determined, inwhich the leader not only is knowledgeable about substance abuse but also actsas a facilitator of interpersonal process, and in which the group members seek tounderstand each other from their own perspective.

504 V. TREATMENTS FOR ADDICTIONSTABLE 23.1. Different Group Modalities for Treatment of AlcoholicsCategory Technique Goals Curative factorsInteractionalInterpretation ofinteractional process;promotion of selfdisclosureandemotion expressionPromotion ofunderstanding andresolution ofinterpersonalproblemsIncreased awareness ofown relatednessModifiedinteractionalProcessing ofinteractionalproblems, but strongemphasis on ancillarysupports forabstinence such asAA and AntabusePromotion ofabstinence andimprovement ofinterpersonaldifficultiesIncorporation of specificresources to supportabstinence andimprovement ofinterpersonal relatednessBehavioralReinforcement ofabstinence-promotingbehaviors;punishment ofundesirable behaviorsSpecific behaviormodificationPrevention of specificresponsesInsight-orientedpsychotherapyExploration andinterpretation ofgroup and individualprocessesPromotion of abilityto tolerate distressingfeelings withoutresorting to alcoholIncreased insight andimproved ability totolerate stressSupportiveSpecific supportoffered to individuals,to enable them todraw on their ownresourcesPromotion ofadaptation to alcoholfreelivingImprovement in selfconfidence,andincorporation of specificrecommendationsGroups differ in their aims and the style of their leaders. Some groups allowfor discussion of issues other than addiction in the hope that group memberswill identify the association between the addictive behavior and all otherproblems. Other groups focus primarily on relapse prevention through the identificationand discussion of all problems, even if unrelated to the addictivebehavior. Groups also vary according to the degree of support offered tomembers—from confrontational groups that give support only when a patientespouses the views of the group leader to supportive groups that accept andexplore individual attitudes and beliefs.Despite the obvious importance of group style and the need for clearlydescribed group techniques, little has been written that provides group leaderswith specific group strategies (Vannicelli, Canning, & Griefen, 1984). Thequestion of the group’s style (defined as the way in which the group’s goals and

23. Group Therapy, Self-Help Groups, and Network Therapy 505processes are linked) is not merely one of academic importance. For example,Harticollis (1980) found that psychoanalytical groups are widely regarded asinadequate and are not recommended for active substance abusers because ofthe counterproductive degree of anxiety that they generate. An early study byEnds and Page (1957) demonstrated that the style of a group of alcoholics predictedtreatment outcome. In this study, alcoholics were assigned to one of severalgroups of different design. Group styles varied from one group described asrelatively unfocused and “client centered,” whose leader avoided a dominantrole and instead promoted interpersonal processes among the group members,to another group based on learning theory, whose leader assumed a dominantrole, offered only conditional support, and focused strongly on punishment andreward. At follow-up, those alcoholics treated in the client-centered groupfared far better than those included in the confrontational group.Descriptions of Some Representative Group ModelsExploratory and Supportive GroupsAn interesting model, the modified dynamic group psychotherapy, developedby Khantzian allows for the identification of individuals’ vulnerabilities andproblems within a context of “safety.” Abstinence is strongly endorsed, and thegroup, which requires an active style of leadership, promotes mutual supportand outreach, and constantly strives to identify and manage contingencies forrelapse (Khantzian, Halliday, & McAuliffe, 1990). According to Cooper(1987), psychotherapeutic groups based on exploration and interpretation aimat forging an increased ability in their members to tolerate higher levels of distressingfeelings, without resorting to mood-altering substances. In contrast,purely supportive treatment groups aim at helping addicted group members totolerate abstinence and assist them in remaining chemical-free, without necessarilyunderstanding the determinants of their addiction.Interactional Group ModelYalom, Bloch, and Bond (1978) described an important group style in whichtherapy is conducted in weekly, 90-minute meetings of 8–10 members who,under the leadership of two trained group therapists, are encouraged to exploretheir interpersonal relationships with the group leaders and the other members.An effort is made to create an environment of safety, cohesion, and trust, wheremembers engage in in-depth self-disclosure and affective expression. The goalof the group is not abstinence but the understanding and working through ofinterpersonal conflicts. (However, “improvement” without abstinence is oftenillusory.) In fact, groups of alcoholics are oriented away from an explicit discussionof drinking. The leaders emphasize that they do not see the group as the

506 V. TREATMENTS FOR ADDICTIONSmain instrument for achieving abstinence, and patients are encouraged toattend AA or to seek other forms of treatment for this purpose. Within this format,a group member can be described as “improved” along a series of 19 possibleareas of growth, irrespective of the severity of his or her drinking.This interactional model was further developed by Vannicelli (1982;Vannicelli et al., 1984), who, unlike Yalom and colleagues (1978), recommendsthat the group leaders strongly support abstinence as being essential tothe patient’s eventual emotional stability. The group leaders firmly endorsesimultaneous use of other supports, such as AA and Antabuse (disulfiram) therapy.In contrast to working with neurotics, whose anxieties provide motivationand direction for treatment, the leaders of such a group of alcoholics are forcedto intervene to provide limits and focus, without generation of more anxietythan necessary. The group therapists resist members’ inquiries into the leaders’drinking habits by instead exploring the patients’ underlying concerns aboutwhether they will be helped and understood. Patients who miss early group sessionsare actively sought out and brought back into the group. Confrontation(particularly of actively drinking members) is used sparingly and only with theaim of providing better understanding of the behavior, thus promoting growthand the necessary goal of activity changes.Interpersonal Problem-Solving Skill GroupsAccording to Jehoda (1958), interpersonal problem-solving skill groups arebased on the premise that the capacity to solve problems in life determinesquality of mental health. Several empirical studies lend some support to thisassumption, suggesting that there is a relation between cognitive interpersonalproblem-solving skills and psychological adjustment. These groups have beenimplemented for alcoholics (Intagliata, 1978) and heroin addicts (Platt, Scura,& Harmon, 1960) with some degree of success. Usually problem-solving skillsgroups are run for a limited number of sessions (frequently 10) and are organizedto teach a multistep approach to interpersonal problem solving. Mostoften, such steps include the following: (1) Recognize that a problem exists; (2)define the problem; (3) generate several possible solutions; and (4) select thebest alternative after determining the likely consequences of each of the availablepossible solutions to the problem. Follow-up studies determined thatgroups with this format were effective in generating specific skills such as anticipatingand planning ahead for problems, even following participants’ dischargefrom the treatment programs. The value of problem-solving skills groups withrespect to other primary modalities of addiction treatment, however, remains tobe determined. It is unclear, for instance, whether these groups contribute tothe overall rates of abstinence achieved in inpatient and outpatient treatmentprograms.

Educational Groups23. Group Therapy, Self-Help Groups, and Network Therapy 507Educational groups represent important ancillary treatment modalities in substanceabuse treatment, not only for addicts but also for their relatives andother social contacts. The obvious purpose of these groups is to provide informationon issues relevant to specific addictions, such as the natural course andmedical consequences of alcoholism, the implications of intravenous addictionfor sexual contacts and the family, the availability of community resources, andso forth. Often, educational groups provide opportunities for cognitive reframingand behavioral changes along specific guidelines. These groups areoften welcomed by some treatment-resistant addicts and alcoholics who cannotcooperate with other forms of therapy. More often than not, educational groupsoffer structured, group-specific, didactic material delivered by different means,including videotapes, audiocassettes, or lectures; these presentations are followedby discussions led by an experienced and knowledgeable leader.Activity GroupsLike educational groups, activity groups constitute another important ancillarymodality in the treatment of alcoholics and other addicts. Unlike educationalgroups, however, patient participation is the main goal of activity groups, whichcan evolve around a variety of occupational and recreational avenues. In a safeand sober context, the addict can expedite socialization, recreation, and selfandgroup expression. Activity groups are often the source of valuable insightinto patients’ deficits and assets, both of which may go undetected by treatmentstaff members concerned with more narrowly focused treatment interventions,such as psychotherapists and nurses. When appropriately designed, activitygroups may constitute invaluable sources of self-discovery, self-esteem, andnewly acquired skills that facilitate sober social interactions.Other groups also promote the acquisition of specific skills, such as thosedevoted to reviewing relapse prevention techniques and those aimed at buildingsocial skills. These groups are particularly helpful in the early stages of therehabilitation process of the alcoholic patient.Groups with Methadone-Maintenance PatientsGroups with methadone-maintenance patients experience problems that relatemore to the structure of the therapy than to the group content. Encouragementis always needed for patients to participate in these groups. Often, groups forthese patients are an efficient way of coping with problems under professionalguidance and peers’ support (Ben-Yehuda, 1980). These groups generally gothrough several stages: the development of esprit de corps, the division of labor,

508 V. TREATMENTS FOR ADDICTIONSthe establishment of group cohesion, and the development of outside-the-grouprelations.Relationship of Group Therapy to Individual TreatmentIt is not a surprise that group therapists maintain that group treatment is thetreatment of choice for alcoholics and other addicts (Matano & Yalom, 1991).In support of this, group therapists such as Kanas (1982) stress not only the difficultythat these patients have in developing an “analyzable transference neurosis”in individual therapy but also their tendency to display impulsive actingout—both of which are characteristics better addressed in the anxiety-diffusingcontext of a group setting. Alcoholics, for example, are often seen as beingorally fixated, with resulting narcissistic, passive–dependent, and depressivepersonality traits (Feibel, 1960). Platt and colleagues (1960) and Feibel (1960)pointed out that individual insight-oriented psychotherapy is often said to becontraindicated in addicts, because the following problems often present inthese patients: intolerance of anxiety, episodes of rage and self-destructivebehavior as a result of frustrated infantile needs, poor impulse control, and(probably most important) the tendency to develop a primitive transferencetoward the therapist.Pfeffer, Friedland, and Wortis (1949) described an undeniable advantageof group therapy over individual treatment, namely, the easily generated peerpressure, which can often promote behavioral changes and a reduction of denialof addiction and interpersonal difficulties. In addition, peer-generated supportoften satisfies narcissistic and dependence needs. Primitive, intense transferencesare often avoided in the group setting because of diffusion among theother members of the group and the “relative transparency of the group leaders”(Kanas, 1982, p. 1016). The tendency to leave treatment prematurely in individualtherapy is often countered by the group’s ability to promote a reductionof anxiety and to generate a therapeutic alliance not only with the leader butalso with the other group members. As stated previously, it is important whendeciding between group and individual therapy to assess both the patient’s abilityto tolerate and benefit from social interactions and his or her level of cognitiveand psychological functioning. Patients with moderate cognitive deficits,or paranoid or other psychotic disorders, are likely to become isolated or hostileand to leave the group setting prematurely.The following is a clinical example of the success of group therapy in a casein which individual therapy had no impact:At the time of referral, Mr. A, a 45-year-old white male, was employed asan administrator. He was married and had children. His chief complaintswere frequent mood changes of many years’ duration and unprovoked

23. Group Therapy, Self-Help Groups, and Network Therapy 509bouts of anger, often directed at his wife, children, and coworkers.Although he had no history of psychiatric or medical problems, he reluctantlyacknowledged that his wife thought he drank too much and that hisboss had strongly demanded that he do something about his angry outburstsand poor job attendance. The patient was referred for individualtherapy, but initial attempts at establishing a therapeutic relationshipfailed. He displayed markedly narcissistic personality traits, which resultedin an often disruptive relationship with the therapist, and he had difficultyin recognizing any interpersonal and mood problems associated with hisalcohol consumption. The patient, however, acknowledged drinking moreand more often than was “healthy” for him. His motivation for treatmentderived from his determination to maintain his current employment andhis interest in learning how to avoid depressive thinking.Both the patient and the therapist felt that no progress was beingmade in individual therapy, and the therapist then referred the patient toalcoholism group treatment. In the group, the patient was exposed to othergroup members’ descriptions of their problems of mood and social relations.On two occasions during the beginning phases of his involvementwith the group, he came to the group while intoxicated. The threat ofexpulsion from the group in the face of these intoxications brought intofocus the similar situation he faced at work, where his drinking was alsojeopardizing his ability to remain employed. Confronted by group membersand therapists alike, he eventually identified a relationship between hisdrinking and his angry outbursts at home and at work. From the outset, hisdrinking was interpreted by other group members as a reflection of hisalcoholism rather than the expression of psychological conflicts. After afew months in treatment, this patient finally felt that he indeed was analcoholic. The absence of drinking was associated with a total remission ofdepressive moods. He eventually made a commitment to abstinence, andhe remained in group treatment for several years.Management of Group Members Who Do NotRemain AbstinentDrinking by some group members is to be expected in alcoholic groups. Fullblownslips or covert drinking by any group member interrupts the group process,elicits drinking-related thoughts and behaviors in other members, andrequires specific and prompt intervention by the group leader. Often, however,a well-managed drinking episode represents an invaluable learning opportunityfor all group members. A slip is not in itself cause for dismissal from the group.A resumption of drinking illustrates to all members the importance of promptidentification and interruption of denial, and the need constantly to ensure theeffectiveness of selected measures for maintaining abstinence. Responsibility forthe slip should be defined to the group as resting entirely on the patient who is

510 V. TREATMENTS FOR ADDICTIONSdrinking and not on any past event or interaction between other group members.Drinking can assume different forms, depending on whether it is acknowledgedor denied by the person and whether or not, despite the drinking, thegroup member professes adherence to the group norms regarding abstinenceand self-disclosure. Those patients who keep drinking and express no intentionto stop should be asked to leave the group. Dismissal from the group isbest explained to the patient and to the other group members as justified bythe person’s present drinking behavior. Readmission into the group once thepatient is willing to accept the group norms, including a commitment toachieving abstinence, should always be offered to a patient who is leaving thegroup. A different approach is to be adopted with patients who express adesire to end the relapse and agree to participate in a discussion within thegroup of their active drinking. Initially, any information from any source(within or outside the group) that a group member is drinking should beimmediately shared with all members. If the patient is intoxicated, he or sheneeds to be asked to leave the group and to return sober to the following session.The next meeting should serve as an occasion to explore feelings aboutdrinking behavior and denial. At this point, the group norms are reiterated;if necessary, specific contingency contracts with the drinking member aredrawn up.Another presentation of the problem is the patient who drinks yet refusesto acknowledge it. It should be part of the group contract that any importantinformation concerning drinking behavior by a group member should be sharedwith the group. In the face of contrasting versions of a patient’s behavior, clarificationshould be sought from the patient in a way that facilitates “voluntary”disclosure. Eventually, it may be necessary to confront the patient directly; ifdenial persists, the patient should leave the group.Other Group Treatment ConsiderationsGroup psychotherapy based on interpersonal and interpretive approaches restsin part on the self-medication hypothesis, which contends that substance abuseshould be understood as the outcome of efforts at self-medication of distressingsymptoms (Cooper, 1987; Khantzian, 1989). Recent challenges to this theory,however, suggest that drug abuse (particularly abuse of cocaine) may not necessarilybe related to attempts at self-medication (Castañeda, Galanter, & Franco,1989). Accordingly, it is advisable that group leaders be knowledgeable aboutaddiction and able to anticipate that addicted group members may display drugseekingbehaviors that can best be regarded as conditioned responses (triggeredby specific internal or environmental cues, such as the sight of a bottle or feelingsof euphoria and celebration) rather than attempts on the part of the addictat dealing with emotional conflict (Galanter & Castañeda, 1985).

23. Group Therapy, Self-Help Groups, and Network Therapy 511SELF-HELP, 12-STEP GROUPS, AND 12-STEP FACILITATIONRole of Self-Help Groups in Addiction TreatmentSelf-help groups represent a widely available resource for the treatment of alcoholism,as well as other forms of chemical dependence. AA and other 12-steporganizations such as NA and Cocaine Anonymous (CA) have not only provideda large population of addicts with support and guidance but also havecontributed conceptually to the field of understanding and treating substanceabuse. However, important questions for the clinician and the researcher needto be answered before the proper role of 12-step programs in the treatment ofaddicts can be established. In what ways are such self-help programs compatiblewith professional care? In what ways do these groups achieve their effects? Forwhich patients are they most useful? Familiarity with self-help groups is essentialboth for the clinician providing care for substance abusers and for theresearcher attempting to understand psychosocial factors involved in the outcomeof addictions.History of Self-Help ProgramsSelf-help groups can be understood as a grassroots response to a perceived needfor services and support (Levy, 1976; Tracy & Gussow, 1976). In this sense, AAis the prototypical organization; it provided a model for the other successfulgroups such as NA and CA, as well as for its more closely related offspring suchas Al-Anon, Alateen, and Children of Alcoholics. Levy (1976) proposed arough division of self-help groups in two types of organizations: type I groups,which are truly mutual help organizations and include all 12-step programs, andtype II groups, which more frequently operate as foundations and place moreemphasis on promoting biomedical research, fundraising, public education, andlegislative and lobbying activities. Type I and type II groups are by no meanstotally exclusive, because type I associations promote public education, andtype II groups sometimes provide direct services.The development of AA has exerted a major influence on the self-helpmovement in general. The next section is concerned only with the developmentof AA and related 12-step programs for addictions, which are clearlydefined as type I associations.Origins and Growth of Alcoholics AnonymousAA’s principal founder, “Bill W,” in accordance with the AA tradition of anonymity,was himself an alcoholic. Bill was spiritually influenced by a drinkingfriend, Edwin Thatcher, who belonged to the Oxford Group, an evangelical religioussect (Kurtz, 1982). Thatcher, usually referred to as Ebby, attributed hisabstinence to his involvement with the Oxford Group, which displayed many of

512 V. TREATMENTS FOR ADDICTIONSthe characteristics later adopted by AA, such as open confessions and guidancefrom members of the group. Bill W continued to drink despite his encounter withEbby in 1934, but he felt that there was a kinship of common suffering amongalcoholics. During his final hospital detoxification, he experienced an alteredstate of consciousness characterized by a strong feeling of proximity with God,which gave him a sense of mission to help other alcoholics to achieve sobriety.Bill’s initial efforts to influence other alcoholics were unsuccessful until, inMay 1935, he met another member of the Oxford Group, “Dr. Bob,” who amonth later achieved sobriety and became the cofounder of AA. The numberof alcoholics who experienced spiritual recovery and achieved sobriety in AAprogressively increased; in 1939, when group membership reached 100, theypublished Alcoholics Anonymous, the book that became the bible for the movement(Galanter, 1989). AA institutionalized practices such as a 90-day inductionperiod, sponsorship relationships, the “12 Steps,” and recruitment for thefellowship. The expansion and stability of the organization resulted from its “12Traditions,” which avoid concentration of power within the organization, preventinvolvement of AA with other causes, maintain the anonymity of itsmembership, and preserve the neutrality of the association in relation to controversialissues. Its membership continued to grow; AA, now a global organization,is reported to have more than 75,000 informal groups in the United Statesand 114 other countries, with a membership estimated at 1.5 million. The birthand development of NA illustrate how AA provided a model to other self-helpprograms for addictions.History and Approach of Narcotics AnonymousAlthough the NA program was first applied to drug addiction at the U.S. PublicHealth Service Hospital at Lexington, Kentucky, in 1947, it was an NA groupindependent of any institution and formed by AA members who were addictsin Sun Valley, California, in 1953, that expanded and gave NA its current form(Peyrot, 1985). The Sun Valley NA group did not identify itself with a programorganized in New York City in 1948 by Dan Carlson, an addict formerlyexposed to the Lexington program, because the Sun Valley founders felt thatNA should strictly adhere to AA’s 12 Steps and 12 Traditions by not identifyingitself with any specific agency and not accepting government funds.There are a few differences between AA and NA. NA members usually useillegal drugs, in contrast to most AA members until recently, who could bedescribed as traditional alcoholics. Also, instead of using the term “alcoholism,”NA refers to its problem as “addiction” and addresses the entire range of abusablepsychoactive substances. There is, however, a clear overlap of approachand membership between the organizations, despite their complete independenceof each other. Following in the footsteps of AA, NA has experiencedfast-paced growth. It became an international organization, present in at least

23. Group Therapy, Self-Help Groups, and Network Therapy 51336 countries, with a probable membership of 250,000. According to the NAWorld Service Office, which publishes NA literature and centralizes informationwithin NA, the growth rate of the organization’s membership has been 30–40% a year (Wells, 1987). The growth of NA and other 12-2tep programs demonstratesthe organizational strength and appeal of the AA model.How 12-Step Programs WorkParticipation in a 12-step program can start at the moment the addict meets amember of an organization, reads its literature, or simply attends meetings (e.g.,an open meeting or an institutional meeting run by AA or NA speakers)(Galanter, 1989). A desire to stop drinking and/or abusing other drugs is theonly requirement for membership. Total abstinence becomes a goal from theoutset of the participation in the fellowship. Initial participation turns into aninduction period, which, in the case of AA, for instance, lasts 90 days andencourages daily attendance at meetings. The member is exposed to the 12-stepapproach to recovery; the first step consists of admitting powerlessness over theaddiction, and consequently breaking with denial. Seeking sponsorship fromanother member who has been sober for months (preferably more than a year)is also encouraged. Sponsors are usually of the same sex if the group is largeenough, so that emotional entanglements can be avoided to keep from distractingmembers from the purpose of attaining and maintaining sobriety. Openmeetings usually consist of talks by a leader and two or three speakers who sharetheir experiences of how the 12-step program related to their recovery.The 12-step program is an attempt to effect changes in addicts’ lives thatgo beyond just stopping the use of substances—changes in personal values andinterpersonal behavior, as well as continued participation in the fellowship.The 12 steps are studied and followed with the guidance of a sponsor and participationin meetings focused on each step. Each step involves changes inbehavior and attitudes that may profoundly affect the addict’s life. To achievethe ninth step, for instance, the addict makes amends to people formerlyharmed by his or her behavior. These amends may result in changes in the waythe person relates to others and interprets the problems that have affected pastand present relationships. For instance, an alcoholic man may “talk” to adeceased father whom he formerly hated and attempt a “conciliation” with hisimage of his dead father. The 12th step encourages propagation of the group’sphilosophy and consequently fosters the individual’s recovery by providingopportunities to others to recover and expand the fellowship.Traditionally, 12-step meetings are open to all members, but they may bedirected to special-interest groups (e.g., gays, women, minority groups, and physicians).Meetings can be of different types, such as discussions, 12-step study,and testimonials; some may be open to nonmembers, and others may be formembers only. If the recovery progresses, the member will learn strategies to

514 V. TREATMENTS FOR ADDICTIONSavoid relapse (e.g., “One day at a time”), obtain help from other members, andeventually help fellow addicts in their recovery. By helping other addicts and bysponsoring newcomers to the program, the individual is helping him- or herselfby becoming more involved with the recovery process and the organization’sphilosophy.Why 12-Step Programs WorkIt is still unclear why 12-step programs can help people exposed to them. Froman existential perspective, AA, for instance, encourages acceptance of one’sfinitude and essential limitation by conveying the idea of powerlessness overalcohol. On the other hand, one can go beyond this limitation by relating toothers and sharing some of the painful aspects of human existence. Kurtz(1982) emphasized that consistency in thought and action is crucial to maintaininga conscious effort to be honest with oneself and others. This effort producesan increased awareness of one’s own needs for growth. AA stresses theneed for consistency in thought and action in all stages of its recovery program.From a learning theory perspective, the group selectively reinforces socialand cognitive behaviors that usually are incompatible with the addictivebehavior. Attendance at meetings is basically incompatible with using the sametime to drink or abuse other drugs. Achievements resulting from sobriety aregenerously praised, and strategies of self-monitoring and self-control are constantlyreinforced through constant interactions with others attempting toremain sober. AA enhances self-monitoring of emotions and behaviors by helpingthe addict to detect reactions to certain internal and external stimuli (craving,distress with interpersonal problems, denial in the presence of depressivefeelings, unrealistic goals when under pressure, etc.). In addition to selfmonitoring,self-control is enhanced as alcoholics learn a new repertoire of cognitiveand social behaviors, such as attending more meetings when cravingincreases, using the 12 steps to cope with stressful life events, and obtain groupsupport to face painful feelings about themselves and others. Other theoreticalperspectives used to understand 12-step programs include operant and sociallearning views; however, because experimentation with the processes involvedin participation in 12-step programs is an almost impossible proposition, the useof learning models remains largely descriptive and speculative.OUTCOME STUDIESGroup Treatment OutcomesThe immense popularity of group treatment and self-help for alcoholics andother substance abusers preceded the availability of significant numbers of controlledoutcome studies (Bowers & al-Rheda, 1990; Cooney et al., 1991; Kang,

23. Group Therapy, Self-Help Groups, and Network Therapy 515Kleinman, & Woody, 1991; Poldrugo & Forti, 1988; Yalom et al., 1978). Yalomand colleagues (1978) reported significant improvement at 8-month and 1-yearfollow-ups of both alcoholics and neurotics treated in weekly interactionalgroup therapy. Improvement was measured along specific variables, however,and not according to the quality of abstinence eventually attained by the groupmembers. In an early report, Ends and Page (1957) compared the outcomeeffects on alcoholics of several group therapy designs, including groups based onlearning theory, client-centered (supportive) groups, psychoanalytical groups,and nonpsychotherapy discussion groups. They found that both client-centeredand psychoanalytical groups yielded better outcomes than did discussion groupsand groups based on learning theory, as measured by improvement in selfconceptat a 1-year follow-up. Client-centered groups also were associated withlower rates of readmission than all other groups in this and a subsequent study.Mindlin and Belden (1965) studied the attitudes of hospitalized alcoholicsbefore and after participation in group psychotherapy, occupational groups, orno-group treatment, and found that group psychotherapy significantly improvedmotivation for treatment and attitude toward alcoholism.The 1998 report by the Institute of Medicine, Bridging the Gap betweenResearch and Practice, has spurred on the development and evaluation ofevidence-based therapies (Marinelli-Casey, Domier, & Rawson, 2002). Thepast 10 years have seen a large increase in the number and quality of clinicaltrials (e.g., Charney, Paraherakis, & Gill, 2001; Magura et al., 2003; Marques& Formigoni, 2001; Meyers, Miller, Smith, & Tonigan, 2002; Ouimett et al.,2001; Petry, Martin, & Finocche, 2001). Many of these studies examine heretoforeunderstudied populations, such as those with co-occurring substancedependence and other major mental illness, serious medical conditions, andor polysubstance dependence. Studies have been designed to test the effectivenessof a variety of group treatment approaches. The feasibility of theirtransfer from both research to clinical settings and individual to group formatshas been investigated (Carise, Cornely, & Gurel, 2002; Carroll et al.,2002; Foote et al., 1999; Hanson, Leshner, & Tai, 2002; Petry & Simcic,2002; Van Horn & Bux, 2001). While some of the more ambitious protocols,such as those developed via the Clinical Trials Network (CTN), are stillundergoing various phases of implementation, there is widespread optimismthat group therapy will soon be established on much firmer empirical foundationthan was true in the past.Some of the approaches that have been receiving significant attention interms of adaptation to group format, standardization, and dissemination, includemotivational enhancement therapy (MET; Miller, Zweben, DiClemente,& Rychtarik, 1994), cognitive-behavioral coping skills therapy (CBST, oftenreferred to as “relapse prevention”; Kadden et al., 1995; for an update, seeLongabaugh & Morgenstern, 1999), and 12-step facilitation (TSF, discussedbelow).

516 V. TREATMENTS FOR ADDICTIONSSelf-Help and Treatment OutcomeAlcoholics AnonymousAA has received more attention from investigators studying outcome variablesthan other 12-step programs. Consequently, most of our knowledge about theimpact of 12-step programs on the lives of addicts is limited to the effects of AAon some samples of alcoholics. The structure of 12-step organizations and theiremphasis on anonymity make scientific research on these groups a very difficulttask (Glaser & Osborne, 1982). Investigators have studied outcome variablesrelated to participation in AA, such as severity of drinking, personality traits,attendance at meetings, total abstinence versus controlled drinking as a therapeuticgoal, and concomitance of AA attendance with professional care (Elal-Lawrence, Slade, & Dewey, 1987; Seixas, Washburn, & Eisen, 1988; Thurstin,Alfano, & Nerviano, 1987; Thurstin, Alfano, & Sherer, 1986).The first variable to deserve attention is that those alcoholics who joinAA are not representative of the total population of alcoholics receiving treatment(Emrick, 1987). AA members tend to be, as common sense would indicate,more sociable and affiliative. Studies also suggest that AA members havemore severe problems resulting from their drinking and experience more guiltregarding their behavior. Attendance at meetings has been associated in somestudies (Emrick, 1987) with better outcome, although the nature of this associationremains unclear. Thurstin and colleagues (1986) found no clear personalitytraits that might seem to be associated with AA membership, but theyreported that success among members appears to be related to less depression,less anxiety, and better sociability. AA seems not to benefit those who canbecome nonproblem users, and it may actually be detrimental to patients whocan learn to control their drinking (Emrick, 1987). AA members who receiveother forms of treatment concomitantly with their participation in AA meetingsprobably do better.As noted earlier, several problems make it difficult to study outcome factorsrelated to participation in 12-step programs. One is the changing compositionof AA membership: more women, younger people, and multiply addictedalcoholics that have been joining the organization. The heterogeneity of addictivedisorders, the anonymity of membership, the impossibility of experimentationwith components of the programs, the self-selection factor in affiliation,and the lack of appropriate group controls all impose serious methodologicaldifficulties in evaluating outcome variables. For clinical purposes, the benefit ofmembership in self-help groups has to be empirically evaluated for each individualpatient.12-Step FacilitationTSF is a manualized individual counseling method developed for use in ProjectMATCH (Anonymous, 1997), a large multicenter study of the effect of cus-

23. Group Therapy, Self-Help Groups, and Network Therapy 517tomizing alcoholism treatment to individual needs. It describes a type of therapyin which the goal is to engender patients’ active participation in AA. Itregards such active involvement as the main treatment element promotingsobriety. The study found it to be effective and equal to other treatmentsemployed, namely, MET and CBST (Nowinski, Baker, & Carroll, 1995).Institutional Self-Help Treatment GroupsMost ambulatory programs for substance abuse treatment are modeled afterones used in general psychiatric clinics. They rely primarily on professionallyconducted individual and small-group therapy. Whether there are more costeffectiveoptions or more potent ones has yet to be fully explored. One alternativeapproach to conventional institutional treatment is based on psychologicalinfluence in a self-help group context and is designed to allow for decreasedstaffing. Such an approach to group treatment is designed to draw on the principlesof zealous group psychology observed in freestanding self-help approachesto addictive illness, such as those of AA and the drug-free therapeutic communities,but at the same time serves as the primary group-based modalityemployed in an institutional treatment setting. In other words, it can beemployed in institutional settings, such as hospitals and clinics, and still capturethe psychological effect of freestanding self-help groups.In a study conducted on this treatment model (Galanter, 1982, 1983), primarytherapists were social workers and paraprofessionals experienced in alcoholismtreatment, supervised by attending psychiatrists. One social worker andone paraprofessional treated patients in the experimental self-help treatmentprogram, and two members of each of the latter disciplines treated the controls;the self-help program therefore operated at half the usual staffing level. Theprogram included an alcohol clinic attached to an inpatient detoxification unit.The control and the experimental self-help programs illustrate the contrastbetween institution-based self-help groups and conventional care. In the study(Galanter, 1982, 1983), the programs operated simultaneously and independentlyin the outpatient department. Therapists in each program were encouragedto perfect their respective clinical approaches, and each group of therapistsreceived clinical supervision appropriate to its needs and experience. Differencesbetween the two programs are outlined here to illustrate the operation ofinstitutionally grounded self-help group care.ORIENTATION PROGRAMIn the control (traditional) group setting, two primary therapists served ascoleaders of a group for their own patients, and attendance in each sessionranged between 8 and 15 patients. In the self-help program, the same formatwas used, but groups were led by patients of the primary therapists who hadestablished sobriety and had demonstrated a measure of social stability over sev-

518 V. TREATMENTS FOR ADDICTIONSeral months. These “senior patients” monitored the progress of patients in theorientation group and were supervised by the primary therapists, who attendedthe orientation for part of each session, participating in a limited fashion only.A patient in crisis might be invited to return to the orientation group, if thisinvitation was seen as helpful.GROUP THERAPYWeekly group meetings were oriented toward practical life issues among controls,but insight was encouraged; progress toward abstinence was a majortheme. The two primary therapists served as facilitators for the group, usingtheir own empathic manner to encourage mutual acceptance and support.When confrontation was necessary, the therapists undertook it in a forthrightbut supportive manner. In the self-help program, groups met with the same frequency,but senior patients assumed the leadership role. Primary therapistsattended part of each session and participated intermittently; they served, however,primarily in a coordinating capacity for these groups and supervised thesenior patients. Patients were encouraged to deal with unusual problems byrecourse to their peers in the program, either in their therapy group or throughsenior patients.PEER THERAPYSelf-help program patients were made aware that the primary source of supportin the clinic was the peer group. New patients were encouraged to seek outpeers and senior patients who would be available to assist them through theprogram. Senior patients were supervised in assisting with crises when this assistancewas judged clinically appropriate by the primary therapists. The seniorpatient program was operated in the self-help modality. Potential seniorpatients were screened for sobriety and social stability, and assisted in patientmanagement of the program for a time-limited period. Those who served asgroup leaders met weekly as a group with the primary therapists, focusing ontheir therapeutic functions in the unit. Under supervision of the therapists,they directed orientation, therapy, and activity groups. Their interventions inmore difficult patients’ problems were reviewed with the primary therapists, andthey referred self-help patients to their respective primary therapists for moretroublesome problems. Other senior patients had administrative functions inthe program.Meetings of the full patient complement also took place in the self-helpprogram. A monthly evening meeting open to all patients served as a focus forgroup spirit and as a context for organizing recreational activities. The meetingswere run collaboratively by staff and senior patients, with programwide activitiesand patients’ progress as the focus. Socialization at the time of these meetingsfocused on the status of patients’ recovery.

23. Group Therapy, Self-Help Groups, and Network Therapy 519OUTCOME AND COMMENTSTwo outcome studies (Galanter, 1982, 1983) of this project found that theexperimental program, with half the staffing of the traditional modality, wasquite viable in a municipal hospital alcoholism treatment program. Furthermore,retention of inpatients upon transfer to the alcohol clinic was 38%greater than in the control (non-self-help) program; rates of abstinence in outpatientswere no less, and social adjustment over the course of a 12-monthfollow-up was enhanced. The self-help format appears therefore to offer a formatfor institutional treatment that is less expensive and potentially more effective.The following case example illustrates the ethos of the self-help program:A 36-year-old outpatient came to the clinic intoxicated, without a scheduledvisit, and asked to speak with a senior patient whom he knew well. Hehad been in outpatient treatment for 8 months, and had been abstinent forthe last 4 months. Five days earlier, he had begun drinking subsequent to acrisis in his family and had missed his group meeting. He gave a history offalling down a staircase earlier in the day, bruising his head. The seniorpatient he had asked to see and another senior patient were present, andthey encouraged him to seek a medical evaluation. The case was thenreviewed with the primary therapist, who saw him briefly, wrote a referralfor medical assessment, and returned him to the two senior patients’ care.After an hour, the senior patients prevailed on him to go with one of themto the emergency service. One of them took him on the following afternoonto a meeting of an AA group he had previously attended. Thepatient was able to maintain abstinence until his next weekly group therapymeeting, at which time a group member offered to get together withhim during the ensuing week to provide him with some encouragement.Given a need for increased substance abuse treatment services, it is importantto note that counseling staff members (social workers and counselors)comprise 66% of the staffs in all federally assisted alcoholism treatment facilities,which constitute the bulk of publicly supported programs (Vischi, Jones,Shank, & Lima, 1980). The question then arises as to whether these counselingstaffers are used in the most cost-effective way. One problematic aspect of thisissue is illustrated by the finding of Paredes and Gregory (1979) that in alcoholismtreatment programs, the economic resources invested in alcoholism treatmentare not positively correlated with outcome. They concluded that the typeand quantity of therapeutic resources invested are related to the characteristicsof the agencies themselves rather than to a treatment strategy conceived foroptimal cost-effectiveness.Two issues common to most small-group therapies for substance abuse inthe clinic setting are relevant here. In the first place, whether behavioral,

520 V. TREATMENTS FOR ADDICTIONSinsight-oriented, or directive, they all focus on the concerns of a relativelysmall number of patients involved in the therapy group (typically 6 to 10), tothe exclusion of other program participants. Second, it is generally agreed thatsuch small-group therapy for alcoholics offers a better outcome when conductedin the context of a multimodal program. Such a program may integrate treatmentcomponents to implement a carefully structured plan, as described byHunt and Azrin (1973).These two aspects of small-group therapy may be considered in relation toa self-help–oriented treatment program such as the one described previously.With regard to group size, such a program introduces the option of the patients’strong identification with and sense of cohesion in a treatment network ofmany more than 6 to 10 patients. In fact, it encourages affiliative feelingsamong the full complement of self-help patients, providing an experience of alarge, zealous group (Galanter, 1989). This cohesion is promoted by therapeuticcontact with a number of senior patients who are involved in the therapygroups; by programwide patient-run activities, such as the orientation groupsopen to patients in crisis; and in monthly large-group meetings, also open to allpatients. This broader identification forms the bulwark of a self-help orientation.Self-Help Groups and the ClinicianThe relationship between professional treatment and membership in a 12-stepgroup has been less than systematically addressed. Clark (1987) proposed guidelinesto orient the clinician. Clearly, acquaintance with 12-step programs isessential for the clinician to orient patients regarding their needs and torespond to possible conflicts between the nature and goals of professional careand the demands of participation in self-help organizations. Clinicians treatingaddicts can learn about 12-step programs by attending local meetings, bybecoming familiar with the fellowship’s literature, and by exploring theirpatients’ experiences in the context of their membership in these organizations.One point deserving emphasis is that physicians should be aware of the dangerof prescribing habit-forming substances to addicts because of not only theinherent dangers involved in the use of these substances but also the goals of programsthat demand complete avoidance of chemical solutions for life’s problems(Zweben, 1987). When psychotropic medication is strongly recommended, thebenefits and risks involved in their use should be carefully discussed with thepatient in the context of the goals of 12-step programs. An occasional sponsormay be opposed to any medication, even when a patient clearly needs pharmacologicaltreatment to alleviate disabling behavioral or physical conditions. In thissituation, the clinician has to address the nature of the conflict involved in thetreatment by making the needed medical treatment compatible with the programphilosophy. This desirable goal can only be achieved when the clinician is wellinformed about the nature of 12-step programs and can help the patient to inte-

23. Group Therapy, Self-Help Groups, and Network Therapy 521grate the rationale for medical treatment with the general goals of his or hermembership in the self-help program. Avoidance of prescribing drugs with habitformingpotential, willingness to educate patients about the nature of their problems,and a positive attitude toward 12-step organizations make it easier for cliniciansto integrate their interventions with the orientation of the fellowship.Candidates for controlled drinking should not be encouraged to participate inabstinence-oriented programs, because the incompatibility of the goals of professionaltreatment with a 12-step orientation may prove to be very detrimental totherapy (Emrick, 1987).Clinicians should, in general, encourage their patients to get exposed to12-step programs, but they should remember that a large number of addicts whonever participate in these organizations can make good use of professional treatmentand successfully recover. Because the composition of the membership ofself-help groups continually changes, it is possible for patients treated withpsychotropic medication, including methadone, to benefit from participationin these groups (Obuchowsky & Zweben, 1987).OverviewTHE NETWORK THERAPY TECHNIQUEThis approach can be useful in addressing a broad range of addicted patientscharacterized by the following clinical hallmarks of addictive illness: First,when they initiate consumption of their addictive agent, be it alcohol, cocaine,opiates, or depressant drugs, they frequently cannot limit that consumption to areasonable and predictable level; this phenomenon has been termed “loss ofcontrol” by clinicians who treat alcohol- or drug-dependent persons (Jellinek,1963). Second, they consistently demonstrate relapse to the agent of abuse,that is, they attempted to stop using the drug for varying periods of time butreturned to it, despite a specific intent to avoid it.This treatment approach is not necessary for those abusers who can, infact, learn to set limits on their use of alcohol or drugs; their abuse may betreated as a behavioral symptom in a more traditional psychotherapeutic fashion.Nor is it directed at those patients for whom the addictive pattern is mostunmanageable (e.g., addicted people with unusual destabilizing circumstancessuch as homelessness, severe character pathology, or psychosis). These patientsmay need special supportive care (e.g., inpatient detoxification or long-termresidential treatment).Key Elements of Network TherapyThree elements are essential to the network therapy technique. The first is acognitive-behavioral approach to relapse prevention, independently reportedto be valuable in addiction treatment (Marlatt & Gordon, 1985). Emphasis in

522 V. TREATMENTS FOR ADDICTIONSthis approach is placed on triggers to relapse and behavioral techniques foravoiding them, rather than on exploring underlying psychodynamic issues.Second, support of the patient’s natural social network is engaged in treatment.Peer support in AA has long been shown to be an effective vehicle forpromoting abstinence, and the idea of the therapist’s intervening with familyand friends in starting treatment was employed in one of the early ambulatorytechniques specific to addiction (Johnson, 1986). The involvement of spouses(McCrady, Stout, Noel, Abrams, & Fisher-Nelson, 1991) has since been shownto be effective in enhancing the outcome of professional therapy.Third, the orchestration of resources to provide community reinforcementsuggests a more robust treatment intervention by providing a support for drugfreerehabilitation (Azrin, Sisson, & Meyers, 1982). In this relation, Khantzian(1988) points to the “primary care therapist” as one who functions in directcoordinating and monitoring roles in order to combine psychotherapeutic andself-help elements. It is this overall management role over circumstances outside,as well as inside, the office session that is presented to trainees to maximizethe effectiveness of the intervention.Starting a NetworkPatients should be asked to bring their spouse or a close friend to the first session.Alcoholic patients often dislike certain things they hear when they first come fortreatment and may deny or rationalize, even if they voluntarily sought help.Because of their denial, a significant other is essential to both history taking andimplementing a viable treatment plan. A close relative or spouse can often cutthrough the denial in a way that an unfamiliar therapist cannot, and can thereforebe invaluable in setting a standard of realism in dealing with the addiction.Once the patient comes for an appointment, establishing a network is atask undertaken with active collaboration of patient and therapist. The two,aided by those parties who join the network initially, must search for the rightbalance of members. The therapist must carefully promote the choice of appropriatenetwork members, however, just as the platoon leader selects those whowill go into combat.Defining the Network’s TaskAs conceived here, the therapist’s relationship to the network is like that of atask-oriented team leader rather than that of a family therapist oriented towardinsight. The network is established to implement a straightforward task: aidingthe therapist in sustaining the patient’s abstinence. It must be directed with thesame clarity of purpose that a task force is directed in any effective organization.Competing and alternative goals must be suppressed or at least prevented frominterfering with the primary task.

