Treatment for Stimulant Use Disorders
Treatment Improvement Protocol (TIP) Series 33
Richard A. Rawson, Ph.D.
Consensus Panel Chair
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service
Substance Abuse and Mental Health Services Administration
Center for Substance Abuse Treatment
Rockwall II, 5600 Fishers Lane
Rockville, MD 20857
DHHS Publication No. (SMA) 99-3296
This publication is part of the Substance Abuse Prevention and Treatment Block Grant technical assistance program. All material appearing in this volume except that taken directly from copyrighted sources is in the public domain and may be reproduced or copied without permission from the Substance Abuse and Mental Health Services Administration's (SAMHSA) Center for Substance Abuse Treatment (CSAT) or the authors. Citation of the source is appreciated.
This publication was written under contract number 270-95-0013 with The CDM Group, Inc. (CDM). Sandra Clunies, M.S., I.C.A.D.C., served as the CSAT government project officer. Rose M. Urban, M.S.W., J.D., C.S.A.C., served as the CDM TIPs project director. Other CDM TIPs personnel included Cara Smith, editorial assistant; Raquel Ingraham, M.S., project manager; Mark A. Meschter, former editor/writer; Mary Smolenski, Ed.D., C.R.N.P., former project director; and MaryLou Leonard, former project manager. Special thanks go to consulting writers Warren Bickel, Ph.D.; Gregory L. Greenwood, Ph.D., M.P.H.; Mitchell Markinem, M.A., N.C.A.C. II; Sara Simon, Ph.D.; and Ronald D. Stall, Ph.D., M.P.H., for their considerable contributions to this document.
The opinions expressed herein are the views of the Consensus Panel members and do not reflect the official position of CSAT, SAMHSA, or the U.S. Department of Health and Human Services (DHHS). No official support or endorsement of CSAT, SAMHSA, or DHHS for these opinions or for particular instruments or software that may be described in this document is intended or should be inferred. The guidelines proffered in this document should not be considered as substitutes for individualized client care and treatment decisions.
Treatment Improvement Protocols (TIPs) are best practice guidelines for the treatment of substance use disorders, provided as a service of the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (CSAT). CSAT's Office of Evaluation, Scientific Analysis and Synthesis draws on the experience and knowledge of clinical, research, and administrative experts to produce the TIPs, which are distributed to a growing number of facilities and individuals across the country. The audience for the TIPs is expanding beyond public and private substance use disorder treatment facilities as alcoholism and other substance use disorders are increasingly recognized as major problems.
The TIPs Editorial Advisory Board, a distinguished group of substance use experts and professionals in such related fields as primary care, mental health, and social services, works with the State Alcohol and Other Drug Abuse Directors to generate topics for the TIPs based on the field's current needs for information and guidance.
After selecting a topic, CSAT invites staff from pertinent Federal agencies and national organizations to a Resource Panel that recommends specific areas of focus as well as resources that should be considered in developing the content of the TIP. Then recommendations are communicated to a Consensus Panel composed of non-Federal experts on the topic who have been nominated by their peers. This Panel participates in a series of discussions; the information and recommendations on which they reach consensus form the foundation of the TIP. The members of each Consensus Panel represent substance use disorder treatment programs, hospitals, community health centers, counseling programs, criminal justice and child welfare agencies, and private practitioners. A Panel Chair (or Co-Chairs) ensures that the guidelines mirror the results of the group's collaboration.
A large and diverse group of experts closely reviews the draft document. Once the changes recommended by these field reviewers have been incorporated, the TIP is prepared for publication, in print and online. The TIPs can be accessed via the Internet on the National Library of Medicine's home page at the URL: http://text.nlm.nih.gov. The move to electronic media also means that the TIPs can be updated more easily so they continue to provide the field with state-of-the-art information.
Although each TIP strives to include an evidence base for the practices it recommends, CSAT recognizes that the field of substance use disorder treatment is evolving and that research frequently lags behind the innovations pioneered in the field. A major goal of each TIP is to convey "front line" information quickly but responsibly. For this reason, recommendations proffered in the TIP are attributed to either Panelists' clinical experience or the literature. If there is research to support a particular approach, citations are provided.
This TIP, Treatment for Stimulant Use Disorders, supplies substance use disorder treatment providers with vital information on the effects of stimulant abuse and dependence, discusses the relevance of these effects to treating stimulant users, describes treatment approaches that are appropriate and effective for treating these clients, and makes specific recommendations on the practical application of these treatment strategies. Research on animals has demonstrated the profound effects that stimulants can have on the central nervous system, and new technologies have begun to document the stimulant-induced neurological impairments in humans. Researchers now believe that these impairments underlie the cognitive deficits that are often seen in chronic stimulant users.
Effective treatment strategies must recognize the impact that stimulant abuse and dependence have on the user's ability to respond to treatment. The treatment strategies that are described in this TIP have been scientifically validated as effective in treating people with stimulant use disorders. These strategies address the specific problems and needs that are inherent to chronic stimulant users.
This document discusses in detail the practical application of these treatment strategies and makes recommendations to improve treatment outcomes for stimulant abuse and dependence. The document also provides for clinicians and primary care providers an overview of the medical aspects of stimulant use. Furthermore, treatment issues for special groups and settings are reviewed.
This TIP represents another step by CSAT toward its goal of bringing national leaders together to improve substance use disorder treatment in the United States.
Other TIPs may be ordered by contacting SAMHSA's National Clearinghouse for Alcohol and Drug Information (NCADI), (800) 729-6686 or (301) 468-2600; TDD (for hearing impaired), (800) 487-4889.
Karen Allen, Ph.D., R.N., C.A.R.N.
President of the National Nurses Society on Addictions
Department of Psychiatry, Community Health, and Adult Primary Care
University of Maryland
School of Nursing
Richard L. Brown, M.D., M.P.H.
Department of Family Medicine
University of Wisconsin School of Medicine
Dorynne Czechowicz, M.D.
Treatment Research Branch
Division of Clinical and Services Research
National Institute on Drug Abuse
Linda S. Foley, M.A.
Project for Addiction Counselor Training
National Association of State Alcohol and Drug Directors
Wayde A. Glover, M.I.S., N.C.A.C. II
Commonwealth Addictions Consultants and Trainers
Pedro J. Greer, M.D.
Assistant Dean for Homeless Education
University of Miami School of Medicine
Thomas W. Hester, M.D.
Former State Director
Substance Abuse Services
Division of Mental Health, Mental Retardation and Substance Abuse
Georgia Department of Human Resources
Office of Substance Abuse
American Psychological Association
Douglas B. Kamerow, M.D., M.P.H.
Office of the Forum for Quality and Effectiveness in Health Care
Agency for Health Care Policy and Research
Stephen W. Long
Office of Policy Analysis
National Institute on Alcohol Abuse and Alcoholism
Richard A. Rawson, Ph.D.
Matrix Center and Matrix Institute on Addiction
Deputy Director, UCLA Addiction Medicine Services
Los Angeles, California
Ellen A. Renz, Ph.D.
Former Vice President of Clinical Systems
MEDCO Behavioral Care Corporation
Richard K. Ries, M.D.
Director and Associate Professor
Outpatient Mental Health Services and Dual Disorder Programs
Harborview Medical Center
Sidney H. Schnoll, M.D., Ph.D.
Division of Substance Abuse Medicine
Medical College of Virginia
Richard A. Rawson, Ph.D.
Matrix Center and Matrix Institute on Addiction
Deputy Director, UCLA Addiction Medicine Services
Los Angeles, California
Felipe G. Castro, M.S.W., Ph.D.
Hispanic Research Center
Department of Psychology
Arizona State University
James W. Cornish, M.D.
Assistant Professor of Psychiatry
Director, Division of Pharmacotherapy
Treatment Research Center
University of Pennsylvania
Department of Veterans Affairs Medical Center
Frances R. Levin, M.D.
Clinical and Educational Activities
Division on Substance Abuse
New York, New York
Michael J. McCann, M.A.
Los Angeles, California
Arlene Hall, R.N., M.S., C.D.
Director of Nursing
Stephen Higgins, Ph.D.
Departments of Psychiatry and Psychology
Ira Allen School
University of Vermont
Kyle M. Kampman, M.D.
Assistant Professor of Psychiatry
Treatment Research Center
University of Pennsylvania
Lame Deer, Montana
Judy Knobbe, M.S.W., L.I.S.W., C.A.D.C.
Heart of Iowa
Area Substance Abuse Council
Cedar Rapids, Iowa
Bureau of Alcohol and Drug Abuse
State of Nevada
Carson City, Nevada
Scott M. Reiner, M.S., C.A.C., C.C.S.
Substance Abuse Program Supervisor
Substance Abuse Services Unit
Virginia Department of Juvenile Justice
Ewa Szumotalska Stamper, Ph.D.
Honolulu Police Department
Private Practice in Clinical and Addictions Psychology
Arnold M. Washton, Ph.D.
Private Practice of Addiction Psychology
Dennis A. Weis, M.D.
Powell Center for Disease Control
Iowa Lutheran Hospital
American Society of Addiction Medicine
Des Moines, Iowa
The Treatment Improvement Protocol (TIP) series fulfills SAMHSA/CSAT's mission to improve treatment of substance use disorders by providing best practices guidance to clinicians, program administrators, and payors. TIPs are the result of careful consideration of all relevant clinical and health services research findings, demonstration experience, and implementation requirements. A panel of non-Federal clinical researchers, clinicians, program administrators, and client advocates debates and discusses their particular area of expertise until they reach a consensus on best practices. This panel's work is then reviewed and critiqued by field reviewers.
The talent, dedication, and hard work that TIPs panelists and reviewers bring to this highly participatory process have bridged the gap between the promise of research and the needs of practicing clinicians and administrators. We are grateful to all who have joined with us to contribute to advances in the substance use disorder treatment field.
Nelba Chavez, Ph.D.
Substance Abuse and Mental Health Services Administration
H. Westley Clark, M.D., J.D., M.P.H., CAS, FASAM
Center for Substance Abuse Treatment
Substance Abuse and Mental Health Services Administration
Over the last 20 years, the use of stimulants has risen to national and international prominence. Stimulant use and its consequences have brought havoc to many communities across the United States and have prompted strong responses from Federal, State, and local governments and organizations. For example, the relatively minor problems of cocaine use in the 1960s and 1970s have grown to become major medical, legislative, and law enforcement issues in the 1990s. The devastation wrought by the crack cocaine epidemic is familiar to most Americans.
Similarly, the use and abuse of another stimulant, methamphetamine (MA), have risen dramatically in recent years. Widespread use and abuse of MA have led to a greater awareness of the problem and have inspired policymakers, legal officials, and service providers to focus increased efforts toward the personal and societal effects of this drug. Concerns that MA abuse may result in another epidemic led to passage of the Comprehensive Methamphetamine Control Act of 1996.
The explosive growth of stimulant use triggered a flurry of research. The results are tremendous advances in fundamental knowledge of stimulant use disorders and on the basic function of the brain and addictive disorders in general. Yet today, there are few reports that describe either the fundamentals of stimulant use disorder treatment or the success of various treatment interventions.
This Treatment Improvement Protocol (TIP) describes basic knowledge about the nature and treatment of stimulant use disorders. More specifically, it reviews what is currently known about treating the medical, psychiatric, and substance abuse/dependence problems associated with the use of two high-profile stimulants: cocaine and MA.
The scientifically based information in this TIP is presented in a manner that makes it available and relevant for clinicians and other "front line" substance use disorder treatment providers. It offers recommendations on treatment approaches, recommendations to maximize treatment engagement, strategies for planning and initiating treatment, and strategies for initiating and maintaining abstinence. Also included are recommendations for the medical management of stimulant users and recommendations regarding special groups and settings.
The Consensus Panel that developed this TIP tried to emphasize those treatment techniques and principles that have been established with empirical support. However, because the "science" of treating stimulant use disorders is barely a decade old, the Panel also reviewed and synthesized a set of techniques and principles developed and supported by leading addiction specialists, but with less empirical support. This document delineates those treatment suggestions and recommendations that are empirically supported and those that are currently based on consensus opinion.
The purpose of this TIP is to advance the understanding of treating the substance use disorders associated with the abuse of cocaine and MA. The Consensus Panel's recommendations summarized below are based on both researched and clinical experience. Those supported by scientific evidence are followed by (1); clinically based recommendations are marked (2). Citations to the former are referenced in the body of this document, where the guidelines are presented in full detail. To avoid sexism and awkward sentence construction, the TIP alternates between "he" and "she" in generic examples.
For purposes of this TIP, the substances included in the category of "stimulants" include the derivatives of the coca plant (cocaine hydrochloride and its freebase form, "crack") and the synthetically produced amphetamines, with a primary emphasis on illicitly produced MA (and its smokable form, "ice"). Certainly there are other stimulants that are more widely used (e.g., caffeine) or that produce major health problems (e.g., nicotine); however, an extensive discussion of issues associated with these substances is beyond the scope of this document.
Because of recent health care reforms, most individuals who seek help for stimulant dependence now receive treatment at structured outpatient treatment programs. Accordingly, this document provides recommendations for treatment strategies and techniques that are most relevant to the treatment of stimulant-dependent patients in structured outpatient treatment programs. However, many, if not most, of these strategies and techniques can be integrated into other types of programs, regardless of the setting or therapeutic orientation.
Psychosocial treatment approaches that incorporate well established psychological principles of learning are appropriate for and effective in treating stimulant users. In an effort to make these approaches consistently effective, the Consensus Panel recommends the use of carefully prepared treatment manuals to minimize differences among therapists. (2) Treatment manuals increase the likelihood that therapists will deliver a uniform set of services to their clients. However, the therapist's clinical judgment and flexibility are extremely important to the treatment process.
The Consensus Panel recommends a contingency management approach for treating stimulant users. (1) A particularly successful version is the community-reinforcement-plus-vouchers approach in which couples counseling, vocational training, and skills training are combined with rewards for negative drug tests (i.e., "clean" urinalysis results).
Relapse prevention systematically teaches clients
The Consensus Panel recommends this approach for use with stimulant users. (1)
Research indicates that the following may be appropriate interventions for stimulant users:
A number of other psychosocial models and approaches have been described, and some used widely, for the treatment of stimulant use disorders, including:
To maximize treatment engagement, programs must make treatment accessible. Having treatment programs in areas convenient to clients is associated with lower attrition rates. (1) Treatment should be provided during the hours and on the days that are convenient for clients. (2) Programs should be located near public transportation and in a part of town viewed as safe for evening visits. (2)
Address clients' concrete needs, including transportation, housing, and finances. (1) Some logistical barriers can be overcome by onsite services, through agreements with subcontractors, or by referrals. These can include onsite child care services, referrals to temporary shelters, vouchers for lunches, targeted financial assistance, assistance with paperwork regarding insurance, or filing for disability benefits. (2)
Because ambivalence about treatment is common among treatment-seeking stimulant users, methods to "screen out" those who are "in denial" are counterproductive and impede treatment entry. (2) The initial interview should be scheduled within 24 hours after the client initially contacts the program. (2)
Initial assessments should be brief, focused, and nonrepetitive. (2)
Individuals need a thorough, clear, and realistic orientation about stimulant use disorder treatment. Clients should acquire a good understanding about the treatment process, the rules of the treatment program, expectations about their participation, and what they can expect the program to do for them and in what time frame. (2)
Addiction treatment is more effective when a client chooses it from among alternatives than when it is assigned as the only option. Thus, it is important to provide clients with options and negotiate with them regarding the treatment approaches and strategies that are the most acceptable and promising. (1)
Whenever possible, family and significant others who support the treatment goals should be involved in the treatment process. (2)
Counselors should be warm, friendly, engaging, empathetic, straightforward, and non-judgmental. Authoritarian and confrontational behavior by the staff can substantially increase the potential for violence. (2)
To organize treatment strategies, it can be helpful to view the treatment process as consisting of
The Consensus Panel recommends treatment for 12 to 24 weeks followed by some type of support group participation. (2)
Clients should have a written schedule of expected attendance they can keep and give to family members who may be involved in treatment. It does not appear appropriate to deliver these services on an ad hoc or as needed basis. (2)
The initial period of stimulant abstinence is characterized by symptoms of depression, difficulty concentrating, poor memory, irritability, fatigue, craving for cocaine/MA, and paranoia (especially for MA users). The duration of these symptoms varies; in general, symptoms typically last 3 to 5 days for cocaine users and 10 to 15 days for MA users. (2)
The first several weeks of treatment have some relatively simple and straightforward priorities.
During the first 2 or 3 weeks, clients should be scheduled for multiple weekly visits, even if the visits are 30 minutes in duration or less. (2)
Immediately upon entering the treatment program, clients should be placed on a mandatory, vigilant, and frequent urine testing schedule. This schedule should continue throughout the treatment process, although the frequency of testing can be tapered as treatment progresses. Urine samples should be taken every 3 or 4 days so as not to exceed the sensitivity limits of standard laboratory testing methods. (2) Participation in self-help groups should be strongly encouraged but not required.
During the initial 2 weeks of treatment, it is important to assess the possible existence of other psychiatric conditions and, if present, initiate appropriate treatment, including medication. (2)
Research has revealed an association between stimulant use and a variety of compulsive sexual behaviors. These behaviors include promiscuous sex, AIDS-risky behaviors, compulsive masturbation, compulsive pornographic viewing, and homosexual behavior for otherwise heterosexual individuals. In order for treatment to be effective, these issues must be discussed openly and nonjudgmentally. (2)
Remind clients that proper sleep and nutrition are necessary to allow the neurobiology of the brain to "recover." Giving them "permission" to sleep, eat, and gradually begin a program of exercise, can help establish some behaviors that will have long-term utility. These behaviors will help them begin to think more clearly and begin to feel some benefit from their initial efforts in treatment. (1)
Establish structure and support. After the initial treatment engagement of 1 to 2 weeks, the focus is on the achievement of abstinence. Although there is no clear delineation between clients who are initiating abstinence and those maintaining abstinence, the initiating period occurs roughly from 2 to 6 weeks into treatment. (2)
Short-term goals should be set immediately and should be reasonably achievable. One such goal is complete abstinence from all substances for 1 week. (2)
Brief, frequent counseling sessions can reinforce the short-term goal of immediate abstinence and establish a therapeutic alliance between the client and counselor. Events of the past 24 hours are reviewed in each session and recommendations are provided for navigating the next 24 hours. (2)
For many clients, their secondary substance use may not have been associated with adverse consequences or compulsive use. As a result, such clients need help to identify the connections between the use of other substances and their stimulant addiction. (2)
Clients should be encouraged to throw out all substance-related items. (2) Family members, sober friends, or 12-Step sponsors should help with this task.
Clients must develop specific action plans to break contacts with dealers and other stimulant users and to avoid high-risk places that are strongly associated with stimulant use. (2)
Educate clients about learning and conditioning factors associated with stimulant use and the impact of stimulants and other substances on the brain and behavior, such as cognitive impairments and forgetfulness. (2)
Other steps to initiate abstinence include
Early slips should not be considered tragic failures but rather simple mistakes. When slips occur, counselors can make a verbal or behavioral contract with clients regarding short-term achievable goals. (2)
The core components of a functional analysis are
Relapse prevention techniques fall into the following categories:
Once clients learn to identify, manage, and avoid high-risk situations, the counselor and client should try to determine if the client is confident in her ability to use those skills in the real world through role-playing and other therapeutic techniques. (2)
So-called "war stories" that include euphoric recall and selective memory are powerful relapse triggers and should be strongly discouraged in recovery groups. (2)
The following recommendations are for medical personnel to help them recognize and treat problems that may arise for stimulant users with acute or chronic intoxication or in various phases of withdrawal.
The most common reasons for emergency room visits by cocaine users are cardiopulmonary symptoms (usually chest pains or palpitations); psychiatric complaints, ranging from altered mental states to suicidal ideation; and neurological problems, including seizures and delirium.
The major presenting symptoms for MA users pertain primarily to altered mental status, including confusion, delusions, paranoid reactions, hallucinations, and suicidal ideation. The rapid development of tolerance to its physiological effects among chronic MA users may explain the relative infrequency of cardiac complications in this group. (1)
The lethal dose of cocaine for 50 percent of novice users (LD50) is 1.5 grams. The LD50 for MA has not specifically been established, and there is significant individual variability to its toxicity. For example, doses of 30 milligrams can produce severe reactions, yet doses of 400 to 500 milligrams are not necessarily fatal. (1)
Uncomplicated intoxication requires only observation and monitoring in a subdued environment until symptoms subside over several hours.
Physical exertion and an overheated room can potentiate adverse effects because stimulants affect the body's heat-regulating mechanism at the same time that blood vessel constriction conserves heat.
Indications that agitation is escalating and moving toward paranoia and potential psychosis (losing touch with reality), with increasing risk for violence, may warrant pharmacological intervention. Fast-acting benzodiazepines such as lorazepam (Ativan) or diazepam (Valium) are useful for calming an anxious, agitated client. (1)
The greatest risk from the distinctive stimulant abstinence syndrome is that one may do harm to oneself or others. Because withdrawal-related dysphoria and depression can be particularly severe in stimulant users, risk of suicide is intensified, and sensitive management is essential. (1, 2)
Continuing agitation and persistent inability to fall asleep during withdrawal may also be treated symptomatically by using the antidepressant trazodone (Desyrel). Diphenhydramine (Benadryl) can also be used for its sedating properties. (1, 2)
Medical personnel must be prepared for the paranoia, aggression, and violence that often accompany stimulant use. These personnel should
There are a number of medical and psychiatric disorders that frequently accompany stimulant abuse and dependence. An awareness of these conditions is important for the safe and effective treatment of stimulant disorders. The conditions include
A diagnosis can be based on established DSM-IV criteria for amphetamine or cocaine use/abuse/dependence and other listed composites. (1)
An appropriate substance use history should include the substance(s) and medications used during the last 30 days; the specific substance(s) or combinations typically used with the usual dose, frequency, and route of administration; the duration of use/abuse; and the time and amount of last use as well as when the symptoms or complaints developed and how they have progressed. (2)
Stimulants typically can be detected in urine for approximately 24 to 48 hours following use and, maximally, for 3 days.
The Consensus Panel feels strongly that cultural competence in treatment extends beyond racial/ethnic sensitivity to understanding the mores of groups bound together by gender, age, geography, sexual preferences, criminal activity, substance use, and medical and mental illnesses. The Consensus Panel therefore recommends the following:
In stimulant use disorder treatment today, providers have the opportunity to move the role of scientifically based approaches into the forefront of the treatment effort. Recent findings from basic and clinical research serve as the foundation of the evolving treatment system for stimulant use disorders and have yielded an entirely new set of strategies and tools to assist in the treatment of stimulant-related clinical disorders.
As knowledge of stimulants and brain functioning continues to grow, new approaches are likely to be forthcoming.
The development of pharmacotherapies for the treatment of stimulant use disorders is a major priority of current research efforts, and it is likely that these efforts will provide some important new options in the near future. As these new treatments are introduced into the service delivery system and integrated into mainstream care, it will be essential for training tools, including this TIP, to be regularly updated.
In the early 1980s, thousands of people began to seek treatment to help them with their struggle to stop using cocaine. The U.S. health care system was rapidly overwhelmed. To many treatment experts who had spent their careers treating heroin addicts and alcoholics, the idea that someone would require "treatment" to discontinue cocaine use was a novelty. Among the first questions asked of the individuals seeking treatment were, "What do you need treatment for?" and "Why don't you just stop using?" Today, much more is known about addiction to cocaine and other stimulants. Although researchers, clinicians, and treatment providers have gained insights into why it is so difficult for stimulant users to stop using and why they need treatment, it is only recently that the substance use disorder treatment field has determined the most appropriate treatment approaches for these individuals.
When the U.S. cocaine epidemic was just beginning, there was a generally held assumption, even among addiction experts, that cocaine was not "truly addicting." A popular joke during this period was that "cocaine is God's way of telling you that you have too much money."
The cocaine epidemic that began in the 1970s peaked in the 1980s and slowly declined in the mid 1990s (Golub and Johnson, 1997). The pattern was similar to the first epidemic that occurred 30 years after cocaine hydrochloride was first isolated from coca leaves in 1885. During the first epidemic, physicians mistook cocaine's powerful stimulant properties as a cure for depression, morphine addiction, chronic tuberculosis, and a long list of other disorders. Physicians and other "healers" prescribed the drug for a range of maladies, and cocaine soon became the major active ingredient in many popular medicines, tonics, and elixirs (including the original formulation of Coca-Cola ®).
Eventually, however, the adverse effects of high-dose and consistent use were recognized. This recognition soon led to legislative responses. First, the Pure Food and Drug Act of 1906 required the proper labeling of cocaine "and other narcotics" on proprietary medicines. Second, the Harrison Act of 1914 virtually eliminated the use of cocaine-containing patent medicines by forbidding their manufacture and sale. But cocaine did not simply go away, and sometime after 1970, a complex set of social and economic circumstances conspired to prompt its return. Increased demand for the drug initially drove supply, and subsequently, its widespread availability and reduced cost fostered greater demand and abuse.
The cocaine epidemic of the 1980s and early 1990s affected a broad spectrum of American society, with the advent of crack cocaine hitting major cities the hardest. A less publicized and more geographically circumscribed stimulant epidemic is the rise of methamphetamine (MA) in the West and Midwest. The spread of MA has brought many of the health, legal, and social problems like those associated with cocaine to smaller and more rural communities.