23. Group Therapy, Self-Help Groups, and Network Therapy 523Unlike family members involved in traditional family therapy, networkmembers are not led to expect symptom relief for themselves or self-realization.This lack of expectation prevents the development of competing goals for thenetwork’s meetings. It also provides the members protection from having theirown motives scrutinized, and thereby supports their continuing involvement,without the threat of an assault on their psychological defenses.Adapting Individual Therapy to the Network TreatmentOf primary importance is the need to address exposure to substances of abuseor to cues that might precipitate alcohol or drug use (Galanter, 1993). First,both patient and therapist should be sensitive to this matter and explorethese situations as they arise. Second, a stable social context in an appropriatesocial environment—one conducive to abstinence with minimal disruptionof life circumstances—should be supported. Considerations of minor disruptionsin place of residence, friends, or job need not be a primary issue forthe patient with character disorder or neurosis, but they cannot go untendedhere. For a considerable period, the substance abuser is highly vulnerable toexacerbations of the addictive illness and in some respects must be viewedwith the considerable caution with which one treats the recently compensatedpsychotic.Study on Training Naive TherapistsA course of training for psychiatric residents naive to addiction and ambulatorytreatments was undertaken over a period of 2 academic years. Before beginningtreatment, the residents were given a structured treatment manual for networktherapy and participated in a 13-session seminar on application of the networktherapy technique. Cocaine-abusing patients were eligible for treatment in thisstudy, if they could come for evaluation with a friend or family member whocould participate in their treatment. In all, 22 patients were enrolled. The treatingpsychiatric residents were able to establish requisite networks for 20 of thesepatients (i.e., a network with at least one member). The networks had an averageof 2.3 members, and the most typical configuration included family membersand friends. Supervisors’ evaluation of videotapes of the network sessionsemploying standardized instruments indicated good adherence to themanualized treatment, with effective use of network therapy techniques. Theoutcome of treatment (Galanter, Dermatis, Keller, & Trujillo, 2002; Galanter,Keller, & Dermatis, 1997; Keller, Galanter, & Weinberg, 1997) reflected retentionand abstinence rates as good as, or better than, comparable ambulatorycare carried out by therapists experienced in addiction treatment. The studydemonstrated the feasibility of teaching the network technique to therapistsnaive to addiction treatment.

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CHAPTER 24Family-Based TreatmentStages and OutcomesM. DUNCAN STANTONANTHONY W. HEATHThe importance of the family in the genesis, maintenance, and alleviation ofsubstance abuse has been well established. Although it is widely acknowledgedthat genetic and/or other biological components are important in the etiologyof many alcohol and drug abuse cases, addiction generally develops within afamily context, frequently reflects other family difficulties, and is usually maintainedand exacerbated by family interaction. Other factors can also be critical(e.g., environmental, economic, cultural), but family variables hold a positionof salience in addiction.Not surprisingly, treatment focused on changing family dynamics has afirm footing in the substance abuse treatment field. Family-based therapy iscommonly part of most successful substance abuse treatment programs and isusually considered an essential element in relapse prevention. As Craig (1993)has noted in an overview of the field, “The need to address family issues in acomprehensive treatment program is now widely recognized in drug abuse treatment”(p. 185). More specifically, a national survey by Fals-Stewart andBirchler (2001) of 398 randomly selected adult outpatient alcohol and/or drugtreatment programs found that 82% offered family- or couples-based counseling.Regarding younger patients, a review of treatments for adolescent substanceabusers by Williams and Chang (2000) concluded that “outpatient familytherapy appears superior to other forms of outpatient treatment” (p. 138),and that it should be a component of any treatment program for such youth. It528

24. Family-Based Treatment 529is therefore no accident that, of 10 adolescent substance abuse treatment programsidentified as exemplary models by the U.S. Department of Health andHuman Services (three of which were modified therapeutic communities), allinclude family members, particularly parents: seven apply family therapy, twoincorporate multifamily therapy, and one has groups for parents (Stevens &Morral, 2003).Over two dozen books have been written about family therapy for adultand/or adolescent substance abusers. These books, plus hundreds of chapters,journal articles, and papers, have described many different modalities of familytherapy, including couple therapy, parents’ group therapy, concurrent parentand index patient therapy, therapy with individual families (both inpatient andoutpatient), sibling-oriented therapy, multifamily therapy, social network therapy,and family therapy with one person. However, rather than reviewing thisvast literature, the intent in the present chapter is, first, to set forth some of thefundamental methods, or principles, of family/couples assessment and treatmentwith substance abusers and their families, and, second, to summarize thedocumented effectiveness of family- and couples-based therapies for this patientpopulation. Readers interested in further pursuit of this subject matter arereferred to overviews by O’Farrell and Fals-Stewart (2002, 2003) and Rowe andLiddle (2003), plus other literature cited later, for a more detailed understandingof the full range of theoretical and clinical approaches within the overallfamily/couples therapy approach to substance abuse. In addition, a brief synopsisof family systems concepts and theory is given in Stanton (1985), while aclinically oriented presentation of the foundations and key elements in familytherapy, per se, may be found in Hanna and Brown (1999).FAMILY PATTERNS OF ADDICTIONAddicted people are commonly in close contact with their families of origin orthe people who raised them (Bekir, McLellan, Childress, & Gariti, 1993; Cervantes,Sorenson, Wermuth, Fernandez, & Menicucci, 1988; Douglas, 1987/1988; Stanton, 1982). Either they live with one or both parents (at five timesthe national rates for same-age adults) or are in touch on a daily or weekly basis.This pattern extends to adult alcoholics (Stanton & Heath, 2004). Overall, 30of 32 reports, across seven countries, attest to such living arrangements or regularityof contact (Stanton, 2004; Stanton & Heath, 2004). These data indicatethat addicted people’s families are important to them, and that they are importantto their families.Stanton, Todd, and Associates (1982) summarized a number of other characteristicsthat distinguish drug-abusing families from other seriously dysfunctionalfamilies. The distinguishing qualities include the following:

530 V. TREATMENTS FOR ADDICTIONS1. A higher frequency of multigenerational chemical dependency, particularlyalcohol, plus a propensity for other addictive behaviors, such asgambling. Such practices model behavior for children and can developinto family “traditions.”2. More primitive and direct expressions of conflict in addictive families.3. More overt alliances (e.g., between addict and overinvolved parent).4. “Conspicuously unschizophrenic” parental behavior.5. A drug-oriented peer group to which the addict retreats following familyconflict, thus gaining an illusion of independence.6. “Symbiotic” child-rearing practices on the part of addicts’ mothers,lasting longer into the addicts’ adulthood.7. A preponderance of death themes and premature, unexpected, anduntimely deaths in the addict’s family.8. “Pseudoindividuation” of the addict across several levels, from the individualpharmacological level to that of the drug subculture.9. More frequent acculturation problems and parent–child cultural disparitywithin families of addicts.This list should be considered no more than a sketch of the addictive family.Readers are referred to Stanton, Todd, and colleagues (1982) for referencesto the original studies on which the outline is based, plus an update by Lawsonand Lawson (2004). For thorough summaries of family dynamics in alcoholism,see Steinglass, Bennett, Wolin, and Reiss (1987), as well as Lawson and Lawson(1998).INDICATIONS FOR THE USE OF FAMILY THERAPYIN ADDICTIONFamilies suffer when one or more members abuse drugs and/or alcohol. Parentsworry about whether their abusing children will come home alive. They rage attheir lack of control, suffer the guilt of the damned, and grasp at any suggestionof hope. Spouses shamefully hide advancing drinking/drugging problems fromtheir neighbors and employers, struggle to maintain their illusions that drinking/druggingis temporary, and wonder what they have done wrong. Children ofalcoholics/addicts also wonder what they did wrong and assume the burdens ofmaturity at startlingly young ages. They beg their parents to come home withoutstopping at the tavern or meeting the dealer. Grown children of alcoholics/addicts are haunted by their pasts, despairing in relationships that inflict substantialpain. Substance abuse affects every member of the family for decadesand for generations.Family therapy offers family members an opportunity to resolve the problemsthat plague them. Family therapists believe that family treatment is indi-

24. Family-Based Treatment 531cated when any man, woman, or child has a complaint concerning alcohol ordrug abuse, whether the individual is the abuser or the “abused.” Because theyfiguratively cast such a large net, family therapists encounter and serve manyclients who initiate therapy for other reasons but later present concerns aboutsubstance abuse in their families. These concerns include issues of abuse, addiction,and recovery for adult and adolescent substance abusers, as well as correspondingissues for “codependents,” children of alcoholics, and adult childrenof alcoholics for several generations (Elkin, 1984; Treadway, 1989).Substance abusers themselves rarely seek the services of therapists. In fact,the most characteristic feature of substance abuse may be the abuser’s denialthat the use of the substance is a problem at all. Similarly, it is almost universallyaccepted that family members often overlook substance abuse; some familiesunintentionally encourage it. Recognizing this fact, family therapists offertheir services to anyone who wants to discuss substance abuse and often inquireabout the individual’s use of alcohol and drugs. As in Al-Anon and related selfhelpprograms, family therapists generally believe that every family member canbe helped to “recover” from the abuse, whether the substance abuser stopsdrinking/drugging or not.Family therapy begins when a family member, a therapist, a treatment program,or a social institution, such as a court, initially identifies the problem.Family treatment is indicated (a) when the family is mustering its forces to convincethe abuser of the extent of the problem and the need for change, (b) duringresidential treatment for the substance abuse (when it is used), and (c) duringrecovery, when the family learns new ways to go on in life withoutchemicals. We offer guidelines for each of these stages of treatment later in thischapter.An absence of family-oriented services in substance abuse treatment canhave calamitous consequences. Without concurrent treatment for nonabusingmembers, families have been known to attempt sabotage of treatment effortswhen those efforts begin to succeed (Brown & Lewis, 1999; Stanton, Todd, etal., 1982). Examples of sabotage are commonly cited in the literature. Theexamples range from the spouse who gives a holiday bottle of liquor to a recoveringalcoholic, to the parents who refuse to work together in maintaining rulesfor their substance-abusing adolescent. On the other hand, Steinglass and colleagues(1987) asserted, at least regarding alcohol treatment, that the evidenceis compelling that “involvement of a nonalcoholic spouse in a treatment programsignificantly improves the likelihood that the alcoholic individual willparticipate in treatment as well” (pp. 331–332).Problems also occur after residential treatment, if families are left out ofthe treatment process. Sobriety for an individual often has difficult consequencesfor other family members, who may gain sudden awareness of their ownproblems or of other family problems. Divorce is not uncommon when adultsubstance abusers “dry out” or “clean up” (Stanton, 1985). The family is crucial

532 V. TREATMENTS FOR ADDICTIONSin determining whether or not someone remains addicted, and the social contextof the abuser must be changed for treatment to “take hold.”Families can prove to be a highly positive influence in recovery as well.Eldred and Washington (1976) found that heroin addicts rated their families oforigin or their in-laws as most likely to be helpful to them in their attempts togive up drugs; the addicts’ second choice was their partner. Similarly, Levy(1972) found, in a 5-year follow-up of narcotics addicts, that patients who successfullyovercame drug abuse most often had family support, while Simpsonand Sells (1990) got 75% crediting family as a major reason for their enteringtreatment. In short, family therapists enlist the inherent leverage of familymembers.Like other treatment professionals who have worked with substanceabusingfamilies, family therapists know the difficulty involved in treating substanceabuse. Only by working together with extended families, specialists in thefield of chemical dependence, physicians monitoring pharmacotherapy, andself-help programs, can substance abuse and its related problems be ameliorated.Finally, professionals must talk to each other, if therapy is to succeed. Forexample, outpatient family therapists must visit local treatment centers and getto know the treatment teams. This investment facilitates referrals to residentialtreatment and subsequent referral for continued therapy upon release.STAGES OF FAMILY THERAPYOur purpose here is to present a model of the stages of family therapy thatsynthesizes much of the literature on family/couple therapy with (1) alcoholicadults (e.g., Berenson, 1976a, 1986, 1992; Davis, 1987; O’Farrell, 1993;O’Farrell & Fals-Stewart, 2000, 2001, 2002; Steinglass et al., 1987), (2) drugabusingadults (e.g., Fals-Stewart, O’Farrell, Birchler, Cordova, & Kelley, 2005;Kosten, Jalali, & Kleber, 1982–1983; Stanton & Todd, 1992; Stanton, Todd, etal., 1982), and (3) substance-abusing adolescents (e.g., Alexander & Parsons,1982; Fishman, Stanton, & Rosman, 1982; Henggeler & Borduin, 1990; Landau& Garrett, 1998; Liddle & Hogue, 2001; Piercy & Frankel, 1989; Stanton& Landau-Stanton, 1990; Szapocznik & Kurtines, 1989; Todd & Selekman,1991; Waldron, Slesnick, Brody, Turner, & Peterson, 2001). One reason wecan do this is because there is already a relatively high degree of consensusamong many of these authors. Although detailed descriptions of the techniquesof family therapy are, again, beyond the scope of this chapter, the literaturecited herein comprises a veritable treasure chest of useful family therapy methods.This presentation will, however, additionally incorporate a more recent,integrative model, developed in great part from working with substance abusers,

24. Family-Based Treatment 533called transitional family therapy, or TFT (Horwitz, 1997; Landau & Stanton,2000; Landau-Stanton, Clements, & Stanton, 1993; Landau-Stanton, Griffiths,& Mason, 1982; Seaburn, Landau-Stanton, & Horwitz, 1995; Stanton, 1981a,1984; Watson & McDaniel, 1998). Based both on structural-strategic (Stanton,1981a; Stanton & Todd, 1992) and intergenerational (e.g., Guerin & Pendagast,1976) methods, it integrates (1) the management of the substance abuse problem,(2) the larger psychosocial environment (ecosystem and network)—inline with Henggeler and Borduin (1990), Liddle and Hogue (2001), and Speckand Attneave (1973; Speck, 2003)—and (3) exploration and interventionspertaining to how the problem originated in the family’s history. TFT’s“geodynamic balance” theory of change (Stanton, 1984) posits that all therapeuticinterventions can be subsumed within a complementary dichotomy of“compression” and “diversion” techniques. Compression (e.g., strategic, paradoxical)methods push a family interaction sequence further in the way it normallyunfolds, that is, exaggerating it so as to get a counteraction—and thus anew sequence—among family members. Diversion (e.g., structural, behavioral)methods introduce competing behaviors that block the family’s typical sequenceand induce it to experience, and then to practice, a different and morefunctional pattern.Stage 1: Problem Definition and ContractingThe first stage of family therapy begins when someone contacts a therapist andrequests help from the full range of service settings and treatment providers.Family therapists also work in therapeutic communities, where families oncewere excluded. By making family therapy available, such therapeutic communitiesbring the “real world” into the center and help each family prepare for itsreunion.The therapist’s first step is to convene enough of the family to gain adequateleverage to initiate change in family interaction regarding the substanceabuse. As previously discussed, this may involve 1, 2, or 30 family members, andmay include other members of the substance abuser’s community. Family therapistsgenerally start by working with the most motivated family member ormembers, convening other family members as necessary (Berenson, cited inStanton, 1981b).Next, family therapists attempt to understand and define the problem.When substance abuse is suspected, many therapists ask simple questions, suchas “Who drinks?” or “What medications are used in your family?” We ironicallyrefer to these as loaded questions and ask them of all our clients.To assess the degree of substance abuse, particularly with adult clients,Davis (1987) suggests the use of a standardized questionnaire, such as the MichiganAlcoholism Screening Test (Selzer, 1971). History of the abuse, degree ofphysiological addiction, organic consequences of long-term addiction, prior

534 V. TREATMENTS FOR ADDICTIONStreatment contacts, family perception of the abuse and its consequences,codependence, and coping behaviors are also topics that deserve careful assessmentby qualified practitioners (Steinglass et al., 1987). If the therapist is notmedically trained, clients are commonly referred to a physician for diagnosisand medical treatment when substance abuse has been chronic and/or whenthere is any indication of organic impairment due to substance abuse or disease.Family therapists often suggest that another family member accompany the substanceabuser to the physician, to offer support and to inform the physician ofthe history of the abuse. Efforts must be made to get the consent of the patientto involve and to communicate with family to satisfy Federal and other privacystatutes and regulations.The therapist can use the information gathered during the assessment toconclude and to state with confidence that—by some objective standards—thefamily has a serious drug or alcohol problem. Such confidence is necessary toovercome denial that a substance abuse problem exists, a common reaction insuch families (Bepko & Krestan, 1985).Once the problem is defined, the therapist and family identify and prioritizetheir goals for treatment, starting with the primary goal of helping the substanceabuser become “clean and sober,” and directly relating each subsequentgoal to this primary one. When families bring up additional issues, the therapistmay ask family members to justify them as relevant to the main goal of sobriety(Stanton & Todd, 1992). Considered together, these goals form the basis fordetermining whether an acceptable treatment contract can be agreed on withthe family (Steinglass et al., 1987).If the decision is made to work with an adult couple, the behavioral coupletherapy approach works toward implementing, within the first two sessions, adaily Sobriety Contract (O’Farrell, 1993; O’Farrell & Fals-Stewart, 2000,2002)—a method that has accreted empirical support in 11 of 12 studies whereit was examined (O’Farrell & Fals-Stewart, 2003). When applicable, the contractmay also incorporate daily Antabuse (disulfiram) ingestion. The procedure,applied on a day-to-day basis, involves the substance-abusing patient’sagreeing not to use alcohol or drugs during that day (in line with the “one dayat a time” tradition), while the spouse/partner expresses support for thepatient’s efforts to stay abstinent. The spouse/partner then records the patient’sperformance on a daily calendar. The partners also agree to reserve for therapysessions, and not to discuss at home, either past substance abuse or fears aboutfuture alcohol/drug abuse, since such conflictual conversations can precipitaterelapse. At each therapy session the couple both reviews the contract calendarwith the therapist, and actually practices the behaviors included in the contract.In other words, they engage in what Minuchin and Fishman (1981) termed“enactment” of the new interactional pattern, thus expanding both their repertoireand their options as to how they deal with one another.

24. Family-Based Treatment 535From the beginning, family therapists work to establish alliances with thesenior sober family members. If the abuser is an adolescent or young adult, thetherapist tries to engage both parents in these alliances whenever possible. Parentsare kept working together and are steered away from discussing their maritaldifficulties, which could divide them and deter them from the primary objectiveof therapy (Stanton & Todd, 1992). This alliance forms the basis for establishingappropriate parental influence in families with substance-abusing adolescents(Alexander & Parsons, 1982; Fishman et al., 1982; Henggeler & Borduin,1990; Landau & Garrett, 1998; Liddle & Hogue, 2001; Piercy & Frankel, 1989;Stanton & Landau-Stanton, 1990; Szapocznik & Kurtines, 1989; Todd &Selekman, 1991).Family therapists’ alliances with sober family members and parents of substanceabusers help them motivate their clients. Family members are the mosteffective motivators known. Even the most evangelistic therapist cannot do aswell. Thus, by forming alliances and encouraging sober family members to stepup the pressure, family therapists help motivate substance abusers to pursue andmaintain sobriety. Similarly, other professional helpers (e.g., school counselors,teachers, police officers, and probation officers) can be enlisted to exert benevolentinfluence. Here, the family therapist serves as coach, promoting the effectiveuse of every reasonable threat, promise, and consequence to encourageabstinence. Later, therapists encourage families to serve as recovering addicts’sponsors to help prevent relapse. For an interesting example of the motivatinginfluence of a family member, we recommend Heard’s (1982) rich descriptionof how a deathbed wish of a deceased grandfather was used to promote recoveryin a 23-year-old heroin addict.Family therapists consider it extremely important during this stage toassume a nonblaming stance (Alexander, Waldron, Barton, & Mas, 1989;Stanton & Todd, 1992) toward the entire family. We find that the confrontingtechniques used in group therapy with substance abusers tend to fan the fires ofresistance and to inspire counterattack. Challenges can still be offered to families,but they must be expressed in nonpejorative ways. Many family therapistsuse positive interpretation when they comment on family members’ behavior.Stanton and Todd (1992) have referred to this as “ascribing noble intentions”or “noble ascriptions” (see also, Stanton, Todd, et al., 1982). Examples includestatements such as “He’s defending the family like any good son would” and“You’re trying your best to be a good mother.” Such statements tune into boththe caring and frustration that most family members experience, and seem tolessen client resistance and promote compliance.Steinglass and colleagues (1987) emphasized that it is essential to label thesubstance abuse as a family problem and to convince the family members thatthey are all essential players in the recovery process. Writing about alcoholism,these authors stated that whenever alcoholism is identified as a problem, the

536 V. TREATMENTS FOR ADDICTIONStherapist must, in the same session, “get across to the family that there is noissue more important at this stage of the work than the cessation of drinking,and that the family and the therapist must mobilize all resources toward thatgoal and that goal alone” (p. 354). Family therapists characteristically invitefamily members to become part of the solution to problems.A powerful, ecosystemic expansion of the above notion is to apply themethods of psychiatrist Ross V. Speck (2003; Speck & Attneave, 1973) andinvolve the family’s social network in the treatment endeavor. This can includeextended family, friends, work associates, and, commonly, other professionalsinvolved with the case. Callan, Garrison, and Zerger (1975) described such anapproach with adults who are addicted to drugs, while van der Velden, Ruhf,and Kaminsky (1991) have applied it with adolescents who abuse substances. Itis also regularly used in TFT (Landau & Garrett, 1998; Landau & Stanton,2000; Seaburn et al., 1995; Stanton & Landau-Stanton, 1990), in which amajor thrust of the first session or two is to attain consensus across the networkon what the primary goals of treatment are, and how change in each can beobjectively defined. Thus all members are working in accord, and (often unintentional)competing agendas among subsystems are minimized: Everybodyagrees both on what needs to be done and on how to know when that hasoccurred.By the second session, TFT also begins to build three graphic constructionswith the family, all of them printed with a marker on a large newsprint flipchart mounted on an easel. These are: (1) a list of the goals of treatment; (2) alist of the tasks to be performed toward meeting those goals, including who is todo them and, if applicable, by when; and (3) a three-generational genogram(Guerin & Pendagast, 1976; McGoldrick, Gerson, & Shellenberger, 1999) thatincludes all members, living and deceased. These graphics are brought to eachsession and hung on the walls (e.g., with masking tape) so as to be readily availablefor reference. Such techniques help to clarify, make more concrete, andprovide perspective on the problem(s)—both as to how they developed and theways the family has devised to contend with them.The therapist should also be aggregating information for a fourth graphic,the family “time line” (Stanton, 1992). This method clearly spreads out facts asto, for instance, when the substance abuse problem, and the latest relapse,began and what changes (e.g., illnesses, unemployment, relocation, immigration),losses (e.g., deaths, divorces, breakups of relationships), or other familystressors were occurring around those times. However, it may be too early atthis stage in therapy to construct the time line publicly with the family. Therefore,the technique is discussed at greater length below.Many families—in attempting to answer the question, “Why did this happento me?”—accept that genetics and/or a disease process is responsible forsubstance abuse, particularly when the problem is alcoholism (see below). Atbest, these theoretical explanations can reduce guilt, blame, and shame in fami-

24. Family-Based Treatment 537lies, facilitate participation in therapy, and promote recovery. Genetic or diseaseexplanations are almost always more useful than moralistic explanations.At worst, though, these explanations (1) provoke fear and enable discouraged,wallowing inaction and irresponsible behavior in the family; and (2) engenderinaction in a therapist who can only envision a medical pathway for change.Incidentally, it is wise for family therapists not to allow themselves or theirclients to become discouraged by the disease explanation of the cause of drugand alcohol addiction. They cannot afford to wait for a pill or a tissue implantto cure the disease. Instead, they help families to understand that by workingtogether, they can overcome the disease’s symptoms, reverse the ostensible destiny,and lead happy, chemical-free lives.Of course, there are—and probably always will be—people who rejectgenetic and disease explanations for addiction. Regarding the former, they maybe at least partly justified, since the majority of people who develop drinking ordrug problems do not demonstrate a genetic predisposition. Only 15–36% ofchildren of alcoholics develop drinking problems (Stabenau, 1988). A highproportion of the people who become problem drinkers—including at least halfof those who are actually hospitalized for alcoholism—have no obvious geneticloading (Goodwin & Warnock, 1991; Searles, 1991). Furthermore, most of thegenetic effects that have been identified for alcoholism in males tend to besomewhat weaker, or less clear, both for females and for other substances ofabuse (Anthenelli & Schuckit, 1997; Cadoret, Yates, Troughton, Woodworth,& Stewart, 1995; van den Bree, Svikis, & Pickens, 1998). But in any case, peoplewho do develop addiction problems can learn to live responsibly and avoidblame and shame. They can work together with their loved ones to overcometheir problems.Stage 2: Establishing the Context for a Chemical-Free LifeWhen substance abuse is identified as a problem, and a therapeutic contract isnegotiated, family therapy enters a second stage in which a context for sobrietyis established. Berenson (1976b) stated that this stage involves “management ofan ongoing, serious drinking problem and setting up a context so that the alcoholicwill stop drinking” (p. 33).Family therapists generally accept cessation of substance abuse as a prerequisitefor further treatment (e.g., Bepko & Krestan, 1985). Furthermore, manybelieve that therapists must consistently demonstrate conviction of the importanceof abstinence over the course of therapy (e.g., Davis, 1987). In the wordsof Steinglass and colleagues (1987):Meaningful therapy with an Alcoholic Family cannot proceed if the therapistadopts a laissez-faire attitude about drinking behavior and acquiesces in a decisionto allow the identified alcoholic to continue drinking. The therapist must take a

538 V. TREATMENTS FOR ADDICTIONSfirm stand on this issue at the start of therapy, while at the same time acknowledgingthat it may not be an easy task and that there may be a number of slips beforeabstinence is achieved. (p. 343)On the other hand, Berenson, whose innovative work was described byStanton (1981a), believes that therapists should concern themselves withachieving substantial changes in drunken behavior instead of abstinence fromdrinking. Berenson considers it tactically unwise to take a resolute stand infavor of total abstinence, even though abstinence is usually the ultimate goal.This position on abstinence runs counter to the beliefs of several others, includingDavis (1987) and Bepko and Krestan (1985). It is consistent, however, withthe problem-solving models that have been applied to drug problems by Haley(1997), Stanton and Todd (1992), and others (e.g., Heath & Ayers, 1991),who often prefer to leave the decision about the importance of total abstinenceto parents or others. These authors believe that therapists who assume a lessadamant, less certain position on the necessity of abstinence enjoy moremaneuverability in therapy. For example, a therapist who states that he or she isnot sure whether abstinence will prove necessary may be able to stay out of acouple’s argument over the issue long enough to help them try out several newsolutions to the problems brought on by the substance abuse (e.g., Berg &Miller, 1992).Independent of the issue of abstinence, Berenson believes that the therapistmust exert a major effort to get the family system calmed down, ergo reducingthe emotionality and increasing the psychological distance between familymembers. Families at this stage of therapy are often overwrought and involvedin intense battles and patterns of over- and underresponsibility that lock memberstogether. (See Bepko & Krestan, 1985, for a thorough discussion of thetherapeutic process of assessing and interrupting overresponsible and underresponsiblebehaviors.)On another tack, behavioral couple therapy for substance abuse is directedtoward increasing positive behaviors as a means for countering the kind ofnegativity—particularly surrounding drinking or drug-taking—which usuallycreeps into, and may even predominate, the partners’ relationship. Early on intherapy each partner is encouraged to acknowledge pleasing behaviors in theother, such as through homework assignments to, each day, “catch your partnerdoing something nice” and record it on a special sheet provided by the therapist(O’Farrell, 1993; O’Farrell & Fals-Stewart, 2000, 2002). This exercise is eventuallyguided toward the implementation of “love days” (Weiss, Hops, &Patterson, 1973) or “caring days” (Stuart, 1980), in which each person plansahead to surprise their partner during the week “with a day when they do somespecial things to show their caring” (O’Farrell & Fals-Stewart, 2000, p. 52). Asexamples, Paolino and McCrady (1977) note the set of special behaviors“might include such minor actions as saying hello when the husband comes

24. Family-Based Treatment 539home at night, clearing the table, rinsing out a glass after having a drink of milkrather than leaving the glass on the counter, asking how the other’s day was,giving a back rub, and so on” (p. 161). These various pleasure-inducing actionshelp to increase “the overall rewardingness of the relationship, which wouldenable the couple to more willingly work on problematic aspects of the relationship,while making the overall relationship more fun” (p. 161). In a sense,the newer, positive experiences compete with and crowd out the older, “nastier”ones.Regarding self-help groups, family therapists often refer family members toAl-Anon, Nar-Anon, Alateen, Alatot, and related programs at this stage,encouraging clients to shop around until they find groups that are “sociallycompatible and geographically accessible” (Davis, 1987, p. 56). According toBepko and Krestan (1985), the goal of this involvement is to help the familymembers “shift their role behavior significantly both in the interest of theirgreatest well-being and with the expectation that a change in their part of thefamily interaction will eventually lead to the drinker’s sobriety” (p. 104). Davis(1987) suggests that therapists must consistently assign visits to self-helpgroups, because participation in groups enhances family therapy in severalways. Participation in self-help groups encourages detachment from substanceabusingbehavior, provides validating experiences and 24-hour crisis supportthrough sponsors, and emphasizes personal responsibility (Davis, 1987).Many family therapists supplement the work of self-help groups by helpingthe spouses of substance abusers to achieve a greater degree of emotionaldetachment. Berenson begins by getting spouses of alcoholics into supportgroups, usually Al-Anon or other spouses’ groups (Stanton, 1981b). Next, heprepares spouses for the impending period of pain and depression, perhaps evennoting that they may have suicidal thoughts as a part of “hitting bottom.”Finally, Berenson helps spouses gain distance from their alcoholic partners,often by suggesting brief separations (e.g., a week away from home) in order topromote differentiation. Berenson warns spouses that their alcoholic partnersmay try to get them back by intensifying the symptom, usually by increaseddrinking.At this point Berenson may involve the alcoholics more in therapy, empathizingwith how isolated and alone they may feel. Concomitantly, he helpsspouses stick to the plan, so that the drunks have a chance to get sober. He tellsspouses that they should not expect the alcoholic to improve but suggests thatwhen they realize that the alcoholics cannot be controlled, the alcoholics maybe able to make a change for the better. Berenson does not support hostilemoves against the alcoholic but only supports moves the spouses make forthemselves.Berenson has suggested several helpful rules for therapists working throughthis stage of family therapy (Stanton, 1981b). First, therapists must have noexpectations that change will occur; rather than “hoping,” they must be “hope-

540 V. TREATMENTS FOR ADDICTIONSless.” Second, therapists should want family members to feel both helpless andhopeless—that is, to “hit bottom,” if they have not done so already. Third,therapists must not look for a single strategic intervention to reverse the multitudeof problems in these families but should work patiently in a simple,straightforward manner.It is also during this stage that the TFT therapist considers publicly constructinga time line with the family (Stanton, 1992). By now, enough informationabout both the nuclear and the extended family should have been collectedto provide a clear picture of how family life events have contributed tothe onset of the family’s problems. Stanton (1992) gives as an example a 17-year-old male, “Pat,” who initiated substance abuse when an aunt with whomhe was very close went through a divorce, and whose abuse became heavy whenhis close, 19-year-old cousin (the aunt’s son) died suddenly in a traffic accident.The family finally entered therapy when his paternal grandmother and her liveinboyfriend of many years broke up, and she tried to induce Pat to leave hisnuclear family and move 1,000 miles away to live with her.Finally, many family therapists work to get the substance abuser to AA,Narcotics Anonymous (NA), or Cocaine Anonymous (CA) as the final step inthe second stage of therapy. Bepko and Krestan (1985) suggest that it is notadvisable for therapists to argue with clients about the value of AA, but theyshould describe AA and its purpose “in a way that is palatable to the particularclient” (p. 103). Most family therapists emphasize that AA is one of the mosteffective treatments for addiction. We help each substance abuser find a groupwith which he or she feels comfortable, then encourage attendance for a whilebefore making a decision whether to continue. For the individuals who feeluncomfortable with AA’s use of the “Higher Power,” we recommend secularsobriety groups (Christopher, 1988).Stage 3: Halting Substance AbuseIn family therapy, there always comes a moment of truth. As a result of thechanges in their family members’ behavior and the firm position of the therapist,substance abusers suddenly become aware that they are going to have tochoose between their families and their drugs. Substance abusers, when consistentlyconfronted (or abandoned) by parents, spouses, children, friends,employers, and perhaps even recovering people in self-help groups and/or atherapist, often “hit bottom” and turn to the therapist for help in changingtheir ways.At this juncture, Steinglass and colleagues (1987) suggest that there arebasically three ways for therapists to proceed. First, when physical dependenceon alcohol or drugs is identified, the therapist should arrange safe detoxificationfor the addicted person and refuse to continue therapy unless this option iscompleted. Without medical intervention, the addict’s independent with-

24. Family-Based Treatment 541drawal is unlikely and possibly dangerous. Second, the therapist can agree to letthe family attempt detoxification on an outpatient basis, on the condition thatif there has been no meaningful progress made toward detoxification in 2 weeks(maximum), medical treatment will be pursued. Third, except in cases wherethe dependence is on sedative hypnotics (e.g., alcohol, barbiturates), and givenproper medical backup, the therapist can work with the family as the “treatmentteam” and conduct the detoxification in the home environment (Scott &Van Deusen, 1982; Stanton, Todd, et al., 1982). In fact, home detoxificationappears to be a cost-effective option in many cases, with savings of 70–85% ofthe cost of hospitalization (Stanton & Shadish, 1997; Stanton, Steier, Cook, &Todd, 1997).Whichever of these courses of action is selected, family therapists try tokeep family members involved in the change process. One benefit is that themembers will be able to realize some responsibility for the success of the treatment(Stanton & Todd, 1992). When treatment is left to the “professionals,”families often fail to realize their responsibility for change. And later, shouldthe recovery process go awry, they blame the setback on the treatment program.Finally, a parallel activity engaged in during this stage by transitional familytherapists is to begin to expand the family genogram to include four, five, ormore generations. The idea is to engage the family in an examination of its pedigreetoward answering certain key questions (which were developed by psychiatristJudith Landau) about the etiology of the problem, that is: When did thesubstance abuse start? With which generation? What was happening across theextended family at that time? In other words, when, in this family’s history, wasthe family so stressed that it had to change its relational patterns or organizationand develop a drinking or drug problem (Landau & Stanton, 2000)?Stage 4: Managing the Crisis and Stabilizing the FamilyWhen the substance abuser becomes “clean and sober,” the family therapistshould be prepared for a new set of problems (Brown & Lewis, 1999). Familymembers, stunned by the unfamiliar behavior of the sober or clean family member,and often frightened, have been known to make seemingly irrational statements,such as “I liked you better when you were drinking.” One woman weknow gave a bottle of bourbon to her recently sober husband for his birthday.No wonder the rate of relapse is high in this stage.In discussing alcoholic families, Steinglass and colleagues (1987) identifiedan analogous stage, “the emotional desert.” In their rich qualitative description,families that have been organized around alcohol for many years experience aprofound sense of emptiness when the drinking stops. Steinglass and colleaguesexplain that these families “have the sensation of having been cut adrift, loosenedfrom their familiar moorings, lost in a desert without any landmarks uponwhich to focus to regain their bearings” (p. 344). Instead of experiencing joy

542 V. TREATMENTS FOR ADDICTIONSover the newfound sobriety, the family members feel empty and depressed. It isnot surprising that members of newly sober families tend to interact in the sameway they did while one of their own was abusing alcohol and/or drugs.Couples often experience a feeling of “walking on eggshells” at home anddrift into a kind of emotional divorce. Both partners want to preserve sobrietyand peace, so they interact sparingly and hesitantly, unwittingly reestablishingthe same patterns of closeness and distance that they enacted previously. Forexample, a recently sober alcoholic, wanting to talk with his wife about his feelings,approached her late at night, waking her from a sound sleep, just as he didwhen he was drunk. She, in turn, rebuffed his awkward attempt at communication,leaving him to go sulk alone, just as once he went off to drink alone. Thus,when recovering couples get to know each other anew, they often find themselvesbored, irrationally angry, and unable to resolve problems that were onceavoided with the help of intoxicants (e.g., O’Farrell, 1993).In the case of addicted young people, a family crisis can be anticipated 3 or4 weeks into this part of treatment (Stanton & Todd, 1992). Commonly, thecrisis occurs in the marital relationship of the parents, who take steps towardseparation. Many addicts have become “dirty” again to reunite their families.Siblings and children of recovering substance abusers also can exert unintentionalpressure to revert to old ways. Gradually, families begin to noticeother problems, long hidden from attention by the magnitude of substanceabuse. As the blur of intoxication clears, children who were once consideredhelpful are suddenly seen as withdrawn and depressed; children who were onceseen to be doing fine in school may be seen as just getting by, and the teenager’smarijuana smoking may be noticed for the first time.Family therapists disagree about how quickly family problems should beresolved in this stage. Berenson suggested that it is advisable to begin this stagewith a hiatus from therapy while things calm down; thus, he does not scheduleregular appointments but tells clients, “Get back to me in a month or so”(Stanton, 1981b). Meanwhile, he encourages his clients to continue their selfhelpgroup activities, with the understanding that if their distress continuesbeyond 6–12 months, family therapy will resume on a more regular basis. Then,after a period of sobriety, Berenson returns to a more orthodox therapy schedule.Others (e.g., Bepko & Krestan, 1985; Steinglass et al., 1987) believe thatregularly scheduled family therapy sessions can be very helpful at these times,especially if they focus on solving the series of problems that hound these familiesand wear them down.Therapy in this stage should be focused on keeping family members as calmas possible (Bepko & Krestan, 1985), while they establish a newfound stabilitythat is not based on substance abuse (Steinglass et al., 1987). Toward this end,therapists work to minimize stress and deescalate conflict, congratulate individualsfor their contributions to family recovery, encourage individuals to focuson their own issues, predict and address common difficulties in recovery and

24. Family-Based Treatment 543fears about relapse, and facilitate minor structural changes in the family toallow adequate parenting (Bepko & Krestan, 1985). Changes in parenting practicesare especially vital when the recovering substance abuser is an adolescent(Alexander & Parsons, 1982; Fishman et al., 1982; Henggeler & Borduin, 1990;Landau & Garrett, 1998; Liddle & Hogue, 2001; Piercy & Frankel, 1989;Stanton & Landau-Stanton, 1990; Szapocznik & Kurtines, 1989; Todd &Selekman, 1991; Waldron et al., 2001).Whenever a relapse into drinking or drug taking occurs, the question ofresponsibility arises. Who is responsible for the relapse? Although conventionaldrug treatment programs and many individual therapists either thrust theresponsibility on the substance abuser or accept it themselves, family therapiststend to assign the responsibility to the abuser’s family. As Stanton and Todd(1992) suggested, “It should be remembered that the addicted individual wasraised by, and in most cases is still being maintained by, his family of origin. It isthus with the family that responsibility rests, and the therapist should help thefamily either to accept it or to effectively disengage from the addict so that theaddict must accept it on his or her own” (p. 55, original emphasis).Similarly, the therapist must assign credit to the entire family when creditis due (Stanton, 1981c). Each member, particularly the often-neglected spouse,is praised for his or her contribution to the growing “health” of the family. Byidentifying and rewarding individual contributions, family therapists spread theglory that is usually bestowed on recovering abusers and promote long-lastingchanges in family interaction.Stage 5: Family Reorganization and RecoveryWhereas families in Stage 4 remained organized around substance abuse andtherapy was focused on resolving difficulties with substance abuse, Stage 5 isconcerned with helping families move away from interaction focused on substanceabuse issues and toward fundamentally better relationships. Here, thesubstance abuser is stabilized and “clean and sober.” Therapy now focuses ondeveloping a better marriage, establishing more satisfactory parent–child relationships,and perhaps confronting long-standing family-of-origin and codependenceissues.Steinglass and colleagues (1987) called this process “family reorganization”(p. 344). Although some families restabilize before reaching this phase andremain organized around alcohol issues (“dry alcoholic” families), we haveobserved that for others, the previous stages of therapy culminate in a seriousfamily crisis. This crisis then leads to disorganization and ultimately to a fundamentallydifferent organizational pattern that is encouraged in this stage oftherapy.Bepko and Krestan (1985) enumerated four goals for their analogue of thisstage, which they have termed “rebalancing” (p. 135):

544 V. TREATMENTS FOR ADDICTIONS1. Shift extremes of behavior from rigid complementarity to greater symmetryor more overt complementarity (improved complementarity for the specificrelationship).2. Help the couple/family to resolve issues of power and control.3. Directly address the pride structures of both partners, so that new forms ofrole behavior are permitted without the need for alcohol.4. Help the couple to achieve whatever level of closeness and intimacy is desirablefor them. (pp. 135–136)See Bepko and Krestan (1985), O’Farrell (1993), Fals-Stewart and colleagues(2005), and O’Farrell and Fals-Stewart (2000, 2002) for detailed discussions oftherapeutic methods used to implement these and related goals.Davis (1987) also emphasized that therapists must help family members toreconsider and redefine the substance abuser’s role in the family at this stage oftherapy. Old expectations and behavioral patterns, based on living with addiction,must be replaced by new adaptive ones. For example, a family that hasgrown used to an alcoholic husband/father may continue to withdraw everytime he shows a hint of anger, leave him out of family decisions, and disregardhis parenting efforts. In this stage of therapy, the father must learn to deal withhis anger, to participate in making responsible decisions, and to function as afather, and the family members must let him change.In the treatment of a family with a young addict during this stage, the therapyevolves beyond Stage 4 crisis management and toward other issues, such asfinding the recovering addict gainful employment and a place to live away fromhome (Stanton & Todd, 1992). Family therapists work to involve parents inthese “launchings,” so they will share the addict’s eventual success. Over time,it becomes increasingly possible to shift the parents’ attention to other siblings,grandchildren, or retirement planning, thereby allowing both the parents andthe recovering addict to let go. Should marital issues surface, as they often do,family therapists try to keep young addicts out of their parents’ marriage issues.Berenson focuses his work in this stage on the couple’s relationship, withthe aim of increasing emotional closeness within the couple, without a returneither to drinking or to discussions centered on alcohol (Stanton, 1981b). Inconjoint sessions with couples and/or multiple-couple groups, Berenson andother family therapists often focus on the severe sexual problems that are commonin such marriages (Stanton, 1981b) and teach new skills for dealing withstress and conflict (Bepko & Krestan, 1985; Fals-Stewart et al., 2005; O’Farrell& Fals-Stewart, 2000, 2002). Therapy sessions with the extended family arescheduled when relatives or in-laws are disruptive (Speck, 2003; Stanton &Landau-Stanton, 1990).Finally, it is also during this stage that a number of family therapists (e.g.,Bowser, Word, Stanton, & Coleman, 2003; Coleman, Kaplan, & Downing,1986; Horwitz, 1997; Reilly, 1975, 1984; Rosenbaum & Richman, 1972) dealwith the often unexpected and unresolved losses and deaths that so many

24. Family-Based Treatment 545chemically dependent families have experienced. These issues may not need tobe covered to effect abstinence initially, but unresolved grief can “eat away” atprogress unless it is brought to terms.More particular to this issue, it is important to recognize that most substanceabusers have been fulfilling a script prescribed by family history. Similarto Walsh’s (1978) finding that, in comparison with “normals,” people whobecome schizophrenic are more likely to have been born close to the time whena grandparent died, Reilly (1975) has noted that addicted people are frequentlydealt with as replacements, or “revenants,” of other family members who werelost, often unexpectedly. Reilly also observed a tendency for adolescents whoabuse substances to be named after a relative who was an alcoholic. His observationis supported by a national survey of adults in the United States byStanton, Adams, Landau, and Black (1998) in which it was found that drug- oralcohol-dependent people were three times more likely to be named after a relativewith a substance abuse problem than were people named after relativeswith no such problem. An example is the case of the young man, “Pat,” mentionedearlier: He was named after, and viewed as very similar to, his paternalgrandfather who manufactured illegal alcohol during the Prohibition period.Pat was later pressured by his paternal grandmother—who called Pat her “prideand joy”—to fill in as a replacement for the longtime boyfriend who had lefther (Stanton, 1992; Stanton & Landau-Stanton, 1990).Transitional family therapy specifically deals with the kinds of loss andscripting dynamics mentioned above. The material revealed in the genogram asto when the problem began in the family’s history, and the loss and grief thatlikely attended that onset, are dealt with in a direct manner. The family istaken back to the point of loss and symbolically “goes through” it again from apresent-day vantage point. This joins the poles of past, present, and future—spanning the family’s generations. The process also depathologizes those membersfrom the past who had problems, and reinstates them, instead, as peoplewho may have been pained and besieged. By granting the forebears their honorableplace, honor is also bestowed on the living, their descendants. Suchuncovering and rebuilding gives the family members the kind of informationthat can free them up to make a choice: Whether to keep, revise, or replace theintergenerational instructions (scripts) that have been carried down. In otherwords, it helps the family come to grips with the question of whether, and how,to move on in life. In experience with several thousand cases, as well as moresystematic qualitative study with over 200 clinical and nonclinical families,TFT has shown great promise in bringing about long-term change in the intergenerationalfamily addiction pattern (Landau & Stanton, 2000).Stage 6: Ending TherapyIn the ideal course of therapy with substance-abusing families, treatment comesto an end when the clients and therapist agree to stop meeting regularly. Family

546 V. TREATMENTS FOR ADDICTIONStherapists tend to agree to stop when they believe that the serious structuraland functional problems that have maintained substance abuse have beenreplaced with new family rules, roles, and interactional patterns. Optimally,substance abuse has not been replaced with other addictive behaviors. Familytherapists tend to tolerate socially acceptable “addictions” (e.g., “workaholism”)as long as family members tolerate them.In TFT, as the therapist hands over control to the family, a renewed commitmentfor support is requested from the network. Strategic predictions aremade, helping the family to understand the likelihood that the substance abusermay once again test their commitment to his or her abstinence. Plans are madefor dealing with this possibility. Finally, a formal, end-of-treatment ritual isdesigned and orchestrated by the family (Landau & Stanton, 2000).The length of therapy and the specific definition of successful treatment varywidely among models of therapy and among individual families. Stanton andTodd (1992), in describing their brief therapy model for treating drug addicts,have broadly stated that therapy is appropriately concluded when “adequatechange has occurred and been maintained long enough for the family to feel asense of real accomplishment” (p. 56). Adherents of other models would not evenattempt to reorganize family structure in the ways prescribed in our fifth stage.Instead, they conclude treatment when family members feel satisfied that theproblems originally presented have been resolved (e.g., Heath & Ayers, 1991).Once all parties agree to cease regularly scheduled sessions, occasionalinoculatory follow-up sessions (“checkups”) may be scheduled, one at a time, atintervals of 2–6 months. Therapists make it clear that clients are welcome toschedule future appointments at any time and to cancel sessions that seemunnecessary. Therapy clients, like medical patients, are not necessarily madepermanently “healthy,” even after a course of treatment. The door to the therapist’soffice, like that of the family physician, remains open (Heath, 1985).Family therapy sometimes ends unexpectedly and prematurely, at least asseen by the therapist. No matter how skilled the therapist, and no matter whatthe stage of treatment, families generally stop coming to therapy when theywant. In such circumstances, responsible therapists make every reasonableeffort to determine whether client families are satisfied or dissatisfied with servicesrendered and to respond accordingly. They offer additional services orreferrals for any family member, as well as professional opinions about remainingproblems and caveats, when appropriate.In conclusion, the six-stage model presented here is intentionally inclusive.We have made no effort to spell out or resolve differences among modelsof family therapy, or to examine the differences between treating drug addictsand alcoholics. Instead, we have broadly sketched a viable course of treatmentfor families with substance-abusing members. Clinicians may wish to emphasizesome stages of therapy more than others.