These stimulant epidemics have had a devastating impact on American society. The impact of illicit stimulant abuse has affected international politics, the U.S. legal system, and the U.S. health care system. "Freebasing," "crack houses," and "coke fiend" have all entered the American lexicon to describe elements of the stimulant epidemic. As the end of the 20th century nears, the powerful psychostimulants cocaine and MA and their derivatives have joined opiates and alcohol as primary targets in the efforts to combat substance abuse and dependence. But on the positive side, the pressing need to effectively deal with stimulant epidemics and treat people with stimulant use disorders has produced a tremendous amount of scientific and clinical research. The results of this research have broadened our knowledge of the human brain and expanded our understanding of substance use disorders.
The slow response of major U.S. institutions to the dangers of cocaine and MA was partly due to an ignorance of the basic biological and psychological effects of these powerful psychostimulants. The knowledge gained over the past two decades on the properties of these substances can help treatment providers and other health professionals to understand, prevent, and treat the problems created by the use and abuse of cocaine and MA. This Treatment Improvement Protocol (TIP) summarizes the latest research as well as first-hand clinical experience of substance use disorder treatment professionals.
Since the mid-1980s, there has been an explosion of knowledge about the effects of cocaine and MA. Because these psychostimulants alter the functioning of the body and the brain so profoundly, physicians, nurses, psychologists, social workers, marriage and family counselors, and substance abuse counselors must understand the profound biological aspects of stimulant addiction. New areas of expertise include the relevant pharmacology, neurobiology, psychiatric and psychological manifestations, and appropriate treatment approaches for stimulant abuse and dependence. The new findings suggest that neurological impairments may last up to 2 years after cessation of stimulant use (Hoff et al., 1996; Melega et al., 1997a).
This TIP presents current knowledge of the nature and treatment of stimulant use disorders. The TIP is designed to be a resource that provides scientifically established information and presents it in a manner that makes it available and relevant for both clinicians and "front line" treatment providers. In addition, the document reviews what is known about treating the medical, psychiatric, and substance abuse/dependence problems associated with the use of cocaine and MA. The treatment section emphasizes those approaches that have been established with empirical support. However, because the field of treating stimulant use disorders is barely a decade old, a set of treatment techniques supported by leading addiction specialists has been included after review and synthesis by the members of the Consensus Panel.
The Consensus Panel believes that scientifically derived knowledge should serve as the foundation of treatment for stimulant use disorders. Findings from basic and clinical research efforts funded by the National Institute on Drug Abuse (NIDA), as well as other government and private institutions, have given treatment providers an entirely new set of strategies and tools to assist those with stimulant-related clinical disorders. The field of stimulant use disorder treatment presents the perfect opportunity to move the role of scientifically based approaches into the forefront of the treatment effort. There is very little in the way of a "traditional treatment system" for stimulant use disorders, and therefore, there should be fewer "turf battles" over the implementation of new treatment approaches.
The Consensus Panel recognizes that most traditional treatment approaches are still viable and highly regarded by providers, and that new treatment techniques may be initially viewed with distrust. Continuing research and clinical experience will ultimately reveal the efficacy of such treatments.
At this time, the approaches with the greatest empirical support are a variety of psychosocial-behavioral strategies, delivered in outpatient settings. However, as knowledge of stimulants and brain functioning rapidly increases, thanks to active research funded by Federal agencies and private foundations, new approaches will soon be forthcoming. The development of pharmacotherapies for the treatment of stimulant use disorders is a major priority of the current research efforts, and it is likely that these efforts will provide some important new options in the near future.
For purposes of this TIP, the substances included in the category of "stimulants" include the derivatives of the coca plant (cocaine hydrochloride and its derivatives) and the synthetically produced amphetamines, with emphasis on the major illicitly produced and abused drug of this category, MA (in its various forms). Certainly there are other stimulants that are more widely used (e.g., caffeine) and that produce major health and social problems (e.g., nicotine); however, an extensive discussion of issues associated with these substances is beyond the scope of this document. Although considered drugs of abuse, MA analogs--compounds with similar molecular structures but not necessarily similar effects, sometimes called "designer drugs"--such as MDA (3,4-methylenedioxy-amphetamine) and MDMA (3,4-methylene-dioxymethamphetamine)--have not been studied adequately for inclusion in this document.
Cocaine hydrochloride is extracted from the leaves of the coca plant (Erythroxylon coca), which is indigenous to the Andean highlands of South America. In its extracted and purified form, it is one of the most potent stimulants of natural origin (Drug Enforcement Agency [DEA], 1995). For thousands of years, the Native Americans in the Andean region have chewed coca leaves to relieve fatigue, much as present-day Americans chew tobacco. Just as tea and coffee are brewed as refreshments or "pick-me-ups," the Andean natives brewed coca leaves into a tea. Furthermore, Andean groups have historically burned or smoked various parts of the coca plant as part of their religious and medicinal practices (Siegel, 1982). However, none of these other uses has had the same impact as purified cocaine hydrochloride.
German chemist Albert Niemann recognized the stimulant properties of the cocaine plant, and in the mid-1800s (ca. 1862) extracted the pure chemical, cocaine hydrochloride. In the early 1880s, the drug's anesthetic properties were discovered, and it was soon used in eye, nose, and throat surgery. As physicians and other prescribers became aware of cocaine's psychoactive properties, it was widely dispensed for anxiety, depression, and addiction treatment (primarily for morphine use).
Extravagant claims of its curative powers increased cocaine's popularity; by the early 1900s, it was the main active ingredient in a wide range of patent medicines, tonics, elixirs, and fluid extracts. It is believed that the original formula of Coca-Cola® that was developed in 1886 by Georgia pharmacist John Pemberton contained approximately 2.5 mg of cocaine per 100 mL of fluid (Coca-Cola Bottling of Shreveport, Inc., et al., vs. The Coca-Cola Company, a Delaware Corporation, 769 F.Supp.671). This formula was sold as a headache cure and stimulant. Another pharmacist bought the rights and founded the Coca-Cola Company in 1892.
By the early 1900s, public health officials were becoming alarmed by the medical, psychiatric, and social problems associated with excessive cocaine use. These concerns from health officials and legal authorities played a major role in initiating and supporting the effort to pass the Harrison Narcotic Act of 1914. This Federal legislation severely restricted the legal uses for cocaine and, for all practical purposes, ended the extensive use and abuse of cocaine in the early part of the 20th century. Interestingly, cocaine hit a low during the 1930s when the advent of amphetamine almost eradicated demand.
From the time of the Harrison Narcotic Act until the 1970s, cocaine use was generally limited to groups on the periphery of society. Legal prohibitions and severely restricted supplies of the drug helped to maintain its low profile. But microcultures of cocaine snorters, swallowers, and shooters remained, and cultivation of coca plants continued in the South American countries that traditionally grew them--Bolivia, Peru, Colombia, and Ecuador.
As the cultural proscriptions against the use of drugs for recreational purposes weakened during the 1960s, cocaine again became part of the American drug scene. Its use increased along with the use of many other psychoactive substances. Snorting was the initial mode, and most experimenters were occasional consumers. They experienced the cocaine euphoria and generally went back to their "normal" lives. Because of this casual use, the fictitious notion arose that cocaine was harmless.
In the 1960s, limited supplies and high prices combined to restrict the use of cocaine to relatively small amounts used by a small number of individuals. Although serious clinical problems were being connected with the use of hallucinogens, barbiturates, and amphetamines, little attention was given to the problems associated with cocaine use because they were rarely seen.
As recently as the late 1970s, many experts and public health officials believed that cocaine was a relatively benign substance and primarily of interest as a "recreational" drug. It was thought that only those who had access to very large supplies of the drug and/or those who were somewhat mentally unstable were at risk for developing problems with cocaine. A notable exception among these experts was the voice of two San Francisco addiction experts who sounded a prophetic warning about cocaine:
In summary, cocaine is a central nervous system stimulant of moderately high abuse potential. At the present time the preferred route of administration is intranasal and the dosage patterns are relatively low. The social rituals surrounding the drug endorse primarily recreational use while the high cost and low availability of the drug produce the current low rate of cocaine abuse in the United States...Most users now use cocaine by the intranasal route at moderately low dosages, while a relatively small percentage use cocaine intranasally or intravenously at high dosages. However, if the drug were more readily available at a substantially lower cost, or if certain socio-cultural rituals endorsed and supported the higher dose patterns, more destructive patterns of abuse could develop. (Wesson and Smith, 1977, pp. 149-150)
Within 5 years of the observation by Wesson and Smith, both essential developments they predicted had occurred. The production of coca in South America expanded from a cottage industry of small groups of subsistence farmers into a major agricultural business that was financed by organized families or "cartels." The manufacture and trafficking of cocaine became a multibillion dollar industry, with profit margins high enough that governments and entire legal systems became corrupted by the influx of cocaine industry money. Supplies of cocaine into the United States increased exponentially. During the early to mid-1980s, according to DEA reports, the estimated amounts of cocaine entering the United States doubled and tripled year after year. These supplies of cocaine made the drug available in purer form and at a more affordable cost to consumers.
Cocaine hydrochloride is generally distributed as a white crystalline powder or as an off-white chunky material. The powder form is usually snorted intranasally. As cocaine became plentiful and less expensive in the early 1980s, its users began to experiment with its various forms and with different routes of administration. Some users began to smoke the powder form by mixing it with tobacco or marijuana. However, those who smoked the powder reported little if any intoxication.
At the same time, users in South America began to smoke base (coca paste), which is one of the products from which cocaine powder is derived (Siegel, 1987). Coca paste is more concentrated than the powder form. Paste smokers report immediate intoxication, with effects similar to those reported by intravenous users. The first hospital admissions for adverse effects of coca paste smoking were in Peru in 1972 (Jeri, 1984). The practice of smoking coca paste appears to have traveled to other countries via illicit cocaine trafficking corridors.
Drug traffickers in the United States learned of the effects of smoking base, but they confused its preparation with that of cocaine freebase, in which the cocaine alkaloid in cocaine hydrochloride is "freed" from the other components (Siegel, 1982). So it was quite by accident that this new process of "freebase" cocaine was discovered. However, its properties were quite unlike those of either coca paste or cocaine powder. Freebase cocaine does not dissolve easily in the blood or mucous membranes of the nasal passages, but it is readily volatilized and can be effectively smoked. The phenomenon of smoking this freebase form was first reported in California in 1974, and by 1980, its use was reported throughout the United States (Siegel, 1982). Today, chunks of the freebase form are most often known as "rock" or "crack."
The next phase in the American cocaine epidemic came when cocaine traffickers saw an opportunity to expand the retail market by delivering to the consumer smaller, more affordable packages of the drug. Chunks of rock cocaine were soon being sold in small glass vials or plastic containers at a cost of $10 to $20. This new retailing effort made a product that was extremely desirable and inexpensive readily available to a much wider user base. The strategy worked extraordinarily well for the cocaine industry.
By late 1985 and early 1986, the retailing of freebase cocaine had swept through most urban centers of the United States. This form was introduced into new markets by highly organized and sophisticated distribution networks. In an effort to make the product distinctive, it was marketed under the new name "crack." There are numerous versions of the origin of the term "crack," but the most likely is that as the freebase cocaine is being heated and volatilized into its smokable form, it makes a characteristic crackling or popping sound.
The crack epidemic was at its worst from 1985 through the end of the decade, although it still remains a serious health and social problem. The introduction of crack into urban communities produced devastating consequences. Health-related problems, rapidly escalating rates of addiction, and an extraordinary wave of street crime and property crime swept through most major American cities. In many areas, street gangs of young males were central to the distribution and sales of crack. Warfare between street gangs battling over turf resulted in many fatalities among gang members as well as innocent bystanders in the community. As drug-related crime escalated dramatically, legal penalties for sales of cocaine and crack were increased, and U.S. jails and prisons rapidly filled with crack users, dealers, distributors, and those involved in the violence associated with the crack trade.
At the peak of the cocaine epidemic, a conservative estimate in the mid-1980s suggested that as many as 8 million Americans used cocaine regularly and that 5 to 8 percent of them had developed a serious cocaine dependence (Cregler and Mark, 1986). The 1988 National Household Survey on Drug Abuse (NHSDA) found that the number of heavy crack and cocaine users rose significantly from 1985 to 1988 (Substance Abuse and Mental Health Services Administration [SAMHSA], 1988). During this period, there was a 33 percent increase among those using crack or cocaine once a week or more; for those using crack or cocaine on a daily or near-daily basis, the rate rose by 19 percent (SAMHSA, 1989).
By the mid 1980s, the use of crack cocaine had replaced heroin use as the main illicit drug problem in the United States. According to the 1997 NHSDA, the number of Americans who used cocaine within the preceding month of the survey numbered about 1.5 million; occasional users (those who used cocaine less often than monthly) numbered approximately 2.6 million, down from 7.1 million in 1985 (SAMHSA, 1998). Only recently have researchers been able to demonstrate a clear decline or stabilization in the use of crack cocaine in U.S. cities (Golub and Johnson, 1997).
Amphetamine, the predecessor to MA, was first synthesized in 1887 and became commercially available in 1932 as a nasal spray for the treatment of asthma (Beebe and Walley, 1995). Amphetamine's stimulant properties were soon recognized, which led to additional medical and functional applications. By 1937, amphetamine was available by prescription to treat the sleep disorder narcolepsy and the syndrome that is now called attention deficit/hyperactivity disorder (AD/HD). After the introduction of amphetamine, other more potent forms were developed and made readily available to the public. These new forms included dextroamphetamine sulfate (Dexedrine) and methamphetamine (Methedrine). Because of their stimulant properties, these new forms were also used to enhance performance. During World War II, MA was widely used by soldiers to fight fatigue and enhance performance. Pilots used MA to stay awake for long periods of time. After World War II, intravenous MA abuse reached epidemic proportions in Japan, when supplies stored for military use became available to the public.
During the 1950s, truckers often used legally manufactured tablets of MA to stay awake on long hauls, athletes used them to enhance performance, and students used them to study long hours and maintain busy schedules. The use of these stimulants during this period was typically not associated with the concept of substance abuse. Although the drugs required a medical prescription, their nonmedical use was generally considered to be simply a method of enhancing performance and usually did not lead to severe addiction. This pattern changed drastically in the 1960s with the increased availability of injectable MA. Intravenous abuse spread among a subculture known as "speed freaks." Evidence soon began to mount that the dangers from the abuse of MA and amphetamine outweighed most of their therapeutic uses.
Eventually, many pharmaceutical amphetamine products were removed from the market, and doctors prescribed the remaining products less freely. As the supply of amphetamine and MA decreased, demand in the black market soon increased, which led to increased illicit production of the drugs. In 1965, greater control measures to curb the trafficking in amphetamine began with amendments to Federal food and drug laws, and the 1970 Controlled Substances Act severely restricted the legal production of these stimulants. Throughout the 1970s, the production and distribution of MA declined nationwide. It was, however, still concentrated in a few cities or regions.
For a number of reasons, the 1970 Controlled Substances Act did not succeed in eliminating MA use. First, the materials and equipment required to produce MA are inexpensive. Second, MA is relatively easy to manufacture. Finally, the active ingredients needed to prepare the drug are relatively easy to obtain. Moreover, clandestine manufacturers developed alternative methods of MA production that were not covered under the law. Furthermore, compared with other stimulants such as cocaine, MA is cheaper and its effects longer lasting.
As the demand for MA increased, so did its production in clandestine laboratories. Because two of the precursor drugs (ephedrine and pseudoephedrine) used to manufacture MA are widely available in Mexico and are easily smuggled into the United States, the clandestine manufacture of MA was initially based in the West and Southwest. In this region, the production and distribution of MA have been historically associated with motorcycle gangs (Feucht and Kyle, 1996).
By the mid-1980s, the number of illegal, makeshift MA laboratories in rural communities in western States had mushroomed, especially in California. In certain areas of California (e.g., San Bernardino, San Diego, San Francisco, and Riverside counties), the problem with MA far outdistanced problems with cocaine even as early as the mid-1980s (Huber et al., 1997). These areas were especially saturated with MA because the illicit laboratories set up to manufacture MA were located in the rural desert areas in proximity to these Southern California urban and suburban areas. The manufacture of MA in these rural regions was preferred by drug manufacturers because the "cooking" process of MA produces a very strong chemical smell, making the home laboratories easy to detect. This phenomenon was evidenced by the tremendous number of MA laboratories seized by law enforcement officials in these locations in the latter half of the 1980s.
There were other indicators of MA's continued spread. For example, data from the NHSDA (SAMHSA, 1988, 1989) revealed that 1 in 10 Californians had used MA at least once in their lives, and that 1 in 50 had used MA within the 12 months prior to the survey. Along with the general increases in MA use, striking increases were observed in MA-related hospital admissions, seizure activity, and deaths (Anglin et al., 1998).
In a further attempt to curb MA production, the Chemical Trafficking and Diversion Act of 1988 amended the 1970 legislation to require wholesalers to record imports and exports of some of MA's chemical precursors, including ephedrine, pseudoephedrine, phenylacetic acid, benzyl cyanide, and benzyl chloride. However, these chemicals could still be easily obtained outside the United States. In particular, the continued availability of precursor chemicals in Mexico resulted in increases in illicit production there, and increasing amounts of MA were smuggled into the United States. Today, Mexican drug cartels have increased their share of the U.S. wholesale MA market (Feucht and Kyle, 1996).
By the late 1980s, MA had spread to other areas of the United States. In Hawaii, MA was being smuggled in from Taiwan and South Korea, and by the summer of 1988, MA was relatively widespread throughout that State. By 1990, MA was being distributed from Hawaii to the U.S. mainland. According to information available from the Drug Abuse Warning Network (DAWN), the estimated number of nationwide emergency room substance abuse episodes involving MA has increased steadily since 1992 (SAMHSA, 1996b). In fact, the number of MA-related episodes recorded during 1994 was almost double the number of episodes in 1989. DAWN statistics indicate the areas hardest hit by MA abuse include San Diego, Phoenix, Los Angeles, Dallas, Denver, and Seattle (see Figure 1-1).
MA--which is known by many street names (see Figure 1-2)--can be swallowed in pill or tablet form, snorted (intranasally) in its powdered form, or injected intravenously in its solution form. Of these three routes of administration, injection leads to the quickest and most intense effects, what users call "the rush." However, MA can be transformed into a high-purity solid form that appears as clear, large, chunky crystals known as "ice" or "glass." This form of MA can be smoked, and because it is a more powerful form, the rush can be immediate and more intense than when administered intravenously. The euphoria reportedly lasts longer than that of smoked crack cocaine.
The ice form of MA first appeared in Hawaii and soon thereafter on the West Coast in the late 1980s. It has been reported that the method of manufacturing and processing MA into ice was imported from the Philippines. The extensive use of MA in some parts of Oahu, especially Honolulu, produced extremely serious concerns about the violence and crime associated with ice use. Ice has continued to be a preferred form of the drug in Hawaii for over a decade. Although health officials on the mainland worried that ice would become a major problem, its availability currently appears to be limited to Hawaii and to some Asian-American communities in Seattle and California (Office of National Drug Control Policy [ONDCP], 1998b). At the time of this writing, it is believed that ice trafficking and availability are very limited in the rest of the United States.
The common perception today is that the cocaine epidemic of the 1980s and early 1990s is in decline and that the "war on cocaine" has been won. The most recent data from the Drug Use Forecasting (DUF) Program (National Institute of Justice [NIJ], 1997b) confirm that in 12 of the 23 DUF program cities, the crack epidemic was in decline by 1996. A substantial decline of at least 10 percent in the overall rate of detected crack/cocaine use was observed in Cleveland, Dallas, Detroit, Houston, Los Angeles, New Orleans, Philadelphia, San Diego, San Jose, and Washington, D.C. Other locations exhibited substantial declines in detected crack/cocaine use among youths, which suggested declines in the overall rate were forthcoming.
Other data, however, indicate that the notion of a declining cocaine epidemic is a misperception. According to the 1996 DUF data (NIJ, 1997b), the crack epidemic in some cities rages on as strong as ever. These locations include Atlanta, Denver, Indianapolis, Phoenix, and St. Louis. There were also some remarkable increases in cocaine-positive tests among male arrestees. In Omaha, the rate of positive tests was 24 percent in 1996, up from 19 percent in 1995. In Miami, cocaine positives increased from 42 to 52 percent. In Indianapolis, cocaine-positive tests grew by 3 percent.
Other studies also indicate that cocaine use is still at high levels. In 1997, NHSDA estimated that approximately 1.5 million Americans used cocaine in the past year (SAMHSA, 1998). Of the 18- to 25- year olds surveyed, 8.9 percent reported using cocaine, and of those age 26 to 34, 18.4 percent reported using cocaine.
A recent annual high school survey, the 1997 Monitoring the Future Study, reports that the use of cocaine, in any form, continues to climb (NIDA, 1998b), whereas cocaine remains the most prevalent drug in the DUF monitoring system (NIJ, 1997b). Figure 1-3 shows the percentage of high school seniors who reported using cocaine and other stimulants.
In 1996, the Drug Abuse Warning Network (SAMHSA, 1996b) reported 487,600 drug-related episodes in hospital emergency departments nationwide. Of these, approximately 20 percent were related to the use of cocaine or crack.
According to Pulse Check (ONDCP, 1997b), the market for cocaine/crack appears to have stabilized, but in many areas, the drug remains in great demand. There have been reports of rising cocaine use in specific communities: the suburbs of Birmingham, Alabama, the Hispanic-American community along the Texas border, and young people in the New York/New Jersey area. In several areas, there is the reported reemergence of powder cocaine.
Unlike the cocaine/crack epidemic of the 1980s and 1990s, the MA epidemic has been regional. But in those areas, MA has taken a strong hold. For example, in some areas of the country, MA has surpassed both alcohol and cocaine as the primary substance of abuse among treatment admissions (Center for Substance Abuse Research, 1997; CSAT, 1997). According to the DEA, MA trafficking and use in the United States have been on the rise over the past few years, as indicated by investigative, seizure, price, purity, and abuse data (DEA, 1996). Recent reports of increased MA use are mentioned in several monitoring and forecasting studies (e.g., DAWN, Monitoring the Future, NHSDA, DUF, and the Treatment Episodes Data Set System).
Increases in the seizures of MA serve as an additional measure of the increasing problem (ONDCP, 1996; CSAT, 1997). For example, in 1995, both the number and weight of MA seizures were the highest in over a decade (CSAT, 1997). In Community Epidemiology Work Group (CEWG) cities, MA-related deaths have been steadily increasing (CEWG, 1996a, 1996b). From 1991 through 1994, MA-related emergency department (ED) episodes increased 256 percent (SAMHSA, 1996a), involving more than 17,000 individuals. DAWN data revealed that MA-related ED episodes had increased by 75 percent from 1993 to 1994.
Although recent reports still place the bulk of MA use in western States including Hawaii (NIJ, 1997b; ONDCP, 1997a), concern continues to grow that the increased number of seizures of clandestine operations and MA-related fatalities in other parts of the country may signal an impending MA epidemic. MA trafficking is increasing in the Southwest, the Midwest, and some southeast regions of the United States (DEA, 1996). In 1996, the DEA seized more clandestine MA manufacturing laboratories in Missouri than in any other State (Samber, 1997). It is reported that MA abuse is very prevalent in several U.S.-affiliated territories in the Pacific (e.g., Guam, the Northern Marianas). According to Pulse Check information, MA is increasing in popularity in Atlanta and Seattle, and it is listed as an "emerging drug" for Austin, Texas; Washington, D.C.; and Columbia, Maryland (ONDCP, 1997b).
There is also a growing amount of anecdotal information on MA's spread from the West Coast. Recent information from the 1996 National Narcotics Intelligence Consumers Committee Report, which describes law enforcement data on drug-related arrests and seizures, indicates that in the last 2 years, MA has increased significantly in the Southeast and the Midwest (DEA, 1997). Although there is little current empirical data to indicate the spread of MA into more rural heartland areas, there are indicators and anecdotal evidence that the manufacture and abuse of MA are having a costly effect in States such as Montana and Iowa (e.g., Kirn, 1998). In fact, the extent of the MA epidemic may be far greater than many experts currently recognize.
Former CSAT Acting Director Camille T. Barry has stated that the particular problem groups for MA abuse are women, gay men, and Asian-Pacific Islanders (Barry, 1998). On a national level, approximately 80 percent of those treated are white Americans. In areas such as Arizona and Minnesota, there has been increasing use in Hispanic and Native American populations. In West Coast cities, the use of MA is increasing among gay men, and use by that population is closely associated with sexual practices (Shoptaw et al., 1997).
Concerns that levels and effects of MA abuse will replicate those of the crack epidemic have put this drug under intense national scrutiny. In response to this concern, The White House launched an initiative called The President's National Strategy for Combating Methamphetamine Abuse. This comprehensive national strategy involves enhanced law enforcement efforts, regulation of precursor chemicals, international initiatives, tougher criminal penalties, legislative proposals, and training of investigators and prosecutors, as well as treatment, prevention, and a public education campaign (ONDCP, 1996). This White House initiative led to passage of the Comprehensive Methamphetamine Control Act of 1996, which in turn created the Methamphetamine Interagency Task Force. The Act set out the Task Force's responsibilities as "designing, implementing, and evaluating the education, prevention, and treatment practices and strategies of the Federal Government with respect to methamphetamine and other synthetic stimulants" (Public Law: 104-237 [10/03/96]).
Several national conferences on MA have been held in the last several years (e.g., CSAT, 1997; ONDCP, 1998c). At a 1997 conference, the ONDCP noted the environmental problems that could stem from MA manufacture:
Methamphetamine is a synthetic stimulant that can produce extreme aggressiveness and violence. Historically, concentrated abuse of this drug was in the West and Southwest but is now reported to be spreading to the Midwest and the eastern portion of the United States. Methamphetamine production entails extreme environmental risks. Clandestine laboratories produce large amounts of toxic waste, much of which is dumped into the ground or in waterways. The cost to clean up these chemical toxins can easily run into thousands of dollars. (ONDCP, 1998c, p. v)
According to various Federal sources, MA is the most widely used and abused of the amphetamines, including amphetamine and dextroamphetamine sulfate (CSAT, 1997). According to the DEA, MA has been the most prevalent, clandestinely produced controlled substance in the United States since 1977 (DEA, 1996). Because of the recent resurgence in its use, the development of new data on its effects, and its ever-increasing national attention, MA is the only amphetamine reviewed in this TIP.
During the 1980s and 1990s, the medical, legal, and societal problems created by the importation, manufacture, sale, and use of the powerful psychostimulants cocaine and MA had a tremendous impact on American society. From the devastating crack epidemic in major U.S. urban centers to the MA-produced destruction in small rural communities in the western and midwestern regions of the United States, the damage caused by the stimulant epidemic has been profound. New knowledge about how these substances influence the basic electrical and chemical activity of the human brain has allowed a better understanding of how and why stimulants affect human behavior, and this knowledge has been rapidly absorbed into the development of new treatment efforts. This TIP provides an overview of (1) the new knowledge about stimulants; (2) the treatment efforts to address stimulant abuse disorders; and (3) the other clinical, medical, and social interventions developed in response to the abuse of and dependence on these substances.
Over the last several decades, research on substances of abuse has vastly improved our understanding of human behavior and physiology and the nature of substance abuse and dependence. Basic neurobiological research has enhanced our understanding of the biological and genetic causes of addiction. These discoveries have helped establish addiction as a biological brain disease that is chronic and relapsing in nature (Leshner, 1997). By mapping the neural pathways of pleasure and pain through the human brain, investigators are beginning to understand how abused psychoactive substances, including stimulants, interact with various cells and chemicals in the brain.
This new information has also improved our understanding of appropriate treatment approaches for different substance use disorders. This chapter describes the effects that cocaine and methamphetamine (MA) use have on the user's brain and behavior, which in turn leads to the stimulant users' unique needs. Knowledge of these effects provides the foundation for stimulant-specific treatment approaches. This knowledge will give treatment providers greater insight into stimulant users and why certain treatment approaches are more effective.
According to National Institute on Drug Abuse Director Alan I. Leshner, Ph.D., the fundamental problem in dealing with any substance of abuse is to understand "the target" (i.e., the user). Therefore, to understand why people take drugs such as cocaine and MA and why some people become addicted, we must first understand what these drugs are doing to their target; that is, how stimulants affect the user.
Discussions of substance abuse and dependence often involve some discussion of the root causes--the societal and risk factors that lead to these conditions. To date, investigators have identified as many as 72 risk factors for substance use and dependence (Leshner, 1998). Among them are poverty, racism, social dysfunction, weak families, poor education, poor upbringing, and substance-abusing peer groups. These risk factors--as well as other environmental and genetic factors--only influence an individual's initial decision to use substances of abuse. But after initial use, an individual continues to use a substance because she likes its effects: Use modifies mood, perception, and emotional state. All of these effects are modulated through the brain; in order to understand this phenomenon, it is important to understand some basic neuroscience.
For substances of abuse to exert their effects, they must first get to the brain. The four most common routes of administering psychoactive (mood-changing) substances are (1) oral consumption (i.e., swallowing), (2) intranasal consumption (i.e., snorting), (3) inhalation into the lungs (generally by smoking), and (4) intravenously via hypodermic syringe.
A swallowed substance goes to the stomach and on to the intestinal tract. Some substances easily pass through the digestive tract into the bloodstream. Other substances are broken down into their chemical components (i.e., metabolized) in the digestive system, thereby destroying the substance.
Substances that are inhaled into the lungs adhere to the lining of the nasal passages (the nasal mucosa) through which they enter directly into the bloodstream. Inhaled substances are usually first changed into a gaseous form by igniting (e.g., marijuana) or volatilizing by intense heat (e.g., crack cocaine, the ice form of MA). The lungs offer a large surface area through which the gaseous form may quickly pass directly into the bloodstream.
Injected substances obviously enter the bloodstream directly, although at a somewhat regulated rate. In these last three routes of administration, substances enter the bloodstream in their unmetabolized form.
Once a substance enters the bloodstream, it is transported throughout the body to various organs and organ systems, including the brain. Substances that enter the liver may be metabolized there. Substances that enter the kidney may be excreted. If a female substance user is pregnant, and the substance is able to cross the placenta, then the substance will enter the fetus' bloodstream. Nursing babies may ingest some substances from breast milk.
To enter the brain, a substance's molecules must first get through its chemical protection system, which consists mainly of the blood-brain barrier. Tight cell-wall junctions and a layer of cells around the blood vessels keep large or electrically charged molecules from entering the brain. However, small neutral molecules like those of cocaine and MA easily pass through the blood-brain barrier and enter the brain. Once inside the brain, substances of abuse begin to exert their psychoactive effects.
The human nervous system is an elaborately wired communication system, and the brain is the control center. The brain processes sensory information from throughout the body, guides muscle movement and locomotion, regulates a multitude of bodily functions, forms thoughts and feelings, modulates perception and moods, and essentially controls all behavior.
The brain is organized into lobes, which are responsible for specialized functions like cognitive and sensory processes and motor coordination. These lobes are made up of far more complex units called circuits, which involve direct connections among the billions of specialized cells that the various substances of abuse may affect.
The fundamental functional unit of the brain's circuits is a specialized cell called a neuron, which conveys information both electrically and chemically. The function of the neuron is to transmit information: It receives signals from other neurons, integrates and interprets these signals, and in turn, transmits signals on to other, adjacent neurons (Charness, 1990).
A typical neuron (see Figure 2-1) consists of a main cell body (which contains the nucleus and all of the cell's genetic information), a large number of offshoots called dendrites (typically 10,000 or more per neuron), and one long fiber known as the axon. At the end of the axon are additional offshoots that form the connections with other neurons. Within neurons, the signals are carried in the form of electrical impulses. But when signals are sent from one neuron to another, they must cross the gap at the point of connection between the two communicating neurons. This gap is called a synapse. At the synapse, the electrical signal within the neuron is converted to a chemical signal and sent across the synapse to the target (i.e., receiving) neuron. The chemical signal is conveyed via messenger molecules called neurotransmitters that attach to special structures called receptors on the outer surface of the target neuron (Charness, 1990). The attachment of the neurotransmitters to the receptors consequently triggers an electrical signal within the target neuron. Approximately 50 to 100 different neurotransmitters have been identified in the human body (Snyder, 1986). Figure 2-2 illustrates a typical synaptic connection and depicts the chemical communication mechanism. Neurotransmitters may have different effects depending on what receptor they activate. Some increase a receiving neuron's responsiveness to an incoming signal--an excitatory effect--whereas others may diminish the responsiveness--an inhibitory effect. The responsiveness of individual neurons affects the functioning of the brain's circuits, as well as how the brain functions as a whole (how it integrates, interprets, and responds to information), which in turn affects the function of the body and the behavior of the individual. The accurate functioning of all neurotransmitter systems is essential for normal brain activities (National Institute on Alcohol Abuse and Alcoholism [NIAAA], 1994; Hiller-Sturmhfel, 1995).
The brain circuit that is considered essential to the neurological reinforcement system is called the limbic reward system (also called the dopamine reward system or the brain reward system). This neural circuit spans between the ventral tegmental area (VTA) and the nucleus accumbens (see Figure 2-3). Every substance of abuse--alcohol, cocaine, MA, heroin, marijuana, nicotine--has some effect on the limbic reward system. Substances of abuse also affect the nucleus accumbens by increasing the release of the neurotransmitter dopamine, which helps to regulate the feelings of pleasure (euphoria and satisfaction). Dopamine also plays an important role in the control of movement, cognition, motivation, and reward (Wise, 1982; Robbins et al., 1989; Di Chiara, 1995). High levels of free dopamine in the brain generally enhance mood and increase body movement (i.e., motor activity), but too much dopamine may produce nervousness, irritability, aggressiveness, and paranoia that approximates schizophrenia, as well as the hallucinations and bizarre thoughts of schizophrenia. Too little dopamine in certain areas of the brain results in the tremors and paralysis of Parkinson's disease.
Natural activities such as eating, drinking, and sex activate the nucleus accumbens, inducing considerable communication among this structure's neurons. This internal communication leads to the release of dopamine. The released dopamine produces immediate, but ephemeral, feelings of pleasure and elation. As dopamine levels subside, so do the feelings of pleasure. But if the activity is repeated, then dopamine is again released, and more feelings of pleasure and euphoria are produced. The release of dopamine and the resulting pleasurable feelings positively reinforce such activities in both humans and animals and motivate the repetition of these activities.
Dopamine is believed to play an important role in the reinforcement of and motivation for repetitive actions (Di Chiara, 1997; Wise, 1982), and there is an increasing amount of scientific evidence suggesting that the limbic reward system and levels of free dopamine provide the common link in the abuse and addiction of all substances. Dopamine has even been labeled "the master molecule of addiction" (Nash, 1997).
When the nucleus accumbens is functioning normally, communication among its neurons occurs in a consistent and predictable manner. First, an electrical signal within a stimulated neuron reaches its point of connection (i.e., the synapse) with the target neuron. The electrical signal in the presynaptic neuron triggers the release of dopamine into the synapse. The dopamine travels across the synaptic gap until it reaches the target neuron. It then binds to the postsynaptic neuron's dopamine-specific receptors, which in turn has an excitatory effect that generates an internal electrical signal within this neuron. However, not all of the released dopamine binds to the target neuron's receptors. Extra dopamine may be chemically deactivated, or it may be quickly reabsorbed by the releasing neuron through a system called the dopamine reuptake transporter (see Figure 2-4). As soon as the extra dopamine has been deactivated or reabsorbed, the two cells are "reset," with the releasing neuron prepared to send another chemical signal and the target neuron prepared to receive it. Substances of abuse, and especially stimulants, affect the normal functioning of the dopamine neurotransmitter system (Snyder, 1986; Cooper et al., 1991).
Psychologists have long recognized the importance of positive and negative reinforcement for learning and sustaining particular behaviors (Koob and LeMoal, 1997). Beginning in the late 1950s, scientists observed in animals that electrically stimulating certain areas of the brain led to changes in mental alertness and behavior. Rats and other laboratory animals could be taught to self-stimulate pleasure circuits in the brain until exhaustion. If stimulants such as cocaine or amphetamine were administered, for example, sensitivity to pleasurable responses was so enhanced that the animals would choose electrical stimulation of the pleasure centers in their brains over eating or other normally rewarding activities.
The process just described in which a pleasure-inducing action becomes repetitive is called positive reinforcement. Conversely, abrupt discontinuation of the psychoactive substances following chronic use was found to result in discomfort and behaviors consistent with craving. The motivation to use a substance in order to avoid discomfort is called negative reinforcement. Positive reinforcement is believed to be controlled by various neurotransmitter systems, whereas negative reinforcement is believed to be the result of adaptations produced by chronic use within the same neurotransmitter systems.
Experimental evidence from both animal and human studies supports the theory that stimulants and other commonly abused substances imitate, facilitate, or block the neurotransmitters involved in brain reinforcement systems (NIAAA, 1994). In fact, researchers have posited a common neural basis for the powerful rewarding effects of abused substances (for a review, see Restak, 1988). Natural reinforcers such as food, drink, and sex also activate reinforcement pathways in the brain, and it has been suggested that stimulants and other drugs act as chemical surrogates of the natural reinforcers. A key danger in this relationship, however, is that the pleasure produced by substances of abuse can be more powerfully rewarding than that produced by natural reinforcers (NIAAA, 1996).
On a short-term basis, stimulants exert their effects by disrupting or modifying the normal communication that occurs among brain neurons and brain circuits. Cocaine and MA have both been shown to specifically disrupt the dopamine neurotransmitter system. This disruption is accomplished by overstimulating the receptors on the postsynaptic neuron, either by increasing the amount of dopamine in the synapse through excessive presynaptic release or by inhibiting dopamine's pattern of reuptake or chemical breakdown (Cooper et al., 1991).
The use of cocaine and MA increases the amount of available dopamine in the brain, which leads to mood elevation (e.g., feelings of elation or euphoria) and increased motor activity. With cocaine, the effects are short-lived; with MA the duration of effect is much longer. As the stimulant level in the brain decreases, the dopamine levels subside to normal, and the pleasurable feelings dwindle away.
A growing body of scientific research based on animal research and brain imaging studies in humans suggests that the chronic use of stimulants affect dopaminergic neurons in limbic reward system structures (e.g., the VTA, nucleus accumbens). These effects may underlie addiction to stimulants. Although the neurochemical pathways of stimulant addiction are not definitively established, a few researchers have found evidence of changes in the structure and function of brain neurons after chronic stimulant use in humans. Some researchers propose that the changes may come from dopamine depletion, changes in neurotransmitter receptors or other structures, or changes in other brain messenger pathways that could cause the changes in mood, behavior, and cognitive function associated with chronic stimulant abuse (Self and Nestler, 1995).
Animal studies have demonstrated that high doses of stimulants can have permanent neurotoxic effects by damaging neuron cell-endings (e.g., Selden, 1991). The question of whether stimulants can produce similar effects in humans remains to be answered. Researchers hope that recently developed brain imaging techniques will help provide the answer. At this time, there is only speculation that such permanent damage may underlie the long-term cognitive impairments seen in some chronic stimulant users. The continuing development and application of new technologies will help expand our knowledge of the neurological effects of stimulants in humans. (The medical aspects of stimulant use disorders are discussed in Chapter 5.)
Addiction is a complex phenomenon with important psychological and social causes and consequences. However, at its core, it involves a biological process: the effects of repeated exposure to a biological agent (a substance) on a biological substrate (the brain) over time (Nestler and Aghajanian, 1997). Ultimately, adaptations that substance exposure elicits in individual neurons alter the functioning of those neurons, which in turn alters the functioning of the neural circuits in which those neurons operate. This eventually leads to the complex behaviors (e.g., dependence, tolerance, sensitization, craving) that characterize addiction (Koob, 1992; Kreek, 1996; Wise, 1996; Koob and LeMoal, 1997).
A general definition of substance abuse is the habitual use of a substance not needed for therapeutic purposes, such as solely to alter one's mood, affect, or state of consciousness. The continued abuse of the substance may lead to adverse physiological, behavioral, and social consequences. A substance-dependent individual will continue his use despite these adverse consequences. Moderate chronic use or severe short-term use of substances may lead to abuse, which may eventually lead to addiction components (Ellinwood, 1974; Hall et al., 1988; Kramer, 1969).
Chronic substance abuse results in a complex set of physiological and neurological adaptations. These adaptations are simply the body's attempt to adjust to or compensate for substance-induced impairments. Repeated exposure to a substance can also lead to adaptations in the reward circuitry that opposes and/or neutralizes a substance's effects (i.e., counteradaptation). Substance addiction (or substance dependence) is manifested by (1) psychological craving (see the following section); (2) tolerance (the need for increasing amounts of the substance to reproduce the initial level of response, or sometimes to simply stave off the unpleasant effects of withdrawal); (3) sensitization (discussed in the section on the medical effects of stimulants); and (4) symptoms of withdrawal upon cessation of use, indicating physiological dependence.
Social and behavioral manifestations of dependence include the reduced ability to function at work or home and may include displays of erratic, moody, or anxious behavior.
Similar to other substances of abuse, moderate chronic use or severe short-term use of stimulants in any form may lead to abuse or dependence (Ellinwood, 1974; Hall et al., 1988; Kramer, 1969). Clinical observations of abuse patterns for both cocaine and MA have noted that, in general, there is an estimated 2- to 5-year latency period between first use and full-blown addiction. However, clinical experience and anecdotal evidence suggest that the latency period may be shortened to less than 1 year by rapid routes of administration (e.g., injection, smoking) and increased stimulant purity (e.g., ice, crack). With increasing use, the user may develop tolerance to the effects of stimulants and may need to keep increasing the amount taken to produce the desired psychological effects. As chronic abuse progresses, users prefer the stimulant over enjoyable activities and eventually may prefer it over food and sex (Hall et al., 1988). At that point, the individual will usually continue her use even when faced with continuing adverse consequences--the hallmark of substance dependence. Abrupt discontinuation of the psychoactive substance following chronic use generally results in discomfort, dysphoria, and behaviors consistent with craving. The user is now motivated to use a substance in order to avoid discomfort and dysphoria. This shift from substance use as positive reinforcement to negative reinforcement is, perhaps, one of the foremost characteristics of late-stage addiction.
The degree to which learning and memory sustain the addictive process has only recently been addressed. Researchers believe that each time a neurotransmitter like dopamine floods across a synapse, circuits that trigger thoughts and memories and that motivate action become hardwired in the brain. The neurochemistry supporting addiction is so powerful that people, objects, and places associated with substance use are also imprinted on the brain.
Craving, a central aspect of addiction, is a very strong learned response with powerful motivational properties often associated with specific memories (i.e., conditioned cues and triggers). Cues--any stimuli (substance-using friends, locations, paraphernalia, moods) repeatedly paired with substance use over the course of a client's addiction--can become so strongly associated with the substance's effects that the associated (conditioned) stimuli can later trigger arousal and an intense desire for the substance and lead to relapse. High relapse rates are common in cocaine addiction even after physical withdrawal and abstinence have been achieved.
Brain-imaging studies have shown that cue-induced drug craving may be linked to distinct brain systems involved in memory (e.g., London et al., 1990; Stapleton et al., 1995). Brain structures involved in memory and learning, including the dorsolateral prefrontal cortex, amygdala, and cerebellum, have been linked to cue-induced craving (Grant et al., 1995). A network of these brain regions integrates emotional and cognitive aspects of memory and triggers craving when it reacts to cues and memories. These cues and memories also play an important role in reinforcing substance use (Grant et al., 1995).
Most substance treatment programs recognize the power of these factors in triggering relapse and warn clients to avoid everything previously associated with their substance use--a tall order for a client in an urban environment saturated with the substance and its associated reminders. Treatment approaches that address these learning and memory issues of addiction may prove effective. For example, Childress developed treatment strategies to help clients reduce craving and arousal during encounters with substance-related stimuli (Childress, 1994). In the laboratory, clients are given repeated, passive exposure to substance-reminding cues in a substance-free protected environment. The research finds that initial arousal and strong craving produced by the cues eventually decrease (Childress, 1994). Better understanding of the relationship of learning and memory to the addiction process may lead to new treatment approaches.
The recent development of noninvasive brain imaging has created a powerful new tool for demonstrating not only the short-term effects of substance use, but also the longer term consequences of chronic substance abuse and addiction. These tools have allowed researchers to boldly go where they previously could not--literally into the depths of a living human brain. Such noninvasive techniques can depict normal and abnormal functioning of different brain areas by measuring metabolic activity (i.e., glucose utilization). They can identify substance-induced structural changes and physiological adaptations. Through a combination of techniques, they can observe the altered "processing" of information in various circuits as the brain responds to substance use.
Using these techniques, investigators have been able to identify brain structures involved in craving, map the emotions of substance users, plot the neurobiological basis of substance-induced euphoria, and more. For example, researchers have used magnetic resonance imaging (MRI) and spectroscopy to see how brain structures change as substances produce their effects. Others have used a functional imaging technique called phosphorus magnetic resonance spectroscopy (31P MRS) to show that chronic substance abuse is accompanied by abnormal metabolism in some areas of the brain that seems to return to normal when people stop using substances (Christensen et al., 1996). Positron emission tomography (PET) has revealed subtle alterations in the dopamine receptors of stimulant users' brains (Iyo et al., 1993). More recent PET studies have demonstrated long-term vulnerability to chronic stimulant abuse (Melega et al., 1997a; Volkow et al., 1996, 1997b). Another PET study has established a dose-response relationship between cocaine and the drug's subjective effects: The greater the amount of cocaine that is administered, the greater the high experienced by the user (Volkow et al., 1997a).
Other researchers combined electroencephalograms (EEGs) and MRI to produce a topographic brain map showing increased electrical activity (in the form of beta waves) during stimulant withdrawal (Herning et al., 1997). Mapping EEG activity during stimulant use and withdrawal may allow researchers to further document substance-induced neuropsychological impairments.
Although much is known about the effects of stimulants in animals, there is little such knowledge of these effects in humans (CSAT, 1997). The continuing development and application of new technologies such as noninvasive brain imaging will allow researchers to improve their understanding of how stimulants affect the human brain. Greater understanding of the underlying neuronal impairments of stimulant abuse will aid in the development of new, more effective treatment approaches.
Substances of abuse--and stimulants in particular--appear to increase the brain's levels of free dopamine in a dose-dependent manner; that is, more dopamine is available when higher doses of the substance are administered (Nash, 1997). The higher the substance dose, the greater the feelings of elation, euphoria, and satisfaction, and as the dopamine levels and pleasurable feeling subside, there is an intense desire to replicate the feelings of pleasure by administering another dose of the substance. This tendency toward repeated administration is characteristic of stimulant abuse and underlies most of the other effects of stimulants, as well as most other addictive substances.
Continued use often leads to adverse consequences, which may include neuropsychological impairment and diminished physical health. Work performance and social and family relations can be adversely affected, and the risk of arrest and conviction on drug-related charges increases. Even after a stimulant user discontinues use, impairments in cognition and functioning may persist, and there may even be persistent psychiatric symptoms (Wada and Fukui, 1990). Cravings for the stimulant's effects tend to linger, even after abstinence has been achieved, and the potential for relapse is high.
The general acute effects of stimulants have been well documented. Among a range of physiological responses, stimulants are known to raise both systolic and diastolic blood pressure, increase heart rate, increase respiration rate, increase body temperature, cause pupillary dilation, heighten alertness, and increase motor activity (CSAT, 1997).
Acute effects from excessive doses include dangerously rapid and erratic heartbeat, cerebral hemorrhaging, seizures/convulsions, respiratory failure, stroke, heart failure, brain damage, coma, and death (CSAT, 1997).
Stimulants are also known to cause sensitization (i.e., the opposite of tolerance), for which multiple drug exposures eventually produce some new adverse reaction. For example, in animals, seizures do not typically occur after single low-to-moderate doses. But with repeated exposure, an animal can become sensitized to the stimulant and may have a seizure after a single, previously harmless, dose.
Although the effects of chronic stimulant abuse in humans has not been well documented, some of the chronic effects include organ toxicity, compromised health (e.g., underfed, malnourished, poor hygiene), dental problems, and dermatitis. (For a complete discussion of the medical aspects of stimulant use, see Chapter 5.)
The immediate psychological effects of stimulant administration include a heightened sense of well-being, euphoria, excitement, heightened alertness, and increases in motor activity. Stimulants also reduce food intake, reduce sleep time, and may increase socialization activities. Stimulants may also enhance performance of certain types of psychomotor tasks.
High doses may result in restlessness and agitation, and excessive doses may produce stereotypic behaviors (repetitive and automatic acts). Chronic psychological effects of stimulant use include various psychiatric disorders such as psychosis, paranoia, and suicidal tendencies.
There may also be neurological impairments and cognitive deficits. Tolerance eventually develops to many of the behavioral effects of stimulants, so that increasing doses are required to achieve the same effect.
The administration of stimulants--particularly if smoked or injected intravenously--can have immediate and often very intense effects on the user. However, the "rush" and subsequent feelings of euphoria may just as quickly fade. The intense effects can be followed by a dysphoric "crash." To stave the crash, the user will administer another dose of the stimulant, which again produces a rush and subsequent crash.
This cycle will go on again and again. This pattern of frequently repeated dosing known as bingeing may continue for up to 3 sleepless days. During this period, the user may not eat and may lapse into a severe depression, followed by worsening paranoia, belligerence, and aggression--a period known as tweaking.
Bingeing eventually ends when the user depletes his supply of stimulants or simply collapses from sheer exhaustion. The stimulant user may then sleep for several days, only to awaken and begin the cycle again.
There is a great amount of anecdotal evidence on the relationship of stimulant use and various sexual behaviors. Stimulants may be used during sexual activities to intensify sexual acts, heighten pleasure, lengthen the duration of intercourse, and lessen inhibitions. The abuse of stimulants is also known to lead to uncharacteristically aberrant or deviant sexual behaviors, the use of prostitutes, and HIV high-risk behaviors (Rawson et al., 1998b).