24. Family-Based Treatment 547SPECIAL CONSIDERATIONS IN FAMILY THERAPYA number of special clinical considerations concern family therapists whenthey work with substance abusers and their families. The most salient of theseconsiderations are discussed next. Interested readers will find insightful discussionsof many of the day-to-day issues that face family therapists in the varioustexts referenced previously.Engaging the Substance Abuser in Treatment or Self-HelpIt is well known within the substance abuse field that, at least in the UnitedStates and Canada, in any given year the vast majority (90–95%) of peoplewho are actively abusing drugs or alcohol do not obtain help for their problems(e.g., Kessler et al., 1994; Sobell, Cunningham, & Sobell, 1996). Consequently,recent years have seen considerable attention devoted to the means for gettingreluctant substance abusers either to enroll in treatment, or to begin attendinga self-help group such as Alcoholics Anonymous or Narcotics Anonymous. Atleast 11 different approaches have been developed that involve family membersand/or significant others toward this end. Ten of the approaches have beenexamined in 19 outcome studies (nine of which included Hispanic cases) acrossthree countries. Reviews of this literature (e.g., O’Farrell & Fals-Stewart, 2003;Rowe & Liddle, 2003; Stanton, 1997, 2004) indicate that significant progress isbeing made in terms of certain of these approaches both becoming more effective,and explicating their methods so others may apply them.Regarding the results from the aforementioned 19 engagement outcomestudies, Stanton (2004) has both summarized the various methods themselvesand compared them as to results. His review applied an “intent-to-treat” criterion,that is, that a method’s effectiveness should be gauged on the proportionof cases that become engaged of those to whom it is offered. Otherwise, if only10 of 100 cases agree to attempt an approach, and nine of those succeed, theapproach may claim “90% success” for what is actually 9% success.Some rather surprising findings emerged from this synopsis. For instance,the well-known Johnson Institute “Intervention” actually succeeds in engagingin treatment/self-help only 0–36% of cases (average across studies = 20%).These low rates seem to be due to the fact that many of the people, such as familymembers, who are trying to get help for a substance abuser believe that theconfrontive and secretive Intervention process is too stressful and damaging torelationships. Thus, many families have refused to proceed with Intervention.Some other findings from this review of outcome studies are as follows:1. Later (1995 on) studies generally attained higher engagement successrates than earlier studies (69 vs. 52%).2. Adult drug users appear to be easier to engage than adult alcoholics (78

548 V. TREATMENTS FOR ADDICTIONSvs. 49%), although this may be confounded by age, because the alcoholicsamples tended to be older.3. The overall engagement success rates for adolescent and adult drugabusers do not differ significantly.4. When a parent is the primary, or only, person mounting the engagementeffort (vs. a spouse/partner, other relative, or friend), the likelihoodof success is increased. This holds for both adolescent and adultcases.5. Engagement is also more likely, and requiring of less effort on the partof the engagement professional, when more people (family, friends,work associates, etc.) are actively involved in the effort. In particular,Landau and colleagues (2004) found a high, and statistically significant,correlation between (a) the number of people involved and (b)scores on an engagement success/efficiency index (r = .69, p < .0001).Stanton’s (2004) review also singles out the approaches that appear to bethe “best options” with particular kinds of cases (e.g., adult drug abusers, adultalcohol abusers, adolescent substance abusers) in terms of both success rate andcost-effectiveness. Regarding cost-effectiveness, specifically—that is, havingthe highest success rate for the least amount of professional effort—twoapproaches stand out, both of which are nonsecretive (in other words, the substanceabuser is informed of the effort from the very beginning). Both involvean average of only 1.5–2 hours of staff time to get most substance abusers intotreatment/self-help, and they generally accomplish this within 1–2 weeks.These approaches are: (1) for adolescents, the behaviorally based “intensiveparent and youth attendance intervention” by Donahue and colleagues (1998),which attained an 89% success rate through the use of a standardized telephoneprogram orientation with the parent to set up an appointment, plus motivationaltelephone reminder calls to both the parent and the youth 2–3 daysbefore the scheduled intake session; and (2) for adults, a TFT-based approachcalled “A Relational Intervention Sequence for Engagement” (ARISE; Garrett,Landau-Stanton, Stanton, Stellato-Kabat, & Stellato-Kabat, 1997), which hadengagement rates of 87% for drug abusers and 77% for alcohol abusers (Landauet al., 2004). ARISE uses a manual-guided, rapid-response, stepped approach inhandling the first call from someone who is concerned about a substanceabuser, as well as quickly expanding the system involved to both increase leveragewith the substance abuser and provide additional support to the person whooriginally called (Garrett et al., 1998, 1999; Landau et al., 2000).Convening DifficultiesOne of the problems identified by therapists working with substance abusersand their families is the difficulty in convening the whole family for therapy

24. Family-Based Treatment 549(Stanton & Todd, 1981; Stanton, Todd, et al., 1982). The families of addictsare particularly difficult to engage in such an endeavor. Fathers, in particular,often appear threatened by treatment and defensive about their contribution tothe problem. Because many have drinking problems themselves, they may alsofear being blamed.Experienced family therapists, recognizing this hesitancy to participate intherapy, work hard to recruit families into therapy. They do not rely on otherfamily members to do the recruiting, because this approach often fails. Instead,they work energetically and enthusiastically to extend personal invitations tothe reluctant. With emotionally healthier families, one telephone call mayenable a therapist to reassure family members that their contributions areimportant to the solution of the substance abuse. With less healthy families, itmay be necessary to meet on “neutral turf” (e.g., a restaurant), to write multipleletters, or even (Stanton, Steier, & Todd, 1982) to pay family members for participationin treatment. Wermuth and Scheidt (1986) and Stanton and associates(Stanton & Todd, 1981; Stanton, Todd, et al., 1982) have describedengagement procedures in considerable detail, the latter group also presenting21 principles for getting reluctant families into therapy.Control of the CaseTo shift the responsibility for dealing with the substance abuser’s problems tothe family, a family therapist needs to have command of the case. The familytherapist must be allowed (e.g., by other elements in the treatment system) todirect the overall case management, including the treatment plan, the use ofmedication and drug tests (see below), and decisions about hospitalization.When one therapist is in charge, substance abusers are less likely to manipulaterelationships among treatment professionals.Stanton, Todd, and colleagues (1982) estimated that approximately halfthe effectiveness of treatment of drug addicts and their families depends on theefficiency and cohesiveness of the treatment system. If family members receivevaried advice, they often end up arguing about the therapy rather than workingtoward recovery. Cohesion in the treatment system of substance abusers necessarilyincludes the self-help programs used by their families. Again, it is vital fortherapists to know the local self-help groups and to collaborate with them forthe sake of their clients.Medication and ManagementFamily therapists who work with substance abusers and their families must haveat least a basic knowledge of pharmacology. This information aids them duringthe detoxification process and reduces the overcaution in the use of medicationsthat sometimes occurs among less informed therapists.

550 V. TREATMENTS FOR ADDICTIONSWith regard to the use of pharmacotherapy, it is vital that physicians, familytherapists, and drug counselors work as a treatment team. Cooperation andopen lines of communication help to counteract the manipulative behaviors ofmany substance abusers. Within that team, the family therapist and physicianhave to work together to encourage family or spouse/partner compliance withprescribed medications, as well as to share information on patient and familyfunctioning (Fals-Stewart et al., 2005; Woody, Carr, Stanton, & Hargrove,1982).Family therapists must have influence over the use of methadone. Familiestend to believe that their recovering members are inherently helpless, fragile,handicapped people; thus, families forgive the most outrageous behavior. Forfamily therapists to argue effectively that addicts can be competent and functionadequately without drugs, they must assert that they are primarily concernedwith the addicts’ detoxifying and getting off all drugs, including methadone.To encourage the cessation of methadone use, family therapists and thefamilies themselves must have significant input into how it is dispensed(Stanton, Todd, et al., 1982; Woody et al., 1982).Epidemiologists have taught us that 30–60% of substance abusers haveconcurrent mental health comorbidities that include major depression, majoranxiety, and personality disorders (Leshner, 1999). Since effective treatmentfor mental health comorbidities typically involves pharmacotherapy, manyquestions occur about how to use medications in substance-abusing populations.Suffice it to say that family therapists must work closely with clients, psychiatrists,substance abuse treatment specialists, and family physicians to determinethe optimal treatment approach for every patient.Involving Parents in DecisionsWhen a substance abuser is an adolescent or a young adult, family therapistsbelieve that parents must be involved in all decisions about the treatment oftheir children. Parents should be included in decisions about hospitalization,medication, and drug tests. Family therapists make parents part of the treatmentteam, because it helps to get couples working together, and the responsibilityfor the resolution of the problem is rightly theirs. When the parents of theyoung person are divorced or unmarried, the same holds true. Furthermore,given the evidence that the majority of all adult substance abusers are in closecontact with one or both of their parents, it makes sense to include the parents.OUTCOMES WITH FAMILY/COUPLE THERAPYConsistent with the greater emphasis given to evidence-based treatments in thebehavioral health industry (mental health and addiction treatment), family/couples treatment outcomes for substance abuse have received increased atten-

24. Family-Based Treatment 551tion in recent years. As we have documented elsewhere (Stanton & Heath,2004), since 1997, at least 16 reviews have been published incorporating 65randomized clinical trials of the effectiveness of family/couples treatment foralcohol and/or other drug problems. The clinical trials are about equally distributedbetween alcohol and other drug abuse samples. About two-thirds of thealcohol treatment studies evaluate couples approaches, and two-thirds of thedrug abuse treatment studies—many of which are with adolescents—examineconjoint family approaches.O’Farrell and Fals-Stewart (2001) have updated the Edwards and Steinglass(1995) meta-analysis of the outcomes of family treatment for alcohol use disorders.The authors obtained a highly significant effect size in favor of familyinvolvedtreatment relative to individually based treatment or wait-list controlconditions (median effect size = .30, p < .00001). The authors found furthersupport for these conclusions in a subsequent review that included more clinicaltrials (O’Farrell & Fals-Stewart, 2003), and noted that the evidence for couplesapproaches was somewhat stronger than for conjoint family approaches.Additional confirmations emerged from an evaluation of the efficacy offamily/couples approaches to alcohol abuse by Miller, Johnson, Sandberg,Stringer-Seibold, and Gfeller-Strouts (2000). These authors determined thatfor adults, effectiveness is now (1) “established” for behavioral couples treatment,and (2) “probable” for psychodynamic/eclectic conjoint couples groups.Stanton and Shadish (1997) reviewed and meta-analyzed the randomizedclinical trials for family therapy with drug abuse and concluded the following:1. Studies that compared family/couples treatment for drug abuse withnonfamily treatment (e.g., individual, group, or psychoeducationaltreatment) found better results for family therapy. Family therapy wasfound to be more effective, less expensive, or both, than the othertreatment types.2. Family therapy works equally well for adolescent and adult drug abusers.3. Comparisons between different “schools” of family therapy were notconclusive.4. Family therapy has shown higher rates of engagement and retention intreatment than nonfamily approaches.Since the Stanton and Shadish (1997) meta-analysis, the number offamily/couples clinical trials for drug abuse has more than doubled, with anincrease, in particular, in couples treatment studies. Sixteen of the 17 newer trialssupported the conclusions of the 1997 review. Furthermore, in conjunctionwith and expanding upon the Miller and colleagues (2000) review of the effectivenessof specific approaches, Stanton and Heath (2004) have concluded thateffectiveness is now “established” for three family approaches and one couplesapproach, and “probable” for a fourth family approach. In summary, these, and

552 V. TREATMENTS FOR ADDICTIONSthe other reviews cited by Stanton and Heath make the case that involvingfamilies/partners in treatment of substance abuse can both reduce treatmentdropout and improve outcomes.The family has also been found to be an essential factor in evidence-basedsubstance abuse prevention programs. Using 20 years of social science research asa foundation, the U.S. National Institute on Drug Abuse has identified risk andprotective factors that predict substance abuse in adolescence and early adulthood(Cire, 2002). Today, an increasing number of prevention programs relateto family form and function in both their content and their activities. Forexample, family risk factors for substance abuse include chaotic home environments,ineffective parenting, and lack of parent–child attachments. Protectivefactors include strong and positive family bonds, parental monitoring of children’sactivities, clear rules of conduct that are consistently enforced, andinvolvement of parents in the lives of their children (Risk and Protective Factors,2002).Research has shown that the same family risk factors apply to the preventionof other social problems, including youth violence, delinquency, schooldropout, risky sexual behaviors, and teen pregnancy. There is also evidence ofthe economic value of evidence-based prevention. One dollar spent in preventionsaves four dollars in the cost of substance abuse treatment (Pentz, 1998).CONCLUSIONSubstance abuse affects everyone in the family. Family therapy is an ecologicaland inclusive intervention that can benefit all those involved and change themultigenerational dynamics of substance abuse. Research now supports family/couple therapy as an effective and efficient approach to both treatment and prevention.Given society’s overt concerns about substance abuse and its incrediblecost to our country, family/couple therapy appears to be making a significantcontribution to the well-being of our people.REFERENCESAlexander, J. F., & Parsons, B. V. (1982). Functional family therapy. Monterey, CA:Brooks/Cole.Alexander, J. F., Waldron, H. B., Barton, C., & Mas, C. H. (1989). Minimizing blamingattributions and behaviors in delinquent families. J Consult Clin Psychol, 57, 19–24.Anthenelli, R. M., & Schuckit, M. A. (1997). Genetics. In J. H. Lowinson, P. Ruiz, R.B. Millman, & J. G. Langrod (Eds.), Substance abuse: A comprehensive textbook (3rded., pp. 41–51). Baltimore: Williams & Wilkins.Bekir, P., McLellan, T., Childress, A. R., & Gariti, P. (1993). Role reversals in familiesof substance misusers: A transgenerational phenomenon. Int J Addict, 28, 613–630.

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CHAPTER 25Treating Adolescent Substance AbuseYIFRAH KAMINEROSCAR G. BUKSTEINThe consequences of substance use, as well as substance use disorders (SUDs),continue to present a major public health concern. Level of substance use isassociated with leading causes of adolescent morbidity and mortality in theUnited States, including motor vehicle accidents, suicidal behavior, violence,delinquency, drowning, and unprotected sexual behavior. Adolescent SUDs,which include substance abuse and substance dependence as defined in thefourth edition of the Diagnostic and Statistical Manual of Mental Disorders(DSM-IV-TR; American Psychiatric Association, 2000), are also associatedwith drug-related chronic problems in several life domains, including psychiatriccomorbidity, school or employment performance, family function, peersocial relationships, legal status, and recreational activities.Regional studies reveal that between 7 and 10% of adolescents are inneed of treatment (Harrison, Fulkerson, & Beebe, 1998; Lewinsohn, Hops,Roberts, & Seeley, 1993; Reinharz, Giaconia, Lefkowitz, Pakiz, & Frost, 1993;Ungemack, Hartwell, & Babor, 1997). However, due to limited resources, onlya small segment of the adolescent subpopulation with alcohol and other substanceuse disorders (AOSUDs), in particular, those with high severity ofAOSUDs, comorbid psychiatric disorders, and legal problems, usually end up intreatment (Kaminer, 2001).Our objectives in this chapter are to review the trends in adolescent substanceuse, nosology, etiology of substance use and its transition to adolescentSUDs, psychiatric comorbidity, prevention, assessment, and the treatment–aftercare continuum. As a point of clarification, the generic term “substanceuse” refers here to nonpathological use of any licit drug (tobacco, alcohol, and559

560 V. TREATMENTS FOR ADDICTIONSinhalants) or illicit drug (controlled substances, both those that are essentiallyproscribed for everyone and those that are available by prescription). The term“substance abuse” is used generically to indicate pathological use. Terms such as“substance abuse,” “substance dependence,” and “SUDs” are specifically mentionedas part of a formal classification system (e.g., DSM-IV-TR).EPIDEMIOLOGYSubstance use among American youth in the 1980s and early 1990s dropped toa low point, then rose continuously between 1992 and 1997; since then, the useof several specific drugs has leveled off or has declined. The main consistentsource of information on adolescent substance use has been the Monitoring theFuture (MTF) surveys, which in 2002 covered nationally representative samplesof 43,000 8th, 10th, and 12th graders in 394 schools (National Institute onDrug Abuse, 2002). Although the prevalence rates derived from the survey failto reflect adequately the magnitude of high-risk behaviors, clinical significance,and adolescent health problems, they may serve at best as a periodic “snapshot”of adolescent substance use.In the 2002 MTF, specific decreases were noted in the use of marijuana,cigarettes, alcohol, inhalants, D-lysergic acid diethylamide (LSD), amphetamines,and Ecstasy. Abuse of anabolic steroids, methylphenidate, and heroinremained stable. The only significant increase in drug use in 2002 was past yearcrack use by 10th graders and sedative use by 12th graders. Attitudes and beliefsabout drugs, which may play a critical role in deterring use, began to change inall three grades, because perceived risk of harm, personal disapproval, and perceivedavailability are associated with the level of drug use.There are surprisingly few community epidemiological studies on the prevalenceof SUDs in adolescents. In community studies, lifetime diagnosis of alcoholabuse ranged from 0.4% in the Great Smoky Mountain Study (Costello etal., 1996) to 8.2 and 9.6% in the Pittsburgh Adolescent Alcohol Research Center(Martin, Kaczynski, Maisto, Bukstein, & Moss, 1995) and the NationalCormorbidity Study (Kendler, 1994), respectively. Lifetime diagnoses of alcoholdependence ranged from 0.6% (Costello et al., 1996) to 4.3% in the OregonAdolescent Depression Project (Lewinsohn, Hops, Roberts, & Seeley,1993; Lewinsohn, Rohde, & Seeley, 1996). The lifetime prevalence of drugabuse or dependence has ranged from 3.3% in 15-year-olds to 9.8% in 17- to19-year-olds (Kashani et al., 1987; Reinherz et al., 1993).Age of InitiationBased on retrospective reports of grade level of first use, the data provided byeighth graders indicated that three substances were initiated by more than 50%

25. Adolescent Substance Abuse 561of users in sixth grade or earlier. These “gateway drugs” were alcohol, tobacco,and inhalants (O’Malley, Johnston, & Bachman, 1995).Gender and Ethnic GroupIn general, male students use more substances of all kinds than female students;however, the differences are consistently getting smaller (Wallace et al., 2003).O’Malley and colleagues (1995) suggested that “closing the gap” by adolescentfemales may have to do with slightly earlier female maturation and with theirtendency to associate with older male students. Excluding Native Americanyouth, Hispanic students score highest among all other ethnic subpopulationsat 8th grade for all illicit drug classes. At 12th grade, they are the highest forcocaine, heroin, and steroids. Hispanic males and females manifest the highestlevels of marijuana use and binge drinking similar to white youth (in excess of40% for 10th graders). Asian American students manifest the lowest rates ofuse.NOSOLOGYSubstance use and abuse occurs on a continuum, and the cutoff point for makinga diagnosis of abuse/dependence is somewhat arbitrary, particularly in adolescents(Rohde, Lewinsohn, & Seeley, 1996). Clinical psychiatry has traditionallyfollowed the dichotomous paradigm of the DSM nosology regardless ofits limitation providing information in terms of pathogenesis and treatmentresponse (Bukstein & Kaminer, 1994). In addition, the serious negative impactof drugs on adolescents or adults who experience subdiagnostic levels of problematicsubstance use has been recognized but has not been addressed by theDSM system (Lewinsohn et al., 1996).The same DSM-IV-TR diagnostic criteria are utilized for both adolescentsand adults in the diagnosis of substance abuse and dependence. Empirical datagenerally support the utility of DSM-IV-TR criteria for alcohol dependenceamong adolescents (Martin et al., 1995). Lewinsohn and colleagues (1996)reported on the strong similarity between adolescents and adults in the frequencyof 8 of the 11 symptoms in DSM-IV-TR criteria for abuse and dependence.Among adolescents with a diagnosis, the most frequently reported symptomswere reduced activities, tolerance, consuming more than intended, anddesire to cut down (Lewinsohn et al., 1996; Stewart & Brown, 1995).Abuse and dependence are distinctly separate (Hasin, Grant, & Endicott,1990). A majority of adults diagnosed as abusers never progress to dependence.Abuse is not necessarily a prodrome, and it may be developmentally limited inmany adolescents. “Diagnostic orphans” are those youth who have subthresholdsymptomatology of alcohol dependence (i.e., one or two symptoms only) but no

562 V. TREATMENTS FOR ADDICTIONSabuse symptoms (Pollock & Martin, 1999). A 3-year follow-up study demonstratedthat this entity has a unique trajectory that is not dissimilar to eitherabuse or dependence.ETIOLOGY AND PATHOGENESISGenetic and biological factors, as well as environmental variables, have beenextensively researched to address questions regarding the etiology of SUDs.Most researchers acknowledge a multifactorial consensus, as presented in thebiopsychosocial paradigm for the etiology and pathogenesis of these disorders.Genetic and Biological FactorsMost of the data regarding the genetic and biological contribution to the developmentof substance abuse are derived from alcoholism research. It has beensuggested that individuals may enter life with a certain level of genetic predispositiontoward AOSUDs. Convergent evidence from twin, adoption, and biologicalresponse studies suggests that genetic factors may indeed play a rolein the etiology of alcoholism (Bohman, Sigvardsson, & Cloninger, 1981;Cloninger, Bohman, & Sigvardsson, 1981). Investigations of neuropsychologicaland physiological precursors or markers of alcoholism, conducted with sonsof alcoholics and nonalcoholics, suggest some possible biological differencesthat may increase vulnerability to alcoholism. For example, children of alcoholicsmay be deficient in serotonin or may have an increased level of serotonin inthe presence of alcohol (Goodwin, 1985). The “addictive cycle”—a pattern inwhich a person initially drinks to feel good and then later has to resume drinkingafter an abstinence period to stop feeling bad—may result from such a problemwith serotonin. Children of alcoholics are also suspected to have increasedtolerance to alcohol.There are indications that adolescent substance abuse may be part of abroader genetic constellation. Some theorists suggest that polydrug abuse(abuse of a wide variety of substances) constitutes evidence against a geneticinterpretation of addiction. Cadoret, Troughton, O’Gorman, and Heywood(1986) suggest instead that some underlying biochemical route may be involvedboth in substance abuse and in problem or deviant behavior, especiallydelinquency, and that at least one genetic pathway occurs through antisocialbehavior.Temperament deviations are associated with an increased risk for psychopathologyand substance abuse (Reich, Earls, Frankel, & Shayka, 1993). Forexample, children with a “difficult temperament” more commonly manifestexternalizing and internalizing behavior problems by middle childhood(Earls & Jung, 1987) and in adolescence (Maziade, Caron, Cote, Boutin, &Thivierge, 1990) compared to children whose temperament is normative.

25. Adolescent Substance Abuse 563Increased behavioral activity level is noted in both youth at high risk for substanceabuse and those having an SUD (Tarter, Laird, Mostefa, Bukstein, &Kaminer, 1990). Other temperamental trait deviations found in high-risk youthinclude reduced attention span persistence (Schaeffer, Parson, & Yohman,1984), increased impulsivity (Noll, Zucker, Fitzgerald, & Curtis, 1992; Shedler& Block, 1990), and negative affect states such as irritability (Brook, Whiteman,Gordon, & Brook, 1990) and emotional reactivity (Blackson, 1994).Tarter, Kirisci, Hegedeus, Mezzich, and Yanyukov (1994) developed a difficulttemperament index to classify adolescent alcoholics. Those adolescents with adifficult temperament displayed a high conditional probability to develop psychiatricdisorders such as conduct disorder, attention-deficit/hyperactivity disorder,anxiety disorders, and mood disorders (Tarter et al., 1994).Environmental TheoriesThe evidence supporting genetic and, presumably, biological factors in alcoholismand substance abuse is paralleled by evidence supporting the role ofpsychosocial, familial, peer, and other environmental and interactional variables.Problem behavior theory, formulated by Jessor and associates, explains substanceuse as a component of a “deviance syndrome” or “proneness” to problembehavior (Jessor, 1987). Together, the personality system, the perceived environmentsystem, and the behavior system generate a dynamic state called“proneness,” which specifies the likelihood of occurrence of normative developmentor problem behavior that departs from the social and legal norms.Also, longitudinal studies have documented that personality characteristicssuch as aggressiveness and rebelliousness are predictive factors that precedethe use of substances and can be identified in preschoolers. Kandel (1982)made two pivotal contributions. She formulated four broad classes of predictors:(1) parental influences, (2) peer influences, (3) adolescent beliefs and values,and (4) adolescent involvement in various shared activities. Kandel also conceptualizedthe “gateway” theory to adolescent substance use and abuse.According to Kandel (1982, 2003), alcohol and marijuana are pivotal “gateway”substances, and she formulated several distinct developmental stages inthe initiation and progression of substance use by adolescents, including (1)beer or wine, (2) cigarettes or hard liquor, (3) marijuana, and (4) other illicitsubstances. Participation in each stage is a necessary but not a sufficient conditionfor progression into a latter stage. Problem drinking may take placebetween marijuana and other illicit drug use; therefore, it represents an additionalstage in the transition of substance use (Donovan & Jessor, 1983).Morral, McCaffrey, and Paddock (2002) argued that a marijuana gateway effectto hard drugs might exist, particularly among specific ethnic groups such asAfrican Americans, although a common factor model may suffice to explainthis association.

564 V. TREATMENTS FOR ADDICTIONSParental InfluencesThree different types of parental characteristics predict initiation of adolescentsubstance use: parental substance use/abuse behaviors, parental attitudes towardsubstances, and parent–child interactions, which include quality of parent–child communication and parental supervision and monitoring. Studies suggestthat a caretaker who exposes a child (particularly a young child) to substanceabuse behavior, and to the nonfulfillment of parental responsibilities that follows,affects the child by providing models and by reinforcement of relatedbehaviors. In a study of environmental influences, the number of householdusers of substances and the degree of children’s involvement were found to bethe best predictors of both expectations of use and actual abuse of alcohol, aswell as a strong predictor of children’s cigarette and marijuana use (Ahmed,Bush, Davidson, & Iannotti, 1984). Among the environmental characteristicsof these families, the following factors were noted to predict adolescentsubstance use: high stress, poor and inconsistent family management skills,increased separation, divorce, death, parental prison terms, and decreased familyactivities.Families with addicted members are often socially isolated from the community,partly because of their need for secrecy and partly because of communityrejection. Parents in substance-abusing families have fewer friends and areless involved in recreational, social, religious, and cultural activities (Kumpfer& Demarsh, 1986). Because of such families’ social isolation, the children havefewer opportunities to interact with other children, have fewer friends, and thechildren express a desire to have more friends but doubt their abilities to makefriends. Emotional neglect is frequently reported; substance-abusing parentshave only a limited ability to involve themselves meaningfully and emotionallywith their children and also have been found to spend less time in planned andstructured activities with their children (Kumpfer & Demarsh, 1986). In addition,more psychopathology and significantly more depression have beendetected in substance-abusing parents. The emotional impact on children fromthese families results in the children’s difficulty with identifying and expressingpositive feelings. Substance-abusing parents are also characterized by difficultyin coping with everyday realities and responsibilities, the presence of comorbidpsychiatric disorders, decreased ability to supervise and monitor their children’sactivities or appreciate that their children may be participating in deviantactivities such as substance use, and lack of energy for better parenting, becauseof the drain on the family’s time, finances, and emotional–social resources createdby the substance abuse (Kumpfer & Demarsh, 1986).Resentment, embarrassment, anger, fear, loneliness, depression, and insecurityare often identified or reported among these children. Intense fear of separationand abandonment is very common. Because psychopathology and emotionaldisturbances often precede substance abuse, these children are at highrisk for the development of substance abuse and dependence.

25. Adolescent Substance Abuse 565Peer InfluencesPeer influences play a crucial role in the process of involvement in the use andabuse of all substances—tobacco, alcohol, and illicit substances (especially marijuana).Because only a small fraction of adolescent substance users may progressto substance abuse, it is of a significant clinical importance to differentiatebetween the causes for substance use and substance abuse. Most substance useoccurs due to social influences and can be attributed to the adolescent’s immediatesubculture and lifestyle. Substance abuse is more strongly tied to a developmentalprocess involving biobehavioral factors (Glantz & Pickens, 1992),and it occurs as a part of a cluster of behaviors that form a syndrome of problembehavior (Jessor & Jessor, 1977) or general deviance (Newcomb, 1995).Peer relationships have a significant effect on the initiation, development,and maintenance of substance abuse. The most consistent and reproduciblefinding in substance abuse research is the strong relationship between an individual’ssubstance use behavior and the concurrent substance use of his or herfriends (Jessor & Jessor, 1977). Such an association may result from socialization,as well as from a process of interpersonal selection (assortative pairing), inwhich adolescents with similar values and behaviors seek each other out asfriends (Kandel, 1982). Susceptibility to peer influence is related to earlierinvolvement in peer-related activities and to a greater degree of attachmentand reliance on peers rather than parents (Kandel, 1978).Regarding values and attitudes in adolescent substance abusers, substanceabuse is correlated negatively with conventional behaviors and beliefs, such aschurch attendance, good scholastic performance, value of academic achievement,and beliefs in the generalized expectations, norms, and values of society(Jessor, 1987). Substance abuse is correlated positively with risk-taking behavior,sensation-seeking behavior, early sexual activity, higher value of independence,and greater involvement in delinquent behavior (Jessor, 1987).Delinquent peer groups may engage in many shared deviant behaviors,such as using the same drugs of choice, Satanism and related rituals, drug trafficking,and violence. Such activities are deeply rooted in the identity-creatingprocess of these groups and are inseparable components of their code of values.PSYCHIATRIC COMORBIDITYThe presence of one or more comorbid psychiatric disorders, both internalizingand/or externalizing types, is often noted in populations of adolescents withSUDs (Bukstein, Glancy, & Kaminer, 1992; Riggs, Baker, Mikulich, Young, &Crowley, 1995). Psychiatric disorders in childhood, featured by disruptivebehavior disorders, as well as mood or anxiety disorders, confer an increased riskfor the development of SUDs in a majority of the cases in adolescence(Bukstein, Brent, & Kaminer, 1989; Christie et al., 1988; Loeber, 1988). The

566 V. TREATMENTS FOR ADDICTIONSetiological mechanisms have not been systematically researched. However, anumber of possible relationships exist between SUD and psychopathology. Psychopathologymay precede SUD, may develop as a consequence of a preexistingSUD, may influence the severity of an SUD, may not be related, or may originatefrom a common vulnerability (Hovens, Cantwell, & Kiriakos, 1994).African American and Hispanic youth may both present with high-abovethresholdsymptom rates of co-occurring disorders, while Hispanic youths mayhave higher rates of externalizing symptoms than African American youths(Robbins et al., 2002). Among youth with SUDs, males have higher rates ofdisruptive disorders, while females have higher rates of depression (Latimer,Stone, Voight, Winters, & August, 2002).A number of psychiatric disorders are commonly associated with SUDs inyouth (Bukstein et al., 1989). Conduct disorder and constituent criteria,such as aggression, usually precede, predict, and accompany adolescent SUDs(Ferdinand, Blum, & Verhulst, 2001; Loeber, 1988). Clinical populations ofadolescents with SUDs show rates of conduct disorder regularly ranging from50% to almost 80%. Conduct disorder is a poor prognostic sign for treatment(Hser et al., 2003; Kaminer, Tarter, Bukstein, & Kabene, 1992). Althoughattention-deficit/hyperactivity disorder (ADHD) is commonly noted insubstance-using and -abusing youth, the observed association is likely due tothe high level of comorbidity between conduct disorder and ADHD (Barkley,Fischer, Edelbrock, & Smallish, 1990; Kaminer, 1992a; Levin & Kleber, 1995;Wilens, Biederman, Spencer, & Frances, 1994). An earlier onset of conductproblems and aggressive behavior, in addition to the presence of ADHD, mayincrease the risk for later substance abuse (Loeber, 1988). Adolescents with andwithout ADHD may have a similar risk for SUDs mediated by conduct andbipolar disorders (Biederman et al., 1997).Aggressive behaviors are present in many adolescents who have SUDs.Consumption of substances such as alcohol, amphetamines, and phencyclidinemay increase the likelihood of subsequent aggressive behavior (Moss & Tarter,1993). The direct pharmacological effects resulting in aggression may be furtherexacerbated by the presence of preexisting psychopathology, the use of multipleagents simultaneously, and the frequent relative inexperience of the adolescentsubstance user. Other compulsive deviant behaviors such as gambling andpathological gambling are common among adolescents with SUDs (Griffiths,1995).Mood disorders, especially depression, frequently have onsets both precedingand consequent to the onset of substance use and SUD in adolescents(Bukstein et al., 1992; Deykin, Buka, & Zeena, 1992; Deykin, Levy, & Wells,1987; Hovens et al., 1994). The prevalence of depressive disorders in thesestudies ranged from 24% to more than 50%.The literature supports SUDs among adolescents as a risk factor for suicidalbehavior, including ideation, attempts, and completed suicide (Bukstein et al.,

25. Adolescent Substance Abuse 5671993; Crumley, 1990; Kaminer, 1996). Possible mechanisms for this relationshipsinclude acute and chronic effects of psychoactive substances. Adolescentsuicide victims are frequently using alcohol or other drugs at the time of suicide(Brent, Perper, & Allman, 1987). The acute substance use may produce transientbut intense dysphoric states, disinhibition, impaired judgment, and increasedlevel of impulsivity or may exacerbate preexisting psychopathology,including depression or anxiety disorders.A number of studies of clinical populations show high rates of anxiety disordersamong youth with SUDs (Clark et al., 1995; Clark & Sayette, 1993). Inclinical populations of adolescents with SUDs, the prevalence of anxiety disorderranged from 7% to over 40% (Clark et al., 1995; DeMilio, 1989; Stowell,1991). The order of appearance of comorbid anxiety and SUD appears to bevariable, depending on the specific anxiety disorder. Social phobia usually precedesabuse, whereas panic and generalized anxiety disorder more often followthe onset of a SUD (Kushner, Sher, & Beitman, 1990). Adolescents with SUDsoften have a history of posttraumatic stress disorder (PTSD) following acute orchronic physical and sexual abuse (Clark et al., 1995; Van Hasselt, Null, Kempton,& Bukstein, 1993). Bulimia nervosa is also commonly associated with adolescentshaving substance use disorders (Bulik, 2002). SUDs are very commonamong individuals diagnosed with schizophrenia (Kutcher, Kachur, & Marton,1992; Regier et al., 1990). Personality disorders (Cluster B in particular) amongadolescents with SUDs are highly prevalent (Grilo et al., 1995). Finally, as suggestedby studies showing language deficits in youth affected by or at high riskfor SUDs, learning disabilities or disorders may also show an increased incidenceof comorbidity (Moss, Kirisci, Gordon, & Tarter, 1994). Patients withcomorbid psychiatric disorders continue to be a challenge for clinicians andresearchers in the assessment and treatment domains.PREVENTIONEfforts to curtail substance abuse concentrate on activities designed for supplyand-demandreduction. It has been reported that the use of alcohol by youthsdeclines when either the price of alcoholic beverages or the legal drinking ageincreases (Coate & Grossman, 1987). Similarly, a reduction in car accidentsamong youth resulted from the increase of the minimum drinking age to 21(O’Malley & Wagenaar, 1991).The goal of primary prevention among children and adolescents is to deferor preclude initiation of gateway substances such as cigarettes, alcohol, andmarijuana. The traditional education program is a prevention strategy used toincrease knowledge of the consequences of drug use. Investigators (Schinke,Botvin, & Orlani, 1991) found the assumption that increased knowledgedecreases drug use to be invalid. Affective education, which increases self-

568 V. TREATMENTS FOR ADDICTIONSesteem and enhances responsible decision making, and alternative activitiesprograms for adolescents were found to be ineffective in the prevention of druguse based on meta-analysis of the literature (Bangert-Drowns, 1988; Tobler,1986). Furthermore, all the prevention strategies noted previously were reportedto increase interest in drugs among some of the participants (Schinke etal., 1991). A more advanced prevention strategy is based on a psychosocialapproach. These prevention programs are aimed at enhancing self-esteem(Schaps, Moskowitz, & Malvin, 1986), social skills, and assertive skills forresisting substance use (Botvin, Baker, Filazola, & Botvin, 1990). However,these techniques failed to be successful in enhancing secondary prevention(Pentz, Dwyer, & MacKinnon, 1989).A study by Botvin, Baker, Dusenbury, Botvin, and Diaz (1995) implementeda curriculum covering life skills training (LST) and skills for resistingsocial influences to use drugs. This curriculum included booster sessions duringthe 2 years after completion of the intervention. The investigators reported asignificant and durable reduction in drug use 6 years later. The generalizabilityof the LST prevention approach for African American and Hispanic youth hasbeen supported (Botvin & Griffin, 2001). Most middle schools however, useproven prevention programs that combine effective content and delivery.Universal prevention programs may delay onset of drinking among low-riskbaseline abstainers; however, there is little evidence supporting their utility forat-risk adolescents (Masterman & Kelly, 2003). Brief interventions such asmotivational interviewing within a harm reduction framework may be wellsuited to for many adolescents.The challenge for health care providers is to identify individuals at highrisk before or shortly after initiation of substance use and to intervene to reducetransitional risk. One of the largest subpopulations of children at risk are thosewith at least one biological parent diagnosed with alcohol or substance dependence.These individuals are at greater risk of developing the same disorder, fourfoldand 10-fold, respectively (Goodwin, 1985; Tarter, 1992). Children ofopioid-dependent parents were reported to have high rates of psychopathologyand significant dysfunction in the academic, family, and legal life domains(Kolar, Brown, Haertzen, & Michaelson, 1994; Wilens, Biederman, Kiely,Bredin, & Spencer, 1995). Contrary to public perception, there is a need for amore balanced view regarding the natural history of children of alcoholics(COAs) primarily because (1) regardless of popular models of dysfunctionalCOAs, the majority of offspring raised with a dysfunctional alcoholic parent donot develop alcoholism (Wilson & Crowe, 1991) and (2) the negative labelingof adolescent COAs regardless of their current behavior was reported to berobust and potentially harmful (Burk & Sher, 1990). Resilence and protectivefactors are also important to consider (Wolin & Wolin, 1996).The heterogeneity of adolescent subpopulations needs to be recognized tobetter understand substance use and its transition to substance abuse and