Cocaine and MA can be smoked, snorted, injected, or ingested orally. These various routes of administration differ in dosage and in the rapidity and intensity of effect, which may affect the course of abuse and dependence. Some evidence suggests that the onset of dependence varies according to the route of administration (DEA, 1995). The route of administration affects the amount (i.e., the dosage) of stimulant delivered to the brain, the speed at which it is delivered, and the resulting intensity of the stimulant's effects.
The intensity of the psychological effects of stimulants, as with most psychoactive drugs, depends on the dose and rate of entry to the brain. For example, when snorted, stimulants generally reach the brain within 3 to 5 minutes, and the resulting rush or "high" may not be perceived as immediate; intravenous administration produces a rush in about 15 to 30 seconds; whereas smoking produces an almost immediate effect (ONDCP, 1998a).
Because of the rapidity of delivery and higher dosages, the smoking of stimulants produces a high that is said to be far more intense than those produced through other routes of administration.
Route of administration has been shown to affect the resulting level of stimulant in the body. In a comparison of oral ingestion versus smoking, Cook measured plasma levels of MA after oral administration and after smoking (see Figure 2-5) (Cook, 1991). For the oral dose of 0.25 mg/kg, plasma levels began to rise 30 minutes after ingestion and reached peak levels (approximately 38 ng/mL) at about 3 hours after ingestion. Plateau levels were maintained until about hour 4 and then slowly declined over the next 4 hours. After smoking (dose of about 21 mg/subject), MA plasma levels approximated 80 percent of peak levels within minutes, peaked (approximately 42 ng/mL) at about 2 hours after administration, maintained a peak plateau for another 2 hours, and then slowly declined over the next 4 hours. By comparison, plasma levels of smoked cocaine and smoked MA both peaked rapidly (Cook, 1991). Plasma levels of smoked cocaine (dose of 21 to 22 mg/subject) peaked at approximately 240 ng/mL at about 5 to 10 minutes after administration. Cocaine plasma levels then declined rapidly, dropping to 50 percent of maximum level (half-life) within 1 hour. Smoked MA (dose of 21 to 22 mg/subject) neared peak levels (approximately 50 ng/mL) within minutes and continued to climb until about 2 hours after administration before slowly tapering off. However, half-life levels were not reached until 11 to 12 hours after administration (see Figure 2-6). The long plateau effect and the much longer half-life of MA versus cocaine suggests considerable dangers in repeated smoking of MA because remarkably higher plasma concentrations could be expected to occur if the dose is repeated, even at fairly long intervals (Cook, 1991). Because stimulants exert their effects in a dose-dependent manner, the route of administration has serious neurological, medical, psychiatric, and neurocognitive implications for the stimulant user and the treatment provider. The intense highs produced by smoking crack cocaine or ice MA can lead to equally intense "lows" during withdrawal (e.g., dysphoria, depression, irritability, anxiety, paranoia, dramatic mood swings). The subsequent cravings can also be extremely intense. Prolonged high doses of stimulants (e.g., during bingeing) may cause greater and longer lasting neurological damage, which in turn may lead to greater and longer lasting cognitive deficits. The onset of stimulants' chronic effects varies across individuals, and although there are few data to predict how long it will take for any user to begin suffering from the chronic effects of stimulant abuse and dependence, onset is probably related to the size of the doses, the frequency of dosing, and the route of administration. However, in general, the higher the doses and the more frequently the doses are administered, the more quickly the chronic effects will appear. From a treatment provider's perspective, a stimulant user's preferred route of administration affects the extent and depth of chronic effects and, therefore, has implications for choosing the most appropriate treatment approach. (See Chapter 4 for a full discussion on the practical applications of treatment strategies. For a discussion on route-of-administration effects on toxicity and adverse reactions, see Chapter 5.)
Cocaine has two main pharmacological actions. It is both a local anesthetic and a central nervous system (CNS) stimulant--the only drug known to possess both of these properties. Cocaine exerts its local anesthetic actions by blocking the conduction of sensory impulses within nerve cells. This effect is most pronounced when cocaine is applied to the skin or to mucous membranes. Cocaine hydrochloride has approved medical use as a local anesthetic in surgery of the nose, throat, and larynx.
As a CNS stimulant, cocaine affects a number of neurotransmitter systems, but it is through its interaction with the dopamine and the limbic reward system that cocaine produces some of its most important effects, including its positive reinforcing effects. The major influence of cocaine on the dopamine system is its ability to block the synaptic reuptake of dopamine. As shown in Figure 2-7, cocaine does not directly "stimulate" the dopamine system; rather, it causes the system to be stimulated by preventing dopamine from being removed from the intracellular space. Cocaine blockade of the dopamine reuptake transporter extends the availability of dopamine in the synaptic space where it continues to occupy the dopamine receptor and causes the postsynaptic neurons to fire for a longer than normal period. This extended firing of the postsynaptic neurons resulting from prolonged dopamine receptor activity is initially experienced subjectively by the cocaine user as a positive sensation involving increased energy, arousal, and stimulation. A recent study has demonstrated a relationship between the intensity of cocaine's subjective effects and the degree to which the dopamine reuptake transporter is blocked (Volkow et al., 1997a). The effects experienced by users of cocaine during the initial period of their use are generally mood-altering in a positive manner (Washton, 1989). For most individuals, the subjective experience of the acute effects includes a generalized state of euphoria in combination with feelings of increased energy, confidence, mental alertness, and sexual arousal.
Under the proper environmental circumstances, individuals also report that cocaine heightens their ability to concentrate, increases sexual excitement, increases their sociability, and decreases any preexisting shyness, tension, fatigue, depression, or boredom. Many people feel more talkative, more intensely involved in their interactions with others, and more playful and spontaneous when high on cocaine. As they come down from their cocaine high, some users experience temporary unpleasant reactions and aftereffects, which may include restlessness, anxiety, agitation, irritability, and insomnia. During this "rebound" period, suspiciousness, confusion, hyperarousal, and other elements of paranoid thinking may also appear.
With continued escalating use of cocaine, the user becomes progressively tolerant to the positive effects while the negative effects steadily intensify (Washton, 1989). Users report that the highs are not so high anymore and the rebound aftereffects increasingly lead to a dysphoric, depressed state. These new "lows" may reinitiate the desire for more cocaine in a futile attempt at mood normalization. The search for the previously experienced high will eventually leave the user in the depths of depression and despair.
When snorted, smoked, or injected intravenously, cocaine quickly produces an intense high. But because it is rapidly metabolized in the body, this high is short-lived. Efforts to replicate the initial high prompt users to take it often and repeatedly. Because of its mechanism of action, cocaine may produce strong craving and strong conditioning of cues associated with its use. The results of a recent brain imaging study revealed that cocaine's fast uptake in the brain has a major role in its rewarding effects and that its fast clearance from the brain sets the stage for frequent abuse, craving, and the binge pattern in cocaine addiction (Volkow et al., 1996). These researchers postulated that dopaminergic activation of the limbic reward system is involved in the rewarding effects of cocaine (and perhaps most, if not all, substances of abuse) and that continued activation of this system may lead to long-term changes in the associated neural circuits that perpetuate the compulsive administration of this drug (see below).
Cocaine use also has acute adverse physiological effects involving the respiratory, cardiovascular, and central nervous systems. Systemic toxicity to cocaine is characterized by profound sympathetic stimulation of the respiratory, cardiovascular, and central nervous systems, producing a combination of medical and psychological effects sometimes known as the "cocaine reaction." (For additional details on the medical aspects of cocaine abuse, see Chapter 5.)
For many cocaine users, the initial experimental use begins to give way to more frequent or regular use. With continued, intensified use, the "casual" user will progress to the abuse stage, requiring larger and larger doses to achieve the desired effects. The abuser may become obsessed with the rituals of cocaine administration and may find that many common items or situations trigger cravings for the drug. For some, abuse will lead to full-fledged addiction. There will be overwhelming urges and cravings for cocaine, and there may be an inability to self-limit or control use. The cocaine addict will deny that she has a drug use problem and will continue use of cocaine despite the negative consequences. At this stage, the adverse consequences of cocaine addiction have probably affected all aspects of the user's life. The addict has succumbed to what Dr. Sidney Cohen called cocaine's "pharmacological imperative" (Washton, 1989). Figure 2-8 lists the characteristics of the stages of cocaine addiction.
The timetable for the onset of the chronic effects of cocaine use varies across individuals and may depend on the size of the doses, the frequency of dosing, and the route of administration. There are no data to base a prediction on how long it will take for any individual to begin to suffer from the chronic effects of cocaine use. However, similar to the effects of MA, the higher the doses and the more frequently the doses are administered, in general, the more quickly the chronic effects of cocaine will appear. In addition, intranasal administration (snorting) is associated with slower onset of chronic effects than if cocaine is smoked (freebase or crack) or injected intravenously. Clearly, there are tremendous individual differences in this timetable, with some individuals reporting an ability to use for extended periods with few signs of negative consequences and others reporting a very dramatic onset of severe detrimental effects as soon as a few weeks or months after initiation of cocaine use.
Physically, the cocaine addict may appear thin or even emaciated. Personal hygiene and self-care may be neglected, and medical and dental needs may go unmet. Because cocaine suppresses appetite, the user fails to eat properly and may suffer from vitamin deficiencies. Severe addicts may ignore food, clothing, shelter, and sexual needs.
Psychologically, cocaine's chronic effects are exactly the opposite of the desired initial effects. Continued cocaine use increases paranoia and confusion and causes an inability to concentrate and an inability to perform sexually. The same substance that acutely produced a mild sensation of arousal and decreased fatigue, on a chronic basis results in chest pain, insomnia, anorexia, episodic depression, and extreme fatigue.
From a treatment perspective, the curious thing is that the user often accurately perceives and attributes the pleasurable, acute effects to the use of cocaine. However, he frequently is unable or unwilling to recognize the relationship of the negative, chronic effects to the use of cocaine. Although it may be dramatically apparent to family and friends that the effects of cocaine are highly detrimental and destructive to the user, the user may insist that the use of cocaine is very helpful and beneficial. The extensive health-compromising effects of cocaine abuse are apparent when examining the behavioral and psychological profile of clients as they enter substance treatment. Generally, these clients exhibit a pronounced disruption in healthy behaviors and an elevation in dysphoric emotions including anxiety, depression, and paranoia (Castro et al., 1992).
Chronic abuse of cocaine may cause neuropsychological impairments (O'Malley et al., 1992) as well as neuropsychiatric syndromes (Herning et al., 1997). Cocaine-induced cognitive deficits can last up to 3 months after heavy use before baseline functioning is restored. In their review, Weinrieb and O'Brien found a strong association between the chronic use of cocaine and deficiencies in short-term auditory recall, memory, concentration--especially for nonverbal abstracting and problem solving--and slowed reaction time (Weinrieb and O'Brien, 1993).
The physical, psychological, and cognitive effects of chronic cocaine use reflect the underlying physiological effects; at the heart of these effects is cocaine's impact on the neurotransmitter dopamine.
Although research efforts continue to focus on the effects of MA, there are limited data on MA's effects on humans (CSAT, 1997). Much of the available information has been surmised from the literature on cocaine. However, the physiological effects of MA are generally similar to those of cocaine: increased heart rate, elevated blood pressure, elevated body temperature, increased respiratory rate, and pupillary dilation. Other acute effects include rapid heart rate, irregular heart rate, and irreversible, stroke-producing damage to small blood vessels in the brain.
MA's psychological effects, like those of cocaine, include a heightened sense of well-being or euphoria, increased alertness, increased vigor, decreased food intake, and decreased sleep time. Acute administration has been shown to increase socialization in humans. High doses may produce repetitive and automatic acts in both humans and animals, and in humans, may cause irritability, aggressive behavior, excitement, auditory hallucinations, and paranoia (delusions and psychosis). Dangerously elevated body temperature and convulsions occur with MA overdoses, and if not treated immediately, can result in death. With continued use, tolerance develops to the behavioral effects, and repeated exposure may produce sensitization. MA users tend to engage in violent behavior. Mood changes are common, with the user rapidly changing from friendly to hostile.
The course of addiction to MA is believed to be similar to that of cocaine. Even the underlying neurological effects of MA are similar to the effects produced by cocaine: increased levels of free dopamine in the brain's limbic reward system. The MA "withdrawal syndrome" is like that of cocaine, but due to the longer effects of MA, withdrawal may be more intense and protracted. Several hours after last use, the MA user experiences a drastic drop in mood and energy levels. Sleep--which may be promoted by the use of secondary substances such as alcohol, barbiturates, and benzodiazepines--finally begins and may last for several days. Upon awakening, the user may experience severe depression, perhaps lasting for several weeks. While in this depressed state, the user has an increased risk of suicide. But once the user feels that she "has recovered" from a bingeing episode, cravings set in, and the cycle often begins again.
There are three essential differences between cocaine and MA. First, MA is thought to enhance CNS neurotransmission by increasing the presynaptic release of dopamine within the limbic reward system. Second, recent research has demonstrated MA's neurotoxicological effects in animals and has begun to support the hypothesis that MA is neurotoxic in humans. Unlike cocaine, MA does cross neuronal cell membranes and will enter into the microscopic sacs (called vesicles) where neurons store dopamine. MA is believed to damage the storage sacs and the neurons' axonal endings such that dopamine leaks uncontrollably into the synapse (see Figure 2-9). MA can also cause neurotoxicity indirectly by mobilizing dopamine out of the safe storage vesicles within the neuron and into the neuron's cytoplasm (i.e., the cell's internal material) where it is converted to toxic and reactive chemicals. Third, cocaine is rapidly metabolized by plasma and tissue enzymes, whereas MA is metabolized at a much slower rate, which results in a longer duration of action (Cook, 1991; ONCDP, 1998b). Although the half-life (effective duration of action) of cocaine is 1 to 2 hours, a single dose of MA may produce an effect for 8 to 12 hours. The fact that MA is metabolized at a slower rate also allows more time for MA to exert its neurotoxicological effects.
The sustained high plasma levels suggest considerable dangers in repeated smoking of MA because remarkably higher plasma concentrations could be expected to occur if the dose is repeated, even at fairly long intervals (Cook, 1991).
Chronic abuse of MA may result in inflammation of the heart lining and, among users who inject the drug, damaged blood vessels and skin abscesses. Chronic users may also have episodes of violent behavior, paranoia, anxiety, confusion, and insomnia. Heavy users show progressive social and occupational deterioration. Psychotic symptoms may sometimes persist for months or years after use has ceased.
Some of the most frightening research findings about MA suggest that its prolonged use not only modifies behaviors, but literally changes the brain in fundamental and long-lasting ways. Animal studies have shown that chronic use of MA can significantly reduce brain dopamine levels for up to 6 months after last use, with less significant reductions persisting for up to 4 years. MA impairs the functioning of both the dopamine system and the serotonin system (serotonin is another important CNS neurotransmitter). MA-induced neuronal toxicity is specific to certain brain regions (primarily the limbic reward system), and this toxicity is reflected both biochemically and anatomically. The adverse effects produced by MA are often long-lasting, and there is some speculation that some types of damage may be permanent. Finally, these impairments in brain functioning may underlie the cognitive and emotional deficits seen in many MA users. Understanding the chronic effects of MA use is essential for treatment providers who serve this population.
Animal studies have shown that high dose regimens of MA significantly deplete neurotransmitter levels, particularly those of dopamine (e.g., Seiden et al., 1976). Subsequent studies replicated these findings (e.g., Ricaurte et al., 1980) and demonstrated that these depletions were evident up to 4 years after cessation of MA administration (Woolverton et al., 1989). A more recent study demonstrated that chronic amphetamine exposure in monkeys could produce long-term effects on the brain's ability to produce dopamine (Melega et al., 1997a). Significant depletion of dopamine persisted 6 months later; even after 1 year, the brain dopamine levels were only at 80 percent of their preexposure levels. In a radiotracer study of humans, Iyo and colleagues (Iyo et al., 1993) revealed reductions in dopamine receptor binding availability in brain areas such as the frontal cortex and striatum in MA users. Although there is little current evidence on MA's chronic effects in humans, animal research has proven that prolonged or heavy use of MA dramatically reduces the brain's ability to produce dopamine.
Numerous animal studies have demonstrated that MA can damage both dopamine and serotonin systems (e.g., Peat et al., 1983; Robinson and Becker, 1986; Seiden et al., 1976; Trulson and Trulson, 1982a, 1982b; Wagner et al., 1979). MA toxicity occurs after repeated high-dose administration, and it is selective for certain neuronal systems, particularly those in the limbic reward system (e.g., striatum, substantia nigra, nucleus accumbens). Within these brain circuits, MA has been shown to reduce the number of nerve fibers, impair normal physiological functioning, and destroy both axons and axon terminals (i.e., at synaptic junctions). These studies have also shown that MA toxicity is highly dependent on dose, route of administration, and frequency with which the drug is given.
Prolonged or heavy use of MA decreases the brain's ability to manufacture dopamine. This impairment may persist for up to 1 year after the user has stopped taking MA. Researchers now believe that those changes in dopamine and the damage done to dopamine and serotonin neurons are responsible for the chronic effects of MA use that are much more pronounced than the acute effects.
If MA does indeed cause damage to dopamine and serotonin systems in humans, then there are ramifications to consider. One of the outcomes of chronic MA use is psychosis. Psychotic individuals are often treated with drugs to reverse or return their brain functions to normal, and most antipsychotic medications work by changing the activities of the dopamine and serotonin neurons. The unanswered question is: Will antipsychotic medications be able to effectively treat MA-induced psychoses in individuals whose dopamine and serotonin systems have been impaired by chronic MA abuse? To date, there have been few, if any, studies investigating antipsychotic medications for the treatment of chronic MA abuse and dependence.
In summary, although there is much evidence of MA's neurotoxicity in animals, the issue of whether MA causes permanent damage to dopamine and serotonin neurons in humans remains very much an unanswered question. Because of the inherent dangers associated with this type of research, the information will have to come from postmortem studies, advanced neuroimaging studies, and the development of new strategies for detecting neurotoxicity--possibly through the use of operant behavioral pharmacology. Finally, the degree of neurotoxicity must be placed in perspective, and the functional consequences require further scrutiny to determine the impact of chronic MA abuse on human brain function.
Recent research has shown how stimulants such as cocaine and MA exert their effects on the user's nervous system and change the user's feelings, emotions, and behavior. There is now a greater understanding of neurological reinforcement systems, how substance use can lead to dependence, and the roles that craving and memory play in sustaining addiction. Although there is currently a dearth of research regarding the neurologic, medical, psychiatric, and neurocognitive effects of stimulants in humans (CSAT, 1994b, 1997), animal studies have demonstrated cocaine's and MA's ability to disrupt normal brain function and cause long-lasting and perhaps permanent neurological impairments. With continuing research and the development of new imaging technologies, the full extent of these stimulants' effects on humans will eventually be revealed. This new information should continue to assist in the development of new and improved approaches for treating stimulant use disorders.
As large numbers of people with substance use disorders began to seek treatment in the early and mid-1980s, "treatment" for stimulant abuse and dependence was invented. The treatment system that responded most quickly was the 28-day Minnesota Model hospital industry. The number of these 28-day, for-profit treatment units grew at an astonishing rate. Tens of thousands of cocaine users were treated in these programs with strategies adapted from the treatment of alcoholics. Today, there is little empirical evidence to assess the efficacy of these efforts.
During this same period, all sorts of unconventional remedies, including health foods, amino acids, hot tubs, electronic brain tuners, and other "New Age" treatments emerged and disappeared. Research efforts to develop scientifically based treatments began during this period with behavioral techniques like contingency contracting (Anker and Crowley, 1982) and medication evaluations including the use of desipramine (Norpramine) (Tennant and Rawson, 1983; Gawin and Kleber, 1984). Over the 15-year period since these early efforts, an entire stimulant use disorder treatment literature has developed.
This chapter reviews the current state of knowledge on the treatment of stimulant use disorders, beginning with the approaches that have the most rigorous empirical support. Other approaches with less support in the scientific literature are presented later in the chapter. At the end of the chapter is a review of the current state of medications research in the treatment of stimulant use disorders. Although at the time of this writing there were no medications with demonstrated clinical efficacy, the ongoing program of research sponsored by the National Institute on Drug Abuse (NIDA) holds great promise for important treatment advances. For this reason, the current state of this research effort will be reviewed.
This chapter reviews what is scientifically known about effective treatments for stimulant use disorders. To be judged effective, a treatment must have been tested and demonstrated to be effective in a randomized clinical trial. Many psychosocial and pharmacological treatments have been investigated in such trials. Several psychosocial treatments for stimulant abuse and dependence have been found to be effective, but to date, no reliably effective pharmacological treatments have been found. What has been learned so far about the use of psychosocial and pharmacological treatments for stimulant use is summarized below. Almost all of the information has been gleaned from studies conducted with cocaine users. Similar studies with methamphetamine (MA) users have not been reported. However, evidence from at least one study indicates that cocaine and MA users respond similarly to psychosocial interventions, suggesting that what has been learned from cocaine users may be applicable to MA users (Huber et al., 1997).
Randomized clinical trials are the best available method for determining whether an intervention improves health. A randomized clinical trial is a prospective study comparing the effect of some intervention against a control intervention in groups of clients who are assigned randomly to the respective treatment groups (see Friedman et al., 1983). In such trials, clients from a particular population sample (e.g., all admissions to clinic X during 1998 meeting a particular list of inclusion and exclusion criteria) are randomly assigned to the intervention under study or to a control condition. Random assignment ensures against possible bias in assigning particular kinds of clients to the respective groups and helps to distribute evenly between the groups any subject characteristics that might influence outcomes.
Prospective means that clients in the groups are studied from the start of the intervention as opposed to retrospectively compiling the information after the intervention is completed. Retrospective observations tend to be less accurate because of relevant information not being collected, getting lost, or being distorted through reliance on people's recall. Having a comparison or control group is essential because most problems have some level of variability (i.e., they wax and wane over time) and because many health problems resolve over time without any formal treatment. The most effective way to determine whether any observed changes are due to the treatment being investigated rather than natural variability is by comparing against a similar group of clients who either received no treatment or received a standard treatment.
Some of the alternatives to randomized clinical trials common in the substance use disorder treatment field can provide useful information but have serious limitations that must be recognized. For example, following a group of clients who received a particular treatment in the absence of a comparison group can be informative in terms of characterizing what has happened to them (e.g., percentage relapsed, percentage who received additional treatment, amount of change from pre- to posttreatment), but such observations do not permit any scientifically valid inferences regarding the role of the treatment provided to any of the changes observed during followup. For that purpose, a comparison group is necessary. Any changes observed might have occurred in the absence of treatment. Without a comparison group there simply is no way to rule out that possibility. Similarly, when clients themselves select group membership, as opposed to being assigned by the researcher, one cannot make valid inferences about the role of treatment to outcome. For example, comparing treatment completers to dropouts is common and may be informative in terms of characterizing how the groups fared, but it is not scientifically valid to infer that any differences observed between them were due to the different amounts of treatment received. It very well could be that some other factor (e.g., differences in the amount of other demands on their time) was responsible both for the differential retention rates and for the subsequent differences observed at followup.
The psychosocial interventions demonstrated thus far to be efficacious in randomized clinical trials with stimulant users share a common feature of incorporating well established psychological principles of learning.
It is impossible to quantify all aspects of psychosocial treatment. Often therapists working in the same clinic and using the same treatment approach differ greatly in terms of the progress their clients make. Put simply, some therapists appear to be very effective and others relatively ineffective. The use of carefully prepared treatment manuals reduces such between-therapist differences. Treatment manuals increase the likelihood that therapists will deliver a uniform set of services to their clients. That does not come at the cost of eliminating therapists' clinical judgment or flexibility. A carefully prepared manual recognizes the importance of clinical judgment and flexibility in addressing the individual needs of clients and incorporates those features into the manual. Considering that effective treatments and associated manuals are available, using them is prudent and will help ensure that clients receive the services that research has shown to be effective.
Community reinforcement is an individualized treatment designed to promote lifestyle changes in several key areas that are conducive to successful recovery (see Meyers and Smith, 1995; Sisson and Azrin, 1989). First, clients with spouses who are not themselves users are offered marital therapy to improve the quality of their relationships in a reciprocal and rewarding manner. Second, clients who are unemployed, employed in jobs that are high-risk for substance abuse, or need vocational assistance for some other reason receive help in that domain. Third, clients are counseled and assisted in developing new social networks and recreational practices that promote and support recovery. Self-help participation is not mandatory but is often used as an effective means of developing a new social network. Fourth, various types of skills training are provided depending on individualized client needs, including substance refusal and associated skills, social skills, time management, and mood regulation training. Finally, clients with alcohol use disorders and no medical contraindications are offered a program of disulfiram (Antabuse) therapy coupled with strategies to support medication compliance.
Voucher-based incentive programs are designed to facilitate retention in treatment and to promote initial abstinence from stimulants. Such incentive programs are known as contingency management interventions, which are discussed further below. In this treatment, clients earn vouchers that are exchangeable for retail items contingent on stimulant-free urinalysis results during the initial 12 weeks of the 24-week treatment. Urinalysis monitoring is conducted thrice weekly during that period. The voucher system used in studies evaluating this treatment included incentives worth a maximum of approximately $980 across the course of treatment. Since those studies were completed, others have reported effective voucher programs using lower cost incentives (Tusel et al., 1995); another program obtained all its incentives via donations from community businesses (Amass, 1997), although the efficacy of this program was not evaluated. How valuable the incentives must be to significantly improve outcomes has not yet been evaluated.