25. Adolescent Substance Abuse 569dependence. This recognition is followed by determining the level of interventionrequired, whether primary, secondary, or tertiary prevention. The preventioneffort must also address adolescent needs in all domains of life, includingattitudes, expectations, and interactions with the community.Implications for policy-related initiatives have to do with supply reduction.Effective prevention programs are cost-effective. For every $1 spent ondrug use prevention, communities can save $4–5 in costs for drug abuse treatmentand counseling. The National Institute on Drug Abuse (NIDA; 2001) hasestablished a set of prevention principles, based on research of effective modelprograms. These principles state that prevention programs should (1) enhance“protective factors” and reverse or reduce known “risk factors”; (2) target allforms of drug abuse, including the use of tobacco, alcohol, marijuana, andinhalants; (3) teach skills to resist drugs when offered, strengthen personalcommitments against drug use, and increase social competence (e.g., in communications,peer relationships, self-efficacy, and assertiveness), in conjunctionwith reinforcement of attitudes against drug use; (4) use interactive methods,such as peer discussion groups, rather than didactic teaching techniques alone;(5) include a parent or caregiver component that reinforces what the childrenare learning and opens opportunities for family discussions about use of legaland illegal substances, and family policies about their use; (6) last long termover the school career, with repeat interventions to reinforce the original preventiongoals; (7) use family-focused prevention efforts that have a greaterimpact than strategies that focus on parents only or children only; (8) use communityprograms that include media campaigns and policy changes, such asnew regulations that restrict access to alcohol, tobacco, or other drugs; (9) usecommunity programs to strengthen norms against drug use in all drug abuse preventionsettings, including the family, the school, and the community; (10)offer school-based opportunities to reach all populations and also serve asimportant settings for specific subpopulations at risk for drug abuse, such aschildren with behavior problems or learning disabilities and those who arepotential dropouts; (11) be adapted to address the specific nature of the drugabuse problem in the local community; (12) be more intensive for high-risk targetpopulations, and the earlier age it must begin; and (13) be age-specific,developmentally appropriate, and culturally sensitive.ASSESSMENTA significant step toward addressing the need for better therapeutic interventionsfor adolescents with SUDs has been the recognition of the assessment and treatmentof SUDs as potentially a multistep task. The expert committee of the Instituteof Medicine report (1990) of the adolescent assessment/referral system developedby the NIDA (Rahdert, 1991; Tarter, 1990) recommend a three-phase

570 V. TREATMENTS FOR ADDICTIONSprocess. An initial screening phase involves identification of health disorders,psychiatric problems, and psychosocial maladjustment. Based on the screeningphase, a minority of adolescents are required to go through the second extensiveassessment phase. This assessment provides a diagnostic summary that identifiesthe adolescent’s treatment needs within specific life domains, such as substanceuse, psychiatric status, physical health status, school adjustment, vocational status,family function, peer relationship, leisure and recreation activity, and legalsituation. The third phase involves the preparation and implementation of anintegrated, problem-focused, and comprehensive treatment plan.Substance use and SUDs are multidimensional behaviors that demand athorough assessment of several dimensions of substance use behavior in additionto quantity and frequency of use. Within the domain of substance usebehavior, important dimensions include the pattern of use (quantity, frequency,onset, and types of agents used), negative consequences (school–vocational,social–peer–family, emotional–behavioral, legal and physical), context of use(time–place, peer use–attitudes, mood antecedents, consequences, expectancies,and overall social milieu), and control of use (view of use as a problem,attempts to stop or limit use, other DSM-IV-TR dependence criteria).Clinicians frequently question whether any self-report by an adolescentabout substance use is accurate. Self-reports may, however, provide reliable andvalid information, particularly when no legal contingencies for drug use arepending (Barnea, Rahav, & Teichman, 1987; Winters, 1992). The clinicianmay attempt to substantiate suspected use by reports from third parties orthrough the use of urine or blood toxicology. Parents, however, tend tounderreport their child’s level of drug involvement and resulting problems(Burleson & Kaminer, in press; Winters, Stinchfield, & Opland, 2000).A variety of instruments are available and others are being developed toassist in the screening and detailed assessment of substance use, and relatedbehaviors and problems. Although readers are referred elsewhere for a moredetailed discussion of individual instruments (Leccese & Waldron, 1994; Winters,Latimer, & Stinchfield, 2001), we provide several examples of types ofinstruments.Screening instruments are used to identify the potential presence of SUDas a preliminary step toward a more detailed, comprehensive assessment,although many substance use/abuse screening instruments are designed to measurethe substance use domain only, such as the CAGE (cut down, annoyed,guilty, eye opener) developed by Ewing (1984). The CRAFFT (car, relax,alone, forget, friends, trouble), a longer, modified version of the CAGE,has shown superior psychometric properties (Knight, Sherritt, Shrier, Harris,& Chang, 2002). Other instruments screen other domains for psychosocialfunctioning; Problem-Oriented Screening Instrument for Teenagers (POSIT;Rahdert, 1991); Drug Use Screening Inventory (DUSI; Tarter, 1990); PersonalExperience Screening Questionnaire (PESQ; Winters, 1992); and Substance

25. Adolescent Substance Abuse 571Abuse Subtle Screening Inventory—Adolescent Version (SASSI-A; Miller,1990). Comprehensive assessment instruments usually provide more detailedinformation about substance use behavior, as well as other domains offunctioning. The formats for comprehensive instruments vary, with some beingself-report questionnaires (e.g., Personal Experience Inventory [PEI]; Winters& Henly, 1988), others being structured interviews (e.g., Adolescent DrugAbuse Diagnosis [ADAD]; Friedman & Utada, 1989), and still others beingsemistructured interviews (e.g., Adolescent Problem Severity Index [APSI];Metzger, Kushner, & McLellan, 1991; Teen Addiction Severity Index [T-ASI];Kaminer, Bukstein, & Tarter, 1991; Kaminer, Wagner, Plummer, & Seifer,1993); and the Global Appraisal of Individual Needs [GAIN]; Dennis, Titus,White, Unsicker, & Hodgkins, 2003).Toxicology of bodily fluids, usually urine, but also blood and hair samples,can be used as a screen to detect the presence of specific substances for both initialassessment and as an ongoing check for substance use. The optimal use ofurine screens requires proper collection techniques, including visual proof ofsample authenticity, evaluation of positive results, and a specific plan of actionshould the specimen be positive for the presence of substance(s) (Casavant,2002; Cole, 1997). Clinicians should establish rules regarding the confidentialityof the results prior to testing.LEVEL OF CAREPlacement of adolescents with SUDs at a particular level of care is based onseveral factors. Dispositional options (triage) involve a variety of possibilities,which may also depend on service availability. Despite certain inherent advantagesof residential programs in terms of intensity and control, the generalizationof improvement made during these programs is uncertain. More emphasisshould be given to community-based programs that may guide the adolescentand his or her family through their real-life problems and experiences.Appropriate referrals to an inpatient unit or residential program mayinclude (1) adolescents with SUDs who have either failed or do not qualify foroutpatient treatment; (2) dually diagnosed adolescents with moderate or severepsychiatric disorders; (3) adolescents who display a potentially morbid or mortalbehavior toward themselves or others (e.g., suicidal and self-injurious behavior);(4) adolescents who are intravenous drug abusers, drug dependent, or needto be detoxified; (5) patients with accompanying moderate-to-severe medicalproblems; (6) adolescents who need to be isolated from their community toensure treatment without interruptions; and (7) pregnant adolescents whomanifest SUDs that endanger the fetus (Kaminer, 1994).Enrollment criteria in a drug-free outpatient or partial hospitalization settinginclude (1) SUDs and other psychiatric disorders that do not require inpa-

572 V. TREATMENTS FOR ADDICTIONStient treatment (i.e., psychiatric disorder severity less than moderate); (2) previoussuccessful outpatient treatment follow-up after completion of inpatienttreatment; and (3) agreement to a contingency contract that will delineate frequencyof visits, compliance with curriculum, including random urine screening,consequences of noncompliance and relapse, and participation in the communitynetwork, including self-help groups. Similar placement criteria foradolescents with SUDs, such as the American Society for Addiction Medicine(ASAM) criteria tailored from the Cleveland Criteria (Hoffmann, Halikas, &Mee-Lee, 1987), have some level of face validity; however, no research regardingtheir reliability or predictive validity supports them. The ASAM PlacementCriteria (2001), specify five broad levels of care for each group: Level 0.5, EarlyIntervention; Level I, Outpatient Treatment; Level II, Intensive Outpatient/Partial Hospitalization; Level III, Residential/Inpatient Treatment; and LevelIV, Medically Managed Intensive Inpatient Treatment. Within these broadlevels of service is a range of specific levels of care. Admission criteria for theselevels of care are based on severity scores for the following six dimensions: acuteintoxication/withdrawal potential; biomedical conditions and complications;emotional, behavioral, or cognitive conditions and complications; readiness tochange; relapse, continued use, or continued problem potential; and recoveryenvironment.TREATMENTAlthough there are over 1,000 studies on drug and alcohol treatment in adults(Kranzler, Amin, Modesto-Lowe, & Onken, 1999), there are a relatively smallnumber of adolescent treatment outcome studies. The limited literature on efficacystudies is characterized, however, by significant methodological limitations(Kaminer, 2000), including small sample size, lack of placebo-controlledcondition, different selection criteria, inadequate measurement of psychosocialand comorbid psychiatric conditions, failure to indicate compliance and attritionrates, little description of actual treatment involved or measures to maintaintreatment fidelity by counselors, unmanualized interventions (making replicationdifficult), therapist variability, lack of or deficiency in objectivemeasurement, such as drug urinalysis for treatment outcome, and inadequatefollow-up of both treatment completers and noncompleters.Catalano and associates’ (1990–1991) review of adolescent treatment outcomein 16 studies concluded that treatment is better than no treatment. Pretreatmentfactors associated with outcome were race, seriousness of substanceuse, criminality, and educational status. The in-treatment factors predictive ofoutcome were time in residential treatment, involvement of family, use of practicalproblem solving, and provision of comprehensive services, such as housing,academic assistance, and recreation. Posttreatment variables, which werethought to be the most important determinants of outcome, included associa-

25. Adolescent Substance Abuse 573tion with nonusing peers, involvement in leisure time activities, work, andschool.In more recent reviews of the literature (Deas & Thomas, 2001; Williams& Chang, 2000; Winters, 1999), similar variables were reported to be mostconsistently related to successful outcome: treatment completion, low pretreatmentuse, peer and parent social support, and nonuse of substances. These morerecent reviews also found evidence that treatment was superior to no treatment.Although insufficient evidence was found to compare the effectiveness of treatmentmodalities, early reports indicated that outpatient family therapy appearedto be superior to other forms of outpatient treatment. These findingshowever, have not been supported by most recent studies.The Drug Abuse Treatment Study for Adolescents (DATOS-A) is amultisite, prospective treatment outcome study of 1,732 adolescent admissionsto 23 programs in four U.S. cities (Grella, Hser, Joshi, & Rounds-Bryant, 2001;Hser et al., 2001). In the year following treatment, patients reported decreasedheavy drinking, marijuana and other illicit drug use, and decreased criminalinvolvement, as well as improved psychological adjustment and school performance.Although the length of time in treatment was generally short, longertreatment stays were associated with several favorable outcomes. Nearly twothirds(63%) of the sample reported at least one comorbid DSM-IV-TR disorder.At baseline, when compared with noncomorbid youth with SUDs, theseyouth with comorbid disorders were more likely to be alcohol- or other-drugdependentand to have more problems with family, school, and criminalinvolvement. Although comorbid youth reduced their drug use and problembehaviors after treatment, they were more likely to use marijuana and hallucinogens,and to engage in delinquent behavior in the 12 months after treatmentwhen compared with noncomorbid adolescents (Grella et al., 2001).Data indicate that most adolescents return to some level of alcohol orother drug abuse following treatment (Brown, Vik, & Creamer, 1989; Brown etal., 1990). Adolescents in substance abuse treatment begin substance use at anearlier age and progress rapidly to the use of multiple drugs, followed by thedevelopment of SUDs (Brown et al., 1989; Myers & Brown, 1990). Other clinicalfeatures of adolescents entering treatment include high levels of coexistingpsychopathology or early personality difficulties; deviant behavior; school difficulties,including high levels of truancy; and family disruption and substanceabuse (Bukstein et al., 1992; Doyle, Delaney, & Trobin, 1994). Several pretreatmentcharacteristics predict completion of treatment by adolescents, includinggreater severity of alcohol problems; greater use of drugs other thanalcohol, marijuana, and tobacco; a higher level of internalizing problems; andlower self-esteem (Blood & Cornwall, 1994; Doyle et al., 1994, Kaminer,1992a). Premorbid psychopathology (e.g., conduct disorder) is negatively correlatedwith treatment completion and with future abstinence (Kaminer,Burleson, & Goldberger, 2002; Myers, Brown, & Mott, 1995). Although factorssuch as severity of substance use may predict short-term treatment outcomes,

574 V. TREATMENTS FOR ADDICTIONSmost longer term outcomes may depend on social–environmental factors. Thisis consistent with studies of relapse among adolescent populations, which suggestthat relapse in adolescents is more often associated with social pressures touse rather than situations involving negative affect, as is usually found in adultrelapse (Brown, Myers, Mott, & Vik, 1994; Vik, Grisel, & Brown, 1992). Adolescents’attendance at self-support or aftercare groups is associated with higherrates of abstinence and other measure of improved outcome when comparedwith those adolescents who did not attend such groups (Harrison & Hoffmann,1989).Despite a higher level of return to substance use among adolescents aftertreatment, abstinent teens may expect decreased interpersonal conflict, improvedacademic functioning, and increased involvement in social and occupationalactivities (Brown et al., 1994). Patterns of substance abuse among adolescentsappear to become more stable between 6 and 12 months after treatment(Brown et al., 1994). An extensive review of treatment outcome studies conductedin the 1970s and 1980s concluded that treatment can be effective and isbetter than no treatment (Catalano et al., 1990–1991). However, an unequivocalsuperiority of specific treatment modalities or components has not beendemonstrated (Winters, 1999).Psychosocial treatment strategies that have shown promise in reducingSUDs among adolescents include family therapies such as multisystemictherapy (Henggeler, Pickrel, & Brondino, 1996), functional family therapy(Waldron, Slesnick, Brody, Turner, & Peterson, 2001), and multidimensionalfamily therapy (Liddle, Dakov, & Diamond, 2001), as well as behavioraltherapy (Azrin, Donohue, & Besalel, 1994), cognitive-behavioral therapy(Kaminer, Blitz, Burleson, Sussman, & Rounsaville, 1998; Kaminer, Burleson,& Goldberger, 2002), Motivational Interviewing (Monti, 1999), contingencymanagement reinforcement (Corby, Roll, & Ledgerwood, 2000), the Minnesota12-step model (Winters et al., 2000), and integrative models of treatment(Dennis et al., 2004; Kaminer, 2001). A common recommendation for youth isto attend 12-step groups. It is noteworthy, however, that little is known regardingthe effects of this approach on adolescents. Kelly, Myers, and Brown (2000)reported modest beneficial effects of 12-step attendance, which were mediatedby motivation but not by coping or self-efficacy.PHARMACOTHERAPY OF DUAL DIAGNOSESPharmacotherapy or medication treatment potentially targets several areas, includingtreatment of withdrawal, use to counteract or decrease the subjectivereinforcing effects of illicit substance use, and treatment of comorbid psychopathology.Unfortunately, no systematic research evaluates the efficacy and safetyof any psychotropic medication in the treatment of adolescents with SUDs(Kaminer, 1995). Although clinically significant withdrawal symptoms appear to

25. Adolescent Substance Abuse 575be rare in adolescents (Martin et al., 1995), there is little rationale for using differentdetoxification protocols than those used for adults. The use of agents to blockthe reinforcing effects of various substances, as aversive agents (e.g., disulfiram) orto relieve craving during and after acute withdrawal, has been studied in adultsbut has received scant attention in adolescents. Kaminer (1992b) described theuse of desipramine in an adolescent with cocaine dependence. Aversive pharmacologicaltreatment with agents such as disulfiram is rare in adolescents. In twocase studies, Myers, Donaue, and Goldstein (1994) expressed caution in usingdisulfiram in adolescents. The opiate antagonist naltrexone, used safely and effectivelyin adults to reduce cravings for alcohol, may hold promise for the treatmentof adolescents with alcohol use disorder according to a case study reported byWold and Kaminer (1997).The high prevalence of coexisting psychiatric disorders in adolescents withSUD presents additional targets for pharmacological agents (Bukstein &Kithas, 2003; Bukstein et al., 1989). Potential targets for pharmacological treatmentinclude depression and other mood problems, ADHD, severe levels ofaggressive behavior, and anxiety disorders. Unfortunately, few data in the literaturedemonstrate the efficacy of pharmacological agents prescribed for adolescentswith a SUD and comorbid psychiatric disorders. Preliminary data suggestthat selective serotonergic reuptake inhibitors may reduce problem drinking inadult drinkers (Naranjo, Kadlec, Sanheuza, Woodley-Remus, & Sellars, 1990),and both depression and drinking behavior in depressed adult alcoholics(Cornelius et al., 1993). However, a recent study indicates that these agentshave a limited clinical utility (Kranzler et al., 1995). In general, cliniciansshould use the same caution in considering pharmacological treatment for adolescentswith a comorbid SUD and psychiatric disorders, as they do in youthwith psychiatric symptoms alone.Only more recently has there been research evaluating the efficacy andsafety of any psychotropic medication in the treatment of adolescents withSUDs (Bukstein & Kithas, 2003; Kaminer, 2001). Open trials with pemolineand bupropion for ADHD, and fluoxetine for depression, in a population ofdrug-dependent delinquents have shown promise (Riggs, Milkovich, Coffman,& Crowley, 1997; Riggs, Leon, Mikulich, & Pottle, 1998). More recently, adouble-blind, placebo-controlled trial of a stimulant medication demonstratedthe efficacy of medication improving ADHD symptoms in adolescents withcomorbid ADHD and an SUD. This study also demonstrated that medicationtreatment of ADHD alone, without specific SUD or other psychosocialtreatment, did not decrease substance use (Riggs, Hall, Mikulich-Gilbertson,Lohman, & Kayser, 2004). Lithium, in a randomized controlled trial (Geller etal., 1998), and serotonergic reuptake inhibitors, in open trials (Cornelius et al.,2001; Riggs et al., 1997), have produced significant improvements in adolescentswith an SUD and comorbid mood disorders.An SUD may increase the potential for intentional or unintentional overdose.Some pharmacological agents may have inherent abuse potential. Critical

576 V. TREATMENTS FOR ADDICTIONSissues in the use of pharmacotherapy include avoiding the precipitation orexacerbation of psychiatric symptoms by the abused substances and the need toachieve some level of abstinence or control of substance use before a more optimalassessment of symptoms and starting pharmacological treatment, thepotential of acute drug effects resulting in intentional or unintentional overdose,and the potential abuse of the pharmacotherapeutic agents themselves.The treatment of ADHD among populations with SUDs remains problematicdue to the abuse potential of central nervous system stimulants by the patient,family, and peers (Coetzee, Kaminer, & Morales, 2002; Kaminer, 1995). Theuse of therapeutic stimulants by patients correctly diagnosed with ADHDdoes not lead to initiation of an SUD (Wilens, Faraone, Biederman, &Guanawardene, 2003). In addition to close supervision of medication compliance,clinicians should consider the use of effective agents with much lowerabuse potential, such as tricyclic antidepressants, bupropion, and pemoline.Longer acting stimulants, while not immune from being abused, may have alower abuse potential than shorter acting stimulants.Although pharmacotherapy of adolescents with SUDs offers a strongpotential adjunct for treatment, the use of medications does not alleviate theneed for psychosocial treatment that directly addresses substance use andrelated behaviors.Although not specifically studied, the multiple areas of possible dysfunctionin adolescents with SUDs and the many available treatment modalitiessuggest a multimodal approach. Treatment matching, or matching adolescentswith specific characteristics with appropriate levels of care and types of treatmentmodalities, is a concept that has received much attention in the adult literature.Psychiatric severity may be the best identified guide to matching(McLellan, Luborsky, Woody, O’Brien, & Druley, 1983). Despite two decadesof specific treatment for adolescents with SUDs, we know little about the“dose” of treatment necessary for successful outcomes, nor do we know muchabout the specific effects of characteristics such as gender, race, and comorbidpsychopathology on outcome. Research into adolescent treatment lags considerablybehind adult treatment research. As the focus of treatment for adolescentswith SUDs shifts from inpatient and residential settings to outpatient,partial hospitalization, and home/family-based treatments, the need for researchinto treatment effectiveness is critical.DISCHARGE AND AFTERCAREMaintenance of treatment gains in the months after treatment ends has beenproblematic in youth with AOSUDs. An approximately 60% relapse rate wasreported during the first 3 months after treatment completion, and an additional20% relapsed during the rest of the first year (Brown et al., 1989). About60% of adolescents continued either to vacillate in and out of recovery after

25. Adolescent Substance Abuse 577discharge from the Cannabis Youth Treatment study (Dennis et al., 2004) or tomanifest at least some form of substance abuse (Kaminer, Burleson, et al.,2002). Lack of continuity of care or aftercare programs for adolescents withAOSUDs is the rule rather than the exception.Partially overlapping terms such as “aftercare,” “continued care,” or “transitionof care” have been used in the literature interchangeably to describeinterventions used in the postacute treatment period. The Continuity of CareGuidelines for Addiction Services developed by the American Academy ofAddiction Psychiatry (AAAP) defined “continuity” as follows: “Transitionsshould incorporate relevant elements of any preexisting treatment plan. Treatmentplans should be relevant to the entire course of an episode of illness/disabilityso that they can provide a degree of continuity in the context of change”(Sowers, 2003, p. 2).The timing and level of therapeutic services in important. The more ancillarycommunity therapeutic services received during treatment, the better theshort-term outcome (Burleson & Kaminer, in press). The more therapeutic servicesreceived posttreatment, however, the poorer the short-term outcome.Godley, Godley, and Dennis (2002) reported that adolescents referredfrom residential treatment to continuing care services were significantly morelikely to initiate and receive more continuing care services, to be abstinentfrom marijuana 3 months postdischarge, and to reduce their 3-month postdischargedays of alcohol use when assigned to an assertive continuing care protocolinvolving case management and the adolescent community reinforcementapproach as compared to usual continuing care. Because of the statedimportance of aftercare, we need continued exploration of how to improveengagement and retention in aftercare. One of the most prominent aftercareoptions is school-based interventions. Most patients return to school; therefore,school-based tertiary prevention in the form of counseling, peer-led groups, andsupport group for “recovered” adolescents is warranted (Wagner, Kortlander, &Morris, 2001). Adolescents enrolled in these programs may also be instrumentalas role models in school-based primary and secondary prevention groups forhigh-risk youth. Also, continued participation in self-help groups, follow-upwith an outpatient clinic, and rigorous maintenance of a contingency dischargecontract are helpful for relapse prevention.Parents/caretakers should be encouraged to support the recovery processand to maintain a risk-free lifestyle for the adolescent (e.g., be aware of ominoussigns of relapse, keep curfew hours, and avoid enabling behavior).CONCLUSIONDespite the progress achieved in the understanding of different aspects of SUDsin adolescents, more research is needed to advance the field. Among the priorityareas for further research are interventions including prevention, and effec-

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CHAPTER 26Psychopharmacological TreatmentsELINORE F. MCCANCE-KATZTHOMAS R. KOSTENThis chapter reviews pharmacotherapies for abuse of nicotine, alcohol, benzodiazepines,opioids, and cocaine. Pharmacotherapies for substance use disorders(SUDs) have been developed to address two broad treatment categories: (1)acute withdrawal or the initial attainment of abstinence and (2) chronic maintenanceor the prevention of relapse. Agents for acute withdrawal are most relevantto dependence on opioids and alcohol.Maintenance agents might directly benefit any protracted withdrawal syndrome,but the general rationale for maintenance pharmacotherapies is thatthey are either blocking or substitution agents. For example, the competitiveopioid antagonist naltrexone completely blocks the effects of heroin, includingthe subjective euphoria and the production of physiological dependence fromrepeated heroin use. Before administering blocking agents, detoxification isrequired to prevent withdrawal from the abused drug. In contrast, substitutionagents maintain the dependent state and will not cause withdrawal when givento dependent patients. Substitution agents prevent illicit drug use by bothreducing drug hunger and withdrawal and producing cross-tolerance. “Crosstolerance”means that tolerance, which is the diminished intensity of a drug’seffects after repeated and sustained dosing, will develop not only to the precisedrug that is being taken repeatedly but also to other drugs from the same pharmacologicalclass (e.g., methadone and heroin, which are both opioids). Examplesof substitution agents that produce cross-tolerance to heroin and have beenshown to be effective in reducing illicit opioid use are methadone, levo-alphaacetylmethadol (LAAM), and buprenorphine.588

26. Psychopharmacological Treatments 589Blocking and substitution are not necessarily incompatible, and partialagonists provide a pharmacological tool to combine both approaches in treatingdrug dependence. At low doses partial agonists such as buprenorphine, suppresswithdrawal symptoms in dependent patients and produce some subjective reinforcingproperties, whereas at higher dosages, these same medications block thereinforcement from full agonists. Thus, buprenorphine at low doses suppressesheroin withdrawal and at high doses blocks the euphoric Finally, any of thesepharmacotherapies should be administered in the context of psychosocial interventionsdeveloped to encourage adherence to medications to facilitate therehabilitation that is a necessary component to any successful treatment.In the following sections, we review a variety of standard treatments forSUDs, as well as several new agents. The goal is to provide an overview ofcurrent pharmacological treatments for nicotine, alcohol, sedative/hypnotic,opioid, and cocaine use disorders.NICOTINE PHARMACOTHERAPIESA variety of pharmacotherapies are available for the treatment of nicotinedependence. Pharmacotherapies for nicotine dependence, which have beenshown to have some efficacy for smoking cessation and the relief of acute withdrawalsymptoms, include nicotine replacement therapy, several antidepressants,and clonidine. A nicotine antagonist is also available.Acute Withdrawal MedicationsNicotine polacrilex gum contains 2 or 4 mg of nicotine; 50–90% of the nicotineis released, depending on the rate of chewing, and is absorbed through thebuccal mucosa, with peak nicotine concentrations reached in 15–30 minutes(Lee & D’Alonzo, 1993). Scheduled dosing (i.e., 1 piece of gum per hour) ismore effective than using the gum as needed for craving (Hughes, 1996).Absorption of nicotine is decreased in an acidic environment, and patientsshould be instructed not to consume acidic beverages such as coffee, juices, andsoda immediately before, during, or after use of the gum (Henningfield,Stapleton, Benowitz, Grayson, & London, 1993). Nicotine polacrilex has beenshown to reduce withdrawal symptoms of anger, irritability, anxiety, depression,and decreased concentration, although craving for cigarettes is unaffected (Lee& D’Alonzo, 1993). The average length of treatment is 4–6 weeks (Hatsukami,Huber, Callies, & Skoog, 1993). One-year follow-up studies show that quitrates for nicotine polacrilex gum range from 8 to 10% when given with physicianadvice and minimal support. This increases to 29% when combined withbehavioral treatment (Hall, Hall, & Ginsberg, 1990). The 4 mg dose of nicotinepolacrilex gum is more effective than the 2 mg nicotine dose in the treat-

590 V. TREATMENTS FOR ADDICTIONSment of highly dependent smokers who smoke in excess of 25 cigarettes daily(Hughes, Goldstein, Hurt, & Schiffman, 1999).Transdermal nicotine administration is another variation of the nicotinereplacement approach to smoking cessation. These systems are available in regimensthat deliver nicotine over a 16- or 24-hour duration (delivering 15 mgand 21–22 mg, respectively) (Palmer, Buckley, & Faulds, 1992). Nicotine isslowly absorbed, with peak levels reached 6–10 hours after application, and nicotinelevels are about half those obtained through smoking. It is recommendedthat those smoking more than 10 cigarettes daily use the highest dose nicotinepatch, while those smoking fewer than 10 cigarettes per day can use the lowerdose patches. Patch use is generally recommended for 8 weeks, with 4 weeks atthe highest dose, followed by 2 weeks each at the lower doses prior to discontinuation.No advantage has been shown by use of the nicotine patch after 8weeks (Fiore et al., 2000). Abrupt cessation of patch use has not been associatedwith significant withdrawal; therefore, tapering may not be necessary(Fiore, Smith, Jorenby, & Baker, 1994). Transdermal nicotine systems havebeen generally well tolerated, with minor side effects of local irritation at theapplication site, mild gastric disturbances, and sleep disturbances, and their usehas been reported to be associated with delayed weight gain. Nicotine patchesproduce end-of-treatment smoking cessation rates from 18 to 77% (about twicethat of placebo-treated subjects), and 6-month abstinence rates range from 22to 42% (compared to 5–28% for placebo-treated subjects) with some fluctuationdepending on counseling (Fiore, Jorenby, Baker, & Kenford, 1992). Forthose who fail with either gum or patch alone, the two may be combined. Inthese cases, the highest dose of the nicotine patch available should be used withthe 2 mg nicotine gum. Other nicotine delivery systems used less frequently inclinical practice include a nasal spray and an inhaler.The observed relationship between nicotine dependence and mood disordersled to research examining the potential for antidepressant medicationsas effective pharmacotherapies for cigarette smoking cessation (Glassman,1997), including tricyclic, monoamine oxidase (MAO) inhibiting, serotoninreuptake–inhibiting, and other forms of antidepressants. Two large, multicenterclinical trials demonstrated the efficacy of bupropion for the treatment of nicotinedependence, and it is recommended as a first-line treatment for smokingcessation (Fiore et al., 2000). Disadvantages of bupropion include more frequentadverse events of tremor, rash, headache, urticaria, insomnia, and drymouth, resulting in an 8–12% discontinuation rate in clinical trials. Bupropionalso lowers seizure threshold and should not be used in those at risk for seizures(American Psychiatric Association, 1996). The antidepressant dose is the sameas that for the treatment of depression, allowing for the pharmacological treatmentof both disorders simultaneously.Two positive clinical trials (Hall et al., 1998; Prochaska et al., 1998) haveled to the recommendation of nortriptyline as a second-line choice for smokingcessation (Fiore et al., 2000). The target dose of this drug for treatment of nico-

26. Psychopharmacological Treatments 591tine dependence is 75–100 mg daily, but it should be used with caution in thosewith cardiovascular disease given its possible effects on cardiac function. Likebupropion, nortriptyline is an antidepressant and may be useful in the treatmentof depressed cigarette smokers. Another antidepressant related medication,selegiline, an MAO inhibitor, has shown some recent efficacy in reducingsmoking (George et al., 2003).Finally, clonidine, a noradrenergic alpha 2agonist that decreases centralsympathetic activity, may be an effective treatment for those who do not wantnicotine replacement therapy or who have failed other smoking cessationmethods.ALCOHOL PHARMACOTHERAPIESAcute Withdrawal MedicationsAcute withdrawal from alcohol is a serious medical condition that can precipitateadrenergic activation, seizures, or delirium tremens, a condition with up to15% mortality when untreated (Kosten & O’Connor, 2003). The current standardapproach to alcohol detoxification uses tapering dosages of benzodiazepines,such as chlordiazepoxide or clonazepam, which are effective in relievingthe autonomic hyperactivity of withdrawal and will prevent seizures. Benzodiazepinesare initially made available on an as-needed basis, with parameters fordosing based on appearance of withdrawal symptoms including agitation,diaphoresis, tremor, hypertension, and tachycardia. Withdrawal symptoms canbe assessed over the course of the detoxification using the Clinical InstituteWithdrawal Assessment of Alcohol Scale, revised (CIWA-Ar; Sullivan,Sykora, Schneiderman, Naranjo, & Sellers, 1989). This extensively studiedscale has been shown to have good reliability, reproducibility, and validity. Thescale measures 10 symptoms associated with withdrawal, each of which can bescored in increasing severity on a scale of 0–7 (with the exception of orientationand clouding of sensorium, which are scored on a scale of 0–4. Scoresabove 10 indicate a need for medication to treat withdrawal symptoms. Furthermore,the CIWA predicts that those with a score of greater than 15 are atincreased risk for severe alcohol withdrawal, with higher scores conveyinghigher risk. Although detoxification schedules must be individualized, a benzodiazepinetaper can usually be accomplished in 3–4 days. Patients with hepaticdisease should be detoxified with lorazepam or oxazepam, shorter-acting drugsthat, unlike the other benzodiazepines, have no active metabolites requiringhepatic clearance. Lorazepam is also a good choice for detoxification of thepatient with severe vomiting, because it is well absorbed by the intramuscularroute of administration.Anticonvulsants have been shown to be equal in effectiveness to benzodiazepinesin the treatment of alcohol withdrawal (Malcolm, Myrick, Brady, &Ballenger, 2001). Multiple studies support the efficacy of sodium valproate

592 V. TREATMENTS FOR ADDICTIONS(1,000 mg daily in divided doses) in reducing the symptoms associated withalcohol withdrawal. Further double-blind studies are needed before routine useof this drug can be recommended in alcohol detoxification. Several studiesreported on the use of valproate, which appears to show good success when usedalone for alcohol detoxification (Hillbom et al., 1989; Roy-Byrne, Ward, &Donnelly, 1989). Sodium valproate should not be used in those with preexistinghepatic or hematological abnormalities. The extended release formulationof valproate now available may be superior for detoxification in order to haveonce daily dosing, less variation in blood levels, reduction in toxicity (peak levels),and reduced symptom breakthrough during dosing (trough levels).Carbamazepine, an anticonvulsant that has been widely used in alcoholwithdrawal, has been shown to be superior to placebo in the rapidity withwhich it relieves alcohol withdrawal symptoms, including tremor, sweating,palpitations, sleep disturbances, depression, anxiety, and anorexia (Bjorkquistet al., 1976). In outpatient randomized clinical trials comparing carbamazepineto tapering dosages of benzodiazepines, the patients receiving carbamazepinehad higher success rates and fewer withdrawal symptoms during alcohol detoxification(Agricola, 1982; Malcolm, Ballenger, Sturgis, & Anton, 1989). In astudy comparing carbamazepine to lorazepam for treatment of alcohol withdrawal,participants were treated over 5 days with a fixed-dose taper ofcarbamazepine 800 mg versus lorazepam 8 mg on day 1. Follow-up showedthat both drugs effectively suppress withdrawal symptoms, but carbamazepinetreatedindividuals showed less posttreatment drinking behavior, and those whoreported drinking stated that they drank less following carbamazepine treatment(Malcolm et al., 2002). This finding has yet to be replicated in additionalstudies. Carbamazepine has common side effects of dizziness, nausea, and vomiting.It may induce the metabolism of drugs that are substrates of hepaticcytochrome P450-3A4 and should not be used in persons with severe hepatic orhematological disease(s). Its efficacy has also not been established in severealcohol withdrawal. However, carbamazepine can be effective alone as a withdrawalmedication in mild to moderate alcohol withdrawal syndromes.The combination of anticonvulsants and moderate doses of benzodiazepinescan facilitate successful alcohol detoxification in those with a history ofprevious alcohol withdrawal seizures or head trauma (Kasser, Geller, Howell, &Wartenberg, 1997). In these cases, the anticonvulsant should be administeredconcomitantly with benzodiazepines in dosages that will provide therapeuticanticonvulsant blood levels. The anticonvulsant should be tapered within aweek of completion of the benzodiazepine taper. There is no indication for continuationof anticonvulsant therapy in individuals who have experienced generalized,nonfocal seizures secondary to alcohol withdrawal. It is, however,important to assess such patients carefully, because any focal neurological signsmay be indicative of an underlying neurological disorder requiring treatment.Two newer anticonvulsants, vigabatrin and gabapentin, have been exam-

26. Psychopharmacological Treatments 593ined as adjunctive therapies for the treatment of alcohol withdrawal (Myrick,Brady, & Malcolm, 2001; Myrick, Malcolm, & Brady, 1998), but further controlledstudies are needed. Two older medicines, phenytoin and phenobarbitalare not recommended for routine use.Protracted withdrawal consisting of subtle symptoms such as sleep dysregulation,anxiety, irritability, and mood instability lasting weeks to months arereported by some alcohol-dependent patients. Patients experiencing such symptomsare more vulnerable to relapse.Maintenance MedicationsA variety of agents have been used for reducing relapse to alcohol use, includingdisulfiram and naltrexone. Other medications include agents such as serotoninreuptake inhibitors (SRIs), ondansetron, topiramate, buspirone, andacamprosate.Disulfiram is a relatively nonspecific, irreversible inhibitor of sulfhydrylcontainingenzymes (Wright & Moore, 1990). The target enzyme forthe pharmacological effect of disulfiram in the treatment of alcohol addictionis aldehyde dehydrogenase, which converts acetaldehyde to acetate inalcohol metabolism. When ethyl alcohol is present in the liver, disulfiramcauses acetaldehyde to accumulate, leading to the disulfiram–alcohol reaction:flushing, weakness, nausea, tachycardia, and, in some instances, hypotension(Wright & Moore, 1990). Disulfiram has not been shown to be effective inachieving abstinence or delaying relapse (Fuller & Roth, 1979). However, inmotivated patients who are intelligent, not impulsive, and have no comorbidmajor psychiatric disorder, and in combination with psychosocial treatments,disulfiram may be effective (Fuller et al., 1986). Treatment of the disulfiramreaction is primarily supportive and includes fluid hydration, oxygen, andTrendelenburg posture (Elenbaas, 1977). Disulfiram must not be initiated untilalcohol is completely eliminated (usually 24 hours after the last drink). Standarddaily dose is 250 mg orally (range, 125–500 mg daily). The time to onset ofaldehyde dehydrogenase inhibition sufficient to result in a reaction on alcoholconsumption is 12 hours, and aldehyde dehydrogenase recovery is completewithin 6 days of the last disulfiram dose (Helander & Carlsson, 1990). Patientstaking disulfiram must be warned to avoid alcohol-containing products andfoods. Disulfiram may also produce a variety of adverse effects, which are rare,but the most severe are hepatotoxicity and neuropathies. This medicationshould be avoided in patients with moderate to severe hepatic dysfunction,peripheral neuropathies, pregnancy, renal failure, or cardiac disease.Opioid antagonists can be used in the treatment of alcohol dependence.Volpicelli, Alterman, O’Brien, and Hayashida (1992) conducted a doubleblind,controlled study in which 35 male veterans were randomized to naltrexone(50 mg daily) and 35 to placebo. Naltrexone was found to significantly

594 V. TREATMENTS FOR ADDICTIONSreduce alcohol craving, days of drinking per week, and the rate of relapseamong those who drank. The second study (O’Malley et al., 1992) involved 97subjects and used a 2 × 2 design in which two of the groups receivednaltrexone, 50 mg daily, and two of the groups received placebo combined witheither coping skills therapy or a supportive therapy. During this 12-week trial,the rate of relapse in those patients treated with naltrexone was 45%, whereaspatients on placebo had a 90% relapse rate. Naltrexone was well tolerated andappeared to reduce alcohol consumption and relapse rates. The psychotherapyalso had an interesting interaction with naltrexone treatment. Although thepatients in the coping skills group were more likely to initiate drinking, theywere less likely to relapse than were patients treated with supportive therapy.For those subjects who drank during the study, the most success in avoidingrelapse was attained by the naltrexone and coping skills group, which had arelapse rate of less than 35%. The worst outcome was in the placebo and supportivetherapy group, where 90% relapsed, and for this placebo group, most ofthe relapses occurred within 30 days of initiating the study. Thus, the secondstudy showed promise for not only this pharmacotherapy but also its combinationwith a specific psychotherapeutic intervention.A 6-month follow-up study reported on the persistence of naltrexone andpsychotherapy effects following discontinuation after 12 weeks of treatment foralcohol dependence (O’Malley et al., 1996). Subjects who received naltrexonewere less likely to drink heavily (defined as more than 5 drinks/day in men, andmore than 4 drinks/day in women) or meet criteria for alcohol abuse or dependencethan those who received placebo, but only through the first month offollow-up, suggesting that some patients may benefit from a period of naltrexonetreatment exceeding 12 weeks. Others have also demonstrated a modestbut consistent effect of naltrexone treatment on drinking outcomes (Anton etal., 1999).Other drugs and administration forms include long-acting, depot formulationsof naltrexone being developed as an alternative to daily or thrice weeklyoral dosing of the drug. (Volpicelli, Rhines, & Rhines, 1997). The opiateantagonist, nalmefene, is also being examined as a treatment for alcoholdependence. It may have advantages over naltrexone in that it is active notonly at mu opioid receptors but also at kappa and delta opioid receptors. It mayhave fewer gastrointestinal side effects, better bioavailability, and less liver toxicityassociated with its use (Mason, Salvato, & Williams, 1999).Serotonergic agents, including buspirone (5-HT 1Aagonist) (Kranzler et al.,1994), SRIs, and ondansetron (5-HT 3antagonist) (Sellers, Higgins, Tompkins,& Romach, 1992), have been studied as treatments for alcohol dependence butresults have been limited. The possible matching of medications to patient typeor comorbid condition may be an effective approach to treatment of alcoholdependence, but this remains to be demonstrated in clinical trials (Myrick etal., 2001). Studies showed that ondansetron reduced alcohol craving in early-

26. Psychopharmacological Treatments 595onset (but not late-onset) alcoholics, and reduced drinking in these individuals(Johnson et al., 2000), but these results need to be replicated in larger controlledtrials.Not yet available in the United States, acamprosate (calcium acetylhomotaurinate),an analogue of homocysteic acid, has a structure similar togamma-aminobutyric acid (GABA) and, as such, has been reported to stimulateinhibitory GABA transmission and to antagonize excitatory amino acids(Zeise, Kasparov, Capogna, & Zieglgansberger, 1993). These properties havebeen postulated to be important to reduction in alcohol craving (Littleton,1995). Acamprosate has no abuse potential, hypnotic muscle relaxant, oranxiolytic properties. Furthermore, it is not hepatically metabolized and is,instead, excreted as unchanged drug by the kidneys, allowing its safe use inthose with liver impairment, although it should not be administered to thosewith renal insufficiency (Wilde & Wagstaff, 1997). A review of acamprosatestudies showed that in 14 of 16 controlled clinical trials, those treated withacamprosate had higher rates of treatment completion for alcohol dependence,longer abstinence period to first drink, and higher overall abstinence rates thanthose treated with placebo (Mason, 2001; Mason & Ownby, 2000). Acamprosatetreatment in several studies also was associated with decreases in laboratoryindices of alcohol consumption, including gamma-glutamyltransferase andcarbohydrate-deficient transferrin (Graham, Wodak, & Whelan, 2002). Thedrug was found to be well tolerated and acceptable to patients.Several studies have compared naltrexone and acamprosate treatment foralcohol dependence. In a 1-year follow-up study, no differences were observedin time to first drink, but time to first relapse was shorter in acamprosate-treatedpatients, while those treated with naltrexone were found to have a greatercumulative number of days of abstinence, to consume fewer drinks at one time,and to have less craving for alcohol (Rubio, Jimenez-Arriero, Ponce, & Palomo,2001). In a study comparing naltrexone, acamprosate, naltrexone and acamprosatein combination, and placebo, both active drugs and the combination wereassociated with significantly longer time to first drink and relapse to alcohol userelative to placebo. Additionally, there was a trend toward more positive outcomesin the naltrexone-treated group relative to the acamprosate-treatedgroup. The combination was more effective than placebo or acamprosate butnot naltrexone (Kiefer et al., 2003).BENZODIAZEPINE PHARMACOTHERAPIESThe benzodiazepines are some of the most frequently prescribed medications inthe United States due to their efficacy as anxiolytics and muscle relaxants,rapid onset of action, and relatively low risk of toxicity relative to other medicationswith similar indications. However, benzodiazepines, similar to alcohol,

596 V. TREATMENTS FOR ADDICTIONShave abuse liability, and produce physiological and psychological dependence.Physiological dependence occurs with longer term (greater than 30 days) use,requiring tapering of the drug, and tolerance that develops with prolonged usecan lead to escalating dosages. Interestingly, severity of the withdrawal syndromedoes not correlate significantly with difficulty in benzodiazepine taper(Rickels, De Martinis, Rynn, & Mandos, 1999). Personality psychopathologyappears to contribute to withdrawal severity and lack of successful taper. Furthermore,a study examining benzodiazepine taper in a sample of sedative/hypnotic-dependent patients reported that those with personality pathologywere more likely to drop out of the taper in the early stage prior to significantdose reductions (Rickels, Schweizer, Case, & Garcia-Espana, 1988). In a 3-yearfollow-up study of outcomes, it was determined that those who participated in ataper leading to a 50% reduction in daily benzodiazepine use had a 39% rate ofbeing benzodiazepine-free. Eighty-six percent of those who refused a taper continuedbenzodiazepine use at 3 years, and those who successfully ended benzodiazepineuse reported significantly lower levels of anxiety compared to patientswho continued to use benzodiazepines (Rickels, Case, Schweizer, Garcia-Espana, & Fridman, 1991).Benzodiazepine taper can be undertaken rapidly in an inpatient setting orslowly on an outpatient basis. The taper of a benzodiazepine is usually undertakenwith the substitution of another benzodiazepine, particularly if thepatient is dependent on a drug with a short half-life. These drugs can be taperedby converting the daily reported use of a benzodiazepine reduced by 50% to theequivalent dose of chlordiazepoxide, clonazepam, or, in cases where there isconcern for hepatic disease and a decreased ability to metabolize the benzodiazepineand its active metabolites, or concern about inability of the patient totake oral medications, lorazepam. The total daily dose required to stabilize thepatient on the first day of the taper can be reduced by up to 10–20% daily, leadingto detoxification over several days.OPIOID PHARMACOTHERAPIESTreatment of OverdoseOpioid overdose is a medical emergency and can be life threatening when complicationsof coma and/or respiratory arrest occur. Naloxone is an injectabledrug that rapidly reverses effects of opioid overdose by displacing the opioidfrom receptors in the brain. Naloxone may be administered intravenously or, inthose without venous access, by subcutaneous injection. A dosage of 0.4–0.8mg should reverse most opioid overdoses. In dependent patients, lower doses(0.1–0.2 mg) may be sufficient; furthermore, it is not advisable to precipitatewithdrawal in these patients. Therefore, in these cases, treatment should beginwith lower naloxone doses, with the dosage increased as clinically indicated.

26. Psychopharmacological Treatments 597Once the symptoms of overdose have abated, it is important to continue tomonitor level of consciousness and respiratory status, because long-actingopioids may require prolonged naloxone treatment that can be administered byintravenous infusion. Patients with opioid overdose should react within minutesto this treatment. Failure to do so should call into question the workingdiagnosis and prompt additional evaluation.Treatment of Acute WithdrawalClonidine reduces the severity of acute opioid withdrawal. Using the opioidantagonists naloxone or naltrexone to precipitate withdrawal, while simultaneouslytreating the patient with relatively high doses of clonidine, has enabledopioid-dependent patients to become drug free within as little as 3 days,while minimizing the antagonist-precipitated symptoms (Charney et al., 1982;Kleber, Topazian, Gaspari, Riordan, & Kosten, 1987; Vining, Kosten, &Kleber, 1988). The duration of withdrawal using this approach was equivalentfor methadone- or heroin-dependent patients; ordinarily withdrawal symptomslast nearly twice as long after abruptly stopping methadone, just as they do afterstopping heroin (Kleber, 1981).Administering an antagonist such as naltrexone precipitates withdrawalwithin minutes for both types of patients, and this process of precipitationappears to equalize the duration of subsequent withdrawal symptoms. Theamount of clonidine needed to ameliorate these symptoms was also lessened bylarger initial doses of naltrexone. Detoxification with a starting dose of 12.5 mgof naltrexone required clonidine for only 4 days, with a total dose of 1.7 mg anda peak dose of 0.6 mg on day 1 (Vining et al., 1988). Thus, a more rapid andcomfortable procedure has evolved for acute detoxification relative to the useof clonidine alone. Another study showed that clonidine, and clonidine andnaltrexone in combination, are both efficacious regimens for the ambulatorytreatment of opioid withdrawal, with 70% of subjects completing detoxification(O’Connor et al., 1995).Tapering doses of methadone are often used in ambulatory detoxification,but the protracted withdrawal syndrome associated with methadone cessationcontributes to a high rate of relapse to opioid use (Senay, Dorus, Goldberg, &Thornton, 1977). Methadone can be administered in starting doses of 10–20mg to patients showing evidence of opioid withdrawal. Failure to suppress withdrawalsymptoms in 30–60 minutes can be followed with an additional dose of5–10 mg. A dose similar to the initial dose may be given 12 hours later, if necessary,although this is not usually practical in ambulatory detoxification settings.On day 2, the total dose administered on day 1 can be administered in a singledose. The methadone dose can then be decreased by 5 mg daily, or by 5 mgdaily until a dose of 10 mg daily is reached, at which time the dose continues tobe tapered by 2 mg daily (for an additional 5 days).

598 V. TREATMENTS FOR ADDICTIONSKhan, Mumford, Rogers, and Beckford (1997) reported that lofexidine, analpha 2adrenergic agonist that produces less hypotension than clonidine, can bea useful adjunctive medication during methadone detoxification. Lofexidinewas equal to clonidine in reducing symptoms of opioid withdrawal, andside effects of hypotension and lethargy were reported by substantially fewerpatients in the lofexidine group. Clonidine can also be used as an adjunctivemedication to assist with emerging withdrawal symptoms during detoxification,but medical complications related to hypotension and sedation can limit tolerancefor this drug. Methadone detoxification should be completed within 3weeks (Van den Brink, Goppel, & van Ree, 2003). Detoxification protocols aresummarized in Figure 26.1.Opioid detoxification can also be undertaken with buprenorphine, anopioid partial agonist (Kosten & Kleber, 1988; Lewis, 1985). In one study, heroinaddicts and methadone-maintained patients were converted to buprenorphinefor a month of stabilization at once-daily doses ranging from 2 to 8 mgsublingually. Following this period, buprenorphine was abruptly stopped, andthe patient was given a high dose of intravenous naloxone (35 mg) to precipitatewithdrawal from the buprenorphine (Kosten et al., 1989). This withdrawalsyndrome was relatively mild and treated with clonidine, if needed. Followingprecipitated withdrawal, it was possible for the patient to be started onnaltrexone the same day. Additional studies in which the sublingual formulationsof buprenorphine are used for detoxification are ongoing at this time.Buprenorphine can also be combined with clonidine and naltrexone for ahighly successful rapid detoxification that is medically safe and preferred bypatients to the alternative of clonidine alone or clonidine plus naltrexone inheroin- or methadone-stabilized patients. The details for such a buprenorphineprotocol are also provided in Figure 26.1.Another method of opiate detoxification has been termed “rapid” or“ultrarapid” detoxification in which withdrawal is precipitated by administrationof either naloxone or naltrexone, with heavy sedation or anesthesia to easewithdrawal symptoms. This procedure produces more severe withdrawal thanstandard opioid detoxification procedures, but the hypothesis is that the use ofan opioid antagonist to induce withdrawal will curtail the duration of the withdrawalsyndrome. This procedure has been associated with severe adverseevents, including complications of anesthesia, severe withdrawal symptomslasting for several days following the procedure, and, rarely, death (Badenoch,2002; Cucchia, Monat, Spagnoli, Ferrero, & Gertschy, 1998; O’Connor &Kosten, 1998; Rabinowitz, Cohen, & Atias, 2002; Scherbaum et al., 1998).Furthermore, this procedure has not been associated with better long-term outcomesin terms of relapse to opiate dependence, calling into question theexpense and risk of the procedure relative to other procedures for opioidwithdrawal (Cucchia et al., 1998; Lawental, 2000; Rabinowitz et al., 2002;Scherbaum et al., 1998).

Clonidine detoxification (9-day protocol)1 Detoxification day2 3 4Clonidine a,b0.1–0.2 mg Every 4 hours as(oral)neededMax. dose: 1 Max. dose: 1.2 mg onmg on day 1 days 2–45 6 7 8 9Taper to 0 ondays 5–8Naltrexone b 25 mg 50 mgClonidine with naltrexone induction (5-day protocol)Clonidine bPreload: 0.2–0.4 mgTaper to 0 on days 3–5Max. dose: 1.2 mg on days 1–2Oxazepam bPreload: 30–60 mgNaltrexone b 12.5 mg 25 mg 50 mg 50 mg 50 mgNote. As needed: oxazepam 30–60 mg every 6 hours for cramps, insomnia; ibuprofen 600 mg every 6 hours forcramps; prochlorperazine 5 mg i.m. every 6 hours for vomiting.a Hold for systolic blood pressure < 90 mm Hg or diastolic blood pressure < 60.b Oral dosing.MethadonedetoxificationMethadoneDetoxification day1 2 310–20 mg; may giveadditional 5–10 mg 12hours later if symptomsreemergeGive entire day1 methadoneamount as onedoseDecrease by 5 mg daily or decrease by 5mg daily until 10 mg/day; then decreaseby 2 mg daily to complete taperBuprenorphinedetoxification Day 1 Day 2 Day 3 Day 4 Days 5–7Buprenorphineat dose of 8–20mg daily taperedto 4 mg daily for≥ 2 daysDiscontinuebuprenorphinefor 24–96hoursClonidine 0.1 mg × 3 (9,10, and 11A.M.); eachdose spacedby 1 hour astolerated(check bloodpressure andhold iforthostatic);continue every6 hours astolerated; giveone additionaldose beforeleaving clinicNaltrexone12.5 mg atnoon0.1–0.3 mg at9 A.M.; thenevery 6 hours25 mg at 11A.M.0.1–0.3 mg at9 A.M.; beginclonidine taperby 25% daily50 mg at 11A.M.Continue taperby 25% daily50 mg dailyFIGURE 26.1. Ambulatory opioid detoxification medication protocols.599

600 V. TREATMENTS FOR ADDICTIONSSuccess rates for detoxification treatments have generally assessed onlyshort-term outcomes of becoming either opioid-free or opioid-free with concomitantnaltrexone treatment, which is not a widely used treatment. Considerationshould be given to maintaining such patients on an opioid antagonistmedication such as naltrexone, because relapse to illicit opioid use followingmedical withdrawal is frequent (≥ 90%) over a 6- to 12-month period withoutsustained outpatient treatment (Kleber, 1981; Kosten & Kleber, 1984). In astudy of methadone maintenance versus a 180-day methadone detoxificationprogram with enhanced psychosocial treatment services, methadone maintenancetherapy resulted in greater treatment retention and lower heroin usethan did the enhanced detoxification treatment (Sees et al., 2000). This observationunderscores the difficulty of successfully undertaking opiate detoxificationin heroin-addicted patients and speaks to the need to increase theavailability of opiate therapy programs that can provide long-term opiatepharmacotherapy to this population (Rounsaville & Kosten, 2000).Maintenance MedicationsThere are currently four drugs approved for the maintenance treatment ofopioid dependence: naltrexone, methadone, LAAM, and the opioid partialagonist buprenorphine. These medication treatments are summarized below.Naltrexone, an opioid antagonist that is administered orally, can be usedin those patients who do not want to be maintained on opioids. Naltrexoneshould not be initiated until the patient is completely detoxified from opioidsto avoid precipitating withdrawal (with the exception of the use of theclonidine–naltrexone detoxification procedure described earlier). An abstinenceperiod of 7–10 days from short-acting opioids (e.g., heroin) and 10 daysof abstinence from long-acting opioids (e.g., methadone) is usually required. Ifdoubt exists as to the opioid history, a “naloxone challenge” may be given: Lackof withdrawal symptoms indicates the absence of current physiological opioiddependence, and naltrexone can then be administered. To perform a naloxonechallenge, 2 ml of naloxone (0.4 mg/ml) solution is prepared, and an initialdose of 0.5 ml of this solution (0.2 mg of naloxone) is administered intravenously.Symptoms of opioid withdrawal (mydriasis, dysphoria, diaphoresis, andgastrointestinal discomfort) in approximately 30 seconds indicate that thepatient remains dependent. If no withdrawal is observed, the remainingnaloxone solution is administered and observation is continued. If intravenousaccess is not available, 2 ml of the naloxone solution may be administered subcutaneously,with an observation period of 45 minutes (Galloway & Hayner,1993).The standard dose of naltrexone is 50 mg daily, although this drug can alsobe administered less frequently at larger doses (100 mg every 2 days, or 150 mgevery third day). Naltrexone will attenuate/block effects of opioid agonists and

26. Psychopharmacological Treatments 601assist in relapse prevention. Naltrexone should be administered for at least 6months, and discontinuation should be carefully planned. Naltrexone sideeffects are few, but hepatotoxicity has been reported, and hepatic functionshould be monitored before and during administration. The biggest problemwith naltrexone has been a lack of patient and clinician acceptance of thetreatment.For patients who chronically relapse to opioid dependence, the treatmentof choice is maintenance with a long-acting opioid agonist. The goal of treatmentwith any long-acting opioid is to achieve a stable dose that reduces or,ideally, eliminates illicit opioid craving and use, and facilitates the engagementof the patient in a comprehensive program that promotes substance abuse rehabilitation.Because treatment with long-acting opioids results in dependence, itis important to select patients who have a history of prolonged dependence(greater than 1 year) and demonstrate physiological dependence (positive urinetoxicology screen for opioids and evidence of opiate withdrawal prior to initiationof treatment).Methadone, the most widely used of these long-acting opioids, is effectivein decreasing psychosocial consequences and medical morbidity associated withopioid dependence. It is also an important tool in decreasing the spread ofhuman immunodeficiency virus infection in and by injection drug users. Theefficacy of methadone spans a wide range of doses, and each patient’s dose mustbe individually titrated. Methadone, 40–60 mg daily, will block opioid withdrawalsymptoms, but doses of 70–80 mg daily are more often needed to curbcraving. Generally, doses greater than 60 mg daily are associated with betterretention in treatment and less illicit opioid use (Ball & Ross, 1991).LAAM, a methadone congener that is longer acting and was thought tohave had potential advantages over methadone, has been associated with cardiacelectrophysiological complications in some patients, resulting in revisedlabeling that includes a black box warning recommending that an electrocardiogram(EKG) be performed prior to treatment, 12–14 days after initiation ofLAAM, and then periodically thereafter to rule out any alterations in the QTinterval (Orlaam Package Insert, 2001). The finding that LAAM and itsmetabolites, norLAAM and dinorLAAM exert negative chronotropic effectsand negative ionotropic responses in cardiac tissue, and the association ofLAAM with several lethal cardiac dysrhythmias (including torsades de dointes)has resulted in its no longer being a first-line treatment for opioid dependencein the United States (Expert Panel Consensus Guidelines, 2002). LAAM hasbeen removed from the market in the European Union.Buprenorphine, an opioid partial agonist, was approved for use as a treatmentfor opioid dependence in October 2002. Buprenorphine, formulated as asublingual tablet, is available as a single agent or as a combination tablet containingbuprenorphine and naloxone in a ratio of 4:1. The latter combinationproduct was designed to prevent the drug from being diverted to injection drug

602 V. TREATMENTS FOR ADDICTIONSuse. The injection of this drug in those addicted to full mu agonist drugs (e.g.,heroin, methadone, LAAM) would produce opiate withdrawal symptoms.Buprenorphine has been shown to be a safer drug than methadone in that a plateauwas observed for dose effects in terms of subjective responses and respiratorydepression (Walsh, Preston, Stitzer, Cone, & Bigelow, 1994). Several clinicaltrials have been reported in which buprenorphine showed comparableefficacy to other opiate therapies. Johnson and colleagues (2000) reported thatin a 17-week randomized study, compared to low-dose methadone maintenance(20 mg daily), high-dose methadone maintenance (60–100 mg daily), LAAM(75–100 mg daily), and buprenorphine (16–32 mg daily) substantially reducedthe use of illicit opioids. The recommended daily dose of buprenorphine is 16mg, although a range of 12–24 mg daily is possible, and dosage should be individualizedfor each patient.Induction with buprenorphine is a straightforward clinical procedure inwhich the patient is instructed to present for induction not having used opioidsfor at least 4 hours and in mild withdrawal. An initial dose of 4 mg is administeredand may be followed 2 hours later by another dose of 4 mg (not to exceed8 mg on day 1). On the second day, a dose of 12–16 mg may be administered.Once a dose of 16 mg is reached, the patient should be followed for several daysto determine whether the dose is one that suppresses withdrawal and reducesdrug craving. Adjustments up or down should be based on clinical examination.Another potential advantage to buprenorphine is that it can be dosed threetimes per week or daily (Schottenfeld et al., 2000). A study of outcomes after1 year of buprenorphine treatment (16 mg daily) or placebo given withpsychosocial interventions showed a highly significant positive treatment effectof buprenorphine both in terms of retention in treatment and reduction in theuse of illicit drugs (opiates, stimulants, cannabinoids, and benzodiazepines)(Kakko, Svanborg, Kreek, & Heilig, 2003).The significant advantage to buprenorphine is that it is the first opioidtherapy for the treatment of opioid dependence that can be obtained by prescriptionfrom the patient’s primary care physician or psychiatrist. Physicianswho wish to prescribe buprenorphine must have special training to comply withgovernmental regulations.Drug–Drug InteractionsIndividuals with SUDs often suffer with comorbid medical or mental disordersthat themselves require pharmacotherapy. The prescribing of multiplemedications to the same patient can result in adverse interactions betweenmedications, leading to adverse events and, in many cases, nonadherence tomedication regimens, increased use of illicit drugs, drug toxicities, and lack oftherapeutic benefit of treatment regimens. These interactions can be especiallydifficult in the opioid-dependent patient who is maintained on an opiate ther-

26. Psychopharmacological Treatments 603apy. These patients are at risk for opiate withdrawal syndromes when prescribedmedications that induce the metabolism of opioids (e.g., inducers of cytochromeP450-3A4) and for opiate toxicity should a coadministered medicationinhibit opioid metabolism. Similarly, if an opioid delays absorption of a medicationor inhibits the metabolism of the drug; toxicity from the drug may occur.Table 26.1 summarizes drug interactions that have been shown to occur inopioid-maintained patients treated with medications for comorbid medical orpsychiatric disorders.COCAINE PHARMACOTHERAPIESCocaine affects multiple neurotransmitters, including release and reuptakeblockade of dopamine, norepinephrine, and serotonin (Koe, 1976). Many medications,including antidepressants, anticonvulsants, and dopaminergic agents,have been studied as potential treatments for cocaine dependence. However,none has been proven an effective pharmacotherapy in randomized, controlledclinical trials, and none have been approved by the U.S. Food and DrugAdministration (FDA) for this indication (Boyarsky & McCance-Katz, 2000;Jin & McCance-Katz, 2003; McCance-Katz, 1997; Silva de Lima et al., 2002).One outpatient, randomized clinical trial in which disulfiram, 250 mgdaily, was administered in combination with psychotherapies in cocainedependent,alcohol-abusing patients showed that disulfiram significantly reducedcocaine and alcohol use. Few adverse events were observed in this study(Carroll, Nich, Ball, McCance, & Rounsaville, 1998). A 1-year follow-up evaluationwith 96 of the participants in this study showed that the effects ofdisulfiram in reducing cocaine and alcohol use were sustained (Carroll et al.,2000). Subsequently, Petrakis and colleagues (2000) showed, in a double-blind,randomized, controlled study, that disulfiram treatment decreased cocaine andalcohol use in methadone-maintained patients who were also cocaine dependent.George and colleagues (2000) showed similar findings in buprenorphinemaintained,opioid-addicted patients who were also cocaine dependent.Naltrexone, an opioid antagonist approved for the treatment of opioid andalcohol dependence, is also being examined as a treatment for cocaine dependence.Although results of earlier studies in patients with comorbid cocaine andalcohol dependence were not encouraging, Oslin and colleagues (1999) reportedthat dosing of naltrexone, 150 mg daily, in cocaine- and alcoholdependentindividuals was associated with decreased cocaine and alcohol use.Naltrexone, 50 mg daily, was found to be associated with significantly lesscocaine use when administered in combination with relapse prevention therapy(Schmitz, Stotts, Rhoades, & Grabowski, 2001). The results from these studiessuggest that the effectiveness of naltrexone may depend on multiple factors,including other substance comorbidity, dose of naltrexone, length of treatment,

604 V. TREATMENTS FOR ADDICTIONSTABLE 26.1. Drug Interactions between Methadone or LAAM and Medications Usedto Treat Other Common Conditions in Opioid-Dependent PatientsIndicationInteraction with methadone or LAAMPsychotropic medicationsFluvoxamine Depression ↑ Methadone levels with potential toxicity(Eap et al., 1997)Desipramine Depression ↑ Desipramine levels (Gourevitch & Friedland,2000)Sertraline Depression ↑ Methadone levels without reported toxicity(Hamilton et al., 2000)Valproic acidCarbamazepineSeizure disorder, bipolaraffective disorderSeizure disorder, bipolaraffective disorderNone reported (Saxon et al., 1989)↓ Methadone levels (Eap et al., 2002)Other medicationsPhenytoin Seizure disorder ↓ Methadone levels (Eap et al., 2002)Phenobarbital Seizure disorder ↓ Methadone levels (Eap et al., 2002)Rifampin Tuberculosis ↓ Methadone levels (Raistrick et al., 1996)Rifabutin Tuberculosis No change in methadone levels (Brown et al.,1996)Fluconazole Fungal infection ↑ Methadone levels by ≈ 35%; clinicalsignificance unknown (Cobb et al., 1998)Ciprofloxacin Bacterial infection ↑ Methadone levels with toxicity reported(Herrlin et al., 2000)Zidovudine (AZT) HIV ↑ Methadone associated with increase in AZTlevels (McCance-Katz et al., 2002)Didanosine (ddI) HIV ↓ ddI levels by 63% (Rainey et al., 2000)Lamivudine HIV NoneLamivudine/zidovudineHIV None (Rainey et al., 2002)Stavudine (d4T) HIV None (Rainey et al., 2000)Abacavir HIV ↑ Methadone clearance (Sellers et al., 1999)(continued)

TABLE 26.1. (continued)Indication26. Psychopharmacological Treatments 605Interaction with methadone or LAAMOther medications (cont.)Nevirapine HIV ↓ Methadone levels, withdrawal symptoms(Altice et al., 1999)Delavirdine HIV No significant effect on methadone; ↑ LAAMlevels (McCance-Katz et al., 2003)Efavirenz HIV ↓ Methadone levels associated with withdrawal(Clarke et al., 2000; McCance-Katz et al.,2002)Nelfinavir HIV ↓ Methadone levels, but no withdrawalsymptoms observed (Hsyu et al., 2000); casereport of methadone withdrawal (McCance-Katz et al., 2000)↑ norLAAM and ↓ dinerLAAM (McCance-Katz et al., 2003)Ritonavir HIV No significant effect on methadone (McCance-Katz et al., 2003)Lopinavir HIV ↓ Methadone levels, withdrawal symptoms(McCance-Katz et al., 2003)Note. Data from McCance-Katz, Cropsey, and Gourevitch.and type of psychotherapeutic intervention. Naltrexone will need to be examinedin larger, controlled clinical trials to determine its efficacy as a cocainepharmacotherapy.Future Directions for Cocaine PharmacotherapyMedications development continues for the treatment of cocaine addiction.Preclinical research focusing on medications that bind the dopamine D 1,D 2,and D 3receptors is ongoing, although no studies have yet been conducted inhumans. A cocaine vaccine is also in clinical trials. Anticocaine antibodieshave been developed and have been shown in animal studies to inhibit selfadministration.The presence of antibody has also been shown to reduce braincocaine levels following intravenous or intranasal cocaine administration (Fox,Kantak, & Edwards, 1996). The vaccine is structurally similar to cocaine, but iscoupled to a carrier protein that prevents rapid metabolism, thus making it possibleto mount an immune response to cocaine (Fox, 1997). The results of clini-

606 V. TREATMENTS FOR ADDICTIONScal trials for efficacy in humans have shown excellent safety, adequate antibodydevelopment, and reductions in cocaine abuse (Kosten et al., 2002; Kosten &O’Connor, 2003).INTERFACE OF PSYCHIATRIC COMORBIDITYAND SUBSTANCE USE DISORDERSPsychotropic medication treatment of dually diagnosed patients is similar tothat of psychiatric patients without SUDs, with several caveats. Patients withpsychotic disorders treated with medications that block dopamine receptorsmay develop postsynaptic dopaminergic supersensitivity, which has been demonstratedin animal studies (Kosten, 1997). This supersensitivity may enhanceeuphoria from a wide range of abused drugs. Furthermore, patients withchronic psychotic disorders often experience negative symptoms of schizophreniaand dysphoria that may be exacerbated by conventional neuroleptics. Thesepatients will benefit from selection of an atypical neuroleptic that lacks strongdopaminergic antagonism (Kosten & Ziedonis, 1997). Patients with psychoticdisorders who are also alcoholic should be carefully evaluated before beingtreated with disulfiram, a dopamine beta-hydroxylase inhibitor that could exacerbatepsychosis in such patients.Attention-deficit/hyperactivity disorder (ADHD) can occur as a comorbidcondition in cocaine abusers who may self-medicate with this stimulant.Cocaine use in this population is often described as ingestion of small amountsof cocaine taken intermittently throughout the day rather than the classicbinge pattern characterized by use of multiple doses of cocaine in rapid successiondescribed by those with primary cocaine dependence. Treatment withstandard agents used for ADHD, including stimulant medications, may result incessation of cocaine use.Depressive disorders are common in those with cocaine and alcohol usedisorders. SRIs may be a good choice for these patients because they are lesslikely to have significant cardiovascular interactions with cocaine and to belethal in overdose. Monoamine oxidase inhibitors (MAOIs) should never beused in cocaine abusers, because of the risk of hypertensive crisis. Benzodiazepinesshould be used with caution in those with cormorbid psychiatric andSUDs, and particularly in alcoholic patients, because of cross-tolerance withalcohol and additive effects if combined with alcohol. Benzodiazepines may berequired initially to stabilize patients with exacerbation of psychosis or severeagitation but should be tapered as antipsychotics and/or mood stabilizersbecome therapeutic. Alcoholic patients with anxiety disorders can usually beeffectively treated with serotonergic agents (SRIs or partial agonists) or, insome cases, tricyclic antidepressants.

26. Psychopharmacological Treatments 607NEUROLOGICAL AND COGNITIVE EFFECTSOF DRUG ABUSEThe neurocognitive effects of drug abuse, while not yet fully elucidated, arelikely to have several negative sequelae in drug abusers. Cognitive impairmentobserved clinically may be associated with perfusion deficits identified in neuroimagingstudies. Drug abusers with these deficits may have more difficultygrasping concepts imparted in drug abuse psychotherapy important for initiatingand maintaining abstinence. Drug users may be less able to utilize skillstaught in psychotherapy interventions aimed at drug and alcohol abuse. Thesedeficits may underlie the observation that some patients with SUDs have highrelapse rates despite participation in substance abuse treatment. Finally, thesedeficits may place drug users at higher risk for medical complications of drugand alcohol use due to both a primary effect of perfusion deficits and secondaryeffect of cognitive impairment that may contribute to high-risk behaviors leadingto medical morbidity. These findings indicate a need to address the issue ofcognitive impairment in the drug abuser and point to a new direction in thedevelopment of pharmacotherapies for SUDs in the future.SUMMARYSubstantial progress has been made in the development of pharmacotherapiesfor the treatment of SUDs. FDA-approved medication therapies are now availablefor the treatment of nicotine, alcohol, and opiate use disorders. Thesetreatments, utilized in conjunction with a program addressing the psychosocialneeds of the patient, represent the most effective regimens available to treataddictive disorders. Research is ongoing to continue to broaden the number ofpharmacotherapies available for these disorders. The search for effective medicationtreatments for other SUDs, such as stimulant use disorders, continues.ACKNOWLEDGMENTSThis work was supported by Grant Nos. K02-DA00478 (to Elinore F. McCance-Katz)and K05-DA00454 (to Thomas R. Kosten) from the National Institute on Drug Abuse.REFERENCESAgricola, R. (1982). Treatment of acute alcohol withdrawal syndrome with carbamazepine:A double-blind comparison with tiapride. J Int Med Res, 10, 160–165.Altice, F. L., Friedland, G. H., & Cooney, E. L. (1999). Nevirapine induced opiate

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CHAPTER 27Dialectical Behavior Therapy forIndividuals with Borderline PersonalityDisorder and Substance Use DisordersM. ZACHARY ROSENTHALTHOMAS R. LYNCHMARSHA M. LINEHANDialectical behavior therapy for substance use disorders (DBT-SUD) is a comprehensivepsychosocial treatment for substance users with borderline personalitydisorder (BPD). DBT-SUD is an extension of standard dialectical behaviortherapy (DBT; Linehan, 1993a, 1993b), a treatment for BPD that hasbeen investigated to the extent that the treatment can be considered “wellestablished”according to criteria outlined by Chambless and Hollon (1998). Itis the subject of several well-controlled randomized clinical trials (RCTs) forthe treatment of BPD, and efficacy has been demonstrated across independentresearch teams (Koons et al., 2001; Linehan, Armstrong, Suarez, Allmon, &Heard, 1991; Linehan et al., 1999; Linehan, Dimeff, et al., 2002; Verheul et al.,2003). Across studies, the evidence suggests that DBT is an efficacious treatmentfor reducing a variety of problems associated with BPD, including selfinjuriousbehavior, suicide attempts, suicidal ideation, hopelessness, depression,bulimia, and substance use.This chapter provides an overview of the modifications of standard DBTthat comprise DBT-SUD. The philosophy and theory behind DBT-SUD, thebiosocial model of BPD, as well as treatment modes and functions, skill mod-615

616 V. TREATMENTS FOR ADDICTIONSules, and treatment strategies in DBT-SUD are outlined. For a comprehensivedescription of this treatment approach, interested readers are referred to theDBT treatment manual and group skills training manual (Linehan, 1993a,1993b) and the DBT-SUD treatment manual (Linehan, Dimeff, & Sayrs,2004).WHY IS A TREATMENT FOR SUBSTANCE USERSWITH BORDERLINE PERSONALITY DISORDER NEEDED?Separately, SUDs and BPD are serious public health problems associated withsignificant psychosocial impairment. Together, however, the combination ofBPD and SUD is associated with greater problems than substance abuse alone(Links, Heslegrave, Mitton, van Reekum, & Patrick, 1995). For example,substance users with personality disorders are at risk for poor treatment outcome(Moos, Moos, & Finney, 2001). The presence of BPD specifically maylead to a number of impediments in standard substance abuse treatments. Inone study, a diagnosis of BPD among opiate addicts treated with methadonepredicted greater psychiatric problems and alcoholism following treatment(Kosten, Kosten, & Rousaville, 1989). Between 5 and 32% of individualswith SUD meet criteria for BPD (Brooner, King, Kidorf, Schmidt, & Bigelow,1997; Weiss et al., 1993), and the two disorders often share core features(e.g., impulsivity; Trull, Sher, Minks-Brown, Durbin, & Burr, 2001). Theextension of DBT from clients with BPD to those with BPD and SUD can beattributed, in part, to the high severity and comorbidity of the two separatedisorders, along with the evidence that standard DBT is efficacious for individualswith BPD.TARGET POPULATION FOR DBT-SUDDBT-SUD was originally developed and tested with female clients meeting fulldiagnostic criteria for BPD and polysubstance abuse disorder or SUDs for opiates,cocaine, amphetamines, sedative/hypnotics, hallucinogens, or anxiolytics.Individuals with mental retardation, schizophrenia, schizoaffective disorder,bipolar affective disorder, and psychosis disorder not otherwise specified (NOS)have been excluded from studies evaluating the efficacy of DBT-SUD. As aresult, DBT-SUD has been tested in a relatively specific population. Althoughit may be impossible to limit the use of DBT-SUD to such a specific populationin clinical practice, it is recommended that DBT-SUD be used with clients similarto the population from DBT-SUD clinical trials, until future outcome studiessupport the efficacy of DBT-SUD in different populations.

27. Dialectical Behavior Therapy 617EMPIRICAL SUPPORTTwo randomized trials examining DBT-SUD have been conducted. Linehanand colleagues (1999) compared DBT-SUD to treatment as usual (TAU) inthe community in a sample of 28 women diagnosed with BPD and either SUDor polysubstance use disorder. Subjects received 1 year of treatment, and wereassessed at 4, 8, 12, and 16 months after treatment, and were matched at pretreatmenton age, severity of drug dependence, readiness to change, and globaladjustment. Subjects in the DBT-SUD condition attended significantly moreindividual psychotherapy sessions during treatment, dropped out of treatmentless, and, importantly, evidenced significantly less drug use, as determined byurinary analyses. At 16-month follow-up, subjects in the DBT-SUD conditionhad higher scores on measures of global adjustment and social adjustment comparedto subjects in the TAU condition.In a second study, 23 subjects with BPD and heroin dependence were randomlyassigned to receive 1 year of DBT-SUD or comprehensive validationtherapy, a treatment consisting of therapist validation coupled with 12-stepmethods (Linehan, Dimeff, et al., 2002). Subjects also received ORLAAM concurrentlyas an opiate replacement medication, and were matched at pretreatmenton age, cocaine dependence, antisocial personality disorder, and globalfunctioning. Although subjects in both conditions had a small proportion ofpositive urinary analyses at follow-up, in the last 4 months of treatment, thosein the DBT-SUD condition maintained treatment gains, whereas those in thecomprehensive validation condition had a significant increase in opiate useduring this period. In addition, subjects in both conditions reported greatersocial adjustment and general adjustment following treatment. Taken together,these studies suggest that DBT-SUD is an efficacious treatment for substanceusers with BPD.PHILOSOPHY AND THEORYPhilosophers such as Hegel and Kant discussed dialectics as a means of understandingor synthesizing apparent contradictions. Dialectics includes both aworldview and a process of change in DBT-SUD. From a dialectical worldview,behavior is conceptualized as interrelated, contextually determined, and systemic.The dialectical process of change is guided by the fundamental notionsthat (1) for every point an opposite position can be held, and (2) natural tensionscan be resolved and adaptive change can occur when workable synthesesemerge from the consideration of contradicting polarities or opposing ideas. Forexample, clients might insist that substance use helps them feel less bored,whereas the therapist might insist that substance use is the problem. Using a

618 V. TREATMENTS FOR ADDICTIONSdialectical perspective, the therapist and client could jointly create a synthesisby discussing how substance use is both understandable as a means of reducingbordeom and simultaneously a cause of much long-term suffering. Workingtogether, the therapist and client would look for ways to feel better temporarilywithout creating long-term suffering.There are many dialectical tensions in DBT-SUD. However, the centraldialectic is that of acceptance and change. For the therapist, this entails balancingan acceptance of clients as they are in the present moment with an explicit,long-term goal of meaningful change. For clients, changing behaviors must bebalanced by accepting unpleasant thoughts, emotions, or the reality thatunpleasant events have occurred. As an example in DBT-SUD, clients areencouraged to accept the reality that painful emotions will occur, while concurrentlyworking to prevent unnecessary emotional suffering caused by dysfunctionalbehavior. A compromise between acceptance and change is not necessarilythe goal. Instead, a synthesis of polarities may be more acceptance-basedin one moment and more change-focused in another, depending on the contextand what is likely to be effective. This is similar to how a golfer might hit theball toward one side of the fairway or the other, depending on the direction andstrength of the wind in the present moment, the shape of the fairway, and theobstacles that lie to the side. The target is to hit the ball as close to the puttinggreen or cup as possible, without the ball going out of play, not to hit the balldown the exact middle of the fairway.BIOSOCIAL MODELLinehan (1993a, 1993b) suggests that BPD is fundamentally a disorder of theemotion regulation system and results from a reciprocal transaction between anemotional vulnerability, an invalidating environment, and emotional dysregulation(see Figure 27.1). Emotional vulnerability is considered to be the keyFIGURE 27.1. Components of the biosocial theory of borderline personality disorder.

27. Dialectical Behavior Therapy 619diathesis, environmental invalidation is the primary socially mediated process,and emotional dysregulation is the multidimensional construct thought tounderlie BPD criterion behaviors.Emotional VulnerabilityAccording to Linehan (1993a), BPD is characterized by emotional vulnerability,a biologically mediated predisposition for affective instability involvinggenetic, intrauterine, and temperamental factors that is defined by heightenedemotional sensitivity, heightened emotional reactivity, and a slow return tobaseline level of emotional arousal; that is, individuals with BPD respondquickly to stimuli, respond with a high magnitude of arousal, and take a longtime before arousal decreases to baseline. Similar to the intense physical painfelt when someone with a serious lower back injury tries to walk, emotionallyvulnerable individuals often feel acute emotional pain in response to whatappear to others to be ordinary events.The Invalidating EnvironmentBroadly put, the invalidating environment is described by Linehan (1993a) asan environment characterized by pervasive criticizing, minimizing, trivializing,punishing, or erratically reinforcing communication of internal experiences(e.g., thoughts and emotions), and oversimplifying the ease of problem solving.For example, a parent may pervasively communicate, “You’re not hurt, you justthink you are” or “This is easy, just deal with it!” In addition, verbal communicationis indiscriminately rejected, and the individual is chronicallypathologized as having undesirable personality traits (e.g., too sensitive, paranoid,lazy, or unmotivated). Because appropriate emotional expression is chronicallypunished and extreme emotional displays are intermittently reinforced,escalation of emotional expressions (e.g., suicidal behavior) may occur. In additionto emotional invalidation, prototypical examples of invalidation are childhoodsexual or physical abuse (Wagner & Linehan, 1997).Emotional DysregulationIn the context of environmental invalidation and emotional vulnerability, thebiosocial model suggests that emotional dysregulation occurs, leading to problemswith behavioral–motoric, physiological, and cognitive–experiential emotionalsystems. Such problems with emotion are hypothesized by Linehan(1993a) to underlie BPD criterion behaviors, and, as shown in Table 27.1, canbe organized across domains of functioning (emotional, behavioral, cognitive,and interpersonal). Linehan suggests that emotional dysregulation in BPD ischaracterized by problems with up–down regulation of physiological arousal,

620 V. TREATMENTS FOR ADDICTIONSTABLE 27.1. DSM-IV Criteriafor Borderline Personality Disorder• Emotion dysregulationAffective instabilityProblems with anger• Behavioral dysregulationImpulsive behaviorSelf-injurious behavior• Cognitive dysregulationDissociationParanoia• Interpersonal dysregulationChaotic relationshipsFears of abandonment• Self-dysregulationIdentity disturbancesChronic feelings of emptinessinhibiting mood-dependent behavior, excessive reliance on avoidant copingstrategies, attentional control, processing emotional information, self-soothing,and self-validation. For example, an inability to decrease intense physiologicalarousal may precede the behavioral dyscontrol that is a hallmark of BPD, suchas self-injury or impulsive substance use. Although substance use may occur inresponse to dysregulated emotional systems, in DBT-SUD, substance use alsocan be conceptualized as a means of emotion regulation; that is, substance usecan function as an attempt to regulate emotions or as the outcome of emotionaldysregulation.TREATMENTDBT-SUD is a principle-driven, flexible, and comprehensive treatment. As abehavioral therapy, it is change-focused. As an acceptance-based therapy,DBT-SUD incorporates strategies to use when changing behavior may not bepossible or effective. Treatment begins by orienting clients to the therapeuticassumptions, agreements, levels and modes of treatment, and includes obtaininga commitment to treatment.Assumptions and AgreementsIn DBT-SUD, assumptions and agreements are openly delineated with clientsin the first few “pretreatment” sessions (see Tables 27.2 and 27.3). During thesesessions, the therapist discusses the requirement that clients commit to treat-

27. Dialectical Behavior Therapy 621TABLE 27.2. Patient and Therapy Assumptions in Dialectical Behavior TherapyPatients1. Patients are doing the best they can.2. Patients want to improve.3. Patients need to do better, try harder, and be more motivated to change.4. Patients must solve their current problems, regardless of who caused these problems.5. Patients are living lives that are unbearable as they are currently being lived.6. Patients must learn new behaviors in all relevant contexts.Therapy1. Patients can not fail in DBT, but the therapy or therapist can fail the patient.2. Helping patients work toward their ultimate goals in life is the most caring thing atherapist can do.3. DBT therapists need support.4. The therapeutic relationship is a relationship of two equals.5. Principles of behavior are universal, affecting both patients and therapists alike.TABLE 27.3. Patient and Therapist Agreements in DialecticalBehavior TherapyPatient agreements1. Stay in therapy for a specified period of time, usually 1 year.2. Attend all therapy sessions.3. Therapy will be discontinued if four consecutive sessions are missed.4. Work toward terminating self-injurious behavior and other therapeutic targets.5. Participate in skills training.6. Abide by relevant research conditions of therapy.7. Pay agreed upon fees for service.Therapy agreements1. Maintain competence and effort.2. Provide ethical and professional treatment.3. Be available for weekly sessions and phone consultation.4. Treat patients humanely, with respect and integrity.5. Maintain confidentiality.6. Seek appropriate consultation.