The efficacy of the community-reinforcement-plus-vouchers approach, delivered as a comprehensive, stand-alone treatment, is supported by three randomized clinical trials (Higgins et al., 1993b, 1994b, 1997), with several additional trials supporting the efficacy of particular components of that approach (e.g., Silverman et al., 1996). The first trial examined the efficacy of this treatment compared with standard outpatient counseling (Higgins et al., 1993b). Treatment was 24 weeks in duration with 6 months of additional followup. The community-reinforcement-plus-vouchers treatment retained clients significantly longer and documented significantly longer periods of continuous stimulant abstinence than did standard counseling. For example, 58 percent of clients assigned to the community-reinforcement-plus-vouchers treatment completed 24 weeks of treatment compared with 11 percent of those assigned to standard counseling. Furthermore, of the clients in the community-reinforcement-plus-vouchers group, 68 percent were documented to have achieved 8 weeks of continuous cocaine abstinence, and 42 percent had 16 weeks of continuous abstinence. Of the clients in the standard counseling group, only 11 percent were documented to have achieved 8 weeks of continuous cocaine abstinence, and only 5 percent had achieved 16 weeks of continuous abstinence. Followup assessments revealed another important difference: Greater cocaine abstinence was documented--at 6, 9, and 12 months after treatment entry--in the group that received community-reinforcement-plus-vouchers treatment than in those who received standard counseling (Higgins et al., 1995).
A detailed manual (Budney and Higgins, 1998) that was designed specifically to guide clinicians in the day-to-day implementation of this approach was published recently by NIDA and is available at no cost via the NIDA Clearinghouse (1-800-729-6686) or can be downloaded from the website http://www.nida.nih.gov/TXManuals/CRA/CRA1.html
The voucher system mentioned above is a contingency management intervention (also referred to as contingency contracting). Contingency management is a well-known behavioral intervention that is designed to increase or decrease desired behaviors by providing immediate reinforcing or punishing consequences when the target behavior occurs. Contingency management has been used with considerable effectiveness in the treatment of a variety of types of substance use disorders and is very useful for treatment planning because it sets concrete short-term and long-term goals and emphasizes positive behavioral changes (Stitzer and Higgins, 1995). However, relying exclusively on punitive consequences in contingency management interventions is not recommended because doing so can promote early treatment dropout (Stitzer et al., 1986).
The voucher program has been demonstrated to be efficacious when delivered apart from the community reinforcement treatment. Silverman and colleagues, for example, demonstrated that vouchers contingent on cocaine-negative urinalysis results increase cocaine abstinence in methadone maintenance clients who abuse cocaine (Silverman et al., 1996). Tusel and colleagues demonstrated reductions in all illicit substance abuse with contingent vouchers (Tusel et al., 1995).
Although vouchers are a well-supported contingency management intervention for increasing abstinence in stimulant users, other methods are also effective. Examples among methadone maintenance clients are take-home methadone doses (which eliminate the need for methadone clients to visit the clinic daily to consume their medication under staff supervision) (Stitzer et al., 1992), continuance of methadone maintenance treatment contingent on abstinence from cocaine (Kidorf and Stitzer, 1993), and even a simple system wherein publicly displayed gold stars and inexpensive gifts (e.g., coffee cups, gasoline coupons) are earned for substance abstinence and counseling attendance (Rowan-Szal et al., 1994).
Contingent methadone take-home doses have been used effectively when coupled with other treatment services. An excellent example of this was provided by McLellan and colleagues (McLellan et al., 1993). Methadone maintenance clients were randomly assigned to one of three conditions that provided increasing levels of services. Two of the three groups received methadone take-home doses contingent on negative urinalysis results and proof of current employment. These groups also received additional services not provided to the minimal-service group. The two groups given the opportunity to earn contingent take-home methadone doses achieved higher rates of cocaine and opiate abstinence than did clients receiving noncontingent take-home doses.
Iguchi and colleagues investigated whether cocaine abstinence could be increased through contingent reinforcement of compliance with individualized treatment plans rather than negative urinalysis results (Iguchi et al., 1997). Newly admitted methadone maintenance clients were assigned to one of three groups: (1) a control group receiving standard treatment at the methadone clinic (the standard group); (2) a group receiving standard treatment plus monetary vouchers contingent on the submission of substance-free urine specimens (urinalysis-contingent group), or (3) a group receiving standard treatment plus the same monetary vouchers but contingent on completing treatment plan tasks (treatment plan group). The third group demonstrated significantly greater reductions in illicit substance use than did the other two groups.
Contingency management can be effective with more-difficult-to-treat subgroups of stimulant users. For example, a contingency management approach that was efficacious in homeless stimulant users combined nonhospital day treatment with access to work therapy and housing contingent on substance abstinence (Milby et al., 1996). Nearly three-fourths of the subjects in this study were primarily crack cocaine users. They were randomly assigned to receive either enhanced or usual care. Enhanced care consisted of 2 months of clinic attendance for 5.5 hours each weekday, transportation to and from the clinic, lunch, psychoeducational groups, and individualized counseling.
During the last 4 months of the trial, the intensity of day treatment was reduced to allow subjects to participate in a work-therapy program refurbishing condemned houses in which they could live for a modest rental fee. Participation in the work program and housing were contingent on the provision of weekly random urinalysis testing. Drug-positive results precluded subjects from working in the program and required them to vacate the housing within 2 weeks. The work and living arrangements could be resumed on submission of two consecutive substance-free urine specimens. Usual care consisted of twice-weekly, 12-Step-oriented group and individual counseling, medical evaluation and treatment or referral, and referrals to community agencies for housing and vocational services. Enhanced care increased cocaine abstinence significantly at the 2-month assessment, although not at the 6- or 12-month assessments. Enhanced care also produced greater reductions in alcohol use at each assessment and significantly fewer days homeless at the 6- and 12-month assessments.
Pregnant women are another important subgroup with whom contingency management has been evaluated, although only in the form of preliminary studies. In two pilot studies, pregnant women were offered incentives for attendance at prenatal clinics and/or maintaining cocaine abstinence (Elk, in press). Monetary vouchers of increasing value were awarded for each successive substance-free urine specimen and for increased or consistent attendance at prenatal and substance use disorder treatment clinics. Abstinence, retention rates, and compliance with prenatal care visits were generally higher in the contingency groups. In another study, pregnant clients were randomly assigned to receive standard or enhanced methadone maintenance treatment (Carroll et al., 1995a). Standard treatment consisted of daily methadone, weekly group counseling, and thrice-weekly urine testing. Enhanced treatment consisted of weekly prenatal care, weekly relapse prevention groups, and monetary vouchers for every three consecutive substance-free urine samples. Treatment retention was similar in the two groups, and there were no significant differences in the percentage of cocaine-positive urine samples provided by the two groups.
This treatment approach with pregnant women with stimulant use disorders is very preliminary and needs more thorough evaluation. However, these efforts further illustrate the potential utility of contingency management for addressing some of the more daunting clinical challenges in treating stimulant abuse. Other important examples are recent pilot studies (Roll et al., 1998; Shaner et al., 1997) suggesting that contingent monetary reinforcement can reduce cigarette and cocaine use in adult schizophrenic clients and providing evidence that contingent monetary reinforcement can be used to increase medication compliance in tuberculosis-infected stimulant users (Elk, in press).
When considered as a group, contingency management interventions have by far the greatest amount of empirical support for their efficacy in promoting therapeutic behavioral change among stimulant users. Stimulant users are sensitive to systematically applied contingency management interventions. Presently, there is no other treatment strategy about which one can make an equally strong positive statement.
Relapse prevention (RP) systematically teaches clients (1) how to cope with substance craving, (2) substance refusal and assertiveness skills, (3) how seemingly irrelevant decisions can affect the probability of later substance use, (4) general coping and problem solving skills, and (5) how to apply strategies to prevent a full-blown relapse should an episode of substance use occur (Marlatt and Gordon, 1985).
Carroll and colleagues have adapted and demonstrated the efficacy of this treatment approach with cocaine users (Carroll et al., 1991a, 1991b, 1994a, 1994b). In an initial study, RP was compared with interpersonal psychotherapy (IP), which teaches strategies for improving social and interpersonal problems (Carroll et al., 1991a). Retention was better with RP than IP, and trends suggested cocaine abstinence may have been as well, but that difference was not significant.
A subsequent study compared RP and case management (Carroll et al., 1994a); the clients in this study also received either desipramine or placebo. A total of 139 clients were randomized to one of four treatment groups. Case management was designed to provide a nonspecific therapeutic relationship and an opportunity to monitor clients' clinical status. Both treatments were delivered in weekly therapy sessions during 12 weeks of treatment. All clients also received weekly urinalysis testing and other clinical monitoring. All treatment groups improved from pre- to posttreatment on measures of cocaine use and the Addiction Severity Index (ASI) drug, alcohol, family/social, and psychiatric composite scales, but there were no significant main effects for psychosocial (RP vs. case management) or drug treatment (desipramine vs. placebo). At 1-year followup, those clients who received RP reported significantly higher levels of cocaine abstinence than did clients who received case management (Carroll et al., 1994b). Considering RP's focus on teaching skills to prevent a lapse from becoming a full-blown relapse, these delayed effects might be expected. Indeed, similar delayed effects of RP have been reported in studies on treatment of other types of substance use disorders (see Carroll, 1996).
Not all studies with RP have been positive. For example, Wells and colleagues reported negative results in a comparison of RP and 12-Step-based counseling (Wells et al., 1994). No significant differences between the two groups were discerned in retention or cocaine use during the 24-week outpatient trial or at a 6-month followup evaluation.
The Matrix model (originally referred to as the neurobehavioral model) is an outpatient treatment approach that was developed during the mid-1980s for the treatment of individuals with cocaine and MA use disorders (Rawson et al., 1990). The model integrates treatment elements from a number of specific strategies, including relapse prevention, motivational interviewing, psychoeducation, family therapy, and 12-Step program involvement. The basic elements of the approach consist of a collection of group sessions (early recovery skills, relapse prevention, family education, and social support) and 20 individual sessions, along with encouragement to participate in 12-Step activities, delivered over a 24-week intensive treatment period (Rawson et al., 1989).
This treatment model serves as the primary treatment protocol for a network of outpatient treatment offices in Southern California (Matrix Center). In this network of clinics, more than 8,000 people with cocaine and MA use disorders have been treated with this approach since 1985. The client population ranges from professionals and executives to inner-city crack users and indigent rural MA users. In order to adapt to the financial realities imposed by the emergence of managed care, 2-month and 4-month versions of the model have been developed and are currently being evaluated. As the model was developed and refined, an extensive set of data on the value of the treatment approach was collected. The research studies evaluating this treatment approach do not include a randomized clinical trial. However, in seven research projects evaluating the treatment model, application of the model has been shown to be associated with significant reductions in cocaine, MA, and other substance use (Rawson et al., 1993, 1996; Shoptaw et al., 1994). In a project comparing the treatment outcome of 224 cocaine and 500 MA users to the Matrix approach, all indicators suggested a comparable treatment response (Rawson et al., 1996; Huber et al., 1997). Along with a reduction of stimulant and other substance use, treatment participation in the Matrix model has been demonstrated to be associated with a significant reduction in HIV-risky sexual behavior (Shoptaw et al., 1997). See Figure 3-1 for an evaluation of Matrix Center protocols for the treatment of MA abuse and dependence.
People with substance use disorders often have extensive marital, relationship, and family problems. Stable marital and family adjustment is associated with better treatment outcomes. Inclusion of family members in treatment is based on the view that they can provide important support for the client's efforts to change and provide additional information about the client's substance use and other behavior. Interventions directed at improving marital and family adjustment have therefore been judged to have the potential to improve treatment outcome. Studies with alcoholics have supported this hypothesis, at least in part. Few studies have been attempted with stimulant users, however.
One randomized trial conducted with a heterogeneous group of substance users, many of whom were cocaine users, supported marital/family therapy as a means to improve treatment outcome (Fals-Stewart et al., 1996). Subjects were male substance users under current criminal justice supervision, who were living with a spouse during the past year, and who expressed a commitment to sustained substance abstinence. These individuals were randomly assigned to two treatment groups that received an equal number of therapy sessions across 24 weeks of treatment. For one group, those sessions focused exclusively on coping skills. For the other group, sessions consisted of coping-skills training plus behavioral marital therapy. The group that received marital therapy had better relationship outcomes (in terms of more positive dyadic adjustment and less time separated) than did the comparison group, and reported fewer days of substance use, longer periods of abstinence, fewer substance-related arrests, and fewer hospitalizations during the year after treatment. As might be expected, some of those differences dissipated over the course of the followup period, but this study illustrates an important role for behavioral marital therapy for stimulant users who have a relatively stable romantic relationship and who express a commitment to substance abstinence at the initiation of treatment.
Some additional interventions merit mention. Permitting women entering residential treatment to be accompanied by some or all of their children appears to improve retention. In a published controlled study on this topic (Hughes et al., 1995), women entering residential treatment for cocaine use who were permitted to have one or two of their children reside with them were retained significantly longer than women whose children were placed with the best available caretaker (300.4 vs. 101.9 mean days of retention). No other measures of outcome were reported.
Another study described procedures for improving treatment participation (Hall et al., 1994). Clients were cocaine-dependent male veterans. All clients began treatment as inpatients, typically for 2 weeks, and were then encouraged to continue therapy in the outpatient center of the same medical complex. Therapy consisted of individual and group therapy sessions. Participation in the outpatient regimen began either during the inpatient stay, in which case clients kept the same individual and group therapists throughout the inpatient and outpatient phases, or it began after the inpatient stay and subjects were assigned new individual and group therapists on entering the outpatient phase. Having participation in outpatient care begin during the inpatient stay resulted in somewhat better participation after hospital discharge, and significantly better initial (3 weeks) but not later cocaine abstinence.
Woody and colleagues reported that supportive-expressive psychotherapy may help the subset of clients interested in receiving such therapy to reduce their cocaine use (Woody et al., 1995). They studied a subset of newly admitted methadone clients who indicated an interest in receiving psychotherapy and were compliant with attending counseling sessions (less than half the clients admitted). These individuals were randomized to receive supportive-expressive psychotherapy plus substance use counseling or only substance use counseling. Supportive-expressive psychotherapy focused on exploring the role that substances played in relationship problems, troubling feelings, and other problems. Those who received psychotherapy used significantly less cocaine during the 24-week study than those who received only substance use counseling.
Finally, an intervention called "node-link mapping" may be helpful in reducing cocaine abuse (Czuchry et al., 1995; Dansereau et al., 1995; Joe et al., 1994). This intervention uses flowcharts and other methods to diagram relationships between clients' thoughts, actions, feelings, and substance use. Clients were individuals enrolled in methadone treatment who were randomized to receive standard counseling or node-link enhanced counseling. Those who received the node-link mapping appeared to reduce their cocaine use more during 6 months of treatment than those who received standard care, but the effect was not compelling. The node-link-mapping group was using more cocaine at the start of treatment. Although the node-link-mapping group showed a greater reduction from the start to the end of treatment than did the standard group, the absolute amount of cocaine use at the end of treatment was not significantly different. Further studies are needed in which these results are replicated in groups that start treatment with the same level of cocaine use or finish treatment with the node-link-mapping group using significantly less cocaine.
A number of other psychosocial models and approaches have been described, and some used quite widely, for the treatment of stimulant use disorders.
Network therapy is based on the rationale that people can recover from substance use disorders if they have a stable social network to support them in psychotherapeutic treatment. In this model, clients receiving individual psychotherapy develop a network of stable, nonsubstance-using support persons, such as family, partners, and close friends. These support persons learn strategies from the therapist to support the therapeutic process for the individual being treated. They may interact regularly with the therapist, participate in treatment sessions with the client, and be involved in setting up treatment plans for the client.
Empirical evidence for network psychotherapy is scarce. Controlled trials of network therapy for cocaine or other substance use have not yet been published.
Acupuncture is an ancient Chinese therapy in which thin needles are inserted subcutaneously at various points on the body. The technique is based on the belief that the body's normal functioning depends on a balance of two opposite polar energies that flow along lines of the body called meridians. Approximately 1,000 acupuncture points are aligned along these meridians, and their stimulation by the thin needles is believed to correct energy imbalances and enhance the body's natural capacity to heal itself. No controlled outcome studies have been reported supporting the efficacy of acupuncture for the treatment of cocaine or other stimulant use disorders (TIP 10, Assessment and Treatment of Cocaine-Abusing Methadone-Maintained Patients [CSAT, 1994b]).
Inpatient treatment has traditionally consisted of a 28-day stay in a hospital or residential treatment facility, during which daily activities such as self-help groups, group psychotherapy, and relaxation techniques were provided in a structured format. Generally supportive and sometimes confrontational in nature, inpatient treatment was aimed at combating clients' denial and initiating participation in the 12 steps of recovery originally delineated by Alcoholics Anonymous (AA). The major goals of most inpatient treatment programs are detoxification from the influence of chronic substance use and beginning the process of engaging with self-help programs such as AA and Narcotics Anonymous (NA). Treatment components include didactic learning about the processes of addiction and recovery as well as experiential techniques. Often the client's family is involved in special "Family Days" to acquaint them with these issues.
Originally developed for the treatment of alcoholism, the 28-day standard hospital treatment regimen was used especially in the early 1980s, when the numbers of clients seeking treatment for cocaine use disorders began to rise dramatically. This trend peaked in the mid-1980s, when more than half of clients in many private programs were being treated for cocaine abuse and dependence (Rawson, 1986). Most of these inpatient programs were adapted to treat cocaine users with few or no modifications from the alcohol regimens. In the mid-1980s, when cocaine use among middle-class Americans reached epidemic proportions, the standard 28-day inpatient treatment program was the most widely used treatment modality for this population (Rawson et al., 1991a).
Several hospital/residential treatment organizations did attempt to evaluate the effectiveness of their treatment programming for cocaine users. For example, Sierra Tucson, in Tucson, Arizona, conducted a program of outcome research during the 1980s designed to evaluate and improve the efficacy of its treatment efforts for cocaine users. The Hazelden treatment organization compiled an extensive database on the effectiveness of its treatment services with cocaine and other substance users. The Carrier organization has published a series of studies designed to evaluate the effectiveness of their treatment programs (Pettinati, 1991). Although the evaluations were not randomized clinical trials, the information collected in the reports supported the value of the treatment services.
The traditional 28-day inpatient treatment regimen was developed with little input from empirically based research. In the past several years, the use of such inpatient programs has been called into question by insurance providers, and subsequently their use has been steadily declining. As insurance coverage for inpatient treatment likewise began to dwindle, these programs became variable in length. Many programs closed, and others were forced to scale back on the services they provided. Currently, in many cases clients are covered for brief inpatient stays (up to 7 days) for detoxification purposes only, and psychosocial services have been limited. Inpatient treatment programs are widely variable in the credentialing of their staff, but nearly all employ some staff members who are themselves in recovery.
Long-term residential treatment is used for substance users who are deemed to be in need of a structured support system for a sustained period. The structure provided by long-term residential treatment is designed to allow positive changes and stabilization in the client's attitudes and lifestyle. The durations of residential treatment programs vary; at one time, most programs were at least 1 year in duration, but today most are about 6 months, or even only 90 days. Most residential programs, both long-term and halfway houses, are staffed at least in part by people who are themselves in recovery.
Therapeutic communities (TCs), the most common type of long-term residential treatment, are residential treatment programs that usually use group activities directed toward effecting significant changes in the residents' lifestyles, attitudes, and values. They emphasize prosocial behavior and the assumption of responsibility for one's actions. Many referrals to TCs take place through the court system. In fact, TCs originally were designed for heroin-addicted clients with deprived socioeconomic backgrounds and long-term histories of criminal involvement.
Halfway houses are residential treatment programs providing transitional support for individuals who are usually progressing from a more restrictive environment, such as a TC, but who are not yet ready to function independently in the community. These individuals may not need the intensive structured environment of a TC but may not yet be ready for independent living. Requirements of halfway-house programs usually include specified community involvement, such as employment or enrollment in school, and abstinence from mood-altering substances. Evening group activities are structured around residents' work schedules.
Although relatively little empirical evidence exists supporting the efficacy of long-term residential treatment for stimulant use disorders, there is at least some reason to believe that it can be effective (Gerstein et al., 1994; Mueller and Wyman, 1997). Although clinical experience suggests that TCs are effective with a subset of cocaine users, to the Consensus Panel's knowledge no controlled clinical trials have been published supporting their efficacy in the treatment of cocaine-dependent individuals.
There is not yet an effective pharmacotherapy for cocaine use disorders, but this topic is being researched intensively. Because of differences in the neurochemistry of cocaine and MA, there is sound reason to believe that different pharmacotherapies may be needed to treat those two forms of stimulant use (Ling and Shoptaw, 1997). However, because both drugs produce similar effects on the brain's dopamine levels, promising medications for the treatment of cocaine use disorders are also being examined for the treatment of methamphetamine use.
Clinical research on pharmacotherapies for MA use disorders is just getting under way. Medications are being sought to address a range of indications. There is interest in developing agents that can alleviate the medical/psychiatric symptoms caused by MA intoxication and withdrawal. For example, antidepressant medications have been found useful in the treatment of individuals who have discontinued their use of MA (NIDA, 1998c). Also, there is interest in developing medications to treat MA abuse and dependence. Ongoing trials are currently assessing dopaminergic (i.e., dopamine-mediated), serotonergic (i.e., serotonin-mediated), and other compounds (CSAT, 1997).
Pharmacotherapy research for cocaine use disorders was spurred initially by an open-label trial followed by a double-blind, randomized trial supporting the efficacy of desipramine, a tricyclic antidepressant, in producing short-term reductions in cocaine use and craving in outpatients (Gawin and Kleber, 1984; Gawin et al., 1989). In the randomized trial, 59 percent of cocaine-dependent clients treated for 6 weeks with desipramine achieved 3 or more weeks of continuous cocaine abstinence compared with 25 percent of those treated with lithium and 17 percent of those who received placebo (Gawin et al., 1989). Unfortunately, those promising results have not been replicated in subsequent controlled trials with desipramine (e.g., Carroll et al., 1994a; Weddington et al., 1991) or imipramine (Janimine), another tricyclic antidepressant (Nunes et al., 1995). Evidence that clients with less severe cocaine dependence may benefit from treatment with desipramine and imipramine was presented in at least two reports and merits further study (Carroll et al., 1994a; Nunes et al., 1995).
Other antidepressants that have been investigated in primary cocaine users include fluoxetine (Prozac) (Grabowski et al., 1995), maprotiline (Ludiomil) (Brotman et al., 1988), and gepirone (Jenkins et al., 1992). Studies are still in progress with some of these compounds, but none has demonstrated reliable efficacy in reducing cocaine craving or use in controlled trials. Because of cocaine's very pronounced effects in the dopamine system, a variety of different dopaminergic compounds has been investigated, including amantadine, bromocriptine, bupropion, flupenthixol, carbidopa-l-dopa, mazindol, methylphenidate, and tyrosine (see reviews by Gorelick, 1994; Kleber, 1995; Mendelson and Mello, 1996). Open-trial data have sometimes looked promising, but no reliable positive effects have been observed with any of these compounds in randomized trials. The same is true for the anticonvulsant carbamazepine (Kranzler et al., 1995).
Buprenorphine is an opioid drug that is currently being evaluated as a treatment for opiate dependence in the same manner as methadone is used. In the course of this work, observations by several researchers suggested that buprenorphine might be an effective treatment for cocaine use disorders in the population that uses both opiates and cocaine (e.g., Kosten et al., 1992; Schottenfeld et al., 1993). However, other more rigorous clinical studies have failed to find that buprenorphine has efficacy in suppressing cocaine abuse (e.g., Johnson et al., 1995). Research continues on this topic. Currently, there is no convincing evidence showing that buprenorphine causes decreases in cocaine use or is associated with greater reductions in cocaine use than when methadone is used to treat clients who abuse opiates and cocaine (see Silverman et al., 1998).
Use of disulfiram therapy for clients who use both cocaine and alcohol looks promising. The majority of stimulant users meet medical criteria for alcohol dependence, and more than 90 percent are current alcohol users (Grant and Harford, 1990; Higgins et al., 1994a). Disulfiram therapy with social monitoring to ensure medication compliance was used as a standard component in the community-reinforcement-plus-vouchers treatment approach described above. A chart review was conducted on 16 cocaine-dependent individuals who received that treatment (Higgins et al., 1993a). Carroll and colleagues reported results consistent with these findings in a pilot randomized trial (Carroll et al., 1993b). In that study, disulfiram therapy was compared with naltrexone therapy in a population of 18 outpatients who abused cocaine and alcohol. Disulfiram therapy resulted in significantly greater reductions in drinking and cocaine use than naltrexone therapy. Finally, a larger randomized trial on the efficacy of disulfiram therapy was completed recently, and again cocaine use was significantly reduced by disulfiram therapy (Carroll, 1996). A detailed protocol for use of disulfiram therapy with cocaine users is provided in the NIDA manual on community reinforcement plus vouchers mentioned above (Budney and Higgins, 1998).