622 V. TREATMENTS FOR ADDICTIONSment. Although standard DBT often uses a variety of commitment strategiesduring pretreatment sessions, in DBT-SUD, clients must, at a minimum, agreeto work toward abstinence from all drugs. Because commitment to treatmentoften ebbs and flows, it is necessary to monitor ongoing changes in committedbehavior throughout treatment.Treatment TargetsClients with BPD often present for treatment with severe behavioral dyscontrol(e.g., self-injurious behavior), treatment-interfering behaviors (e.g., not showingup to treatment), and problems affecting physical (e.g., sleep problems),emotional (e.g., excessive emotionality), and cognitive (e.g., hopelessness)functioning. To treat this range of therapeutic targets consistently, a hierarchyfor problem behaviors is used in DBT-SUD: (1) Reduce acute life-threateningand intentional self-injurious behaviors; (2) reduce treatment-interfering behaviors;and (3) reduce quality-of-life interfering behaviors, beginning withdrug use, and including such problems as eating disorders, anxiety, depression,and physical health problems. The complete and total cessation of all drug useis the primary target in the quality-of-life interfering behaviors.Within this larger treatment hierarchy, DBT-SUD outlines the “path toclear mind” in order to provide specific treatment targets addressing substanceuse. The overarching, and, accordingly, first SUD-specific target is the reductionof all substance abuse, including illicit and licit drug abuse. In accomplishingthis, the next target in the path to clear mind is to maintain an adequatedose of drug replacement medications, when relevant, and more generally todecrease the physical discomfort associated with abstinence. Physical pain andpsychological distress are targeted for change when possible. However, acceptanceskills are used to tolerate pain that cannot be reduced directly.Clients also learn how to monitor cravings, to evaluate the intensity ofcravings, to identify when cravings are particularly likely to increase drug use,to reduce cravings, and to avoid using drugs once cravings occur. On the onehand, clients learn that cravings should be expected to occur; on the otherhand, they learn how to actively problem-solve ways to cope with cravingswithout using. Unlike standard DBT, in which clients are frequently encouragedto turn their attention toward the experience of aversive emotions, DBT-SUD clients are encouraged to use skills to turn their attention away from cravingsand urges to use. As coping skills are acquired and generalized, DBT-SUDemphasizes community reinforcement of “nonaddict wise-mind” behaviors; thatis, clients increase activities associated with a decreased likelihood for drug use,such as Alcoholics Anonymous (AA) and Narcotics Anonymous (NA) meetings,gaining steady and legitimate employment, and socializing whenever possiblewith nonaddicts in mainstream settings.

27. Dialectical Behavior Therapy 623Next, “apparently unimportant behaviors” are targeted. Patterned afterMarlatt’s work on apparently irrelevant decisions (Marlatt & Gordon, 1985),in DBT-SUD, behaviors (both observable events and privately experiencedevents, such as thoughts) that are links on the chain toward drug use are targeted.Examples range from obvious (e.g., selling drugs) to less obvious (e.g.,going into an environment with many cues associated with drug use). Finally,on the path to clear mind, DBT-SUD targets closing options to use drugs,including, for example, ending contacts and throwing away contact informationwith those who sell and use drugs, getting rid of all drug paraphernalia, andnot lying about drug use.Dialectical AbstinenceThe goal of DBT-SUD is to stop using drugs, with the ideal outcome of treatmentbeing complete and indefinite abstinence. However, the cold reality suggestedby clinical observation and supported by treatment outcome studies isthat even in the best treatments for substance use, abstinence may not lastindefinitely. Harm reduction approaches take into account the likelihood oflapse following treatment (e.g., Marlatt & Gordon, 1985), aiming to reduce theimpact of substance use rather than focus exclusively on abstinence. In DBT-SUD, abstinence is the goal, not harm reduction. However, the synthesisbetween complete abstinence and a harm reduction approach is struck. Theresulting perspective, called “dialectical abstinence,” refers to the position oftargeting complete abstinence on the one hand, while being prepared for andresponding effectively to drug lapse on the other hand; that is, dialectical abstinenceis achieved through the therapist targeting 100% abstinence with theclient, while also planning for the possibility of relapse by developing a relapsemanagement plan.Attachment StrategiesAlthough similar to BPD clients without substance use problems, thosewith co-occurring BPD–SUD disorders appear to have important differences.Linehan (1993a) characterizes individuals with BPD as either “attached” or as“butterflies.” Whereas attached BPD clients communicate often with therapists,rarely miss appointments, and appear closely affiliated to their therapists,butterfly clients do the opposite. Substance-abusing BPD clients are often butterflies,possibly because their drug use has become more reinforcing than socialinteractions, and this clinical observation has led to the addition of a set ofattachment strategies in DBT-SUD. For example, to develop rapport, the firstseveral sessions include a large amount of therapist validation, with less emphasison immediate change and/or interpersonal aversive contingencies than in

624 V. TREATMENTS FOR ADDICTIONSstandard DBT. In addition, because these clients tend to come into and go outof therapy, therapists may become easily demoralized. Thus, a strong emphasisis made on remoralizing and motivating therapists during consultation teammeetings. Other attachment strategies include orienting the client to this problem,increasing contact with clients toward the beginning of treatment, frequentcontacts with clients via voice mail, in vivo therapy sessions, decreasingor increasing session length as needed, family and friends network meetings,and calling clients when they are avoiding them when they repeatedly do notshow up for appointments or respond to telephone calls.Modes and Functions of TreatmentDBT-SUD includes methods for learning adaptive coping skills, generalizingsuch skills into relevant contexts, enhancing commitment to treatment, andpreventing demoralization of both the therapist and client. There are four primarymodes of treatment: group skill training, individual therapy, phone consultation,and consultation team. Because of the need for replacement medicationand the frequent comorbidity of Axis I disorders, DBT-SUD also canincorporate a pharmacotherapy mode. Next, the function, process, and structureof treatment modes are briefly reviewed.Skills TrainingWeekly 2-hour skills training classes occurs in a group format. The primaryfunction of skills training classes is the acquisition of new behavioral and cognitiveskills. Skills training classes are co-led by two skills trainers, and includeboth homework review of previously learned skills and didactic presentation ofnew skills from the skills training manual (Linehan, 1993b). Specifically, thereare separate skill modules for mindfulness, distress tolerance, emotion regulation,and interpersonal effectiveness.MindfulnessDerived from Eastern meditative and Christian contemplative traditions, mindfulnessis the practice of paying attention in a particular way: on purpose, in thepresent moment, and without judgment. In this module, clients learn that theirbehavior is a function of current emotions (emotion mind) or logical analysis(reasonable mind). “Wise mind” knowing and behavior is emphasized as a synthesisof emotion and reasonable minds, such that decisions and actions areboth effective and remain within personal values. For example, in order tochange a client’s identity as an addict, wise mind is emphasized as behaviorsthat are inconsistent with identity as an addict.Mindfulness skills specifically include the ability to observe, describe, and

27. Dialectical Behavior Therapy 625participate fully in one’s actions and experiences in a nonjudgmental, onemindful,and effective manner. Observing refers to noticing experiences withoutbecoming attached, allowing thoughts or other internal experiences to flowfreely with full awareness. Describing follows observing and involves labeling orputting words on experiences. Participating is somewhat different and involvesbehaving effectively, without observing and describing internal experiences(e.g., an athlete at peak performance). Being nonjudgmental, including beingaware of judgments and letting go of their literal truth, is a central skill repeatedlypracticed by DBT clients and therapists. Being one-mindful entails asharpening of attentional focus on one thing or activity at a time. This skillinvolves staying in the present moment and not becoming distracted bythoughts about the past or future. Finally, the focus on effectiveness is a keyaspect of mindfulness. Effectiveness refers to behaving in a flexible manneracross contexts in a way that is consistent with one’s values and long-termgoals. The emphasis on effectiveness as a DBT skill illustrates how mindfulnessis a behavioral, psychological, and spiritual practice, extending beyond formalmeditation practice.Additional mindfulness skills specific to DBT-SUD include “urge surfing”and “alternative rebellion.” Urge surfing stems from Marlatt’s treatment foralcohol abuse (Marlatt & Gordon, 1985) and involves awareness of urges touse, coupled with the use of imagery of a wave as the urge is “surfed.” As isalways the case with waves, urges eventually cease. For many, use of this skillhelps considerably in preventing substance use following cravings to use. Alternativerebellion refers to identifying ways to rebel against society, parents, orothers in a skillful way that does not involve drug use. This skill is relevant forthose drug users whose identity as an addict functions as a way to be differentand unique. As a mindfulness skill, alternative rebellion is linked to being effectiveand could include dyeing one’s hair, getting a tattoo, or wearing unusualclothes.Distress ToleranceThe distress tolerance module is designed to teach clients how to tolerate aversiveemotional experiences without behaving maladaptively. A list of crisismanagement skills is taught, including strategies for effective temporary distraction,such as activities eliciting opposite emotions, and squeezing ice or a rubberball. Self-soothing skills are introduced, whereby clients learn to soothe themselvesintentionally during periods of crisis, with calming visual stimuli, sounds,smells, tastes, and objects to touch. In addition, other skills, such as imaginaland relaxation exercises, are taught to improve the current moment, in order toavert crises. Other distress tolerance skills include awareness, breathing, andhalf-smile exercises, as well as radical acceptance of reality as it is in the presentmoment. Overall, distress tolerance skills are intended to interrupt and change

626 V. TREATMENTS FOR ADDICTIONShabitual, problematic, and often context-insensitive responses to emotionaldistress, allowing the opportunity for new responses to aversive stimulation thatcannot be directly changed and the emergence of a broader repertoire of skillfulbehavior.Two new skills added to the distress tolerance module are “adaptivedenial” and “burning your bridges.” Adaptive denial is a skill that draws onwhat is often considered an inherent problem among many substance users,denial. As a skill, adaptive denial includes identifying a craving to use drugs andrelabeling it as a craving for something that is not harmful and to which onehas access; that is, the idea is to reattribute a drug craving as a craving for somethingelse. For example, clients may be taught to recognize their craving to usedrugs and to practice telling themselves that it is really a craving for a flavoredtoothpick. Of course, in this example, it would be necessary for the client tocarry around flavored toothpicks, putting one in the mouth each time as adaptivedenial of the drug craving.“Burning your bridges” is a skill derived from the notion of willingness. Inorder to help tolerate distress associated with no longer using drugs, burningyour bridges involves radical acceptance that drugs will no longer be used.However, the key component of this skill is that such acceptance is accompaniedcompletely by a willingness, as evidenced by behavior, to cut off all previouslinks to drug use and the identity of being a drug user. This skill is compatiblewith the target on the path to clear mind described as eliminating optionsto use drugs (e.g., telling the truth).Emotion RegulationThe emotion regulation skills module is designed to help clients better understandtheir emotions, reduce emotional vulnerability, and decrease emotionalsuffering. Specific skills taught include an increased awareness of emotions,identifying and challenging distorted ways of thinking about emotions, learninghow emotions are related to problem behaviors, accurately labeling emotions,understanding the functions of emotions, reducing emotional vulnerability,increasing pleasant emotions, and acting opposite to behavioral urges associatedwith emotions. Although all of these skills are useful, the opposite action skill isparticularly helpful, because it can be applied in many contexts to change avariety of problem behaviors.The opposite action skill uses an algorithm for knowing when to changeemotion. This includes first determining whether the emotion is justified, basedon the current situation. Next, it is important to know the action urge of theemotion being experienced. Each emotion has its own urging component(e.g., anger—attack, fear—run, sadness—withdraw, guilt—repair, shame—hide). When the client is experiencing an unjustified emotion that he or shewishes to change, the skill is to go opposite to the action urge of the emotion.

27. Dialectical Behavior Therapy 627For example, if a client is feeling guilty for disagreeing with a friend, the oppositeaction skill would be to teach the client to ask him- or herself first whetherthe behavior was egregious according to his or her own values. If the disagreementwas done in a manner inconsistent with the client’s values (e.g., disrespectfullyand judgmentally disagreeing), then a repair (e.g., apology) would besuggested as a way to lower justified guilt. However, if the disagreement did notviolate the client’s values and guilt was unjustified (i.e., respectfully and nonjudgmentallydisagreeing), then the client would be instructed not to repair butto repeat the behavior (i.e., effective opinion giving) multiple times. As the clientlearns that giving opinions does not always result in negative outcomes,over time, the unjustified guilt response to disagreeing effectively would extinguish.Interpersonal EffectivenessBecause chaotic interpersonal relationships are a key characteristic of BPD, thedevelopment of interpersonal skills is crucial. This skill module teaches clientshow to identify factors interfering with interpersonal effectiveness, challengecommon cognitive distortions associated with interpersonal situations, anddetermine the appropriate level of intensity for making requests or saying “no” agiven situation. Specific guidelines for being taken seriously, attending to relationships,and preserving self-respect are taught, and clients are instructed topractice developing new interpersonal skills based on these guidelines in a widevariety of situations, including frequent rehearsal and role playing during groupand individual sessions. When teaching interpersonal effectiveness in DBT-SUD, the specific skills taught are designed to avoid drug-using contexts (e.g.,drug refusal interpersonal skills) and to respond effectively when such contextscannot be avoided (e.g., craving tolerance skills).Individual TherapyIndividual therapy sessions with a DBT-SUD therapist are typically 50–60 minutesonce per week. The individual therapist provides psychoeducational informationto the client early in treatment, including handouts that describe thepros and cons of participating in DBT-SUD compared to other treatments andfacts about drug addiction. However, a primary function of individual therapy isto develop and maintain client motivation to overcome obstacles to change. Avalidating environment is created, whereby clients are treated with compassionand acceptance in the context of targeting behavioral change. Factors interferingwith progress in treatment are discussed, preventing problems that mightinterfere with the development of new skills and helping clients remain intreatment despite urges to dropout. Episodes of emotional dysregulation fromthe previous week are discussed in light of skills that could have been used. In

628 V. TREATMENTS FOR ADDICTIONSaddition, skills are practiced during session and are woven into plans in anticipationof upcoming events.Diary CardsIn order to monitor a variety of targets, a daily diary card is used. For example,clients may rate their mood, monitor the frequency of self-injurious behaviorand drug use urges, and track other relevant targets. The diary card is reviewedat the beginning of each session, and the therapy session is organized aroundtargets evident on the diary card. Given the plethora of treatment targets andthe possibility that clients will not remember salient events from the previousweek, the diary card is instrumental in directing therapy sessions toward highlyrelevant targets.Behavioral AnalysisTo change dysfunctional behaviors, DBT-SUD uses a number of problemsolvingstrategies. Behavioral analysis is used to identify problem behaviors andto understand the relevant contexts in which these behaviors generally occur.Behavioral analysis involves an active, directive effort by the therapist to identifyspecific antecedents and consequences associated with the problem behavior.A thorough elaboration of events before, during, and after problem behaviorsfacilitates the selection of appropriate treatment interventions. Based on afunctional-analytic approach to behavioral assessment, the goal of behavioralanalysis is prediction and control of functional classes of problem behaviorrather than traditional diagnostic assessment of disease entities (Hayes &Follette, 1992; Kanfer & Saslow, 1969). In other words, in DBT-SUD, borderlinesymptoms and substance use are conceptualized as problem behaviors. Thesemay be external, publicly observable behaviors, such as self-mutilation orimpulsive aggression, or internal, publicly unobservable experiences, such asself-judgmental thoughts or urges to use substances.Because behavioral analysis in DBT-SUD involves explicating the links ina specific chain of events, it is often referred to as a “chain analysis.” During achain analysis, the topography, intensity, and duration of the target problem isdiscussed. As links in the chain of events (including internal experiences andexternal events) before and after the target behavior are explored, the therapistconsiders the role of classical and instrumental conditioning. Classically conditioned(respondent) behaviors are under the control of an antecedent stimulus,and instrumentally conditioned (operant) behaviors are under the control ofconsequent events. For example, strong urges to use substances may be classicallyconditioned to occur after interpersonal conflicts. On the other hand, substanceuse may be instrumentally conditioned by the consequences that follow,such as less hostility or increased attention from others. A chain analysis is a

27. Dialectical Behavior Therapy 629detailed assessment of one instance of a problem behavior. As chain analysesare conducted repeatedly across sessions, an understanding of the relevant controllingvariables (i.e., antecedent or consequence) of a problem behavior isdetermined, informing the choice of interventions. Strategies for changingantecedents include behavioral exposure (e.g., rehearsing saying “no” to a drugdealer) and stimulus control (e.g., avoiding drug dealers). In addition, otherbehavioral principals used during chain analyses are positive and negative reinforcement,punishment, extinction, and shaping.Dysfunctional links uncovered in a chain analysis are examined andreplaced with more adaptive responses during a solution analysis. Typically, thisis guided by three questions:1. Can the client change the circumstance (e.g., flush the drugs down thetoilet, quit the job)?2. Can the client change an emotional reaction (e.g., go opposite to theemotion action urge)?3. Can the client better tolerate the pain associated with the problem(e.g., radically accept the problem)?Together, client and therapist collaboratively develop strategies to replaceproblematic links and then commit to using new solutions the next time theproblem behavior emerges. The solution analysis does not stop there, however.Once the client has committed to using new behavior in future chains of eventsthat could lead to problem behaviors, it is important to continue searching forpossible links in the solution chain that could lead the client back to the problembehavior. This can be challenging, because many therapists may be satisfiedwith their chain analysis and the client’s commitment to skillful solutionstargeting reduced substance use or other problems. From a dialectical perspective,however, the identification and commitment to a specific solution doesnot mean that solution is the best choice of solutions, nor does it mean that thesolution will actually work at all. If solutions were easy to implement, then mostsubstance-abusing clients with BPD might not have such severe and enduringproblems. Accordingly, solutions are analyzed for apparent problems, and newlyimproved solutions emerge. The process is akin to predicting where the leaksmight be when preparing to fix the plumbing under the sink. Although a reasonableplan may exist, the skillful plumber considers where the plan may fail,making adjustments as necessary, before implementing the plan.Skills EnhancementA primary goal of individual therapy is to enhance skills learned during group.One way to do this is to ask clients to rehearse behavior in session. Behavioralrehearsal may occur in the form of covert rehearsing of challenges to distorted

630 V. TREATMENTS FOR ADDICTIONScognitions or by role-playing interpersonal scenarios. Therapists provide reinforcementand coaching during rehearsals and role plays, with an emphasis onskills use. Whenever skillful behavior occurs in session, the therapist reinforcessuch behavior. Ineffective behavior during the session, on the other hand, isoften extinguished. When repeated attempts to extinguish ineffective behaviorin session fail to work, the therapist may use mildly aversive responses to suchbehavior. However, the standard stance of the therapist is to be warm, nurturing,and validating, using aversive contingencies infrequently and only asneeded to evoke skillful behavior.Another method of facilitating skills use is behavioral exposure andresponse prevention in session. Clients will often become angry, ashamed, orfearful in session, and a range of behaviors may be evoked in response to theseemotions. BPD clients who feel angry may lash out, while those who feelashamed may look down or dissociate, and clients who feel fearful may suddenlyleave a session. Behavioral exposure and response prevention applied to theseemotions in session target paying attention to these emotions nonjudgmentally,observing urges to behave ineffectively, and blocking these urges by helping clientsnot to lash out, to keep eye contact, or to remain in the therapy room.ValidationVerification of what the client does effectively and disconfirmation of what isineffective is a commonality across many psychotherapies. Although validationof clients may be defined in various ways, in DBT-SUD, validation is a corestrategy operationalized on several levels (see Table 27.4). Validation may beexplicitly verbal, or it may occur more implicitly and functionally, such as whenthe therapist offers a tissue when an emotionally inhibited client appears on theverge of tears. Validation may be used as pure acceptance, with no directedeffort toward change. In DBT-SUD, there is an explicit emphasis on the thera-TABLE 27.4. Levels of Validation in Dialectical Behavior Therapy1. Listening and observing2. Accurate reflection of patient experiences3. Helping patients articulate unverbalized emotions, thoughts, andpatterns of behavior4. Communicating an understanding of behavior as valid given pastlearning history or biological vulnerability5. Communicating an understanding of behavior as valid given a currentcontext or what is deemed normative6. Therapist providing radical genuineness, treating the individual as anequal and not as a sick and fragile patient

27. Dialectical Behavior Therapy 631pist providing a warm, genuine, and compassionate interpersonal style. In manycases, these clients were raised in invalidating family environments (e.g., physical,sexual, or emotional abuse), continue to be surrounded by invalidating peopleassociated with drug using, and describe their previous mental healthtreatments as invalidating. The DBT-SUD therapist attempts to create a relationshipthat is different from past relationships. The deep pain and sufferingexperienced by these clients is attended to and validated in an authentic andcompassionate way.Importantly, however, therapist validation of client behavior is targetedspecifically to that which makes sense, is legitimate, or is effective. DBT-SUDtherapists attempt to validate what is valid, and, at times, invalidate what isinvalid. This requires the DBT therapist to discern carefully what is valid, andto apply validation in accordance with the conceptualization of each client’sproblem behaviors. For example, after a relapse, the therapist might warmly andcompassionately validate how and why it makes sense that the client used drugsto reduce short-term misery, but would not validate drug use as an effective,long-term solution to reducing pain. In DBT-SUD, validation is essential,because clients often come and go from treatment, and may not be as attachedto therapists compared to standard DBT clients with BPD and no substance useproblems. Consequently, aversive interpersonal contingencies are held to aminimum, unless, of course, such contingencies assist in reducing problembehaviors.Dialectical StrategiesIn DBT, dialectical strategies are fundamentally based around acceptance (e.g.,validation) and change (e.g., problem solving). Dialectical reasoning is pursuedwith the client, whereby the therapist helps the client move from a polarizedposition of “either–or” to a dialectical synthesis of “both–and.” Any therapiststrategy that challenges the client’s position (thesis), and instead involvesactively searching for what might be missing (antithesis), can be considered adialectical strategy if the tension between the thesis and antithesis produces asynthesis, or solution, that is ultimately useful for therapeutic change. There isno assumption that a single synthesis is the “correct” solution to a problem.Instead, the therapeutic process is one that continually works dialectically,yielding a number of possible solutions to a given problem; that is, the underlyingprinciple of dialectical strategies is a focus on the process of change within afluid context. Specifically, however, there are a number of dialectical strategiesused with clients (see Table 27.5; for descriptions, see Linehan, 1993b). Inorder to be effective, these strategies must be used in a manner that is genuine,and not as simple mechanical techniques. In addition, from a dialectical perspective,the therapist must be willing to let go of the truth or rightness of anydialectical strategy, and instead continually search for ways to help clients

632 V. TREATMENTS FOR ADDICTIONSTABLE 27.5. Dialectical Strategies Used in Dialectical Behavior Therapy1. Acceptance and change-focused interventions2. Nurturing the patient and demanding that patients help themselves3. Being stable and persistent, as well as flexible4. Highlighting patient’s strengths and deficits5. Structuring session with an agenda, and responding to in-session patient behaviors asthey occur6. Highlighting both ends of continua, and making synthesizing statements7. Pointing out paradoxes when present (e.g., patient’s behavior, therapeutic process)8. Using metaphors9. Playing the devil’s advocate10. Extending the seriousness or implications of patient’s communication11. Helping patient activate “wise mind”12. Helping make lemonade out of lemons13. Allowing natural changes in therapyNote. Adapted from Linehan (1993a, p. 206). Copyright 1993 by The Guilford Press. Adapted by permission.change problem behaviors. This approach probably helps reduce therapist burnout,and also helps ensure a validating and warm therapeutic environment. Inaddition, dialectical strategies are used in a manner that is often unpredictableto the client, and when any specific strategy does not help bring about new clientbehavior, another strategy is used.Telephone ConsultationClients with BPD and substance abuse problems experience a profound sense ofsuffering. Between treatment sessions, there often are times when emotionalpain (e.g., shame) and dysregulation occur, or events transpire that historicallyhave prompted drug use. To reduce the effects of emotional dysregulation in theclient’s natural environment, to prevent substance abuse, and, more broadly, toenhance generalization of skills, clients are encouraged to contact their individualtherapists on an ad hoc basis for brief telephone consultation between sessions.On the one hand, because these individuals may experience unrelentingcrises, therapists observe personal limits associated with telephone consultation.Clients call for help in implementing skills in necessary situations, ideallybefore crises occur. On the other hand, many DBT-SUD clients, particularlythose who are less attached to their therapists, will infrequently use the telephonefor skills coaching. As a result, some clients not only are encouraged tocall but also will be asked to practice calling their therapist between sessions. Inall consultation calls, therapists assess for immediate danger and provide appropriateassistance if the client is deemed to be in imminent danger of harminghim- or herself or others.

27. Dialectical Behavior Therapy 633TABLE 27.6. Consultation Team Agreements in Dialectical Behavior Therapy1. Meet weekly for 1–2 hours.2. Discuss cases according to the treatment hierarchy (i.e., self-injurious/life-threateningbehavior, treatment-interfering behavior, and quality-of-life interfering behavior).3. Accept a dialectical philosophy.4. Consult with the patient on how to interact with other therapists, and do not tellother therapists how to interact with the patient.5. Consistency of therapists with one another (even across the same patient) is notexpected.6. All therapists observe their own limits without fear of judgmental reactions fromother consultation group members.7. Search for nonpejorative empathic interpretation of patient’s behavior.8. All therapists are fallible.Consultation TeamAs mentioned earlier, the consultation team is a necessary mode of treatment.Team members commit to weekly meetings and agree to a team structure andprocess (see Table 27.6). In important ways, team members treat each other byproviding validation, support, and motivation. This support is invaluable andcan help DBT-SUD therapists have a more balanced approach toward their clients.A consultation team also provides opportunities for fresh perspectives andnew solutions, helping therapists get unstuck and remain hopeful. It is notuncommon for DBT-SUD therapists periodically to become rigid in theirthinking and behavior with a client. The consultation team offers problemsolving and validation for the therapist, and team members actively use a dialecticalprocess to help find effective syntheses between polarized positions. Forexample, the team can help remind the therapist to continue managing contingenciesin session appropriately (e.g., not being warm in response to client hostility).If possible, it is extremely helpful to videotape and watch important segmentsof the therapy session during the consultation team meeting, because thisengenders a full appreciation for the difficulty a therapist may be having, andallows the team to ensure that all members are indeed adhering to the treatment.PharmacotherapyFive principles organize the management of psychotropic medications in DBT-SUD. First, and most importantly, safe and nonlethal medications must be prescribedand used in a safe manner. This principle is considered in light of eachindividual. For those with a history of medication abuse, the DBT-SUDpharmacotherapist would observe the medication being ingested and providethe client with a small supply of take-home medications. Second, simple medi-

634 V. TREATMENTS FOR ADDICTIONScation regimens are used in order to mitigate problems with side effects anddrug interactions, both of which can interfere with treatment. Third, specificsymptoms are targeted first, rather than general problems such as affectiveinstability. Fourth, choice of medications is guided by controlled efficacy studies.Finally, speed of clinical improvement is imperative, with, for example, opiatereplacement rapidly adjusted to the desirable therapeutic maintenance dose.DBT-SUD Case ManagementBecause substance users with BPD often encounter problems obtaining andmaintaining adequate food, housing, and employment, case management canbe added to DBT-SUD. Unlike standard case management approaches thatintervene directly in the environment (e.g., making a phone call on behalf of aclient), however, DBT-SUD case management emphasizes actively coachingthe client to intervene on his or her own behalf. The DBT-SUD case managerdoes not manage clients’ resources; instead, clients manage their resources withskills coaching from the case manager or individual therapist. The case manageris utilized by the individual therapist on an ad hoc basis in one of the followingways: (1) as a resource to the therapist for referrals or advice, (2) to provideinformation or referrals directly to the client, or (3) to provide in vivo skillscoaching in the client’s natural environment.FUTURE DIRECTIONSTo date, the efficacy of DBT-SUD has been demonstrated in two small clinicaltrials. As described earlier, these studies suggest that DBT-SUD is a promising,manual-based treatment for substance users with BPD. The next step in thedevelopment and evaluation of DBT-SUD is a Stage II efficacy trial. Such workis currently underway on a two-site study at the University of Washington(Linehan) and Duke University (Lynch). In this National Institute of DrugAbuse–sponsored project, 172 individuals with BPD and opioid dependencewill be randomly assigned to receive DBT-SUD or Individual Drug Counselingwith Group Drug Counseling (Mercer & Woody, 1999). Both treatment conditionswill receive Suboxone, an opiate replacement medication that consists ofan opiate partial agonist (buprenorphine) and antagonist (naloxone). This willbe the largest study ever to evaluate the efficacy of DBT-SUD.SUMMARYDBT-SUD is a comprehensive psychosocial treatment designed to treat substanceusers with BPD. The philosophy, theory, structure, skills modules, treat-

27. Dialectical Behavior Therapy 635ment modes and functions, and treatment strategies are equivalent to those ofstandard DBT. However, notable additions to DBT-SUD include (1) treatmenttargets that aim to reduce drug-related behaviors, (2) new coping skills for managingdrug cravings and withdrawal, (3) new “wise mind” skills, (4) attachmentstrategies, (5) increased use of validation and less aversive interpersonal contingencies,(6) increased use of case management to assist in housing and othercrises via direct environmental intervention, and (7) a pharmacotherapy mode.Overall, DBT-SUD is a promising new treatment that is grounded in philosophyand theory, supported by preliminary empirical findings, and, importantly,offers hope for substance users with BPD.REFERENCESBrooner, R. K., King, V. L., Kidorf, M., Schmidt, C. W., & Bigelow, G. E. (1997). Psychiatricand substance use comorbidity among treatment-seeking opioid abusers.Arch Gen Psychiatry, 54, 71–80.Chambless, D. L., & Hollon, S. D. (1998). Defining empirically supported therapies. JConsult Clin Psychol, 66, 7–18.Hayes, S. C., & Follette, W. C. (1992). Can functional analysis provide a substitute forsyndromal classification? Behav Assess, 14, 345–365.Kanfer, F. H., & Saslow, G. (1969). Behavioral diagnosis. In C. M. Franks (Ed.), Behaviortherapy: Appraisal and status. New York: McGraw-Hill.Koons, C. R., Robins, C. J., Tweed, J. L., Lynch, T. R., Gonzalez, A. M., Morse, J. Q., etal. (2001). Efficacy of dialectical behavior therapy in women veterans with borderlinepersonality disorder. Behav Ther, 32, 371–390.Kosten, R. A., Kosten, T. R., & Rousaville, B. J. (1989). Personality disorders in opiateaddicts show prognostic specificity. J Subst Abuse Treat, 6, 163–168.Linehan, M. M. (1993a). Cognitive-behavioral treatment of borderline personality disorder.New York: Guilford Press.Linehan, M. M. (1993b). Skills training manual for treating borderline personality disorder.New York: Guilford Press.Linehan, M. M., Armstrong, H. E., Suarez, A., Allmon, D., & Heard, H. L. (1991).Cognitive-behavioral treatment of chronically parasuicidal borderline patients.Arch Gen Psychiatry, 48, 1060–1064.Linehan, M. M., Dimeff, L. A., Reynolds, S. K., Comtois, K. A., Welch, S. S., Heagerty,P., & Kivlahan, D. R. (2002). Dialectical behavior therapy versus comprehensivevalidation therapy plus 12-step for the treatment of opioid dependent womenmeeting criteria for borderline personality disorder. Drug Alcohol Depend, 67, 13–26.Linehan, M. M., Dimeff, L. A., & Sayrs, J. H. R. (2004). Dialectical behavior therapy forsubstance abusers with borderline personality disorder: An extension of standard DBT.Unpublished manuscript.Linehan, M. M., Schmidt, H., III, Dimeff, L. A., Craft, J. C., Kanter, J., & Comtois, K.A. (1999). Dialectical behavior therapy for patients with borderline personalitydisorder and drug-dependence. Am J Addict, 8, 279–292.

636 V. TREATMENTS FOR ADDICTIONSLinks, P. S., Heslegrave, R. J., Mitton, J. E., van Reekum, R., & Patrick, J. (1995). Borderlinepersonality disorder and substance use: Consequences of comorbidity. CanJ Psychiatry, 40, 9–14.Marlatt, G. A., & Gordon, J. R. (1985). Relapse prevention: Maintenance strategies in thetreatment of addictive behaviors. New York: Guilford Press.Mercer, D., & Woody, G. (1999). Individual drug counseling. Rockville, MD: NationalInstitute on Drug Abuse.Moos, R. H., Moos, B. S., & Finney, J. W. (2001). Predictors of deterioration amongpatients with substance-use disorders. J Clin Psychol, 57, 1403–1419.Trull, T. J., Sher, K. J., Minks-Brown, C., Durbin, J., & Burr, R. (2001). Borderline personalitydisorder and substance use disorders: A review and integration. ClinPsychol Rev, 20, 235–253.Verheul, R., van den Bosch, L. M. C., Koeter, M. W. J, de Ridder, M. A. J, Stijnen, T.,& van den Brink, W. (2003). Dialectical behaviour therapy for women with borderlinepersonality disorder: 12-month, randomised clinical trial in the Netherlands.Br J Psychiatry, 182, 135–140.Wagner, A. W., & Linehan, M. M. (1997). Biosocial perspective on the relationship ofchildhood sexual abuse, suicidal behavior, and borderline personality disorder. InM. Zanarini (Ed.), Role of sexual abuse in the etiology of borderline personality disorder.Washington, DC: American Psychiatric Press.Weiss, R. D., Mirin, S. M., Griffin, M. L., Gunderson, J. G., & Hufford, C. (1993). Personalitydisorders in cocaine dependence. Compr Psychiatry, 34, 145–149.

CHAPTER 28Matching and Differential TherapiesProviding Substance Abuserswith Appropriate TreatmentKATHLEEN M. CARROLLBroadly defined, matching individuals to treatment means providing the individualwith the treatment approach that is likely to maximize outcome. Thepast 20 years have been marked by both tremendous progress and increasingmethodological rigor in substance abuse research, and hence, the developmentof a much wider range of empirically supported pharmacotherapies and behavioraltherapies. Availability of a broader range of therapies has likewise heightenedinterest in differential treatment research, whether it be matching individualsto specific treatment approaches, matching patients to different levelsof services, or identifying predictors of response to specific therapies.To date however, empirical evidence supporting specific, a priori matchingstrategies has been modest at best (Magura et al., 2003; McKay, Cacciola,McLellan, Alterman, & Wirtz, 1997; McLellan & McKay, 1998; ProjectMATCH Research Group, 1993, 1997), in part due to the complexity of treatmentdecisions for many patients, who typically present for treatment with acomplex array of substance use, psychiatric, legal, medical, and social problems,as well as limits of the service delivery system in accommodating the needs ofdiverse patients (Gastfriend, Lu, & Sharon, 2000). The complexities and challengingmethodological requirements of matching research have also hamperedprogress in this area (Moyer, Finney, Elworth, & Kraemer, 2001).There is some more consistency in the literature, however, regardingpatient prognostic variables that have emerged across patient populations.637

638 V. TREATMENTS FOR ADDICTIONSBriefly, greater severity of substance dependence, presence and severity ofcomorbid psychiatric problems, lower levels of social support, and unemploymenthave consistently related to poorer outcome reviews (McLellan &McKay, 1998). Larger scale studies have also demonstrated with some consistencythat addressing comorbid issues and problems in treatment is generallyassociated with improved outcome (McLellan, Arndt, Metzger, Woody, &O’Brien, 1993; McLellan, Grissom, Zanis, & Randall, 1997).Thus, appropriate matching to treatment implies provision of an effective,empirically supported therapy, with adjunct therapies appropriate to the specificco-occurring problems, as dictated by careful, thorough, assessment of thepatient functioning and status across a range of domains. This review summarizesempirically supported therapies across the most common substance use disorders(SUDs), with special emphasis on how pharmacological and behavioraltherapies can be combined to enhance outcome. When available, data regardingthe types of individuals who may respond particularly well or poorly to specificapproaches are reviewed. First, however, it is important to understand therespective roles of pharmacotherapy and behavioral approaches in terms of howthese may be tailored, or combined, to meet the needs of specific individuals.ROLES OF PHARMACOTHERAPY IN THE TREATMENTOF SUBSTANCE USE DISORDERSThe target symptoms addressed and roles typically played by pharmacotherapydiffer from those of behavioral treatments in their course of action, time toeffect, target symptoms, and durability of benefits (Elkin, Pilkonis, Docherty, &Sotsky, 1988). In general, pharmacotherapies have a much more narrow applicationthan do most behavioral treatments for SUDs; that is, most behavioraltherapies are applicable across a range of treatment settings (e.g., inpatient,outpatient, residential), modalities (e.g., group, individual, family), and to awide variety of populations. For example, disease-model, behavioral, or motivationalapproaches have been used, with only minor modifications, regardless ofwhether the patient is an opiate, alcohol, cocaine, or marijuana user. On theother hand, most available pharmacotherapies tend to be applicable only to asingle class of substance use and exert their effects over a narrow band of symptomsor clinical settings. For example, methadone produces cross-tolerance foropioids but has little effect on concurrent cocaine abuse; disulfiram producesnausea after alcohol ingestion, but not after ingestion of illicit substances. Anotable exception is naltrexone, which is used to treat both opioid and, morerecently, alcohol dependence.Common roles and indications for pharmacotherapy in the treatment ofsubstance dependence disorders are presented (Carroll, 2001; Rounsaville &Carroll, 1997).

28. Matching and Differential Therapies 639DetoxificationFor those classes of substances that produce substantial physical withdrawalsyndromes (e.g., alcohol, opioids, sedatives/hypnotics), medications are oftenneeded to reduce or control the often-dangerous symptoms associated withwithdrawal. Benzodiazepines are often used to manage symptoms of alcoholwithdrawal. Agents such as methadone, clonidine, naltrexone, and buprenorphineare typically used for the management of opioid withdrawal. Typically,the role of behavioral treatments during detoxification is typically extremelylimited due to the level of discomfort, agitation, and confusion the patient mayexperience. However, studies have suggested the effectiveness of behavioralstrategies in increasing retention and abstinence in the course of longer termoutpatient detoxification protocols (Bickel, Amass, Higgins, Badger, & Esch,1997).Stabilization and MaintenanceA widely-used example of the use of a medication for long-term stabilization ofdrug users is methadone maintenance for opioid dependence, a treatment strategythat involves the daily administration of a long-acting opioid (methadone)as a substitute for the illicit use of short-acting opioids (typically heroin). Methadonemaintenance permits the patient to function normally, without experiencingwithdrawal symptoms, craving, or side effects. The large body ofresearch on methadone maintenance confirms its importance in fostering treatmentretention, providing the opportunity to evaluate and treat other problemsand disorders that often coexist with opioid dependence (e.g., medical, legal,and occupational problems), reducing the risk of HIV infection and other complicationsthrough reducing intravenous drug use, and providing a level of stabilizationthat permits the inception of psychotherapy and other aspects of treatment.Antagonist and OtherBehaviorally Oriented PharmacotherapiesA more recent pharmacological strategy is the use of antagonist treatment, thatis, the use of medications that block the effects of specific drugs. An example ofthis approach is naltrexone, an effective, long-acting opioid antagonist. Naltrexoneis nonaddicting, does not have the reinforcing properties of opioids, hasfew side effects and, most important, effectively blocks the effects of opioids.Therefore, naltrexone treatment represents a potent behavioral strategy: Becauseopioid ingestion is not reinforced while the patient is taking naltrexone,unreinforced opioid use allows extinction of relationships between conditioneddrug cues and drug use. For example, a naltrexone-maintained patient, antici-

640 V. TREATMENTS FOR ADDICTIONSpating that opioid use will not result in desired drug effects, may be more likelyto learn to live in a world full of drug cues and high-risk situations withoutresorting to drug use.Treatment of Coexisting DisordersAn important role of pharmacotherapy in the treatment of SUDs is as treatmentfor coexisting psychiatric syndromes that may precede or play a role in themaintenance or complications of drug dependence. The frequent co-occurrenceof psychiatric disorders, particularly affective and anxiety disorders, with SUDsis well documented in a variety of populations and settings (Kessler et al., 1997;Regier et al., 1990). Given that psychiatric disorders often precede developmentof SUDs, several researchers and clinicians have hypothesized that individualswith primary psychiatric disorders may be attempting to self-medicatetheir psychiatric symptoms with drugs and alcohol. Thus, effective pharmacologicaltreatment of the underlying psychiatric disorder may improve not onlythe psychiatric disorder but also the perceived need for, and therefore the useof, illicit drugs (Nunes & Levin, 2004). Examples of this type of approachinclude the use of antidepressant treatment for depressed alcohol- (Mason,Salvato, Williams, Ritvo, & Cutler, 1999), opioid- (Nunes et al., 1998), andcocaine-dependent (Rounsaville, 2004) individuals.BEHAVIORAL TREATMENTSMost behavioral approaches for SUDs address several common issues and tasks,despite often vast differences in theory, technique, and strategies. Although differentapproaches vary in the degree to which emphasis is placed on these commontasks, some attention to these issues is likely to be involved in any successfultreatment (Rounsaville & Carroll, 1997). Moreover, it should be noted thatcurrently available pharmacotherapies for drug dependence would be expectedto have little or no effect in these areas commonly addressed by behavioraltherapies.Setting the Resolve to StopRare is the substance abuser who seeks treatment without some degree ofambivalence regarding cessation of drug use. Even at the time of treatmentseeking, which usually occurs only after substance-related problems havebecome severe, substance abusers usually can identify many ways in which theywant or feel the need for drugs and alcohol, and have difficulty developing aclear picture of what life without drugs might be like (Rounsaville & Carroll,1997). Moreover, given the substantial external pressures that may precipitate

28. Matching and Differential Therapies 641application for treatment, many patients are highly ambivalent about treatmentitself. Ambivalence must be addressed if the patient is to experience him- orherself as an active participant in treatment; if the patient perceives treatmentas wholly imposed upon him or her by external forces and does not have a clearsense of personal goals for treatment; it is likely that any form of treatment willbe of limited usefulness. Treatments based on principles of motivational psychology,such as motivational interviewing (Miller & Rollnick, 2002), concentratealmost exclusively on strategies intended to bolster the patient’s ownmotivational resources. However, most behavioral treatments include someexploration of what the patient stands to lose or gain through continued substanceuse as a means to enhance motivation for treatment and abstinence.Teaching Coping SkillsSocial learning theory posits that substance abuse may represent a means ofcoping with difficult situations, positive and negative affects, invitations bypeers to use substances, and so on. By the time substance use is severe enoughfor treatment, use of substances may represent the individual’s single, overgeneralizedmeans of coping with a variety of situations, settings, and states. Ifstable abstinence is to be achieved, treatment must help patients to recognizethe high-risk situations in which they are most likely to use substances and todevelop other, more effective means of coping with them. Although cognitivebehavioralapproaches concentrate almost exclusively on skills training as ameans of preventing relapse to substance use (Marlatt & Gordon, 1985; Montiet al., 1989), most treatment approaches touch on the relationship betweenhigh-risk situations and substance use to some extent.Changing Reinforcement ContingenciesBy the time treatment is sought, many substance abusers spend the preponderanceof their time involved in acquiring, using, and recovering from substanceuse, to the exclusion of other endeavors and rewards. The abuser may beestranged from friends and family, and have few social contacts who do not usedrugs. If the patient is still working, employment often becomes only a means ofacquiring money to buy drugs, and the fulfilling or challenging aspects of workhave faded. Few other activities, such as hobbies, athletics, and involvementwith community or church groups, can stand up to the demands of substancedependence. Typically, rewards available in daily life are narrowed progressivelyto those derived from drug use, and other diversions may be neither availablenor perceived as enjoyable. When drug use is stopped, its absence mayleave the patient with the need to fill the time that had been spent using drugsand to find rewards that can substitute for those derived from drug use. Thus,most behavioral treatments encourage patients to identify and develop fulfilling

642 V. TREATMENTS FOR ADDICTIONSalternatives to substance use, as exemplified by the community reinforcementapproach (CRA; Azrin, 1976) or contingency management (Budney & Higgins,1998), which stresses the development of alternate reinforcers for substanceuse.Fostering Affect ManagementAmong the most commonly cited reasons for relapse are powerful negativeaffects, and several clinicians have suggested that failure of affect regulation is acritical dynamic underlying the development of compulsive drug use. Moreover,the difficulty many substance abusers have in recognizing and managingaffect states has been noted in several populations. Thus, an important commontask in substance abuse treatment is to help develop ways of coping withpowerful dysphoric affects, and to learn to recognize and identify the probablecause of these feelings (Rounsaville & Carroll, 1997). Again, whilepsychodynamically oriented treatments such as supportive–expressive therapy(Luborsky, 1984) emphasize the role of affect in the treatment of cocaine abuse,virtually all forms of psychotherapy for substance abuse include a variety oftechniques for coping with strong affects.Improving Interpersonal Functioningand Enhancing Social SupportsA consistent finding in the literature on relapse to substance abuse and dependenceis the protective influence of an adequate network of social supports(Longabaugh, Beattie, Noel, Stout, & Malloy, 1993). Typical issues presentedby drug abusers are loss of or damage to valued relationships occurring whenusing drugs was the principal priority, failure to have achieved satisfactory relationshipseven prior to having initiated drug use, and inability to identifyfriends or intimates who are not themselves drug users (Rounsaville & Carroll,1997). Many forms of treatment, including family/couple therapy (E. E. Epstein& McCrady, 1998; Fals-Stewart, O’Farrell, & Birchler, 1997), 12-step approaches(Nowinski, Baker, & Carroll, 1992), interpersonal therapy (Rounsaville,Gawin, & Kleber, 1985), and network therapy (Galanter, 1993), make buildingand maintaining a network of social supports for abstinence a central focus oftreatment.Fostering Compliance with PharmacotherapyThe difficulties of fostering adequate levels of treatment compliance with substanceusers are well known, so much so that substance abusers are typicallyexcluded from clinical trials of treatments for other disorders. Thus, whenpharmacotherapies are used in the treatment of substance abuse, it is not sur-

28. Matching and Differential Therapies 643prising that high rates of noncompliance are seen. A major role that behavioraltreatments play when pharmacotherapies are used in the treatment of substanceuse is in fostering compliance, because most strategies to improve complianceare inherently psychosocial. These include, for example, regular monitoring ofmedication compliance through pill counts and medication serum levels;encouragement of patient self-monitoring of compliance (e.g., through medicationlogs or diaries); clear communication between patient and staff about themedication, its expected effects, side effects, and benefits; repeatedly stressingthe importance of adherence; contracting with the patients for adherence;directly reinforcing adherence through incentives or rewards; providing telephoneor written reminders about appointments or taking medication; preparingand educating patients about the disorder and its treatment; and frequentcontact and the provision of extensive support and encouragement to thepatient and his or her family.TREATMENT APPROACHES FOR SPECIFIC CATEGORIESOF SUBSTANCE USEBefore moving to a review of empirically supported treatments for specific categoriesof substance use, three general issues regarding the current state of substanceabuse treatment are highlighted. First, nonpharmacological, behavioraltreatments continue to constitute the bulk of substance abuse treatment in theUnited States. Numerous uncontrolled studies, as well as randomized trials,consistently point to the benefits of purely behavioral approaches for manySUDs (McLellan & McKay, 1998; Simpson, Joe, & Brown, 1997), and effectivepharmacotherapies, even in cases where they exist, tend to be underutilizedSecond, for most types of illicit drug use, no effective pharmacotherapies exist.Classes of drug use for which no effective, approved pharmacotherapies havebeen developed include marijuana, hallucinogens, amphetamines, inhalants,phencyclidine, and sedative/hypnotic/anxiolytics. Although major advanceshave been made in identifying physiological mechanisms of action for many ofthese substances, and in a few cases (e.g., marijuana) specific receptors havebeen identified that should accelerate progress in identifying pharmacologicaltreatments, behavioral therapies remain the sole available treatment for manyclasses of drug dependence. Third, there is general consensus that even forour most potent pharmacotherapies for drug use, purely pharmacological approachesare insufficient for most substance abusers and best outcomes are seenfor combined treatments. As described earlier, most pharmacotherapies arecomparatively specific and narrow in their actions, and may help to detoxify,stabilize, or treat coexisting disorders, but are rarely considered “complete treatments”in and of themselves. Furthermore, because few patients will persist orcomply with a purely pharmacotherapeutic approach, pharmacotherapies deliv-

644 V. TREATMENTS FOR ADDICTIONSered alone, without any supportive or compliance-enhancing elements, are usuallynot considered feasible. Even where pharmacotherapy is seen as the primarytreatment approach (as in the case of methadone maintenance), someform of psychosocial treatment is used to provide at least a minimal supportivestructure within which pharmacotherapeutic treatment can be conducted effectively.Furthermore, medication effects can be enhanced or diminished withrespect to the context in which they are delivered; that is, a medication administeredin the context of a supportive clinician–patient relationship, with clearexpectations of possible medication benefits and side effects, close monitoringof compliance, and encouragement for abstinence, is more likely to haveenhanced effectiveness than a medication delivered without such elements.Thus, even for primarily pharmacotherapeutic treatments, a psychotherapeuticcomponent is almost always included to foster patients’ retention in treatmentand compliance with pharmacotherapy, and to address the numerous comorbidpsychosocial problems that occur so frequently among individuals with SUDs(Carroll, 2001).TREATMENT OF ALCOHOL DEPENDENCEThere is now a comparatively wide range of empirically supported behavioraltherapies for alcohol use disorders, including brief intervention, social skillstraining, cognitive-behavioral therapies, family/couple and network therapies,and motivational interviewing (DeRubeis & Crits-Christoph, 1998; Miller &Wilbourne, 2002). The availability of a much broader array of effective treatmentoptions led in part to Project MATCH, a large, multisite study of a prioritreatment-matching hypotheses, in which 1,726 alcohol-abusing or -dependentpatients were randomly assigned to either motivational enhancement therapy(Miller, Zweben, DiClemente, & Rychtarik, 1992), 12-step facilitation(Nowinski et al., 1992), or cognitive-behavioral therapy (Kadden et al., 1992),all delivered as individual treatments over 12 weeks. While the results of thislandmark study indicated few strong indicators of matching or differentialresponse to these treatments, a major finding of Project MATCH was thatthese three therapies were followed by marked and sustained reductions in alcoholconsumption (Project MATCH Research Group, 1997, 1998). To illustrate,in all three conditions, patients, on average, entered treatment drinkingmore than 80% of days, rapidly reduced their consumption to less than 15% ofdays, and kept those levels down at follow-up visits over 3 years. Thus, oneimplication of these findings is that delivery of a high-quality individual behavioraltherapy can be associated with meaningful change in individuals with awide range of alcohol disorders and associated problems.There have been a number of developments in the pharmacotherapy ofalcohol use disorders as well. The most commonly used pharmacological

28. Matching and Differential Therapies 645adjunct for the treatment of alcohol dependence remains disulfiram (Antabuse).Disulfiram interferes with normal metabolism of alcohol, which results inan accumulation of acetaldhyde; hence, drinking following ingestion of disulfiramresults in an intense physiological reaction, characterized by flushing,rapid or irregular heartbeat, dizziness, nausea, and headache (see Nace, Chapter5, this volume). Thus, disulfiram treatment is intended to work as a deterrent todrinking. Despite the sustained popularity and widespread use of disulfiram, alandmark multicenter, randomized clinical trial found that disulfiram was nomore effective than inactive doses of disulfiram or no medication in terms ofrates of abstinence, time to first drink, unemployment, or social stability (Fulleret al., 1986). However, for subjects who did drink, disulfiram treatment wasassociated with significantly fewer total drinking days. Rates of compliancewith disulfiram in the study were low (20% of all subjects), but abstinence rateswere reasonably good (43%) among compliant subjects. This study highlightsseveral important problems with the use of disulfiram: (1) Compliance is amajor problem and must be monitored closely, and (2) many patients areunwilling to take disulfiram (62% of those eligible for the study refused to participate).Thus, several investigators have evaluated the effectiveness of behavioraltreatments to improve retention and compliance with disulfiram. One of themost effective strategies is disulfiram contracts, in which the patient’s spouse ora significant other agrees to observe the patient take disulfiram each day andreward the patient for compliance with disulfiram treatment (O’Farrell, Cutter,Choquette, & Floyd, 1992). Azrin, Sisson, Meyers, and Godley (1982) reportedpositive and durable results from a randomized clinical trial comparingunmonitored disulfiram to disulfiram contracts, where disulfiram ingestion wasmonitored by the patient’s spouse or administered as part of a multifacetedbehavioral program, the CRA. A broad-spectrum approach developed by Huntand Azrin (1973), CRA incorporates skills training, behavioral family therapy,and job-finding training, as well as a disulfiram component. CRA has beenfound to be significantly more effective than traditional group approaches infostering abstinence. Combined disulfiram–behavioral treatment for alcoholdependence illustrates how a pharmacotherapy that may be marginally effectivewhen used alone can be highly effective when used with in combination withtreatments that foster compliance and target other aspects of substance abuse.Another major development in the treatment of alcohol dependence wasthe recent Food and Drug Administration (FDA) approval of naltrexone. Theapplication of naltrexone, an opioid antagonist, to the treatment of alcoholismderives from findings that naltrexone reduces alcohol craving and use inhumans. In randomized clinical trials, naltrexone has been shown to be moreeffective than placebo in reducing alcohol use and craving (O’Malley et al.,1992; Volpicelli, Alterman, Hayashida, & O’Brien, 1992). As with disulfiram,best responses are seen among patients who are compliant with naltrexone

646 V. TREATMENTS FOR ADDICTIONS(Volpicelli et al., 1997), which underscores the importance of delivering naltrexonein conjunction with an effective behavioral approach that addresses compliance.Thus, it is not surprising that naltrexone’s effects have been found to differsomewhat depending on the nature of the behavioral treatment with which it isdelivered. For example, in the O’Malley and colleagues (1992) study, highestrates of abstinence were found when the patient received naltrexone plus a supportiveclinical management psychotherapy condition that encouraged completeabstinence from alcohol and other substances. However, for patients whodrank, the combination of a cognitive-behavioral coping skills approach andnaltrexone was superior in terms of rates of relapse and drinks per occasion.Evaluation of naltrexone’s effectiveness in combination with acamprosate,another promising medication, and with brief versus more intensive behavioraltreatment that should shed light on important data regarding the types ofpatients who respond to lower versus higher intensity behavioral approacheswith naltrexone, is ongoing (COMBINE Study Research Group, 2003).TREATMENT OF OPIOID DEPENDENCEThe inception of methadone maintenance treatment revolutionized the treatmentof opioid addiction, because it displayed the previously unseen ability tokeep addicts in treatment and to reduce their illicit opioid use, outcomes withwhich nonpharmacological treatments had fared comparatively poorly. Beyondits ability to retain opioid addicts in treatment and help control opioid use,methadone maintenance also reduces the risk of HIV infection and other medicalcomplications through reducing intravenous drug use (Ball & Ross, 1991),and provides the opportunity to evaluate and treat concurrent disorders, includingmedical problems and family and psychiatric problems. The bulk of thelarge body of literature on the effectiveness of methadone maintenance pointsto its success in retaining opioid addicts in treatment and reducing their illicitopioid use and illegal activity (Ball & Ross, 1991). Methadone maintenancetreatment, especially when provided at adequate doses and combined with drugcounseling, substantially decreases illicit opioid use, injection drug use, criminalactivity, and morbidity and mortality risk (O’Brien, 1997). However, there is agreat deal of variability in the success across different methadone maintenanceprograms, which appears to be largely associated with both variability in deliveryof adequate dosing of methadone and in provision and quality of psychosocialservices (Ball & Ross, 1991).There remain, however, several problems with methadone maintenance,including illicit diversion of take-home methadone doses, difficulties withdetoxification from methadone maintenance to a drug-free state, and the concurrentuse of other substances, particularly alcohol and cocaine, among

28. Matching and Differential Therapies 647methadone-maintained individuals. Thus, a range of psychosocial treatmentshave been evaluated for their ability to address these drawbacks of methadonemaintenance, as well as to enhance and extend the benefits of methadonemaintenance. Several types of behavioral approaches have been identified aseffective in enhancing and extending the benefits of methadone maintenancetreatment, and these are summarized below (Carroll, 2001).Before describing specific approaches that have been demonstrated to beeffective in enhancing the effectiveness of opioid maintenance therapies, thecontext for such approaches should be set by a brief review of a study thatauthoritatively established the importance of psychosocial treatments evenin the context of a pharmacotherapy as potent as methadone. McLellanand colleagues (1993) randomly assigned 92 opiate-dependent individuals to(1) methadone maintenance alone, without psychosocial services; (2) methadonemaintenance with standard services, which included regular meetingswith a counselor; and (3) enhanced methadone maintenance, which includedregular counseling plus on-site medical/psychiatric, employment, and familytherapy, in a 24-week trial. Although some patients did reasonably well in themethadone-alone condition, 69% of this group had to be transferred out of thiscondition within 3 months of the study inception, because their substance usedid not improve or even worsened, or because they experienced significantmedical or psychiatric problems that required a more intensive level of care. Interms of drug use and psychosocial outcomes, the best outcomes were seen inthe enhanced methadone maintenance condition, with intermediate outcomesfor the standard methadone services condition, and the poorest outcomes forthe methadone-alone condition. This study illustrates that although methadonemaintenance treatment has powerful effects in terms of keeping addicts intreatment and making them available for psychosocial treatments, a purelypharmacological approach is not sufficient for the large majority of patients,and better outcomes are closely associated with higher levels of psychosocialtreatments.More recently, among the most exciting findings regarding how the benefitsof agonist maintenance therapies can be enhanced for a range of individualshas been the use of contingency management to reduce the use of illicit drugsin addicts who are maintained on methadone. In these studies, a reinforcer isprovided to patients who demonstrate specified target behaviors, such as providingdrug-free urine specimens, accomplishing specific treatment goals, orattending treatment sessions. For example, using methadone take-home privilegesas rewards contingent on reduced drug use is an approach that capitalizeson an inexpensive reinforcer that is potentially available in all methadonemaintenance programs. Stitzer, Iguchi, Kidorf, and Bigelow (1993) have doneextensive work in evaluating methadone take-home privileges as a reward fordecreased illicit drug use. In a series of well-controlled trials, this group of

648 V. TREATMENTS FOR ADDICTIONSresearchers has demonstrated (1) the relative benefits of positive over negativecontingencies; (2) the attractiveness of take-home privileges over other incentivesavailable within methadone maintenance clinics; (3) the effectiveness oftargeting and rewarding drug-free urines over other, more distal behaviors, suchas group attendance; and (4) the benefits of using take-home privileges contingenton drug-free urines over noncontingent take-home privileges.Silverman and colleagues (1996), drawing on the compelling work ofSteve Higgins and his colleagues (e.g., Budney & Higgins, 1998), evaluated avoucher-based contingency management system to address concurrent illicitdrug use (typically cocaine) among methadone-maintained opioid addicts. Inthis approach, urine specimens are required three times weekly in order todetect systematically all episodes of drug use. Abstinence is reinforced througha voucher system in which the rewards help patients develop alternative reinforcersto drug use (e.g., movie tickets or sporting goods, but never money). Toencourage longer periods of consecutive abstinence, the value of the pointsearned by a patient increases with each successive clean urine specimen, andthe value of the points is reset when the patient relapses. In a very elegant seriesof studies, Silverman and his colleagues have demonstrated the efficacy of thisapproach in reducing illicit opioid and cocaine use, and in producing a numberof treatment benefits among this very difficult population.Although contingency management procedures appear quite promising inmodifying previously intractable problems in methadone maintenance programs,particularly continued illicit drug use among clients, they have rarelybeen implemented in clinical practice. A major obstacle to the implementationof contingency management voucher approaches in regular clinical settings istheir cost (up to $1,200 over 12 weeks). However, lower cost variable ratio contingencymanagement approaches, in which patients earn opportunities to drawprizes from a bowl contingent on specific behavioral targets, have also receivedimpressive empirical support in a range of populations (Petry, 2000; Petry &Martin, 2002). Moreover, there are indications that the positive effects of contingencymanagement procedures may diminish over time when the behavioralintervention is no longer in effect. Studies evaluating the change in strength orpreference of reinforcers over time within methadone maintenance programsare needed. For example, for clients from the street who enter a methadone program,contingency payments or dose increases may be highly motivating,whereas for clients who have been stabilized and are working, and who mayhave less free time, other reinforcers, such as take-home doses or permission toomit counseling sessions, may be more attractive later in treatment. While contingencymanagement procedures may prove effective only over short periods oftime, they may still be valuable in that they may provide an interruption inillicit drug use (or other undesirable behaviors) that may serve as an opportunityfor other interventions and services to take effect.

Other Psychotherapies28. Matching and Differential Therapies 649Other studies have evaluated other forms of psychotherapy as strategies toenhance outcome from opioid maintenance therapies. The landmark study inthis area was done by Woody and colleagues (1983) and replicated in communitysettings (Woody, McLellan, Luborsky, & O’Brien, 1995). While the originalstudy is now more than 20 years old, it is reviewed in some detail here,because it remains the most impressive demonstration of the benefits and roleof psychotherapy in the context of methadone maintenance programs. Moreover,it has generated several substudies that have added greatly to our understandingof the types of patients who benefit from psychotherapy in the contextof methadone maintenance programs.In this landmark study, 110 opiate addicts entering a methadone maintenanceprogram were randomly assigned to one of three treatments: drug counselingalone, drug counseling plus supportive–expressive psychotherapy (SE), ordrug counseling plus cognitive psychotherapy (CT). After a 6-month course oftreatment, although the SE and CT groups did not differ significantly fromeach other on most measures of outcome, subjects who received either form ofprofessional psychotherapy evidenced greater improvement in more outcomedomains than the subjects who received drug counseling alone (Woody et al.,1983). Furthermore, gains made by the subjects who received professional psychotherapywere sustained over a 12-month follow-up, while subjects receivingdrug counseling alone evidenced some attrition of gains (Woody, McLellan,Luborsky, & O’Brien, 1987). This study also demonstrated differential responseto psychotherapy as a function of patient characteristics, which may point tothe best use of psychotherapy (relative to drug counseling) when resources arescarce: While methadone-maintained opiate addicts with lower levels of psychopathologytended to improve regardless of whether they received professionalpsychotherapy or drug counseling, those with higher levels of psychopathologytended to improve only if they received psychotherapy. In addition,this study provides indications of differential response to psychotherapy by concurrentpsychiatric disorder. For example, depressed addicts improved with psychotherapy,while addicts with antisocial personality disorder tended to showlittle or no improvement, unless they are also had a depressive disorder (Woodyet al., 1995).New Maintenance TherapiesNew maintenance therapies that have recently been developed for opioiddependence hold the promise of making effective maintenance therapies morebroadly available. This is significant, because access to methadone treatment isquite limited; currently, fewer than one in five heroin users receives treatment

650 V. TREATMENTS FOR ADDICTIONSfor drug dependence (Rounsaville & Kosten, 2000). Barriers to access to methadonemaintenance include both limited patient and community acceptance ofmethadone, and regulatory restrictions and the lack of availability in manyareas of the country. Development of alternative maintenance agents, andespecially agents that can be more readily administered with reduced clinicattendance and outside of traditional methadone maintenance settings, mayaddress some of the problems associated with limited access to treatment.Buprenorphine, a partial mu agonist and kappa antagonist, represents apromising alternative to methadone and was recently approved by the FDA.Because of its unique pharmacological properties, there may be a number ofadvantages to its use, compared to either methadone or levo-alpha-acetylmethadol (LAAM), as a maintenance agent for the treatment of opioiddependence settings. Ceiling effects at higher buprenorphine doses result in alower risk of overdose compared with methadone, and buprenorphine may alsohave a reduced abuse liability in opiate-dependent individuals (thus, less likelihoodfor diversion), because its use may precipitate withdrawal symptoms(Strain, Preston, Liebson, & Bigelow, 1995; Walsh, Preston, Bigelow, & Stitzer,1995). Withdrawal symptoms following abrupt discontinuation of buprenorphineare also usually relatively mild (Cowan & Lewis, 1995; Fudala, Jaffe, Dax,& Johnson, 1990). Results of random assignment, double-blind clinical trialsgenerally support the safety and dose-dependent efficacy of buprenorphinemaintenance (Fudala et al., 2003; Ling, Wesson, Charavastra, & Klett, 1996;Schottenfeld, Pakes, Oliveto, Ziedonis, & Kosten, 1997).Because buprenorphine have been made available only recently, very fewstudies have been done to identify predictors of patient response to methadoneversus buprenorphine, or the minimal and optimal intensity of behavioral treatmentto be administered in conjunction with these maintenance agents. However,it is likely that the same principles as those found in the methadone literatureregarding use of behavioral therapies to enhance outcome with theseagents as will emerge over time.Naltrexone–Agonist TreatmentOpioid antagonist treatment (naltrexone) offers many potential advantagesover methadone maintenance: It is nonaddicting and can be prescribed withoutconcerns about diversion, it has a benign side-effect profile, and it may be lesscostly, in terms of demands on professionals and patients’ time, than the dailyor near-daily clinic visits required for methadone maintenance (Rounsaville,1995). Most important are behavioral aspects of the treatment, because unreinforcedopiate use allows extinction of relationships between cues and druguse. While naltrexone treatment is likely to be attractive only to a minority ofopioid addicts (Cornish et al., 1997), naltrexone’s unique properties make it animportant alternative to methadone maintenance.

28. Matching and Differential Therapies 651However, despite its many advantages, naltrexone has not fulfilled itspromise. Naltrexone treatment programs remain comparatively rare and underutilizedwith respect to methadone maintenance programs (Rounsaville,1995). This is in large part due to problems with retention, particularly duringthe induction phase, where, on average, 40% of patients drop out duringthe first month of treatment, and 60% drop out by 3 months (Greenstein,Fudala, & O’Brien, 1997). Naltrexone treatment has other disadvantagescompared with methadone, including (1) discomfort associated with detoxificationand protracted withdrawal symptoms, (2) lack of negative consequencesfor abrupt discontinuation, and (3) no reinforcement for ingestion—all of which may lead to inconsistent compliance with naltrexone treatmentand high rates of attrition.Preliminary evaluations of behavioral interventions targeted to addressnaltrexone’s weaknesses were encouraging. Several investigators (e.g., Grabowskiet al., 1979; Meyer et al., 1976) reported success using contingency payments asreinforcements for naltrexone consumption. Family therapy and counselinghave also been used to enhance retention in naltrexone programs. For example,in a nonrandomized study of multiple family therapy, Anton, Hogan, Jalali,Riordan, and Kleber (1981) reported that during the first month of naltrexonetherapy, addicts in family therapy had a much significantly lower dropout ratecompared to those not in family therapy (92 vs. 62%). More recently, some ofthe most promising data regarding strategies to enhance retention and outcomein naltrexone treatment have come from investigators evaluating contingencymanagement approaches. Preston and colleagues (1999) found improved retentionand naltrexone compliance for an approach that provided vouchersfor naltrexone compliance versus one that provided noncontingent or novouchers.Again, however, it is not clear to what extent these procedures canbe implemented outside of research settings, nor how durable they are after thetermination of the incentive program.TREATMENT OF COCAINE DEPENDENCEIn contrast to the treatment of opioid dependence, where behavioral therapieshave been most effective when combined with pharmacotherapies (particularlyagonist approaches such as methadone maintenance), the cocainetreatment literature is marked by strong evidence that points to the effectivenessof purely behavioral approaches. Despite many clinical trials evaluatingdiverse pharmacological agents, there is currently no effective pharmacotherapyfor general populations of cocaine abusers. In contrast, several studieshave demonstrated that comparatively brief, purely behavioral approachescan be both sufficient and effective for the majority of patients who receivethem.

652 V. TREATMENTS FOR ADDICTIONSVoucher-Based Contingency ManagementPerhaps the most exciting findings pertaining to the effectiveness of psychosocialtreatments for cocaine dependence have been reports by Higgins and colleagues(Higgins et al., 1991, 1994; Higgins, Wong, Badger, Haug-Ogden, &Dantona, 2000) of the effectiveness of a program incorporating positive incentivesfor abstinence, reciprocal relationship counseling, and disulfiram into acommunity reinforcement approach (CRA; Azrin, 1976). The Higgins strategyhas four organizing features, which are grounded in principles of behavioralpharmacology: (1) Drug use and abstinence must be swiftly and accuratelydetected; (2) abstinence is positively reinforced; (3) drug use results in loss ofreinforcement; and (4) emphasis is on the development of competing reinforcersto drug use (Higgins, Budney, Bickel, & Hughes, 1993).In this program, urine specimens are required three times weekly. Abstinence,assessed through drug-free urine screens, is reinforced through a vouchersystem in which patients receive points redeemable for items consistent with adrug-free lifestyle, such as movie tickets, sporting goods, and the like, butpatients never receive money directly. To encourage longer periods of consecutiveabstinence, the value of the points earned by the patients increases witheach successive clean urine specimen, and the value of the points is reset backto its original level when the patient produces a drug-positive urine screen ordoes not provide a urine specimen.In a series of well-controlled clinical trials, Higgins and colleagues havedemonstrated (1) high acceptance, retention, and rates of abstinence forpatients receiving this approach (i.e., 85% completing a 12-week course oftreatment, and 65% achieving 6 or more weeks of abstinence) relative to standardsubstance abuse counseling; (2) rates of abstinence that do not declinesubstantially when less valuable incentives are substituted for the voucher system;(3) the value of the voucher system itself (as opposed to other programelements) in producing good outcomes by comparing the behavioral systemwith and without the vouchers; and (4) the durable effects of the voucher system(Higgins et al., 1993, 2000; Higgins & Silverman, 1999). Higgins’s initialwork with voucher-based contingency management has now been widely replicatedin other settings and samples: homeless substance abusers (Milby et al.,2000), pregnant substance users (Svikis, Haug, & Stitzer, 1997), drug users in atherapeutic workplace (Silverman et al., 2002), alcohol-dependent individuals(Petry, Martin, Cooney, & Kranzler, 2000), and cocaine-dependent individualswithin methadone maintenance treatment programs (Silverman et al., 1998).In regard to matching, there is some evidence that individuals with antisocialpersonality disorder may respond comparatively well to contingency managementapproaches (Messina, Farabee, & Rawson, 2003), and that raising thelevel of reinforcement may improve response among individuals who do notrespond initially to lower levels of reinforcement (Silverman, 1999).

Cognitive-Behavioral Therapies28. Matching and Differential Therapies 653Another behavioral approach that has been shown to be effective in treatingcocaine abusers is cognitive-behavioral therapy (CBT), which is based on sociallearning theories on the acquisition and maintenance of SUDs. The goal ofCBT (also frequently called relapse prevention or coping skills therapy) is tofoster abstinence through helping the patient to master an individualized set ofcoping strategies as effective alternatives to substance use. Typical skills taughtinclude fostering resolution to stop both cocaine and other substance usethrough exploring positive and negative consequences of continued use; functionalanalysis of substance use (i.e., understanding substance use in relationshipto its antecedents and consequences), development of strategies for copingwith high-risk situations, including cocaine craving, preparation for emergencies,and coping with a relapse to substance use; and identifying and confrontingthoughts about substance use.A number of randomized clinical trials among several diverse, cocainedependentpopulations have demonstrated that compared with other commonlyused psychotherapies for cocaine dependence, CBT appears to be particularlymore effective with more severe cocaine users or those with comorbidpsychiatric disorders, especially depression (Carroll, Rounsaville, Gordon, etal., 1994; Maude-Griffin et al., 1998; Rohsenow, Monti, Martin, Michalec, &Abrams, 2000). Moreover, CBT appears to be a particularly durable approach,with several studies suggesting that patients treated with this approach maycontinue to reduce their cocaine use even after they leave treatment (Carroll,Rounsaville, Nich, et al., 1994; D. E. Epstein, Hawkins, Covi, Umbricht, &Preston, 2003; Rawson et al., 2002). Recent evidence also suggests that individualswith cognitive impairment may not respond as well to cognitivebehavioralapproaches (Aharonovich, Nunes, & Hasin, 2003).Manualized Disease Model ApproachesUntil very recently, treatment approaches based on disease models were widelypracticed in the United States, but virtually no well-controlled, randomizedclinical trials had been done to evaluate their efficacy alone or in comparisonwith other approaches. Thus, another important finding that has emerged fromrecent randomized clinical trials and has potential significance for the clinicalcommunity is the effectiveness of manualized disease model approaches. Onesuch approach is 12-step facilitation (TSF), a manual-guided, individual approachthat is intended to be similar to widely used approaches that emphasizeprinciples associated with disease models of addiction. While this treatment hasno official relationship with Alcoholics Anonymous (AA) or Cocaine Anonymous(CA), its content is intended to be consistent with the 12 steps of AA,with primary emphasis given to steps 1–5 and the concepts of acceptance (e.g.,

654 V. TREATMENTS FOR ADDICTIONSto help patients accept that they have the illness, or disease, of addiction) andsurrender (e.g., to help patients acknowledge that there is hope for sobrietythrough accepting help from others and from a “Higher Power”)(Nowinski etal., 1992). In addition to abstinence from all psychoactive substances, a majorgoal of the treatment is to foster active participation in self-help groups, andpatients are actively encouraged to attend AA or CA meetings and becomeinvolved in traditional fellowship activities. In a comparison of TSF, CBT, andclinical management (a supportive approach in which patients receive comparableempathy, support and other “common elements” of psychotherapy butnone of the unique “active ingredients” of TSF or CBT) for alcoholic cocainedependentindividuals, TSF was significantly more effective than clinical managementand was comparable to CBT in reducing cocaine use (Carroll, Nich,Ball, McCance-Katz, & Rounsaville, 1998).The National Institute on Drug Abuse (NIDA) Collaborative CocaineTreatment Study (CCTS), a multisite, randomized trial of psychotherapeutictreatments for cocaine dependence (Crits-Christoph et al., 1999), also offeredstrong evidence of the effectiveness of a similar approach, individual drug counseling(Mercer & Woody, 1999). In this study, 487 cocaine-dependent patientswere randomized to one of four manual-guided treatment conditions: (1) cognitivetherapy plus group drug counseling; (2) SE, a short-term psychodynamicallyoriented approach, plus group drug counseling; (3) individual drugcounseling plus group drug counseling; or (4) group drug counseling alone. Outcomeson the whole were good, with all groups significantly reducing cocaineuse from baseline; however, the best cocaine outcomes were seen for subjectswho received individual drug counseling. Considered together with the recentfindings of the Project MATCH Research Group (1997), where TSF was foundto be comparable to CBT and motivational enhancement therapy in reducingalcohol use among 1,726 alcohol-dependent individuals, the findings fromthese studies offer compelling support for the efficacy of manual-guided diseasemodel approaches. This has important clinical implications, because theseapproaches are similar to the dominant model applied in most communitytreatment programs and may thus be more easily mastered by “real-world” cliniciansthan approaches such as contingency management or CBT, treatmentswhose theoretical underpinnings may not be seen as highly compatible withdisease model approaches.TREATMENT OF MARIJUANA DEPENDENCEAlthough marijuana is the most commonly used illicit drug in the UnitedStates, treatment of marijuana abuse and dependence is a comparatively understudiedarea to date, in part because comparatively few individuals present for

28. Matching and Differential Therapies 655treatment with a primary complaint of marijuana abuse or dependence. Currently,no effective pharmacotherapies for marijuana dependence exist, andonly a few controlled trials of psychosocial approaches have been completed;thus, there is as yet little data on the types of individuals who respond particularlywell or poorly to these approaches. Stephens, Roffman, and Curtin (2000)compared a delayed treatment control, a two-session motivational approach,and the more intensive (14 session) relapse prevention approach, and foundbetter marijuana outcomes for the two active treatments compared with thedelayed treatment control group, but no significant differences between thebrief and the more intensive treatment. More recently, a replication and extensionof that study, involving a multisite trial of 450 marijuana-dependentpatients, compared three approaches: (1) a delayed treatment control,(2) a two-session motivational approach, and (3) a nine-session combinedmotivational–coping skills approach. Results suggested that both active treatmentswere associated with significantly greater reductions in marijuana usethan the delayed treatment control through a 9-month follow-up (MTPResearch Group, 2004). Moreover, the nine-session intervention was significantlymore effective than the two-session intervention, and this effect was alsosustained through the 9-month follow-up. Adding contingency managementhas also been shown to improve outcomes in these populations (Budney, Higgins,Radonovich, & Novy, 2000). Moreover, some early evidence suggests thatindividuals who submit drug-negative urines at treatment inception may havebetter response to treatment (Moore & Budney, 2002), a finding that is consistentwith that of the general drug abuse treatment literature (Ehrman, Robbins,& Cornish, 2001).CONCLUSIONSRecent years have been marked by enormous progress in the identification of awide range of empirically validated pharmacological and behavioral therapiesfor SUDs. Important new treatment options, such as naltrexone and acamprosatefor alcohol use disorders, and buprenorphine for opioid dependence, wereunavailable 20 years ago, as were behavioral therapies, including contingencymanagement, behavioral marital counseling, motivational interviewing, andCBT—all of which have demonstrated efficacy across a range of SUDs andpopulations. Equally promising are the findings that combining pharmacotherapieswith behavioral therapies can extend, strengthen, and make treatmenteffects more durable. Nevertheless, the rapid, recent progress in the identificationof efficacious therapies has not been matched by identification of moderatingvariables or consistent patient predictors of response to specific treatmentapproaches that can guide researchers’ and clinicians’ efforts to match individu-

656 V. TREATMENTS FOR ADDICTIONSals to optimal treatment strategies. Identification of moderators of response toefficacious therapies, as well as identification of the specific mechanisms bywhich those treatments achieve their effects, should be a primary focus in theyears that lie ahead.ACKNOWLEDGMENTSSupport was provided by National Institute on Drug Abuse Grant Nos. K05-DA00457and P50-DA09241, and by the U.S. Department of Veterans Affairs VISN 1 Mental IllnessResearch, Education, and Clinical Center.REFERENCESAharonovich, E., Nunes, E. V., & Hasin, D. (2003). Cognitive impairment, retentionand abstinence among cocaine abusers in cognitive-behavioral treatment. DrugAlcohol Depend, 71, 207–211.Anton, R. F., Hogan, I., Jalali, B., Riordan, C. E., & Kleber, H. D. (1981). Multiplefamily therapy and naltrexone in the treatment of opioid dependence. Drug AlcoholDepend, 8, 157–168.Azrin, N. H. (1976). Improvements in the community-reinforcement approach to alcoholism.Behav Res Ther, 14, 339–348.Azrin, N. H., Sisson, R. W., Meyers, R., & Godley, M. (1982). Alcoholism treatmentby disulfiram and community reinforcement therapy. J Behav Therapy Exp Psych,13, 105–112.Ball, J. C., & Ross, A. (1991). The effectiveness of methadone maintenance treatment. NewYork: Springer-Verlag.Bickel, W. K., Amass, L., Higgins, S. T., Badger, G. J., & Esch, R. A. (1997). Effects ofadding behavioral treatment to opioid detoxification with buprenorphine. J ConsultClin Psychol, 65, 803–810.Budney, A. J., & Higgins, S. T. (1998). A community reinforcement plus vouchersapproach: Treating cocaine addiction. Rockville, MD: National Institute on DrugAbuse.Budney, A. J., Higgins, S. T., Radonovich, K. J., & Novy, P. L. (2000). Addingvoucher-based incentives to coping skills and motivational enhancement improvesoutcomes during treatment for marijuana dependence. J Consult ClinPsychol, 68, 1051–1061.Carroll, K. M. (2001). Combined treatments for substance dependence. In M. T.Sammons & N. B. Schmidt (Eds.), Combined treatments for mental disorders: Pharmacologicaland psychotherapeutic strategies for intervention (pp. 215–238). Washington,DC: American Psychological Association Press.Carroll, K. M., Nich, C., Ball, S. A., McCance-Katz, E., & Rounsaville, B. J. (1998).Treatment of cocaine and alcohol dependence with psychotherapy and disulfiram.Addiction, 93, 713–728.