Finally, an exciting area of research currently being pursued in the basic-science laboratory using nonhuman subjects focuses on the development of potential vaccines against
cocaine use disorders in the form of enzymes or catalytic antibodies. These novel approaches may hold greater promise than more conventional approaches (Ling and Shoptaw, 1997).
The preceding chapter describes what is known about the effectiveness of treatments for stimulant use disorders. This chapter focuses on how to use that information to improve treatment efforts with stimulant users. Whenever possible, treatment recommendations will employ strategies with empirical support. However, because many stimulant use treatment issues have not been systematically researched, the recommendations of the TIP's Consensus Panel as augmented by field review feedback are the basis for other recommendations.
Individuals seeking help for stimulant dependence receive the majority of their treatment in outpatient treatment programs. Accordingly, the treatment strategies described emphasize techniques employed in outpatient treatment programs. However, many if not most of these strategies and techniques can be integrated into programs other than structured outpatient treatment programs.
This chapter describes the key components of the stimulant use disorders in chronological order as they typically unfold to provide clinicians delivering treatment with a clinical road map. Treatment recommendations are offered to systematically address these clinical issues as they emerge.
This chapter is written with the assumption that abstinence from all mood-altering psychoactive drugs is the ultimate treatment and program goal. Although there is debate about the universal appropriateness of this position, the current treatment system in the United States is founded on this philosophy. This chapter also assumes that structured outpatient treatment will be viewed as one interdependent component of a larger substance use disorder treatment process and system. Many stimulant-dependent individuals experience medical problems or emergencies, psychiatric problems or crises, or various social, legal, or employment problems. As a result, although this chapter focuses on outpatient treatment of stimulant abuse and dependence, it acknowledges the critical importance of institutions and processes such as hospitals, medical/psychiatric management, and case management.
This chapter assumes that the client or the potential client is medically and emotionally ready for entry into outpatient care. Chapter 5 describes the medical/psychiatric factors that should be considered to ensure the safe admission of the client into an appropriate care setting. In addition to these safety elements, there are other considerations for some stimulant user groups (e.g., pregnant women, women with children, adolescents, those with coexisting disorders, the severely impoverished, and homeless individuals) in which the use of outpatient strategies may not be appropriate. Treatment considerations for client groups with these special needs are discussed in Chapter 6. Client Worksheets referred to throughout this chapter are located in Appendix B.
Stimulant use disorder treatment is a health care service, and stimulant users are the customers for that service. For a treatment program to effectively meet the needs of stimulant users, it is essential to understand the perspective of the "customer" as she approaches, enters, and participates in treatment. For example, opiate-addicted individuals frequently initiate contact with the treatment system when they have exhausted all resources and are in fear of the discomfort of opiate withdrawal. Their initial overriding priority is for "treatment" to provide medication to prevent or alleviate symptoms of withdrawal. Treatment programs incapable of responding to this client priority are unlikely to successfully engage opiate addicts in treatment.
Stimulant users approach the treatment system with a different set of priorities than opiate users, because for them avoidance of the withdrawal syndrome is not a major motivating factor. The priorities of stimulant users and the assistance they are seeking vary more greatly than those of opiate-addicted individuals. However, there are some common themes in the pretreatment perspective of many stimulant users.
Admission interviews with stimulant users provide substantial evidence that one of the major treatment-seeking considerations for most individuals is that their use of cocaine or methamphetamine (MA) has resulted in negative consequences. These consequences include legal, job-related, medical, family/relationship, financial, and psychiatric problems. Frequently, the treatment-seeking stimulant user is focused more on receiving assistance with these problem areas than on achieving abstinence from cocaine or MA.
Treatment-seeking stimulant users frequently say, "My life is out of control." They point to their excessive behaviors associated with obtaining, using, and recovering from the use of cocaine or MA. These behaviors include, but are not limited to
Accompanying these behaviors is an array of emotional turmoil including but not limited to
As documented in Chapter 5, the use of stimulants produces significant cognitive impairment (van Gorp et al., 1998) and frequently is accompanied by severe paranoia. Users have difficulty concentrating, impaired short-term memory, and a relatively short attention span. Their ability to recognize the interconnectedness of their stimulant use and the chaos occurring in their lives is poor, and the pervading sense of paranoia (especially for MA users) makes the development of a plan to remediate their problems very difficult. In short, it is often difficult for stimulant users to make sense of what is happening to them.
Many uninitiated clinicians are frequently frustrated and angered by what they perceive as a "lack of motivation" or the presence of "denial" in treatment-seeking stimulant users. Few stimulant users enter treatment with unconditional enthusiasm about the goals and methods of treatment. A significant number present for treatment exhibiting hostility, skepticism about the need for treatment, and opposition to fundamental elements of many treatment plans (e.g., cessation of alcohol and secondary substance use, participation in self-help programs). Although many stimulant users profess a strong desire to discontinue stimulant use, their resistance to initiating recommended treatment behaviors is often a source of clinician frustration. The recognition of this ambivalence as an integral part of the stimulant addiction syndrome, rather than as a frustrating impediment to working on "the real treatment issues," can help clinicians recognize the importance of effective techniques to motivate positive behavioral change.
The experience of craving a substance is a hallmark of almost all substance use disorders. However, for stimulant users, the experience of craving plays an important role in the maintenance of drug use. The basic research findings described in Chapter 2 have documented the existence of neurophysiological correlates of stimulant craving. Virtually all stimulant users have experienced craving but have little understanding of the biological underpinnings of this subjective experience. The power and volatility of this craving response can be exceptionally difficult for some stimulant users to resist (especially those who use the rapid delivery ingestion methods of smoking or injection). For many, it is virtually impossible to imagine how "counseling" or some other form of nonresidential treatment will help with this "irresistible force."
This combination of behaviors, attitudes, and emotions is frequently present to varying degrees with the majority of treatment-seeking cocaine and MA users. Other issues that frequently are priorities to treatment-seeking stimulant users include the dysphoria that occurs upon discontinuation of stimulants, often referred to as "the crash" (Gawin and Kleber, 1986); the compulsive sexual behavior of many men (especially MA users), which is often reported as equally or more difficult to control than the drug use (Rawson et al., 1998b); and the discouragement about previous attempts in and outside of treatment to discontinue stimulant use, only to experience relapse to even more severe levels of drug use. This set of attributes is, in many ways, the "raw material" that programs need to address in the treatment of stimulant users.
In one site in Southern California, a group of 500 MA users and a group of 224 cocaine users were treated using the same outpatient protocol (the Matrix manual), in the same office, with the same staff during the same time period (Rawson et al., 1996; Huber et al., 1997). Although there were some substantial demographic and drug use differences between the two groups, their response to the outpatient treatment protocol was virtually identical. MA users presented with higher ratings of depression, hallucinations, and several other symptoms, and exhibited a more prolonged period of symptom remission. Yet the data collected during treatment and at followup suggested comparable response to this outpatient experience.
There appears to be little empirical rationale for designating any one of the following psychosocial approaches as being differentially effective for the two stimulant user groups. Therefore, the following treatment recommendations apply to users of both cocaine and MA.
Programs should maximize treatment accessibility. Research has shown that placing treatment programs in areas convenient to clients is associated with lower attrition rates (Stark, 1992). Treatment should be provided during the hours and on the days that are convenient for clients. If the majority of clients do not work and find boredom and lack of daytime activities a significant contributing factor to substance use, daytime treatment programming may be helpful. For programs with a substantial number of working clients it is essential to have evening hours. Some programs may need multiple sets of hours for different client groups. Programs should be located in the areas that are accessible to clients, such as near public transportation and in a part of town viewed as safe for evening visits. In rural areas, small satellite sites may be needed to bring treatment closer to clients. Facilities should be accessible to individuals with disabilities.
Research has demonstrated the importance of addressing clients' concrete needs, including transportation, housing, and finances (Chafetz et al., 1970). Providers may find it necessary to establish protocols for rapidly addressing transportation barriers, such as by providing bus tokens, bus and cab fare, and vans. Some logistical barriers can be overcome by onsite services, through agreements with subcontractors, or by referrals. These can include providing onsite child care services, referrals to temporary shelters, vouchers for lunches, targeted financial assistance, assistance with paperwork regarding insurance, or filing for disability.
Referrals should not be limited to providing clients with the name, address, and phone number of an agency. Rather, referrals should involve advocacy: networking with agencies and organizations, calling those contacts, and setting up the appointments or visits.
Stimulant users often make their first contact with the treatment system on the telephone or as a result of an exploratory visit to a counselor or treatment program. The manner in which the receptionist, intake worker, counselor, or other staff person handles the initial contact with the prospective client may decide whether or not the individual decides to enter treatment. Timeliness is an important factor too. Having a counselor, intake worker, or other staff person available to answer telephone inquiries immediately for as many hours per day as possible will increase admission rates. Telephone inquiries should be answered without substantial delay (stimulant users are often impatient individuals, who hang up when placed on hold). Taking messages and calling back later will frequently result in a failure to find the individuals; or, when contacted, they may have changed their minds. Having 24-hour hotlines can be useful because some stimulant users or their family members make their initial treatment inquiries during late night and weekend hours.
Seeking help at an addiction treatment program can be a profoundly difficult and painful act. In fact, in many cases, a family member or friend often makes the initial contact with the treatment program. Data from telephone initial contacts to the Matrix Center clinics in Southern California indicate that approximately 45 percent of all initial treatment inquiries are not made by the potential client, but rather are made by a family member or friend.
In some treatment programs, there is a belief that unless the potential client makes the call for the initial appointment, it is inappropriate to schedule one. This policy is apparently based on the belief that requiring substance users themselves to make the initial call helps to reduce client "denial" and decreases the "no show" rate. Analysis of the data from the Matrix calls indicated no significant difference in "no shows" depending on who made the initial appointment. Because ambivalence about treatment is common among treatment-seeking stimulant users, methods to "screen out" those who are "in denial" are counterproductive and impede treatment entry.
The individual's decision to seek help may last for only a brief period of time. As a result, many individuals seeking help fail to show up for their initial appointment if it is scheduled too far in the future. For these reasons, the interview should be scheduled as soon as possible and within 24 hours after clients initially contact the program (Higgins and Wong, 1998). Figure 4-1 discusses the importance of scheduling.
Programs may not always have the resources to conduct thorough intake interviews whenever contacted. However, programs can provide interim services or minimal contact. For example, a brief interview or a partial intake within 24 hours would be preferable to making an appointment several days after the initial contact. The interview might identify any acute needs that require immediate attention. Also, treatment programs can provide orientation meetings in lieu of waiting lists. If a waiting list cannot be avoided, staff members can telephone the individual to express concern for the individual's well-being, conduct mini-assessments, and provide basic recommendations, such as attending a 12-Step meeting. Such efforts can serve as a temporary bridge between the initial contact and a thorough interview and assessment. These interim services can take advantage of fleeting motivations for change.
Many programs conduct multiple assessments, often by several members of multidisciplinary teams. This technique may be useful for some clients, such as those with complex coexisting disorders. However, stimulant-dependent individuals are often irritated by lengthy and repetitive assessments. For such clients, it is essential that client assessments conducted early in treatment not become onerous or barriers to treatment. Accordingly, initial assessments should be brief, focused, and nonrepetitive. There are several clinical assessment questionnaires for stimulant users available in Washton and Rawson et al. (Washton, 1991; Rawson et al., 1991b).
It is important to identify clients' expectations, as well as their fears, concerns, and anxieties. For example, clients with previous treatment experiences may have anxieties about treatment failure. Programs should specifically make efforts to discover clients' worries and identify those issues that can be dispelled through information and education about the program and the treatment process. An important task here is to help eliminate their fear of the unknown.
Individuals need a thorough, clear, and realistic orientation about stimulant addiction treatment. Clients should acquire a good understanding about the treatment process, the rules of the treatment program, expectations about their participation, and what they can expect the program to do for them. They should understand the basic components of treatment, the amount of time that will be involved, and what will happen next. An orientation can help to dispel fears and anxieties and can help to correct misunderstandings. Research has shown that providing effective orientations has a positive effect on program retention (Stark, 1992). Parts of the orientation may need to be repeated, because cognitively impaired stimulant-dependent clients may forget what they have been told.
Motivation research demonstrates strongly and consistently that people are most likely to engage in an action when they perceive that they have personally chosen to do so. In order to perceive that one has a choice, there must be alternatives from which one can choose (Miller, 1985). Research suggests that substance use disorder treatment is more effective when a client chooses it from among alternatives than when it is assigned as the only option (Kissin et al., 1971). The ability to choose also seems to reduce client resistance and dropout (Costello, 1975; Parker et al., 1979). Thus, it is important to provide clients with options and negotiate with them regarding the treatment approaches and strategies that are the most acceptable and promising.
Initial information and instructions should be simple and clear. Although clients with stimulant use disorders will vary, many will have cognitive problems that will limit their ability to follow long and complex instructions or explanations. As noted above, it is valuable to include clients in selecting their treatment plan. However, once the selection is made, it is important to be clear about the specific requirements of the treatment recommendation and the next step in the treatment process.
Whenever possible, family and significant others who support the treatment goals should be involved in the treatment process, including the initial assessment and intake processes. Significant others can provide collateral information regarding the individual's addiction and can be evaluated regarding their potential for helping to promote the treatment goals or for hindering progress.
Significant others should be provided with information about the addictive process, the treatment program, assessment results, and the next steps for themselves as well as for the client. Individuals who walk away from a significant other's assessment process without interacting with program staff members are likely to feel neglected and ignored. Also, significant others can be given information about their role in the addiction process. They also should be provided with information about codependency and self-help for significant others of addicted persons, such as that provided by Al-Anon.
Research has shown that welcoming clients and treating them with respect are important factors in improving immediate and long-term retention (Chafetz et al., 1970). Individuals who contact treatment programs should be treated with courtesy, friendliness, respect, and warmth. The importance of professional demeanor and a respectful attitude toward clients applies to all staff members with whom they have contact, including both clinical and nonclinical staff members. Potential clients should not, for example, be put on hold for long periods of time.
Although it is true that some stimulant-dependent individuals can be difficult and provocative, these clients are often frightened, disoriented, and cognitively impaired. All program staff members should consider the courage that it takes to seek help for treatment and the shame and anxiety that most clients experience entering treatment. Staff members should provide individuals with positive feedback for asking for help and seeking treatment.
A review of treatment research noted that evidence of high levels of therapist empathy is associated with positive treatment outcomes, and empathy was the predominant therapist characteristic associated with positive treatment outcomes (Landry, 1995). Counselors should be warm, friendly, engaging, empathic, straightforward, and nonjudgmental. Although many clients with stimulant use disorders respond poorly to confrontation and pressure, counselors should not hesitate to provide advice, especially behavioral prescriptions. Advice and recommendations should be provided in a caring and helpful way, not in a controlling or confrontational fashion. Counselors should make deliberate attempts to exert calming effects on clients and remain mindful of clients' potential for extreme impulsiveness and irritability.
When stimulant users are treated in a calm and respectful manner, violent reactions are very rare. However, authoritarian and confrontational behavior by the staff can substantially increase the potential for violence.
Aggressive confrontations with clients must be avoided. It is counterproductive to fight resistance to change or resistance to treatment. Rather, take steps that promote the therapeutic alliance. (See Miller and Rollnick, 1991, for an excellent description of these methods.) Confrontational strategies designed to break through the "denial process" are counter-productive and may be dangerous with stimulant users (Lieberman et al., 1973; Milmoe et al., 1967). Client readiness for treatment and motivation for change are not static conditions. Rather, these are dynamic processes that can be increased (or decreased) through counselor efforts. Counselors should cultivate the motivation and readiness of clients for change and growth (Miller, 1995).
Few data support specific recommendations on the appropriate duration for outpatient treatment episodes. Similarly, there is little empirical evidence to guide the selection of session frequency, session duration, or session format (group vs. individual) of outpatient services for cocaine/MA users. However, it does appear accurate to view treatment as a set of procedures that address a series of clinical issues in a fairly predictable sequence. To organize treatment strategies, it can be helpful to view the treatment process as consisting of (1) a treatment initiation period, (2) an abstinence attainment period, (3) an abstinence maintenance phase, and (4) a long-term abstinence support plan.
One important function for any treatment plan is to give clients a clear structure and framework for their treatment experience. This structure sets up specific expectations and provides clients with the benchmarks they need to plan their treatment participation and measure their treatment progress.
There are no data to clearly establish the proper duration for a treatment episode. However, it is necessary to provide clients with a framework for their treatment experience. Many of the research studies and those with extensive clinical experience have used 12 weeks (Carroll, 1996); 16 to 24 weeks (Rawson, 1986; Washton, 1989); or 24 weeks (Wells et al., 1994). In general, it appears that a duration of 12 to 24 weeks, followed by some type of support group participation, is a commonly used framework.
There are reports in the literature that describe treatment plans scheduled from one session per week (Carroll et al., 1995b, 1995c) up to five sessions per week (Washton and Stone-Washton, 1993). One study that reported a negative treatment finding (Kang et al., 1991) reported that once-per-week psychotherapy was not an effective treatment for cocaine users. In general, the majority of reports have used multiple sessions per week (2, 3, 4) for at least the first several months, with a reduction to fewer (1, 2, 3) through month 6.
The session lengths reported in the literature range from 30 minutes to 6 hours. In general, sessions of 45 to 120 minutes in length are most common.
There is tremendous variability regarding the optimal session format. Treatment strategies described in the literature include individual therapy sessions (Higgins et al., 1993a); a specified combination of individual and conjoint sessions (Meyers and Smith, 1995); and a collection of individual, group counseling, classroom didactic sessions, and conjoint session formats (Rawson et al., 1995). Other organizations employ primarily a group approach with individual and conjoint sessions on an ad hoc basis (Washton, in press). There is no research to support the value of one format or combination of formats over another. The most compelling factor in choosing a format may be practical considerations. Individual sessions are generally more flexible for scheduling; group sessions are typically less expensive to deliver. Figure 4-2 presents considerations regarding treatment duration and format.
The only certainty about the treatment framework is that it is critical to give the client clear, specific expectations of his treatment involvement. If the expectation is two individual sessions for 4 weeks followed by one individual session for 8 weeks, or three group sessions per week for 24 weeks, this should be agreed upon in writing by the counselor and client. Clients should have a written schedule of expected attendance they can keep and give to family members who may be involved in treatment.
It does not appear appropriate to deliver these services on an ad hoc or as needed basis. The structure and expectation of a prescribed treatment regimen has clinical value, independent of the contents of the treatment materials. Certainly there may be modifications in the treatment plan as treatment proceeds, based on clinical progress or other considerations; however, the initial contract needs to be specific and clear.
During the first days and weeks of treatment, it is important to remember that although stimulant users do not have to contend with the uncomfortable withdrawal symptoms of the opiate or the alcohol dependent client, they often are experiencing a set of dysphoric symptoms. The initial period of stimulant abstinence is characterized by symptoms of depression, difficulty concentrating, poor memory, irritability, fatigue, craving for cocaine/MA, and paranoia (especially for MA users). The duration of these symptoms varies; however, in general, they typically last for 3 to 5 days for cocaine users and 10 to 15 days for MA users. The severity of these symptoms and the dysfunction they produce may be sufficient to warrant hospital/residential care in order to establish a period of abstinence (see Chapter 5).
The first several weeks of treatment have some relatively simple and straightforward priorities. They are to
The following recommendations for this period can be integrated into a variety of treatment frameworks.
Initiating a routine of treatment attendance involves giving the client a clear expectation of when and where this attendance should occur, what is going to happen when she attends, positive reinforcement when attendance occurs on schedule, and reminders when treatment is missed. During the initial weeks, clients will be early, late, come in under the influence, and frequently be in crisis and confusion. This initial period is an opportunity to "shape" appropriate behavior by reinforcing proper attendance. Staff should remember that simply attending the sessions is a major indication of treatment engagement and should be enthusiastically reinforced. There will be ample time to give clients corrective feedback on being late or missing sessions.
Stimulant-dependent clients appear to benefit from frequent clinic visits, even if the contacts are brief. During the first 2 to 3 weeks, such clients should be scheduled for multiple weekly visits, even if the visits are 30 minutes or shorter (Higgins and Wong, 1998).
One of the most powerful strategies to increase treatment involvement and establish treatment engagement is to use incentives and other tangible positive reinforcers to reward progress in treatment (Higgins and Budney, 1997). The specific reinforcers will differ among client populations. Some clients prefer vouchers for retail items or coupons for fast food; others appreciate clothes for themselves or their children or rebates for payments. Some programs hold brief ceremonies or present certificates. Rowan-Szal and colleagues demonstrated the effectiveness of incentives for attendance at counseling sessions and substance-free urinalyses through the use of "stars" on an awards board (Rowan-Szal et al., 1994).
A primary message that should be conveyed to clients with stimulant use disorders is that they should return to the program, no matter what. Even if they use stimulants or other substances, they should return to treatment. Clients should be given appointment reminder cards, flyers, and schedules, with the message that they are expected to return and that they will always be welcomed back.
Programs should routinely telephone clients who fail to show up for scheduled clinic visits. Clinic staff members should encourage clients to come in for the clinic visit and inquire about any possible crises that may have prevented their participation. Personal letters can also be used as reminders.
Research has demonstrated that providing treatment in smaller groups in friendly, com-fortable environments is associated with lower attrition rates (Stark, 1992). Programs should be prepared for client feedback related to not belonging and not feeling comfortable. Clients with stimulant use disorders often feel that they do not belong in treatment because they are not addicted, because they do not like the appearance of the program, or because they do not feel that they can relate to the other clients.
Rather than simply assuming that these beliefs represent defense mechanisms, programs should take steps to improve the comfort level of the treatment program and experience. For example, whenever possible, programs should take steps to help clients maximize their ability to identify with other clients and not feel alone. This can include establishing a "buddy system" in which a somewhat seasoned client or alumnus is provided with opportunities to dispel fears and concerns about the program and treatment process. If "buddies" are matched according to assumed similarities in background, the process can help clients to feel that they can relate to others in the program.
After an initial assessment interview, it can be useful to ask clients to agree to a "temporary" trial period of abstinence. Counselors can end the first interview with a specific plan for abstinence, such as abstaining from substances of abuse at least until the next clinic visit. Some form of structured preparatory treatment that can act as a bridge to the regular treatment program can be useful for clients who are unwilling to make such a commitment (Obert et al., 1997). These can include a preparatory group therapy that involves motivational enhancement techniques (Miller and Rollnick, 1991). These groups can be brief but frequent, such as three to five times per week, and can include urine testing.
It is important to recognize that an individual may be at different stages of readiness for change (Prochaska et al., 1992) regarding different substances. For example, an individual may have made the decision to stop using stimulants but is still contemplating the decision to stop drinking alcohol. The individual's hesitancy to enter treatment may reflect ambivalence about alcohol, not stimulants. A motivational group may help to move him from the contemplation phase to the decision and action phases with regard to alcohol.
Time planning and scheduling should be promoted as an important way to deter spending a lot of time alone or having big blocks of time without planned activities. Typically, the daily routine of stimulant-dependent individuals revolves around seeking, using, and recovering from the effects of stimulants. To break this pattern, clients can be taught to use basic daily schedules through which they can provide structure and accountability to their lives. Counselors can provide clients with simple daily schedules such as those illustrated in Client Worksheet 1, Daily Schedule and Planner (see Appendix B for client worksheets). Clients should be vigorously encouraged to schedule and plan each day, especially during this early phase of treatment. Clients should be encouraged to plan time for clinic visits, 12-Step meetings, meals, healthy social activities, exercise, recreation, and leisure time.
Immediately upon entering the treatment program, clients should be placed on a mandatory, vigilant, and frequent urine testing schedule. This schedule should continue throughout the treatment process, although the frequency of testing can be tapered as treatment progresses. Urine samples should be taken every 3 or 4 days so as not to exceed the sensitivity limits of standard laboratory testing methods (see the Strategies for Initiating Abstinence Section below for more on urine testing).
Clients should be encouraged to attend a 12-Step program meeting as soon as possible. They should be provided with a schedule of meetings that are easily accessible to them. Participation in self-help groups should be strongly encouraged but not required. Some individuals who refuse self-help participation nevertheless succeed in treatment. Thus, although self-help participation has been shown to be associated with positive treatment outcomes (Landry, 1995) and will be a great resource for many clients, it is not a necessary condition for all clients to succeed.
Many stimulant users, especially those who use MA, will enter treatment exhibiting symptoms of depression and psychosis. Clearly not all stimulant users have co-occurring depressive illness or a psychotic disorder. With most stimulant users these symptoms subside over several days (for cocaine users) or several weeks (for MA users). However, some stimulant users do have a co-occurring depression or thought disorder. During the initial 2 weeks it is important to assess the possible existence of these other psychiatric conditions and, if present, initiate appropriate treatment, including medication. Individuals who express suicidal ideation or planning should be taken very seriously and should be treated as any other potentially suicidal person.
Research demonstrates an association between stimulant use disorders and a variety of compulsive sexual behaviors (Rawson et al., 1998b). These behaviors include promiscuous sex, AIDS-risky behaviors, compulsive masturbation, compulsive pornographic viewing, and homosexual behavior for otherwise heterosexual individuals.
Stimulant-dependent clients can have tremendous concerns and anxieties about the compulsive sexual behaviors that they engage in while using stimulants. Such clients often assume that they are the only ones who have experienced such feelings and engaged in such behaviors. As a result, they may believe that they are perverted sexually or have sexual identity issues. These feelings can be barriers to treatment engagement and retention. Thus, programs can provide education to stimulant-dependent clients about the associations between stimulant abuse and compulsive sexual behavior.
During the initial several weeks of treatment it is important to remind clients that proper sleep and nutrition are necessary to allow the neurobiology of the brain to "recover." Giving clients "permission" to sleep, eat, and gradually begin a program of exercise can help to establish some behaviors that will have long-term utility. These behaviors will also help clients begin to think more clearly and begin to feel some benefit from the initial efforts in treatment.
Clients should leave early treatment sessions with an assurance that the program can provide or secure immediate attention to critical medical and psychiatric problems. Clients should understand that the program will help them to obtain rapid access to medical and psychiatric evaluation and treatment if they need it. Written lists of community and self-help resources are helpful resources. Programs should develop and always have accessible for distribution a variety of self-help and community resource materials to provide to their clients. These materials should include the name, address, telephone number, and descriptions of 12-Step meetings, other self-help resources, medical clinics, social service agencies, temporary housing and shelters, battered women's shelters, and children's resources.
During the first several weeks of treatment, most individuals stop or at least reduce their use of stimulants. However, even if people have difficulty achieving total abstinence, the first several weeks can be considered successful if treatment engagement is established and some initial steps toward abstinence are made. After the initial treatment engagement of 1 to 2 weeks, a clear focus is on the achievement of abstinence. Although there is no clear delineation between clients who are initiating abstinence and those maintaining abstinence, the initiating period occurs roughly from 2 to 6 weeks into treatment.
The primary goals of strategies used in this phase of treatment are to (1) break the cycle of compulsive, repetitive stimulant use, (2) initiate a period of abstinence from all substances of abuse, (3) encourage the establishment of behaviors that support abstinence, and (4) initiate changes in attitude, behavior, and lifestyle that help maintain abstinence. The following section describes techniques for accomplishing these goals.
Initiating abstinence from stimulant addiction is not a mental exercise but a specific plan of behavioral action. To initiate this plan, a basic structure and daily routine must replace the lifestyle dominated by drug seeking, using, and recuperating. Structure, stability, and predictability are provided by a simple plan that clients can follow on a daily basis. The daily structure should incorporate and build around the client's participation in the treatment program. This will include establishing short-term goals, frequent counseling sessions, frequent urine testing, developing a support system, and time planning (Washton, 1989).
Short-term goals should be set immediately and should be reasonably achievable. One such goal is complete abstinence from all substances for 1 week. Because many stimulant-dependent clients engage in binge use, a comparable goal is to achieve a period of abstinence approximately twice as long as the usual time period between binges. Brief, frequent counseling sessions can reinforce the short-term goal of immediate abstinence and establish a therapeutic alliance between the client and counselor. Events of the past 24 hours are reviewed in each session, and recommendations are provided for navigating the next 24 hours. Establishing a social support system and conducting frequent and regular urine testing are also critical to providing structure, support, and accountability.
The daily scheduling exercise described in the previous section continues to be an extremely important organizing strategy through this phase of treatment. Proactively planning time is a direct counterpoint to the impulsive, free-form lifestyle of the substance user. Clients should write down their schedules during session time, and session time should be used to review compliance with the schedule prepared in the previous session. Many clients will find this task difficult and may resist this "regimentation" of their time. However, if counselors reinforce successive efforts to follow such schedules, compliance will improve.
Stimulant-dependent clients in outpatient programs need structure that provides support for engaging in healthy behaviors. Urine testing is part of that structure. It should not be presented or used primarily as an investigative tool or as a method to test the honesty of clients. Rather, it should be used and presented as a means of support for initiating and maintaining sobriety.
Urine testing should be conducted for the primary stimulant and for secondary substances. Testing should be conducted in concert with the clinic visits. During this phase of treatment, urine testing should be conducted no less than once a week. Tests should be spaced so that the results are obtained from a previous test before conducting the next test, which generally means spacing tests no more frequently than every 3 days. Testing should be randomly conducted, although it is advisable to test on days that closely follow periods of high risk, such as holidays, paydays, and weekends. To ensure that the urine is a valid sample from the client, testing should be either observed or monitored through the use of temperature strips.
Most stimulant-dependent clients also use some other substance, such as alcohol or marijuana. They often do not perceive their use of a secondary substance as problematic. Indeed, for many clients, their secondary substance use may not have been associated with adverse consequences or compulsive use. As a result, such clients need help to identify the connections between the use of other substances and their stimulant addiction. Clients should learn that using another substance increases the likelihood of relapse to stimulants (Rawson et al., 1986; Carroll et al., 1993a, 1993b).
Clients should learn that some secondary substances of choice, such as alcohol, can have a disinhibiting effect and lead rapidly to stimulant use (Higgins et al., 1996). A similar finding has anecdotally been reported by MA users with regard to their use of marijuana (Rawson et al., 1996). Clients should learn that the dose or the frequency of use of the secondary substance is not important, but that disinhibiting effects and potent conditioned responses and cues can occur at low doses. Achieving abstinence helps clients learn to develop substance-free coping mechanisms.
Clients can be helped to examine some of the reasons for why they use secondary substances. For example, some stimulant-dependent women use alcohol as a way to tolerate an abusive situation. Also, clients can be taught avoidance strategies for the secondary substance, such as eschewing high-risk situations where alcohol will be served.
Clients are sometimes ready for treatment for the primary substance of choice but not their secondary substance. Thus, secondary substance use is common during this phase of treatment. Although programs should promote abstinence from all psychoactive drugs, clients who use their secondary substance should not be discontinued from treatment solely because of this use. Rather, they should receive treatment strategies to help them decrease the likelihood of doing so in the future.
Contingency management (described in Chapter 3) reinforces desired behavior by providing immediate consequences. It can be used to improve compliance with treatment components and to promote abstinence. It sets concrete goals and emphasizes positive behavior changes.
In contingency management, a specific target behavior, such as providing stimulant-free urine samples, is selected. The target behavior should be easily measured. Next, a specific and desirable contingency is identified and selected as a reward for each time that the target behavior is accomplished. The reward should not be exchangeable for cash, but can have a cash equivalent, such as a cash-equivalent voucher system or nonrefundable movie passes. The link between the targeted behavior and the reward should be specified. Finally, the agreement should be documented in a written contract and should specify the duration and any changes over time in contingencies. Contingency management interventions have been shown in controlled research studies to be effective for helping cocaine users to achieve and sustain abstinence (Higgins et al., 1994b; Silverman et al., 1996).
The process of identifying cues and triggers is dynamic and ongoing and will change over time. For example, as clients learn more about the associations between specific emotional states and stimulant cues, they can become increasingly sophisticated about identifying and avoiding or defusing potential triggers. However, there are several strategies that should be used very early in the treatment process to help clients to avoid certain external or environmental cues that are likely to be potent triggers for stimulant cravings and urges (Washton, 1989). These include discarding drugs, drug paraphernalia, and materials related to substance use; breaking contact with dealers and users; avoiding high-risk places; and developing basic refusal skills.
First, if the client has not already done so, a specific action plan must be developed to find and get rid of all substances (including alcohol) and drug-related paraphernalia. Clients should be encouraged to accomplish this task with the help of a family member, sober friend, or 12-Step sponsor to ensure that all drug-related items are found and permanently discarded. In addition to objects used to prepare or inject stimulants, materials associated with drug use that should be discarded include phone numbers of dealers and prostitutes, pornographic videotapes, containers used to hold drug supplies, mirrors or special tables used to cut stimulants, and weighing scales.
Second, it is essential for clients to develop specific action plans to break contacts with dealers and other stimulant users. When spouses and significant others are themselves stimulant users, it is important to develop a plan to assertively encourage the significant other to also seek help.
Third, an action plan should be developed to help the client avoid high-risk places. This involves identifying places strongly associated with stimulant use and making specific plans to avoid them. This may include taking different routes home from work, going to certain locations at times different than normal, or using a "buddy system" when going to a high-risk area. Finally, a plan of action should be developed to deal with confrontations with acquaintances who are still using stimulants. Clients should prepare specific drug-refusal statements that can be used when they encounter drug-using friends and practice with their counselor and fellow group members. This action plan must include immediately leaving the situation after the encounter. Client Worksheet 5, Action Plan for Avoidance Strategies (see Appendix B), can be used to assist clients develop strategies to avoid potent high-risk cues and triggers.
Clients with stimulant use disorders often do not understand many of the things that they have experienced as a result of their stimulant use, such as impulsive behaviors, anger and hostility, and cognitive deficits. They require education to help them understand the learning and conditioning factors associated with stimulant use. Similarly, they need information about the impact of stimulants and other substances on the brain and behavior, such as cognitive impairment and forgetfulness. Information about stimulant-induced behavior can help them understand the episodes of anger, hostility, and sexual compulsivity.
Clients, especially those with MA use disorders, should be educated about the early abstinence syndrome and protracted abstinence. Also, they should learn how their secondary substance of choice has an important role in relation to relapse to stimulant use. They require education about the biopsychosocial processes of addiction, treatment, and recovery. They should also learn about the stages of treatment and recovery, as well as the specific tasks, goals, and pitfalls of each.
Although many clients with stimulant use disorders in early treatment phases have poor retention of information and temporary cognitive deficits, they can understand basic information about cues and triggers. They can be taught how conditioning factors can elicit drug cravings and urges, that these cravings and urges are a natural part of early abstinence, and that there are methods to deal with them. Clients with stimulant use disorders should be provided with basic education about the conditioning process and how this process is applied to their disorder.
These educational efforts should describe basic conditioning factors related to stimulant use as described in Figure 4-3.
Stimulant (and secondary substance) use becomes strongly associated with certain people, places, objects, activities, behaviors, and feelings. Because clients with stimulant use disorders may have engaged in stimulant use hundreds or thousands of times, their daily life is filled with numerous reminders or cues that can trigger stimulant cravings and stimulant use. Although it is common for many clients to have some of the same cues and reminders, such as seeing the drug or the dealer, there are wide differences among clients regarding the specific type, strength, and number of cues. Accordingly, it is important for counselors to help clients to acknowledge and identify the cluster of cues unique to their lives.
The primary tasks here are to teach clients how cues are developed and how these cues can trigger drug craving and use, and to encourage them to actively identify their cues and triggers. This can be accomplished through exercises and worksheets. Client Worksheet 2, Identifying External Cues and Triggers, and Client Worksheet 3, Identifying Internal Triggers, can be the basis of exercises to help clients accomplish these tasks.
External and internal cues often pervade every aspect of stimulant users' lives. As a result, clients should develop action plans with specific behavioral and mental steps to prevent cues from becoming triggers. They should be taught to avoid, wherever possible, external cues that strongly remind them of stimulant use. They should be taught to leave situations that are making them think about stimulants or experience cravings. They should be taught specific techniques to stop drug thoughts from becoming drug cravings. Finally, they should be taught immediately achievable techniques that can defuse stimulant cravings from leading to drug use. Client Worksheet 4, Action Plan for Cues and Triggers, can be a valuable part of such educational efforts.
Families and significant others should be encouraged to participate in treatment. The family should receive education about the addictive process, its role in the process, and its role in the treatment and recovery processes. Family members also need information about the effects of stimulants on the brain and behavior in order to understand the stimulant-induced behavior. They should receive a primer on the classical conditioning aspects of stimulant use disorders, and look at cravings as a conditioned response.
The information should be clear and simple, and not too conceptual or abstract. The ideal format is a group psychoeducational session, consisting of a brief didactic session, followed by a video and a group discussion. The process should help to elicit discussions and examples about how what they heard and saw applies to them. Also, family participation can be an opportunity to do an informal evaluation of the substance use disorders of other family members. Through this process, program staff members may be able to identify certain treatment needs, which may require treatment or referral.
For clients who are actively working on achieving abstinence and who have a stable marriage or relationship with someone who is not using stimulants, involving the spouse and client in couples or relationship counseling can be valuable. This strategy can help to improve communication skills and the relationship. Research has shown that marital and relationship counseling can have positive effects on substance treatment (Landry, 1995; Stanton and Shadish, 1997). If relationship counseling is considered, the significant other must not have problems with substance use (excepting nicotine), and the significant other must agree with the basic treatment goals of abstinence and be willing to engage in behaviors that support sobriety. Some research results related to behavioral relationship therapy are presented in Figure 4-4.
Clients with stimulant use disorders, especially during the early phases of abstinence, seem to have low frustration tolerance and appear to be restless in group sessions. But as soon as clients are able to do so (generally within a few days), they should be introduced to a structured and therapeutic group process, such as a beginner's recovery group. These groups can provide a preexisting support network and a forum for openly talking about early abstinence problems. At the same time, participation in 12-Step meetings, such as Alcoholics Anonymous (AA), Narcotics Anonymous (NA), or Cocaine Anonymous (CA), should be strongly encouraged. Clients can be given the short-term goal of attending ninety 12-Step meetings in 90 days.
Also, clients can be encouraged to establish or reestablish relationships with nonsubstance-using friends and family and, perhaps, to establish a "buddy system" with a healthy family member, friend, or 12-Step sponsor to call during crises.
Some clients with stimulant use disorders develop significant stimulant-induced compulsive sexual behaviors. These can include compulsive masturbation, compulsive or impulsive sex with prostitutes, and compulsive pornographic viewing. For these clients, interventions can be conducted, the result of which is to decrease the likelihood of both the compulsive sexual behaviors and stimulant relapse.
A first step involves asking clients to agree to a temporary sex abstinence plan for 2 to 4 weeks. Next, clients should be made aware that sexual feelings, thoughts, and fantasies are conceptualized as very high-risk triggers that will be acted out if they are not talked out. For people who have this problem, even normal, routine sexual thoughts and contacts can quickly become major triggers.
Programs should provide a safe environment for such clients to talk about these issues, either within the context of a group session or individual counseling. Discussions should be held about safe and unsafe sexual behaviors in regard to relapse prevention. Specific and clear recommendations should include not having sex with anyone with whom the client has gotten high, and not pursuing sex with anonymous or unknown partners. Client fears should be addressed, such as the fear that sex without drugs will be boring or impossible.
Many of the avoidance strategies used with psychoactive substances can be employed for these clients in relation to sexual cues. For some clients, the sexual behavior has a higher reinforcing effect than the stimulant.
Clients will need reminders to stay away from people, places, and things related to sexual behaviors. These can include porno shops, certain streets with prostitutes, and video shops. Also, clients should be educated about reciprocal relapse, in which one compulsive behavior is inextricably involved with another, and therefore, engaging in the behaviors associated with one condition can cause one to act out behaviors associated with the other condition.
It is rare for clients to go from active, full-blown stimulant addiction to complete abstinence. Rather, most clients go through a phase during which there are days without substance use and occasional days with substance use. In fact, substance use during this early transition from abusive or dependent use to abstinence should not be considered relapse because there was not a genuine period of abstinence from which to relapse.
Thus, substance use during this period of transition should not be characterized as relapse but rather as difficulty in breaking the pattern of stimulant use. Also, clients should understand that substance use is normal during this difficult phase, despite their hard efforts to the contrary. Program staff members should understand that substance use during this phase is not a sign of poor motivation but reflects multiple processes, including cues and triggers and a not-yet-stable brain. Slips can also be thought of as a behavioral indicator of conflict and ambivalence about stopping. At the same time, counselors should clearly communicate that they are not giving clients permission to use. Rather, they are making efforts to keep the client engaged in treatment.
Early slips should be considered opportunities for adjusting the treatment plan and trying other strategies. They can be opportunities for gaining an appreciation of the strength of cravings and triggers, and learning new methods to handle them. They can be an opportunity to examine if the treatment plan is adequate and appropriate or to increase the frequency of contact with treatment and/or the support system, such as self-help meetings and contacts with the sponsor. Some recommendations for guiding group discussions of slips are listed in Figure 4-5.
Early slips should not be considered as tragic failures but rather as mistakes. When slips occur, counselors can make a verbal or behavioral contract with clients regarding short-term achievable goals. This can include such simple tasks as agreeing not to use psychoactive substances for the next 24 hours, to attend a specific number of clinic sessions over the next couple of days, and to bring a significant other to treatment the next day. This process can involve having the client identify areas that need to be addressed or enhanced. It may be important to take a closer look at cues and triggers and determine if anything has changed.
Many stimulant users can discontinue the use of cocaine or MA for periods of time without the assistance of treatment involvement. As previously mentioned, "withdrawal" is a less important consideration for stimulant users than it is for users of substances that produce a physically uncomfortable withdrawal, such as opiates, alcohol, and benzodiazepines. For stimulant users, the trick is not in stopping, but in staying off, or avoiding relapse. In the treatment of stimulant users, achieving abstinence is the "warm-up act"; sustaining abstinence is "the main event."
The dichotomy between strategies to achieve abstinence and strategies to maintain abstinence is somewhat artificial and arbitrary because many of the same principles apply and many of the same techniques are used over the course of treatment. However, there are some issues that appear to increase in importance over the 1- to 4-month period typically needed for learning how to maintain abstinence. These are discussed below.
Once stimulant use is discontinued and a client's sleeping and eating habits are normalized, the majority of symptoms described as the "crash" typically lessens. However, the resolution of the crash symptoms does not signal that the brain is back to normal. Clinical observations show that there are significant biological and psychological symptoms that continue to hamper the functioning of stimulant users 90 to 120 days after discontinuation of substance use. The symptoms described include a mild dysphoria, difficulty concentrating, anhedonia, lack of energy, short-term memory disturbance, and irritability.
The existence of these "protracted withdrawal" symptoms has been the subject of some debate. Recently, evidence from positron emission tomography (PET) scan research has provided tangible evidence in monkeys that MA use produces very significant changes in brain functioning that last for more than 6 months (Melega, 1997a). The brain areas involved and the neurochemical deficits observed in these PET scans are consistent with the clinical symptomatology of this "protracted withdrawal syndrome." Although there is still reason to be cautious about specifying the precise cause or time course of this syndrome, there does appear to be neurophysiological evidence to support the factual basis of this phenomenon.
There are a number of common patterns to the relapse episodes of stimulant users who are attempting to maintain abstinence (Havassy et al., 1993). These include
Many stimulant users have spent a good portion of the years leading up to treatment entry with their lives revolving around substance use. Frequently, during the initial 6 to 12 months of abstinence they have little idea what to do with their lives. In particular, they often have very poor social and recreational behavior repertoires. The creation of new, positively reinforcing activities and interests is an important part of this period of treatment.
The strategies recommended for maintaining abstinence draw primarily from the behavioral and cognitive-behavioral models described in Chapter 3. One overall theme in the following materials is that newly abstinent stimulant users can be taught a set of information and skills that can help them avoid relapse. The following strategies have been found to help stimulant users maintain their abstinence.
The purpose of functional analysis is to teach clients how to understand their stimulant use so that they can engage in problem-solving solutions that will reduce the probability of future stimulant use. The core components of a functional analysis are (1) teaching clients to examine the types of circumstances, situations, thoughts, and feelings that increase the likelihood that they will use stimulants; (2) counseling clients to examine the positive, immediate, but short-term consequences of their stimulant use; and (3) encouraging clients to review the negative and often delayed consequences of their stimulant use. Client Worksheet 29, Components of a Functional Analysis, gives clients an overview of these components.
Employing contingency management agreements can help sustain initial treatment gains. When contingency management is used, the behavioral contract must be based on objective criteria such as urinalysis results and attendance at group therapy sessions. All specifics must be clearly detailed in the written contract. Systematic and consistent implementation of the agreement is crucial: Reinforcement must be delivered promptly when the contract is satisfied and withheld when it is not. Frequent, positive reinforcement of success is critical.
Client Worksheet 28, Sample Behavioral Contract for Stimulant Abstinence, can be modified and used to help meet the treatment needs of specific clients. As this sample contract illustrates, contingency management can involve receiving "points," credits, money, or other benefits or incentives.
Relapse prevention techniques teach clients to recognize high-risk situations for substance use, to implement coping strategies when confronted with high-risk events, and to apply strategies to prevent a full-blown relapse should an episode of substance use occur (Marlatt and Gordon, 1985). The techniques involve several cognitive-behavioral interventions that focus on skills training, cognitive reframing, and lifestyle modification.
Relapse prevention techniques fall into several categories:
As reviewed in the previous chapter, there is a substantial body of literature on the use of relapse prevention techniques with stimulant users. The manual developed by Kathleen Carroll provides an excellent set of relapse prevention exercises, which can be directly applied in treatment settings (Carroll, 1996). The Matrix manual (Rawson et al., 1991b) previously described has a section on conducting relapse prevention training in a group setting and supplies handouts and instructions for their use. Washton has published a set of relapse prevention materials that can be easily incorporated into treatment programming (Washton, 1990a, 1990b). Also, Figure 4-6 sets out basic precepts to be used in addressing relapse. The following treatment themes are critical to the relapse prevention-based treatment strategies.
One major element of a relapse prevention approach is the delivery of information to stimulant users about a variety of use-related topics. One frequently used format for delivering this information is in psychoeducation groups. These groups consist of a mixture of education, peer support, and recovery-oriented therapy. The group leader provides a brief discussion or shows a short videotape on a specific topic that is relevant to the group participants. The group members are encouraged to discuss the topic as it is personally relevant to them. Also, the group leader encourages group members to discuss the problems, challenges, and successes that they are currently experiencing.
The topics typically discussed in a psychoeducation group for clients with stimulant use disorders include
Many of these are addressed in the sections below. Some recommendations for running a relapse prevention group are presented in Figure 4-7.
During the previous phase of establishing abstinence, clients should have learned skills for negotiating high-risk situations. In particular, clients should be able to identify cues and triggers, develop action plans for cues and triggers, and deal with early abstinence symptoms.
Once clients learn to identify, manage, and avoid high-risk situations, the counselor and client should try to determine if the client is confident in her ability to use those skills in the real world. It is important to evaluate and have clients engage in self-evaluation to determine if they are overconfident regarding their avoidance and refusal skills, and to determine if they actually have more skills than they imagine. Client Worksheet 11, Evaluating Your Self-Efficacy Regarding Relapse, can help clients to evaluate how they think they would handle certain high-risk situations that they cannot avoid. Similarly, Client Worksheet 12, Increasing Your Self-Efficacy, involves role-playing exercises designed to simulate real-world high-risk situations and to increase the client's self-efficacy.
Two important risk factors for stimulant relapse are euphoric recall and the desire to test control over stimulant use. Euphoric recall is the act of remembering only the pleasures associated with stimulant use and not the adverse consequences. Euphoric recall is a potent relapse risk factor because it minimizes clients' perceptions of stimulants' danger, promoting an ambivalence about quitting. For these reasons, so-called "war stories" that include euphoric recall and selective memory are powerful relapse triggers and should be strongly discouraged in recovery groups. Client Worksheet 18, Selective Memory About Stimulant Use, can help clients to explore this issue.
After beginning to feel healthier, more in control of their lives, and free of some of their stimulant-related problems, some clients feel that they are ready to try a new approach to stimulant use. For example, some may feel that if they are "careful," they can use stimulants without losing control over their use. Others may feel that this is a good time to try using stimulants "one last time," just to see if they can do it without escalating into compulsive use and loss of control. Clients should be taught that urges to test their control over stimulant use are a powerful relapse warning sign. Client Worksheet 19, Fantasies About Controlled Use, can be part of psychoeducation efforts designed to recognize these fantasies as warning signs that need to be addressed. Also, Client Worksheet 20, Those Ugly Reminders, can help clients make lists of negative consequences of stimulant use, which can be reviewed when they experience cravings, fantasize about controlled use, or romanticize their experiences with stimulants.
Stimulant slips and relapses are mistakes, not failures, and indicate a need to adjust the treatment plan. After a slip, a relapse-specific session should be scheduled as rapidly as possible. The counselor should reassure clients that he has not given up on them. Counselors and clients together review and analyze the events leading up to the slip and identify which warning signs were present. Clients should be encouraged to consider the events of the previous few weeks, such as changes at work, at school, in social networks, or in family situations. Similarly, they should closely examine events and issues that occurred in treatment, such as getting new counselors, moving from one phase of treatment to another, or events happening to another client.
Clients should be helped to identify specific steps that can be taken to avoid future relapses in the event that a similar set of circumstances recurs. Most importantly, slips and relapses should prompt revisions in the treatment plan. Such revisions may include increasing the number of self-help meetings, participating in individual counseling for a brief period of time, or obtaining a 12-Step sponsor. Also, clients should receive recommendations and guidance to handle the negative thoughts and feelings caused by slips. Client Worksheet 7, Permission to Relapse, is a useful client handout for this purpose.
Stimulant users in recovery are often surrounded by individuals who continue to use: dealers, neighbors, friends, or family members. The ability to refuse stimulants when offered requires a special type of assertiveness, hence the need for a special type of assertiveness training. Drug refusal training reminds clients that individuals offering them stimulants do not have the client's best interests in mind. Rather, clients are taught to think of such individuals (even if friends or family members) as "drug pushers" who must be discouraged. Clients are taught that their primary goal is to refuse offers of stimulants. They are taught that their secondary goals are to reinforce their commitments to not use and to feel good about themselves for doing it.