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IndexAcamprosate, 405, 595Acetaldehyde, 84Acetaminophen, 387Addiction, generallychanged set point model, 9–11clinical conceptualization, 370–371developmental progression, 45–46legal conceptualization, 355–356neurobiology, 3–4origins of drug liking, 4–6as psychiatric diagnosis, 222–223See also Substance use disorder; specificsubstanceAddiction Severity Index, 46, 53Adenylate cyclase, 85AdherenceAIDS treatment, 419dropout from substance abusetreatment, 495pharmacotherapy, 642–643Administration, modes ofbenzodiazepine formulations, 237–238cocaine, 185–188historical development, 17, 18methamphetamine, 206–207opioid therapy for pain, 384personality disorders and, 254Adolescent substance use/abuse, 29alcohol, 79assessment, 47, 48, 569–571behavioral correlates, 565biological factors in, 562–563club drugs and circuit parties, 260–262cocaine, 185consequences of, 559diagnosis, 561–562environmental factors in, 563gateway theory of, 560–561, 563gender differences in, 438, 561heroin, 261parental relations and, 564pathological gambling and, 305patterns and prevalence, 559, 560–561peer relations and, 565polysubstance abuse, 249preventive interventions, 567–569psychiatric comorbidity, 565–567,574–576racial/ethnic differences in, 325, 330,561relapse and relapse prevention, 576–577research needs, 577–578school adjustment assessment, 54–55suicidal behavior/ideation and, 566–567tobacco, 114, 117, 438treatment, 572–576treatment outcome predictors, 573–574treatment setting determination, 571–572663

664 IndexAfrican Americansadolescent substance use patterns, 566alcohol use and abuse, 83, 322, 323–324cocaine use and abuse, 185–186, 325determinants of substance usepatterns, 326effects of socioeconomic status, 324gender differences in substance use,322–323health outcomes of substance use,324–325, 326heroin use, 326HIV risk, 326hypertension among, 324law enforcement experiences, 326–327patterns of substance use, 324–326population statistics, 321smoking patterns, 117, 118treatment issues, 327–328Age-related patterns of substance use.See also Adolescent substance use/abuse; ElderlyAIDS/HIV, 96behavior–immune interactions and,419–420epidemiology, 411implications for drug addictiontreatment, 420–421, 423–425legal issues in addiction treatment,425–426mother-to-infant transmission, 422neuropsychiatric complications, 412–414polysubstance abuse and, 262prevention strategies, 426–427racial/ethnic differences, 326risk factors, 411–412, 427–428substance use and risk of, 415–420testing, 421–423women’s issues, 440Alcohol, Drug Abuse, and MentalHealth Administration, 24–25Alcohol abuse treatmentchallenges, 97–98comorbidity considerations, 98–99with elderly patients, 401–407group therapy, 503–510historical evolution, 23–24patient matching, 644–646pharmacotherapy, 644–646preventive intervention with childrenof alcoholics, 568psychiatric comorbidity and, 273psychiatrist role in, 99psychotherapy, 459relapse detection in, 98relapse prevention pharmacotherapy,593–595self-help approaches, 26–27therapeutic relationship in, 97, 98treatment matching, 644–646withdrawal pharmacotherapy, 591–593See also Alcohol use and abuseAlcohol dehydrogenase, 84Alcohol dehydrogenase 2 gene, 324, 329Alcoholics Anonymous, 26, 30, 283,284, 328, 469, 511–512, 513, 514,516Alcohol use and abuse, 17amnestic disorder related to, 87–88among adolescents, 560, 561among elderly, 396, 397, 398–401associated personality traits, 256–257beneficial effects of moderate intake,93, 95benzodiazepine use and, 227–228,230–231, 232, 233, 234, 235–236,288, 398, 401, 404, 407, 591blackouts, 359cancer risk and, 96–97cardiovascular complications relatedto, 92–93cognitive impairments associated with,40–41comorbid cocaine use, 188–189, 193comorbid psychiatric disorders, 78–82,98–99, 253, 254, 277, 443–444co-occurring pathological gambling,308–309delirium related to, 87dementia induced by, 88–89diagnosis of abuse or dependence, 76–77

Index 665dietary guidelines, 75–76endocrine dysfunction related to, 95epidemic abuse, 20, 27fetal alcohol syndrome, 97, 441flushing reaction, 19, 330gastrointestinal complications relatedto, 90–91gateway theory of adolescentsubstance abuse, 560–561, 563gender differences, 439–449genetic factors, 442, 537health effects, 440hematologic complications related to,94–95HIV infection risk and, 415–416,417–418immune function and, 95, 417–418intoxication, 86laboratory testing, 65, 77–78liver complications related to, 91–92musculoskeletal problems related to,95neurobiological effects, 7, 11, 93–94patterns of, 20, 45–47, 75, 76, 78pharmacology, 84–86polydrug abuse, 248, 249, 250, 251,258–259racial/ethnic differences, 82–84, 322,323–324, 329, 330–331, 332–333religious beliefs and attitudes and,330sexual behavior and, 441sexual dysfunction related to, 89–90skin problems related to, 96sleep disturbances associated with, 89social costs, 75treatment. See Alcohol abusetreatmentvehicle operations and, 351, 358violent behavior and, 356–357vitamin deficiencies related to, 88, 90,91, 92withdrawal, 86–87in workplace, 341Alcohol Use Inventory, 46Aldehyde dehydrogenase, 84Alexithymia, 461, 467Alprazolam, 225, 228, 229tine-release formulations, 237withdrawal, 231Americans with Disabilities Act, 341Amitryptyline, 225Amnestic disorder, alcohol-induced, 87–88Amobarbital, 113, 224Amphetaminesadolescent use patterns, 560comorbid alcohol abuse, 79laboratory testing for, 65Anemia, alcohol-induced, 94Antidepressant therapy, 238with ADHD patient, 289cocaine addiction treatment, 202with dually diagnosed patients, 286with elderly patients, 404–405heroin overdose risk and, 260for pathological gambling, 309for smoking cessation, 590–591See also specific drug; specific drug typeAntihistamines, 225Antisocial personality disorder, 11, 357alcohol abuse and, 82comorbid substance use disorder, 253,254, 272, 273Anxiety disordersin addicted persons, 230–231in adolescents, 567alcohol use and, 80, 89, 98benzodiazepine discontinuation inpeople with, 236–237benzodiazepine therapy, 221, 230–231comorbid substance use disorder, 273co-occurring kleptomania, 314co-occurring pathological gambling,308epidemiology, 220gender differences, 253pharmacotherapy with duallydiagnosed patients, 288–289social costs, 220Asian Americansalcohol use and abuse, 83–84, 330–331population statistics, 321, 330

666 IndexAsian Americans (cont.)religious beliefs, 330smoking patterns, 117, 118treatment issues, 331–332Assessmentfor addiction diagnosis, 371–373adolescents, 569–571alcohol abuse disorders, 76–77alcohol withdrawal, 591cocaine abuse, 200–201in cognitive therapy, 477–483, 489,492–493comorbid substance use andpsychiatric disorders, 276–278in correctional facilities, 361–362elderly patients, 399–401in family therapy, 533–534identifying nonmedical drug use, 221–222long-term benzodiazepine use, 233–235nicotine dependence, 116–117for pain management, 374–375, 375–377, 376, 391polysubstance abuse, 245–248pseudoaddiction, 371–372in psychodynamic psychotherapy,463–464substance use disorder, 278women with addictive disorders, 446,447See also Laboratory testing;Psychological assessmentAthletesdrug testing for, 68–69substance use problems among, 348Atomoxetine, 289Attachment disorder, 461Attention-deficit/hyperactivity disorder, 566adolescent pharmacotherapy, 575, 576cocaine use and, 194–195pharmacotherapy with duallydiagnosed patients, 289–290, 606stimulant therapy, 289Attributional style, 40Aversion therapy for pathologicalgambling, 313BBarbituratescomorbid alcohol abuse, 79laboratory testing for, 65pharmacology, 224Behavioral addictions. See Impulsecontrol disordersBehavioral assessment, 44in dialectical behavior therapy, 628–629Benzodiazepines, 6, 113abuse among elderly, 398abuse potential, 226–227, 230, 290,595–596alcohol use/abuse and, 227–228, 230–231, 232, 233, 234, 235–236, 288,398, 401, 404, 407, 591antagonists, 226for anxiety treatment in addictedpersons, 230–231, 288clinical application, 595clinical features, 219–220for cocaine withdrawal management,202comorbidity considerations in use of,606discontinuation, 229–230, 231–232,236–238long-term use, 233–236, 237medical concerns, 223–224methadone boosting effect, 228–229new formulations, 237–238pharmacology, 225–230prevalence and patterns of use, 221,235–236reinforcement effects, 230speed of onset, 226–227tolerance, 232–233withdrawal, 596Bipolar disorderalcohol abuse and, 79–80cocaine abuse and, 194comorbid substance use disorders,272–273co-occurring kleptomania, 314impulse control disorders and, 306

Index 667pharmacotherapy with duallydiagnosed patients, 286–287Blackouts, 359Borderline personality disorders, 255alcohol abuse and, 82biosocial model, 618–620cocaine use and, 195–196comorbid substance use disorders, 253,254, 616dialectical behavioral therapy, 496–497, 615–616. See also Dialecticalbehavior therapyBuprenorphine, 380, 588for cocaine addiction, 202for opioid detoxification, 598opioid maintenance therapy with,601–602, 650therapeutic action, 13, 589Bupropion, 289adolescent treatment, 575, 576cocaine addiction treatment, 202for smoking cessation, 590Buspirone, 231for anxiety treatment in addictedpersons, 288–289clinical features, 238Butabarbital, 224CCAGE interview, 77, 278, 399Canceralcohol use and, 96–97tobacco use and, 106–107Cannabinoids, 6, 7Carbamazepinealcohol withdrawal management, 592cocaine addiction treatment, 202side effects, 592Carbohydrate-deficient transferin, 65,78, 98Cardiovascular systemalcohol effects, 92–93cocaine effects, 189, 190, 196–197methamphetamine effects, 207tobacco effects, 107, 112–113Case management, 494, 549in dialectical behavior therapy, 634Ceremony and ritual, 16, 18, 20, 21–22alcohol use in, 82–83tobacco use in, 105Chain analysis, 628–629Changed set point model of addiction,9–11Child abuse/neglect, 357Child Behavior Checklist, 54Chlordiazepoxide, 225, 591Chromatography techniques, 64Circuit parties, 261–262Cirrhosisalcoholic, 91, 92chronic hepatic encephalopathy, 41ethnic differences, 83Clomipramine, 309Clonazepam, 225, 229, 237–238, 315,591Clonidinefor opioid withdrawal, 597, 598for smoking cessation, 591therapeutic action, 13Clorazepate, 228, 229Clozapine, 287Club drugs, 260–262, 419Cocaine use and abuseaddiction risk, 192, 208–209addiction treatment, 202–206, 209,263, 651–654adulterants, 188, 197assessment, 200–201associated personality traits in, 256–257chronic use, 190–191, 197comorbid alcohol abuse, 79, 188–189,193crack cocaine, 184, 185, 186, 188,197–198, 415, 560elimination half-life, 191fetal exposure, 199–200, 209freebase, 187–188genetic factors in, 192–193health effects, 189, 190–191, 196–198HIV infection risk and, 415, 416,418–419

668 IndexCocaine use and abuse (cont.)ingestion, 197–198intoxication, 190intoxication treatment, 201–202intravenous use, 187, 188, 198laboratory testing for, 65law enforcement, 186mortality and morbidity, 185neurophysiology, 6, 189–190, 197overdose complications, 185, 190overdose treatment, 201pharmacotherapy for, 603–606polydrug abuse, 185, 188, 193–194,249, 250, 251, 259–260, 263preparation and administration, 185–188prevalence and patterns, 184–186, 192psychiatric comorbidity, 193, 194–196, 273, 286–287racial/ethnic differences in, 185–186,325, 326recreational use, 192relapse risk, 190, 191sexual behavior and, 441tolerance, 191withdrawal, 191–192, 202workplace consumption, 344Codeine, 65Cognitive-behavioral relapse prevention,515cocaine addiction treatment, 203,653with dually diagnosed patients, 282Cognitive-behavioral therapy, 475, 476cocaine addiction treatment, 203with dually diagnosed patients, 281methamphetamine addictiontreatment, 208for pathological gambling, 312–313See also Cognitive-behavioral relapseprevention; Cognitive therapyCognitive functioningAIDS/HIV complications, 412–414alcohol-related impairments, 87–89assessment, 50–51blackouts, 359chronic cocaine use effects, 191cocaine intoxication effects, 190cognitive deficits model of addiction,11cognitive style, 40intoxication as defense against legalresponsibility, 357–359methamphetamine effects, 207, 208polydrug abuse effects, 258–259as predictive of drug use, 259prenatal cocaine exposure effects,199–200processes involved in substance abuse,40–43substance abuse effects, 40–42, 607in withdrawal, 42Cognitive therapycase formulation, 477–483case management approach, 494conceptual basis, 482dialectical behavior therapy and, 495–496dropout prevention, 495with dually diagnosed patients, 282,489indications, 474–475model of substance abuse, 475–476,480monitoring progress in, 492–493motivational enhancement therapyand, 495for pathological gambling, 312present focus of, 486relapse prevention, 488–489session structure and schedule, 487–488stages-of-change assessment, 489–490strategies for substance abusetreatment, 491–495therapeutic relationship in, 483–485,490treatment goals, 480, 485, 497treatment planning, 489–491See also Cognitive-behavioral relapseprevention; Cognitive-behavioraltherapyCommunity reinforcement approach,645, 652

Index 669Comorbidity, psychiatric, 31, 43–44, 48–49, 252in alcohol abuse, 78–82, 98–99among adolescents, 565–567among African Americans, 327–328among incarcerated persons, 360–361assessment and diagnosis, 276–278cocaine abuse and, 193–196cognitive therapy, 282, 489compulsive buying behavior, 316epidemiology, 250, 271–273group therapies, 278–279, 283–284,503integrated psychosocial treatments,280–283kleptomania, 314outcomes research, 638pathological gambling, 308–309personality disorders, 253–254pharmacotherapy, 284, 286–292, 606,640predictors of substance abuse, 252relationships between disorders, 273–276, 443–444, 565–566treatment implications, 271, 273,284–285treatment models, 279–280in women, 443–444See also Polysubstance abuseCompulsive behavior, 461–462compulsive buying, 315–317See also Impulse control disordersConduct disorder, 566Confidentialityaddiction treatment with AIDSpatients, 425in drug testing, 346mandated reporting of drug use, 350–351, 357in treatment for physicians withsubstance use problems, 350in workplace intervention, 346, 347Contingency management, 641–642cocaine dependence treatment, 204,652with dually diagnosed patients, 283with methadone maintenance therapy,647–648obstacles to implementation, 648Contract with America AdvancementAct, 341Coping skills training, 641Correctional facilities, 360–363Corticobasal ganglionic–thalamiccircuitry, 305Corticotropin-releasing factor, 190Cortisol, 12Couple therapy, 534, 538–539, 544outcomes, 550–552COX-1/COX-2 inhibitors, 387–389Crack cocaine, 184, 185, 186, 188, 197–198, 415, 560Criminal behavior, substance abuse and,357Cross-tolerance, 588Cue exposurecocaine relapse prevention, 203–204cognitive therapy strategies for dealingwith, 493in pathological gambling, 308Cyclic adenosine monophosphate secondmessenger systemalcohol use and, 85naltrexone effects, 12–13neurobiology of drug liking, 4–5, 6neurobiology of tolerance, 7DDefective stimulus barrier, 460Delirium, alcohol-related, 87Delirium tremens, 591Dementia, alcohol-induced, 88–89Denial, 331, 343, 463–464, 502Department of Transportation, 69Dependenceclinical characteristics, 110–111definition, 369–370neurobiology, 3, 4, 6–9polysubstance, 245–247substance abuse and, 222–223

670 IndexDepressionin adolescents, 566–567alcohol abuse and, 79, 99, 443–444cocaine abuse and, 194in cocaine withdrawal, 202comorbid substance use disorder, 273,277in elderly, 404–405gender differences, 253genetic risk, 442immune function and, 417–418impulse control disorders and, 306pharmacotherapy with duallydiagnosed patients, 286, 606Desensitization therapy for pathologicalgambling, 313Desipramine, 289, 575Detoxificationalcohol, 591–593clinical evolution, 30elderly patients, 401family involvement, 540–541opioid, 597–598pharmacotherapy, 639Dextromethorphan, 65Diagnostic and Statistical Manual of MentalDisorders, 356, 561alcohol abuse disorders, 76nicotine dependence criteria, 110–111polysubstance abuse diagnosis, 245–247Diagnostic Interview Schedule, 48Dialectical behavior therapy, 495–496applications, 615, 616assumptions and agreements, 620–622case management in, 634conceptual basis, 617–618, 634–635conceptualization of borderlinepersonality disorder in, 618–620consultation team, 633effectiveness, 617future prospects, 634–635individual psychotherapy in, 627–632modes of treatment, 624pharmacotherapy in, 633–634rationale, 616skills training groups in, 624–627telephone consultation, 632therapeutic relationship, 623–624,630–631treatment targets, 622–623Diazepam, 225, 228, 401Dietary uses of drugs, 22Diphenylhydrantoin, 65Disability, addiction as, 360Disinhibition, neurobehavioral, 44–45,255, 262Disruptive Behavior Rating Scale, 54–55Disulfiram, 24, 402, 405, 534adolescent treatment, 575behavioral interventions with, 645for cocaine abuse treatment, 603contraindications, 593effectiveness, 593, 645side effects, 593therapeutic action, 593, 645Divorce and child custody issues, 359Domestic violence, 357Dopaminergic systemalcohol use and, 85cocaine action, 189, 190, 191comorbidity considerations inpharmacotherapy, 606in drug reinforcement, 3, 5, 6in impulse control disorders, 307methamphetamine effects, 207–208neurobiology of addiction, 9–10neurobiology of tolerance, 7in schizophrenia, 81Drug and Alcohol Testing IndustryAssociation, 66Drug-free workplace, 68, 69–71Drug-Free Workplace Act, 69, 341Drug interactions, 397–398in opioid-substitute maintenancetherapy, 602–603Drug Use Screening Inventory, 45, 47EEating disorderscomorbid substance abuse and, 81co-occurring kleptomania, 314

Index 671Economics, 28–29alcohol use and socioeconomic status,324cocaine use and socioeconomic status,184–185, 208–209social costs of mental disorders, 220social costs of workplace substanceuse, 340–341Educational attainmentcocaine use and, 184–185tobacco use and, 118Ego deficit psychology, 460–461Elderlydiagnosis of substance abuse among,399–401obstacles to treatment, 396–397patterns and prevalence of substanceabuse, 396, 397–399population trends, 396risk of drug interactions, 397–398treatment of substance use disorders,401–407typology of abuse among, 398–399Emergency department admissionscauses of, 185cocaine-related, 185, 200methamphetamine-related, 206racial/ethnic differences, 325Emotional functioningalexithymia, 461, 467assessment, 43–44in borderline personality disorder,618–620in etiology of substance abuse, 460family therapy issues, 538relapse factors, 642skills training in dialectical behaviortherapy, 626–627Employee Assistance Program, 69, 70,347–348Encephalopathy, chronic hepatic, 41, 94Endocrine function, alcohol-relatedcomplications in, 95Enzyme immunoassay analysis, 64Epidemic substance abuse, 20–21, 27–28Epidemiology. See Patterns andprevalence of useErythrocyte mean corpuscular volume,77–78Excitatory amino acid antagonists, 10–11Expert testimony, 355FFamily Adaptability and CohesionEvaluation Scales, 52Family and Medical Leave Act, 341Family Assessment Device, 52Family Assessment Measure, 52Family Environment Scale, 52Family functioningadolescent substance abuse risk and,564alcohol abuse and, 76–77assessment, 51–52Family therapycase management in, 549characteristics of families withaddicted members, 529–530detoxification stage, 540–541ending therapy, 545–546graphic constructions, 536grief and loss issues, 544–545indications, 530–532maintaining sobriety, 541–545network therapy techniques, 521–523outcomes, 550–552pharmacotherapy management, 549–550problem formulation, 533–534, 535–537rationale, 528–529recovery process, 537–541reorganization stage, 543–545self-help groups and, 539, 540social network involvement, 536special problems in substance abusetreatment, 547–550stages of, 532–533therapeutic alliances in, 535therapeutic contract, 534Federal Testing Guidelines, 69Fentanyl, 65

672 IndexFetal alcohol syndrome, 97, 322, 441Fetal exposureAIDS transmission, 422cocaine, 199–200, 209criminalization of, 449nicotine, 442Flumazenil, 226Flunitrazepam, 419Fluoxetineadolescent treatment, 575for kleptomania, 315Flurazepam, 229Flushing reaction, 330Fluvoxamine, 309, 315, 316Folate deficiency, 94Furosemide, 113GGabapentin, 592–593Gambling, pathological, 303clinical features, 304–305, 308co-occurring disorders, 308–309diagnostic criteria, 304epidemiology, 306treatment, 309–313triggers, 308Gamma-aminobutyric acidalcohol use and, 85, 86–87barbiturate action, 224benzodiazepine interaction, 226cocaine action, 189in cognitive deficits model ofaddiction, 11neurobiology of drug liking, 6neurobiology of tolerance, 7Gamma-glutamyltransferase, 77, 98Gamma-hydroxybutyric acid, 65, 260–262, 419Gas chromatography–mass spectroscopy,64Gastrointestinal system, alcohol effects,90–91Gateway theory of adolescent substanceabuse, 45, 560–561, 563Gender differencesadolescent substance use, 249, 561cocaine use, 185–186depression and alcohol use, 79pathological gambling, 308pharmacology, 439–440polysubstance use, 249, 252–253psychiatric comorbidity implicationsfor treatment, 273racial/ethnic patterns of substance use,322–323, 328–329tobacco use patterns, 117, 118, 439See also Women, addictive disorders inGeneticsadolescent substance abuse risk, 562–563alcohol dehydrogenase 2 genepolymorphism and alcoholism, 324,329alcoholism risk, 537cocaine use and, 192–193gender differences in substance usepatterns, 442impulse control disorders and, 305substance use disorder risk and, 4, 11,257–258Glutamate metabolismalcohol use and, 85cocaine action, 189methamphetamine effects, 208neurobiology of addiction, 10–11Group therapyactivity groups, 507advantages, 502, 508contraindications, 503with dually diagnosed patients, 278–279, 283–284educational groups, 507effectiveness, 514–515elderly patients, 403–404exploratory groups, 505group size, 519–520group style, 504–505individual psychotherapy and, 508–509interactional groups, 505–506

Index 673Hinterpersonal problem-solving skillgroups, 506leadership, 503–505with methadone-maintenancepatients, 507–508modalities, 503nonabstinent members in, 509–510patient selection, 503skills training in dialectical behaviortherapy, 624–627supportive groups, 505therapist role, 502–503, 510treatment goals, 504See also Network therapy; Self-helpgroupsHair analysis, 65Hallucinations/delusions, alcoholinduced,89Hallucinogenics, 333, 419ceremonial use, 21neurobiology of tolerance, 7polysubstance abuse, 251prehistoric use, 17Haloperidol, 201–202Health care workers, 349–350Health Insurance Portability AssuranceAct, 425Health statusalcohol effects, 90–97, 324–325, 417,440assessment, 47–48cocaine effects, 189, 190–191, 196–198gender differences among substanceabusers, 440methamphetamine effects, 207tobacco effects, 106–107, 112–114,115–116See also Fetal exposureHeparin, 113Hepatitis, alcoholic, 91–92Hepatitis C, 95Heroinadolescent use, 261, 560comorbid cocaine use, 193, 259–260comorbid psychiatric disorders amongusers of, 252neurobiological action, 4–5neurobiology of addiction, 11overdose, 260perinatal use, 442polysubstance abuse, 251–252, 259racial/ethnic differences in usepatterns, 326substitution therapy, 588–589. See alsoMethadoneworkplace consumption, 344Hispanic Americansadolescent substance use patterns, 566alcohol use and abuse, 84, 322, 328–329cocaine use and abuse, 185gender differences in substance use,322, 328–329population statistics, 321smoking patterns, 117–118substance use patterns, 329treatment issues, 329–330[5-]Hydroxyindole, 307Hypertensionalcohol-related, 93among African Americans, 324Hypnotics. See Sedative/hypnotic drugsHypothalamic–pituitary–adrenal axis,189–190Hypothalamic–pituitary axis, 95IImmune functionalcohol use and, 96, 417–418behavior–immune interactions, 419–420depression and, 417–418Impulse control disordersclassification, 303. See also specificdisorderepidemiology, 306–307

674 IndexImpulse control disorders (cont.)mood disorders and, 306neurophysiology, 305, 306, 307–308obsessive–compulsive behavior and,305substance use disorders and, 304–305Impulsivity, 255, 262Infectious disease transmissionamong intravenous drug users, 198cocaine use and, 198, 202, 209methamphetamine use and, 207Inhalants, 561Interpersonal relationshipsadolescent substance abuse risk and,564–565assessments, 53–56school adjustment, 54–55skills training in dialectical behaviortherapy, 627social skills deficits, 54treatment considerations, 642Intravenous drug usersAIDS prevention, 420–421, 426–427cocaine, 187, 188, 198infectious disease transmission among,198personality disorders among, 254Inventory of Drinking Situations, 56–57Ion channelsalcohol use and, 85cocaine action, 196–197neurobiology of drug liking, 6KKetamine, 260–262, 419Kleptomania, 313–315epidemiology, 306–307LLaboratory testingadolescent assessment, 571AIDS/HIV, 421–423alcoholism screening, 77–78, 446for athletes, 68–69chain-of-custody procedures, 67–68,70, 71cocaine use, 200, 201in correctional facilities, 362drug testing methodologies, 64–65elderly patients, 399–400evasive techniques and behaviors, 67false positives, 66indications, 63–64informed consent for, 70interpretation, 66–67privacy and confidentiality issues, 346purpose, 63in workplace, 68, 69–71, 341, 346Lamotrigine, 287Law enforcement, 24cocaine-related, 186deinstitutionalization and, 364historical evolution, 19–20, 31prohibition, 25–26racial/ethnic differences in experienceof, 326–327substance use among police, 351–352tobacco prohibitions, 105See also Legal issuesLead poisoning, 207Legal issuesaddiction treatment with AIDSpatients, 425–426alternatives to standard judicialsystem, 363–364civil law, 359–360clinical significance, 354–355disability claims, 360expert witness testimony, 355family and matrimonial law, 359fetal substance exposure, 449insanity defense, 358intoxication as defense againstresponsibility, 357–359liability of providers of intoxicatingsubstance, 359mandated reporting of drug use, 350–351, 357mandated treatment, 364mens rea doctrine, 359

Index 675personal injury cases, 359psychiatric assessment, 356services for incarcerated persons, 360–363substance abuse–crime linkages, 357substance abuse–violence linkages,356–357terminology of addiction, 355–356workplace testing and treatment, 341See also Law enforcementLeukopenia, alcohol-induced, 94–95Levo-alpha acetyl methadol, 588opioid maintenance therapy, 601side effects, 601Life skills training, 568Lithium, 286–287, 575for kleptomania, 315for pathological gambling, 312Liveralcohol effects, 91–92, 94chronic hepatic encephalopathy, 41, 94Locus coeruleusneurobiology of addiction, 9–10neurobiology of dependence, 7–9Lofexidine, 598Lorazepam, 225, 228, 229, 591LSDadolescent use patterns, 560laboratory testing for, 65neurobiology of tolerance, 7MMaintenance therapywith behavioral interventions, 647–648, 649–650, 651blocking agents, 588for opioid dependence, 600–602, 649–651partial agonists, 589substitution agents, 588See also MethadoneManualized therapies, 653–654Marijuanaadolescent use patterns, 560comorbid cocaine use, 193dependence treatments, 654–655gateway theory of adolescentsubstance abuse, 45, 560–561, 563health effects, 418laboratory testing for, 65polysubstance abuse, 251, 260racial/ethnic differences in usepatterns, 325workplace consumption, 344Matching, treatmentalcohol dependence, 644–646cocaine dependence, 651–654definition, 637group therapy selection, 503marijuana dependence, 654–655opioid dependence, 646–651outcomes research, 637–638pain management, 378–380rationale, 637research needs, 655–656MDMA. SeeMethylenedioxymethamphetamine(MDMA)Medical review officer, 68, 70Meperidine, 381Mephobarbital, 224Mescaline, 65Mesocorticolimbic reward system, 189Mesolimbic reward system, 5, 10Methadone, 30benzodiazepine use and, 228–229cannabis use and, 260chronic pain among users of, 373cocaine use and, 193, 259group therapy with methadonemaintenancepatients, 507–508laboratory testing for, 65neurobiological action, 12for opioid detoxification, 597–598opioid maintenance therapy, 600, 601,639, 646–649pain management strategies, 381–384therapeutic action, 588Methamphetamine, 262–263, 419addiction treatment, 208chronic use, 208intoxication, 207

676 IndexMethamphetamine (cont.)neurophysiology, 11, 207–208preparation and administration, 206–207prevalence and patterns of use, 206tolerance, 2073, 4-Methylenedioxyamphetamine, 653, 4-Methylenedioxymethamphetamine(MDMA), 260–262, 419adolescent use patterns, 560laboratory testing for, 65Methylphenidate, 289–290, 560Michigan Alcoholism Screening Test,46, 399Microsomal ethanol-oxidizing system,84–85Military personnel, 351–352Mindfulness, 624–625Minnesota Model of treatment, 30Minnesota Multiphasic PersonalityInventory, 46–47, 49Mixed substance abuse. SeePolysubstance abuseMonoamine oxidase, stimulusaugmentation and, 40Monoamine oxidase inhibitors, 201–202contraindications in cocaine abusers, 606for smoking cessation, 591Mood disordersin adolescents, 566–567alcohol use and, 79–80, 89gender differences, 253impulse control disorders and, 306Morphine, laboratory testing for, 65Mortalitycocaine-related, 185gender differences, 446–447Native American, 332–333Motivational enhancement therapy, 496,515cocaine relapse prevention, 204–205Motivational interviewing, 641cocaine relapse prevention, 204–205with dually diagnosed patients, 282Motor vehicle operationslegal liability of intoxicated persons, 358mandated reporting of substance use,350–351Multidimensional PersonalityQuestionnaire, 49–50Multidrug abuse. See Polysubstance abusemu opioid receptorsbuprenorphine action, 13in impulse control disorders, 307–308naltrexone action, 12–13Musculoskeletal system, alcohol effects, 95NNalmefene, 594Naloxone, 596–597Naloxone challenge, 600Naltrexone, 402, 405adolescent treatment, 575alcohol relapse prevention, 593–594cocaine abuse treatment, 202, 603–605effectiveness, 645–646for impulse control disorders, 309–312, 315, 316neurobiological action, 12–13for opioid relapse prevention, 600–601, 650–651for opioid withdrawal, 597Narcissism of addicts, 460, 508Narcotics Anonymous, 512–513National Institute on Alcohol Abuseand Alcoholism, 24National Institute on Drug Abuse, 24, 66National Institutes of Mental Health, 24Native Americans, 332–333alcohol use and abuse, 83population statistics, 321tobacco use, 105, 118Network therapy, 521–523Neurobehavioral disinhibition, 44–45Neurobiologyalcohol effects, 85–89, 93–94chronic pain, 376–377cocaine effects, 189–191, 197cognitive assessment, 50–51cognitive impairments associated withsubstance abuse, 40–42, 51implications for treatment ofaddiction, 3–4, 12–14

Index 677in impulse control disorders, 305, 306,307–308methamphetamine effects, 207–208models of addiction, 9–11neuropsychiatric complications ofAIDS/HIV, 412–414origins of drug liking, 4–6polysubstance use effects, 258–259predisposition to addiction, 4, 11racial/ethnic differences, 326of withdrawal, 6–9, 10Neuroleptic drugs, 606Nicotine. See TobaccoN-methyl-D aspartatealcohol use and, 85, 86–87methamphetamine effects, 208Nonsteroidal anti-inflammatory drugs,387–389Noradrenalineneurobiology of addiction, 9–10neurobiology of dependence, 7–9Noradrenergic systemin impulse control disorders, 307methamphetamine effects, 208Norepinephrine systemalcohol use and, 85cocaine action, 189, 190, 191Normalization, 3Nortriptylinefor kleptomania, 315for smoking cessation, 590–591Novelty seeking, 82, 255–256Nucleus accumbens, 5, 6OObsessive–compulsive disorders, 305Occupational Safety and Health Act,341Olanzapine, 287cocaine addiction treatment, 202for pathological gambling, 312Ondansetron, 594–595Opioid addiction treatmentdrug–drug interaction risk, 602–603effectiveness, 646–651historical evolution, 24methadone maintenance therapy, 600,601, 639, 646–649normalization in, 3overdose management, 596–597pharmacotherapy, 3, 12–13polydrug use and, 263withdrawal management, 597–600Opioid agonists/antagonistsalcohol relapse prevention, 593–594classification, 380–381for pathological gambling, 309–312See also specific agentOpioidsclassification, 380comorbid alcohol abuse, 79comorbid cocaine abuse, 185, 193dependence, 370epidemics of abuse, 27–28historical use, 17–18, 21HIV infection risk and use of, 416neurobiological action, 4–6overdose, 596–597for pain management, 22, 368, 373–375, 378–387patterns and prevalence of use, 253polysubstance abuse, 251, 259–260side effects, 385–386tolerance, 369tolerance and dependence,neurobiology of, 7–9workplace consumption, 344See also Opioid addiction treatment;specific agentOral contraceptives, 113Osteoporosis, alcohol use and, 95Outpatient treatment, 30–31Overdosebarbiturates, 224cocaine, 185, 190, 201–202heroin, 260mortality, 185opioids, 596–597polysubstance use and, 260Oxazepam, 228, 229, 591Oxycodone, 381

678 IndexPPain managementadjuvant analgesics, 389analgesic administration route, 384assessment for, 375–377, 391assessment of aberrant drug-relatedbehaviors in, 371–373categories of patients, 374–375clinical concerns, 367–368, 386–387,391definition of addiction in, 370–371dosing considerations, 384–385drug dependence and, 369–370drug selection for, 380–384drug tolerance in, 368–369nonsteroidal anti-inflammatory drugsfor, 387–389opioid therapy, 368, 374–375, 378–387patient selection, 378–380in people with substance abusedisorders, 373–374, 376prevalence of chronic pain, 367side effects of opioid therapy, 385–386strategies, 377–378Pancreatitis, alcohol-induced, 91Panic disorderalcohol use and, 80, 99benzodiazepine discontinuation inpeople with, 236–237cocaine use and, 194Paroxetinefor kleptomania, 315for pathological gambling, 309Partial agonist drugs, 589Patterns and prevalence of use, 20–21among adolescents, 559, 560–561among elderly, 396, 397–399associated personality profiles, 256–257benzodiazepines, 221club drugs and circuit parties, 260–262cocaine, 184–186gender differences, 438identifying nonmedical use, 221–222methamphetamine, 206physicians, 350polysubstance, 248–253racial/ethnic differences, 322–323,324–326, 328–331, 332–333sedative/hypnotic drugs, 220–221in workplace, 341Pemoline, 290, 575, 576Pentazocine, 113Pentobarbital, 224Perceptual field dependence, 40Performance-enhancing drugs, 348, 352Personal Experience Inventory, 47Personality disordersalcohol abuse and, 81–82cocaine use and, 195–196comorbid substance use disorder, 253–254co-occurring pathological gambling,308Personality traitsadolescent substance abuse risk, 562–563substance use disorders and, 255–257Pharmacotherapyabuse potential of psychoactiveagents, 290–291adherence, 642–643adolescents with psychiatriccomorbidity, 574–576alcohol abuse treatment, 644–646for alcoholism in elderly persons, 404–405alcohol relapse prevention, 593–595alcohol withdrawal, 591–593applications, 638behaviorally-oriented, 639–640for benzodiazepine withdrawal, 596for cocaine abuse, 603–606comorbidity considerations, 286–292,606, 640for compulsive buying, 316–317for detoxification, 639in dialectical behavior therapy, 633–634drug interactions, 602–603effectiveness, 643–644

Index 679in family therapy, 549–550kleptomania, 314–315maintenance therapy, 588. See alsoMethadonefor nicotine dependence, 589–591opioid addiction, 3, 12–13. See alsoMethadonepathological gambling, 309–313for relapse prevention, 639risk of drug interactions amongelderly, 397–398self-help group acceptance of, 284,520–521for substance use disorders, 291, 588See also Pain management; specificdrugPhencyclidine, 41laboratory testing for, 65Phenobarbital, 224for benzodiazepine withdrawal, 231Phenothiazine, 113Phenylbutazone, 113Phenylpropanolamine, 65Phosphoinositol phosphate secondmessenger system, 7Physicians with substance use problems,349–350, 360Polyneuropathy, 94Polysubstance abuseassociated personality traits, 255–257club drugs and circuit parties, 260–262comorbid personality disorders, 253–254diagnostic conceptualization, 245–248epidemiology, 248–253genetic risk, 257–258group therapy, 503HIV risk in, 262neuropsychological impact, 258–259overdose risk in, 260treatment, 250–251treatment considerations, 263–264See also specific substancePosttraumatic stress disorderalcohol use and, 80cocaine use and, 194comorbid substance use disorder, 277Prazepam, 228, 229Predisposing factorsadolescent substance abuse, 562–565affective, 43alcohol abuse, 86benzodiazepine abuse, 230gender differences, 443–444intellectual functioning, 259neurobiological abnormalities, 4, 11personality disorders, 254psychopathology, 274, 276, 443–444substance use disorder, 257–258in women, 439–440See also GeneticsPrefrontal cortex, 11Pregnancy, 199. See also Fetal exposurePrescription drugs, 22Preventive interventionsabstinence movements, 25–26with adolescents, 567–569in African American communities,327, 328with attention-deficit/hyperactivitydisorder patients, 289cost-effectiveness, 569family involvement, 552historical evolution, 19–20, 31–32HIV transmission, 426–427program design principles, 569smoking initiation, 109strategies for women, 448–449Prisoners, 360–363Propoxyphene, 113laboratory testing for, 65Propranolol, 113Pseudoaddiction, 371–372Psychiatric disorderscocaine-related psychosis, 201–202diagnosis, 48–49severity, as predictive of comorbidsubstance abuse, 252social costs, 220See also Comorbidity, psychiatric;Psychological assessment; specificdisorderPsychological assessmentbehavioral, 44cocaine abuser, 201

680 IndexPsychological assessment (cont.)cognitive, 50–51contextual considerations, 38domains of interest in substanceabuse, 40–43, 44–45emotional functioning, 43–44family functioning, 51–52forensic, 356goals, 37–38, 45history of alcohol and drug use, 45–47personality traits, 49–50psychiatric comorbidity, 48–49recreational/leisure activities, 55–56reliability requirements, 39social adjustment, 53–56treatment linkage, 37, 42, 43, 45, 56–57validity requirements, 38–39vocational, 55during withdrawal, 42Psychotherapyabstinence in, 464–465adolescent substance abuse treatment,574with AIDS patients, 424–425alcohol relapse prevention, 593, 594assessment and diagnosis of addiction,463–464change processes, 458cocaine addiction treatment, 203–206,209, 652–654for compulsive buying, 317with dually diagnosed populations,280–283, 291–292effectiveness, 458–459, 643–644elderly patients, 403–404to enhance pharmacotherapyadherence, 642–643indications, 459for kleptomania, 315with opioid maintenance therapy,649, 651for pathological gambling, 312–313patient ambivalence about abstinence,640–641physical health considerations in,467–468psychodynamic basis, 460–462rationale, 457relapse issues, 468self-help groups and, 469–470, 520–521special aspects of addiction work,462–468structure of, 465–466therapeutic relationship in, 463, 464–465, 467–468, 469transference/countertransferenceissues, 464, 469, 508treatment plans, 458treatment targets, 457, 466–467, 640–643See also Cognitive therapy; GrouptherapyPsychotic disordersalcohol use and, 89, 98pharmacotherapy considerations indually diagnosed patient, 606QQuetiapine, 287Quinine, 65RRace/ethnicityadolescent psychiatric disorders, 566adolescent substance use, 561alcohol use patterns, 82–84cocaine use and, 185–186differences among women, 322individual differences, 321–322overdose deaths and, 185population distribution, 321, 330tobacco use and, 117–118See also specific racial or ethnic groupRaves, 261, 419Recreational drug use, 22cocaine, 192Reinforcement, drugbenzodiazepines, 230neurobiology, 3, 4–6social functioning, 53

Index 681Relapse and relapse preventionadolescent treatment, 576–577affective factors in, 642alcoholism treatment and relapseprevention, 98, 593–595cocaine use, 190, 191, 203, 205–206cognitive therapy strategies, 488–489disease model, 470family therapy, 541–545management of persons released fromincarceration, 363network therapy techniques, 521–522pharmacotherapy for, 639psychotherapy strategies, 468smoking, 111–112, 115stress and, 12See also Cognitive-behavioral relapsepreventionReligion and spiritualityabstinence movements, 25attempts to curtail substance use, 19–20attitudes toward alcohol, 330ceremonial substance use, 16, 18, 21Native American culture, 333See also Ceremony and ritualRespiratory complications, cocainerelated,198Reticulocytosis, 94Risperidone, 287SSaliva analysis, 65Schedule for Affective Disorders andSchizophrenia, 48Schizophreniaalcohol use and, 80–81cocaine use and, 195, 274pharmacotherapy with duallydiagnosed patients, 287–288smoking and, 113Secobarbital, 224Sedative/hypnotic drugsaction, 219adolescent use patterns, 560definition, 219discontinuation, 236–238new formulations, 238–239pharmacology, 224–225polysubstance abuse, 251prevalence and patterns of use, 220–221withdrawal, 231workplace consumption, 344–345See also Benzodiazepines; specificdrugSelective serotonin reuptake inhibitors,238, 606adolescent treatment, 575for impulse control disorders, 309,316–317Self-esteemassessment, 50preventive interventions withadolescents, 567–569Self-help groupsattitudes toward pharmacotherapy,284, 520–521cognitive therapy and, 494dually diagnosed patients, 283–284family therapy and, 539, 540historical evolution, 26–27individual psychotherapy and, 469–470, 520–521in institutional settings, 517–520origins and development, 511–513outcomes, 516–520role in addiction treatment, 511,654See also Twelve-step programsSelf-medication hypothesis, 274, 275,460, 510Self-Report Family Inventory, 52Serotonergic systemalcohol use and, 85–86cocaine action, 189, 190in impulse control disorders, 307in LSD tolerance, 7methamphetamine effects, 208See also Selective serotonin reuptakeinhibitorsSerum gamma-glutamyltransferase, 77

682 IndexSexual behaviorHIV infection risk, 411, 415, 417polydrug use and, 262women with addictive disorders,441Sexual dysfunction, alcohol-related, 89–90Sexual harassment/assault, 357, 360, 439,443, 445Skin problems, alcohol-related, 96Sleep disorders, alcohol-induced, 89Smoking. See TobaccoSocial anxiety disorder, alcohol use and,80Social Relationship Scale, 53Sociocultural contextabstinence movements, 25–26alcohol use patterns, 82–84attitudes toward alcohol use bywomen, 444–445, 448–449benefits of substance use, 16epidemic substance abuse, 20–21, 27–28historical evolution of substance abusetreatment, 23–27, 29–32historical evolution of substance use,17–23, 28–29patterns of substance use, 20–21pharmacodynamics and, 18–19significance of, 16Sports. See Athletes, drug testing forStages-of-change model, 282–283, 465–466, 489–490Steroids, 560Stimulus augmentation, 40Stressin neurobiology of addiction, 12workplace, 55Structured Clinical Interview for DSM-III-R, 48Substance Abuse Problem Checklist,53Substance use disorderassessment and diagnosis, 278clinical features, 222–223co-occurring pathological gambling,308–309impulse control disorders and, 304–305See also Comorbidity, psychiatric;specific substanceSuicidal behavior/ideation, adolescentsubstance use and, 566–567Sweat analysis, 65Symptom Checklist 90–Revised, 49TTelephone consultation, in dialecticalbehavior therapy, 632Temazepam, 229Testicular atrophy, 95Theophylline, 113Therapeutic relationshipin cognitive therapy, 483–485, 490in dialectical behavior therapy, 623–624, 630–631in family therapy, 535in group therapy, 508in psychodynamic psychotherapy, 463,464–465, 467–468, 469racial/ethnic context, 328substance abuse among highresponsibilityworkers and, 350–351in treating alcoholism, 97, 98Thiamin, 88, 92, 94Thin layer chromatography, 64, 65Thrombocytopenia, alcohol-induced, 94,95Thyroid dysfunction, alcohol-related, 95Tobacco, 21, 351acute intoxication, 112addictive potential, 107, 115adolescent use patterns, 560, 561AIDS infection and, 418–419alcohol abuse and, 79anti-smoking movement, 107–108assessment of use, 116–117benefits of quitting, 113–114business interests, 108, 109cocaine use and, 193–194dependence, 110–111drug interactions, 113

Index 683environmental tobacco smoke, 107–108ethnic differences in use, 117–118future prospects, 109gender differences in use patterns, 438health effects, 106–107, 112–113,115–116, 440historical use, 105–106low-tar/low-nicotine cigarettes, 108–109mortality, 107, 108neurobiology of drug liking, 6nicotine gum and patches, 589–590pharmacology, 118–121pharmacotherapy for dependence,589–591polysubstance abuse, 251prevalence and patterns of use, 106,108, 109, 114–116relapse risk, 111–112, 115risk factors for smoking, 114smokeless, 119social costs, 107withdrawal, 111Tolerancebenzodiazepines, 232–233cocaine, 191cross-tolerance, 588definition, 368–369methamphetamine, 207neurobiology, 3, 6–9Topiramate, 315Transference/countertransference, 464,469, 508Transitional family therapy, 532–533Trazodone, 225, 315Treatment, generallyAIDS infection and, 420–421, 423–425of incarcerated persons, 360–363matching. See Matching, treatmentneurobiology of, 3–4, 12–14neurocognitive effects of drug abuseand, 607polysubstance abusers, 250–251, 263–264role of laboratory testing, 63role of psychological assessment in,37, 42, 43, 45, 56–57self-help movement, 26–27technical and conceptual evolution,23–27, 29–32See also Pharmacotherapy;Psychotherapy; specific substance ofabuseTricyclic antidepressants, 113Tryptophan hydroxylase, 208TWEAK interview, 77Twelve-step facilitation, 515, 516–517,653–654Twelve-step programs, 469, 511–514dually diagnosed patients, 283individual psychotherapy and, 520–521UUrine testing. See Laboratory testingVVaccine, cocaine, 605–606Validation, 630–631Valproatefor alcohol withdrawal management,591–592for kleptomania, 315Venlafaxine, 289Ventral tegmental areaneurobiology of drug liking, 5, 6neurobiology of tolerance anddependence, 7, 9–10Vigabatrin, 592–593Violent behavior, 261in adolescents, 566alcohol use and, 356–357substance use among police andmilitary personnel and, 351–352Vitamin deficiencies, alcohol-related, 88,90, 91, 92, 94Voucher and reward therapies in cocainerelapse prevention, 204

684 IndexWWernicke–Korsakoff syndrome, 88, 94Wernicke’s encephalopathy, 87–88White Americansalcohol use and abuse, 323–324cocaine use and abuse, 185–186population statistics, 321smoking patterns, 117, 118Withdrawalalcohol, 86–87, 591–593assessment, 591benzodiazepines, 229–230, 231–232,236–238, 596cocaine, 191–192, 202cognitive capacity in, 42maintenance therapy rationale, 588–589neurobiology, 6–9, 10nicotine, 111, 589–591opioid, 597–600psychological assessment during, 42sedative/hypnotic drugs, 231Women, addictive disorders in, 437–438clinical features, 446–447epidemiology, 438–439health risks, 440prevention, 448–449psychological factors, 443–444reproductive functioning, 441risk factors, 439sociocultural factors, 444–445treatment, 447–448See also Gender differencesWorkplaceathletes, special problems of, 348detecting substance use, 68, 69–71,223, 342–343, 346Xdisability claims, 360drug-free workplace programrequirements, 69–70drug-specific manifestations, 343–345health care settings, 349–350high-responsibility occupations, 350–351historical development of interventionin, 30–31legal issues regarding testing andtreatment, 341mandated reporting of drug use, 350–351negative outcomes of substance use in,340–341organizational factors in substancemisuse, 342, 345–346patterns and prevalence of substanceuse, 341police and military personnel, 351–352practice issues, 340, 345preemployment interview, 342–343,345psychological assessment in, 55substance-abusing executives, 348, 349treatment and interventions, 345–348Xanax, 237–238ZZaleplon, 238–239Zolpidem, 238–239

Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

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