This approach emphasizes the following elements that should be incorporated into encounters with individuals offering stimulants or inviting the client into high-risk situations.
In this approach, the counselor guides the client through three scenarios involving specific individuals, specific times of the day, and specific situations. Based on these scenarios, the client and counselor engage in role-playing exercises so that the client can practice these behaviors. Furthermore, clients are encouraged to engage in additional role-playing exercises with significant others or other appropriate people.
The overall goal of relationship counseling is to develop effective communication skills to help couples achieve and maintain abstinence, change their lifestyle, increase enjoyment in their relationship, and learn better ways to problem solve. Specific exercises for conducting these sessions can be found in the Community Reinforcement Approach Manual (Budney and Higgins, 1998).
These treatment exercises are designed to increase participation in prosocial activities that may serve as alternatives to stimulant use. This includes helping clients to develop interests and participate in recreational and social activities that do not involve stimulant or other substance use. Potential activities can be evaluated by the counselor and client according to how interesting they are to the client, how costly, to what degree they involve others, how much time they require, how likely the client is to engage in them, and how much physical exertion they require. Potential coparticipants are identified. The next step involves the development of an action plan to identify the specific steps necessary to engage in the activities. These should be incorporated into the treatment plan. Examples of these exercises are included in several of the aforementioned manuals.
The social skills training efforts are used to help clients learn and practice skills that will facilitate nonsubstance alternatives for socializing, recreating, and coping with stressful interpersonal situations. The goal is to help clients experience more positive reinforcing effects and fewer negative, adversive effects from social interactions. The training can be especially helpful for clients who have problems meeting nonsubstance-using peers or interacting with coworkers, and who feel uncomfortable in social settings. Social skills training techniques have been developed for anger management, anxiety in social situations, initiating pleasant conversations, and assertiveness training (Alberti and Emmons, 1982; Chaney, 1989; Monti et al., 1995).
This counseling is focused on helping unemployed clients locate a job, and helping improve the employment situations of clients with unsatisfactory jobs or jobs that are high-risk for relapse.
Treatment, recovery, and relapse prevention efforts should address biological, psychological, social, and spiritual areas of life. Clients should be taught the value of recreational and leisure activities and how to incorporate them into their recovery program. Many recreational activities can offer opportunities for clients to learn or practice social skills, such as cooperation, teamwork, healthy competition, and leadership.
Vigorous physical exercise helps clients feel good about themselves, decreases anxiety and depression, increases appetite, and often helps clients sleep better. Clients should be taught the value of regular aerobic exercise and how to incorporate it into their daily or weekly schedule. Clients should be provided with a variety of options for exercise, such as dancing, walking, biking, jogging, tennis, swimming, skating, aerobics, and weightlifting. Client Worksheet 23, Exercise and Recovery, and Client Worksheet 24, Examples of Exercise Activities, can help clients understand the value of exercise in their recovery, review potential types of exercises, and learn to incorporate exercise into their recovery program.
Many clients in treatment for substance use disorders have problems related to nutrition and diet. Stimulants decrease appetite, leading to decreases in the intake of calories and nutrition. Clients with stimulant use disorders eat insufficiently, and when they do eat, often eat impulsively and eat foods with negligible nutritional value. As a result, these clients should receive a formal nutritional assessment conducted by a nutritionist as well as guidance regarding eating a nutritionally balanced diet, discarding patterns of infrequent and impulsive eating, and learning to plan and schedule nutritionally appropriate meals. Client Worksheet 25, Nutritional Self-Assessment, can help clients evaluate their own unhealthy patterns of eating and need for structure regarding nutrition.
In the Community Reinforcement Approach, all clients who meet the diagnostic criteria for alcohol dependence or who report that alcohol use causes problems in their attempts to achieve abstinence from stimulant use are offered disulfiram therapy. A typical disulfiram dose is 250 mg/daily unless the client reports being able to consume alcohol at that dose without a reaction. In such situations, the dose is increased to 500 mg. Disulfiram ingestion is observed by clinical staff members when clients come for urinalysis monitoring. Take-home doses are provided for the other days. (See Figure 4-8 for related research on disulfiram therapy.)
Self-help strategies can be valuable components of all phases of treatment. Self-help strategies, especially those that focus on substance use, are especially valuable as ancillary activities that support the treatment goals of maintaining abstinence. In general, self-help programs help clients to develop appropriate social skills, create healthy social networks, establish healthy intimate relationships, and engage in substance-free healthy activities. They also provide opportunities to learn socially appropriate mores and norms, how to receive and give advice, and how to mentor others.
The most frequently used and available self-help strategy is the 12-Step approach. It is the rare city that does not have many AA group meetings every day, and most larger cities have numerous CA and NA meetings. Clients should be provided with information regarding the 12-Step process, such as meeting format, the spiritual component, the basic content and meaning of the 12 Steps, the role of the 12-Step sponsor, and the role of anonymity.
Although the Consensus Panel recommends participation in a 12-Step group, providers should not require clients' participation. Rather, it is better to encourage and recommend 12-Step participation, especially because 12-Step programs are self-described as voluntary self-help programs of recovery. Similarly, family members of clients should be encouraged to participate in 12-Step programs designed for family members, such as Al-Anon. Such encouragement can be provided by having meetings on site. Both clients and family members should receive lists with the addresses and times of meetings, and provide transportation when necessary.
Also, self-help strategies other than the 12-Step programs can be valuable components of treatment. Some are specifically related to substance use, such as Rational Recovery, Save Our Selves, and Women in Sobriety. These may be particularly helpful for individuals who are reluctant to participate in the 12-Step programs. These include such activities as church-related groups, cancer survivor groups, and domestic violence groups. Some research findings on AA are shown in Figure 4-9.
Substance use counseling generally consists of therapeutic efforts that focus primarily on solving present-day problems that interfere with abstinence and recovery. Although there is variation, counseling generally focuses on current issues and involves advice, guidance, and encouragement. It is typically conducted in group formats.
In contrast, psychodynamic therapy, typically conducted in individual session formats, focuses on intrapsychic processes that impair effective coping and damage relations. Psychodynamic therapies differ greatly, but when used in substance use disorder treatment, they often assume that substance use is at least in part a strategy to self-medicate problems or a coping mechanism to deal with such problems as trauma, victimization, and low self-esteem.
Views differ regarding the appropriateness of individual psychodynamic therapy for clients with stimulant use disorders. As a result, the Consensus Panel makes the following recommendations. First, clients should be thoroughly evaluated to determine their need for this type of treatment. Are the client's individual treatment needs elicited through the treatment planning process best met by individual psychodynamic therapy or by providing basic skills to maintain abstinence? Second, clients should be thoroughly evaluated with regard to their readiness for psychodynamic therapy. Because psychotherapy can stimulate feelings and thoughts that may provoke relapse triggers, clients should be evaluated regarding their readiness to handle such triggers. Do clients have the emotional stability, relapse prevention skills, and social supports to handle this therapy? Third, if individual psychotherapy is introduced, it should be consistent and coordinated with other treatment strategies, especially group counseling and self-help involvement. For example, psychotherapy oriented to the stages of recovery can be especially useful (Wallace, 1992).
Overall, the Consensus Panel suggests that not all clients with stimulant use disorders are appropriate for, need, or want individual psychotherapy to establish or maintain abstinence. When provided, there should be an explicit treatment need, the client should have the requisite skills, and the therapy should support abstinence.
Because treatment should be based on the individual client's unique needs, the length of treatment should not be dictated by the number of weeks in the program. In particular, termination of the abstinence maintenance phase of treatment should be based specifically on achieving the treatment goals documented in clients' treatment plans.
The end of the abstinence maintenance phase is a good opportunity to help clients review their treatment experiences. Counselors should engage in activities and exercises that help clients to critically examine their treatment successes, the areas where they experienced problems, and the ways in which they addressed these problems. Similarly, counselors should help clients to evaluate the strength of their current recovery program and identify areas where they need strengthening. Through this process, the counselor and client should develop a continuing-care treatment plan that identifies remaining treatment needs and strategies that will be used to meet those needs.
Termination of the abstinence maintenance phase of treatment should be a transition to a lower level of care, not a termination per se. Abrupt termination should be avoided. Rather, programs should have or develop strategies that allow and encourage clients to remain connected with the program. Furthermore, programs should develop strategies that specifically educate clients about the continuing care treatment services available to them and that actively encourage clients to utilize these services. Ways in which programs can help clients to remain in contact with the program include
This chapter addresses the symptoms, complaints, and other medical sequelae commonly seen in persons using various forms of stimulants (e.g., cocaine, crack, amphetamines, methamphetamine [MA]) who appear at hospital emergency rooms (ERs) and other medical settings, or who need specialized medical care while participating in residential or outpatient substance use disorder programs. The purpose of the chapter is to assist medical personnel in recognizing and treating problems that may arise for stimulant users with acute or chronic intoxication or in various phases of withdrawal after protracted use of these drugs and differentiating these from similar presentations of other medical and psychiatric conditions. Another emphasis is the need for establishing and ensuring linkages between medical facilities and appropriate, comprehensive substance use disorder treatment/rehabilitation programs.
In a meta-analysis of 555 consecutive cocaine-related visits to hospital ERs in four cities between 1989 and 1992, Schrank concluded that catastrophic complications directly related to the use of this stimulant comprise only a small fraction of the sequelae (Schrank, 1993). Deaths were relatively rare, occurring in only four patients. In this sequence of cases, there were no reports of myocardial infarction, intracranial hemorrhage, ischemic stroke, infarcted bowel, or pulmonary barotrauma. The most common reasons for ER visits by cocaine users were cardiopulmonary symptoms (usually chest pains or palpitations); psychiatric complaints, ranging from altered mental states to suicidal ideation; and neurological problems, including seizures and delirium.
Most of the patients had multiple problems, many related to intravenous substance use. Rapid medical intervention was crucial for cocaine users with seizures, hyperthermia, potentially lethal arrhythmias, or toxic delirium. However, most patients responded well to simple evaluation, observation, and supportive care. Pharmacological intervention was required in less than one-fourth of the 555 cases. Schrank emphasized the importance of recognizing concurrent use of multiple substances and the presence of cocaine or other drugs in victims of traumatic injury and in obstetrical patients.
MA users are much less likely than individuals using cocaine to arrive at the ER with such acute medical problems as cerebrovascular accidents, acute cardiac ischemia and failure, hyperthermia, or seizures. The major presenting symptoms for MA users pertain primarily to altered mental status, including confusion, delusions, paranoid reactions, hallucinations, and suicidal ideation. The rapid development of tolerance to its physiological effects among chronic MA users may explain the relative infrequency of cardiac complications in this group (Heischobar and Miller, 1991).
The precise clinical effects of cocaine and MA depend on a complex mixture of the pharmacological properties and purity of the drug used; the dose, frequency of use, and route of drug administration; the user's state of intoxication or withdrawal and previous experience with the drug; and other concomitant medical and psychiatric conditions, including simultaneous use of other substances as well as personality attributes and expectations regarding drug reactions. All of these factors not only mediate drug effects, but also influence the user's susceptibility to substance abuse or dependence (Ellinwood and Lee, 1989; Gold, 1997).
The method by which stimulants are taken--the route of administration--determines the dosage and the rapidity and intensity of effects. Route of administration also affects the potential for adverse reactions and the likelihood of addiction. The principal routes used to administer cocaine and MA are oral ingestion, nasal insufflation (snorting), intravenous injection, and inhalation of smoke vapors (smoking/inhalation). These stimulants can also be taken vaginally, rectally, or sublingually.
In general, smoking and intravenous use rapidly evoke similarly intense responses, whereas oral ingestion and intranasal administration are slower delivery mechanisms, causing lower and more gradually rising blood levels and less intense subjective responses. Indeed, cocaine is seldom taken by mouth in this country because first-pass hepatic biotransformation metabolizes 70 to 80 percent of the dose and substantially diminishes the drug's effects (Gold and Miller, 1997). When crack cocaine is smoked, a highly concentrated dose is rapidly delivered to the brain. Several studies have reported a close correlation between subjects' plasma levels and the subjective effects from single doses given to relatively naive users who have not developed tolerance (Ellinwood and Lee, 1989; Gold and Miller, 1997; Volkow et al., 1997a). As the efficiency of the delivery system increases, so does the intensity of both the pleasurable and adverse effects. Figure 5-1 depicts these general variations in response times according to the different routes of administration for cocaine and MA.
To some extent, the dangerous consequences and addictive potential of stimulants also reflect the route of drug administration. Oral ingestion of MA is thought to protect the user from cardiotoxicity (Cook et al., 1993), and the lower and more sloped peak blood levels achieved by this route are also thought to be responsible for lower rates of addiction (Gold and Miller, 1997). Also, cocaine appears to be less addictive if doses remain small, peak plasma levels and the onset of drug effects are slow, and unpleasant withdrawal effects are absent or minimal. Oral ingestion and, to some extent, intranasal routes fulfill these criteria of slower, less hazardous consequences (Gold, 1997).
Intravenous use is more toxic than intranasal or oral routes, but inhalation is generally perceived as the quickest and, from the user's perspective, the most desirable delivery method because smoked crack cocaine and ice MA produce the highest peak blood levels and the most potent subjective impact without attendant hazards from syringe needle use (Cho, 1990; Cook, 1991; Gold, 1997). Other investigators report that smoked ice does not seem to produce the same intense "rush" as injection. There is some indication that in utero exposure alters cocaine reinforcement properties for adults or, at least, increases rates of cocaine self-administration in the laboratory (Gold and Miller, 1997).
Different routes of drug administration also produce different side effects. Intravenous users frequently develop illnesses associated with the preparation of drugs for use (i.e., mixing/making) and the use or sharing of unsterile needles, including HIV infection, hepatitis, tuberculosis, lung infections and pneumonia, bacterial or viral endocarditis, cellulitis, wound abscesses, sepsis, thrombosis, renal infarction, and thrombophlebitis (Sowder and Beschner, 1993; Gold, 1997).
Nasal insufflation is associated with sinusitis, loss of sense of smell, congestion, atrophy of nasal mucosa, nosebleeds, perforation or necrosis of the nasal septum, hoarseness, and problems with swallowing. Crack users complain of throat ailments and a productive cough with black sputum (Gold, 1997; Gold and Miller, 1997). Intravenous use of MA is associated with greater severity of medical and social problems compared with other routes of administration (Sowder and Beschner, 1993).
Figure 5-2 compares differences in use and consequent problems between intravenous and nonintravenous MA users. Apparently, MA users recognize these route-related effects and tend to vary the routes of administration because the drug causes irritation to nasal mucosa and lungs (Center for Substance Abuse Treatment [CSAT], 1997). Even prolonged use of amphetamine-containing diet pills has resulted in ischemic colitis and pulmonary edema (Sowder and Beschner, 1993).
The major differences between cocaine and MA pertain to the rapidity of responses and the duration of their effects. The sought-after effects of MA can persist for hours, whereas those from cocaine are over in minutes. This has important consequences for the choice of drug and the patterns of administration adopted by users. The plasma levels from smoked crack cocaine both peak and decline rapidly, whereas those from smoked MA also peak relatively rapidly but decline more slowly because metabolism takes longer. Regularly repeated use may be more common among cocaine users trying to sustain the drug's effects, whereas withdrawal is more protracted for MA users (Cook, 1991; Gold and Miller, 1997). Figure 5-3 shows some of the differences between cocaine and MA.
The plasma levels of cocaine/crack peak and decline rapidly, with a terminal half-life of about 56 to 60 minutes. MA plasma concentrations also peak rapidly but remain high for much longer (Cho, 1990; Cook, 1991). In normal subjects, the plasma half-life of cocaine ranges from 40 to 90 minutes (Rowbotham, 1993).
Because the biological half-life of cocaine is relatively short, repeated dosing is necessary to sustain an effect (Gold and Miller, 1997). By contrast, repeated dosing with MA, before metabolism and elimination are complete, can result in substantial accumulation of the drug in the body with increased likelihood for addiction (Cho, 1990; Cook, 1991).
Other factors in the growing preference for smokable forms of MA, as well as crack cocaine, include availability and price. Crack is generally less expensive and more available than powdered cocaine hydrochloride and produces, in the initial smoker, a very intense but brief rush described by some as a "full body orgasm" (Gold, 1997). Because ice costs less than other forms of MA per dose, and because the euphoria attained may persist for several hours, this form of MA delivers the most "bang for the buck." Because abuse liability increases as time before onset of action decreases, and the concentrations of the drug that reach the brain and receptor sites increase (Cornish and O'Brien, 1996), the current concern about increased use of stimulants pertains to both the smokable preparations (crack and ice) and to continuing intravenous use of both drugs.
The incidence and severity of MA- and cocaine-induced side effects and toxic reactions are also dose-related. As the dose increases, the profile of side effects progresses from mild excitement to more intense reactions, even psychosis (CSAT, 1997). Because tolerance develops rapidly to the desired euphoric effects, stimulant users nearly always escalate dose size and frequency of drug use in pursuit of the vanishing rush. If initial use was by oral or intranasal routes, users also tend to switch to intravenous administration or inhalation, methods that promise more rapid response rates and peak plasma levels (Ellinwood and Lee, 1989).
Chronic MA users may consume as much as 15 grams of the drug per day in doses exceeding 1 gram every 4 hours over a 24-hour period. Because the conventional dose is 10 mg, doses of 150 mg to 1 g would ordinarily be highly toxic to naive users (Cho, 1990). There is, however, considerable individual variation in toxicity and overdose from stimulants. Although general ranges have been established for lethal doses and blood levels, reactions are unpredictable (Gold and Miller, 1997).
The lethal dose of cocaine for 50 percent of novice users (LD50) is 1.5 grams. The LD50 for MA has not specifically been established, and there is significant individual variability to its toxicity. For example, doses of 30 mg can produce severe reactions, yet doses of 400 to 500 mg are not necessarily fatal. Reported tissue levels of MA in fatalities, nonetheless, have ranged from 1µg/mL to over 14 µg/mL. Reported blood levels have also ranged from 27 µg/mL to only 0.6 µg/mL (Mori et al., 1992).
The purity of the stimulant used also influences the rate and completeness of its absorption and effects. The purer the drug, the greater the effects. "Street" drugs, however, are seldom entirely pure. The purity of confiscated cocaine hydrochloride intended for oral or intranasal consumption generally ranges between 20 and 80 percent; the purity of intravenous cocaine preparations can vary between 7 and 100 percent; and for freebase or crack intended for smoking, from 40 to 100 percent (Gold and Miller, 1997). Most seized batches of MA have 40 to 70 percent purity (Burton, 1991; CSAT, 1997).
Adulterants are added to cocaine to increase its weight by cutting or substituting less expensive but similar-tasting and acting products that will maximize profits for the dealer while still satisfying the customer. In general, the adulterants in cocaine do not pose serious health-related problems, although these cannot be completely discounted (Schrank, 1993). Cocaine is most often cut with mannitol, lactose, quinine, glucose, or other inert compounds for weight, and with caffeine, lidocaine, other stimulants, anesthetics, or hallucinogens for taste and effect (Schrank, 1993; Gold, 1997).
The manufacturing processes for illicit MA and ice are often crude and can involve many impurities and contaminants that do pose serious health consequences. Until recently, most of the MA sold on the street was manufactured from phenyl-2-propanone (P2P), a method of synthesis in which lead acetate is used as a chemical reagent. The large quantities of lead in the final product can result in symptoms of hepatitis, nephritis, and encephalopathy (Allcott et al., 1987). Two outbreaks of lead poisoning in Oregon in 1977 and 1988 involving a total of 14 cases among intravenous MA users were blamed on the lead acetate used in the P2P manufacturing process. Testing revealed the presence of 60 percent lead by weight in one case (Irvine and Chin, 1991).
The typical clandestine manufacturing process for MA has changed over the last 12 years--from the P2P method--to an ephedrine-based method and, more recently, to pseudoephedrine and phenylpropanolamine processing (CSAT, 1997). The difference between these two primary synthesis methods is primarily the precursor chemicals used.
The newer and more popular ephedrine method, which accounted for 89 percent of production in 1995, makes it simpler to synthesize MA, uses less strictly controlled ingredients, produces less odor than chemical reactions involving P2P, and yields a more potent and psychoactive form of MA (with a higher percentage of the more active dextro steroisomer, rather than equal proportions of dextro and levo stereoisomers produced by the P2P method) (Burton, 1991; Cho, 1990; CSAT, 1997; Drug Enforcement Agency [DEA], 1996). In addition, dextro-MA is three to four times more potent to the central nervous system than levo-MA (Sowder and Beschner, 1993). Therefore, the MA currently being manufactured has especially potent effects.
Illicit MA is also likely to contain potentially toxic contaminants from unintended reaction byproducts and reagent residuals as well as processing errors. Many clandestine laboratories are operated by uneducated and unskilled chemists who get recipes from unpublished, handwritten sources or through the Internet. As with cocaine, most of the contaminants are intentional fillers used to dilute or cut the product and may include lactose, lidocaine, procaine, caffeine, quinine, or sodium bicarbonate.
Other impurities in illicit MA can cause dangerous toxic reactions. Some identified contaminants have been shown to have great potency for producing seizures in mice. Poisoning from other reagents and organic byproducts, including mercury, has also been suspected but not documented (Burton, 1991).
The effects of stimulant use also reflect the temporal pattern of drug administration and the user's experience history or chronicity. Users describe various motivations for initial experimentation with cocaine or MA, including a desire for heightening a sense of well-being and euphoria, increasing alertness and energy, boosting self-esteem, enhancing sexual desire and responsiveness, dispelling fatigue, improving performance, losing weight, or consuming more alcohol without feeling intoxicated (Hando and Hall, 1997; Sowder and Beschner, 1993). Some users only administer stimulants periodically, although most discover that tolerance builds rapidly to many of the desired effects, particularly euphoria, so that increasing doses are needed to achieve similar effects.
Although serious medical, psychological, and social consequences have followed experimental low-dose use of stimulants, two other patterns of self-administration are of greater concern. The fourth edition of The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American Psychiatric Press, 1994) characterizes these as (1) episodic use, separated by at least 2 days of nonuse, with gradually escalating doses and more potent routes of administration that often culminate in binge use; and (2) daily, or almost daily, use with no wide fluctuations in dose, but a gradual escalation. Actually, compulsive users probably represent only 5 to 10 percent of the total number of MA users and an even smaller percentage of all users of amphetamines (Cho, 1990).
Because of their different pharmacological properties, MA users typically administer the drug on a daily basis, whereas crack cocaine users binge on large amounts for a shorter period, interspersed by periods of nonuse (CSAT, 1997; King and Ellinwood, 1997). Figure 5-4 illustrates rapidly escalating and sustained plasma levels attained by different time patterns of drug administration during cocaine and MA binges. An extremely compulsive pattern of rapidly repeated injections or inhalations is required to sustain high plasma levels of cocaine, in contrast to amphetamine/MA, which has a longer half-life (Ellinwood and Lee, 1989).
The greatest behavioral pathology and most serious medical consequences usually follow compulsive bingeing with high doses of either smoked or injected MA or cocaine (Ellinwood and Lee, 1989). The following paragraphs describe the sequence of phases that typically occur in the establishment of this hazardous, "high-transition" pattern and some of their accompanying side effects (as depicted in Ellinwood and Lee, 1989; King and Ellinwood, 1997). Knowledge of these phases can be useful for the medical practitioner in taking a substance use history and understanding what effects are likely to accompany a particular stage of acute intoxication, withdrawal, or more chronic use patterns.
Chronic users of stimulants develop tolerance to many of the initial effects, often after only a few weeks of drug use. This means that a higher dose is required to achieve the same effects, or markedly diminished effects are attained if the same dose is continued (American Psychiatric Press, 1994). Most notably, tolerance develops rapidly to the euphorogenic effects of stimulants and is the ostensible cause for most dose escalation by stimulant users--although dose increases may also stem from a desire to experience more intense effects. Tolerance also develops to the anorectic effects of MA in humans because weight loss stops after several weeks. Tolerance also appears to develop to the cardiotoxic effects of large doses of MA that many users survive. In fact, many of the initial symptoms of stimulant intoxication disappear with chronic use: Blood pressure may be normal, and nausea and vomiting are seldom seen. This tolerance is not the result of increased MA metabolism because chronic users show metabolic patterns similar to naive users (Angrist, 1994).
Interestingly, chronic, high-dose stimulant users may also become sensitized to the drug, a unique phenomenon characteristic of psychomotor stimulants. Sensitization is essentially the reverse of tolerance and produces undesirable effects with lower doses of the drug than were required to yield these same reactions in an earlier phase of the addiction process. There appears to be some sensitization to the psychosis-inducing effects of stimulants in humans. After one psychotic episode is experienced following chronic, high-dose use, a lower minimal dose of cocaine or MA may induce another psychotic episode, with more rapid onset following drug intake and a longer duration than the initial psychosis. Many sensitized stimulant users experience an almost immediate return of paranoia, psychosis, and stereotyped thinking if drug use is resumed (Angrist, 1994; CSAT, 1997). The sensitization process in stimulant dependence is elaborated in the section on toxic psychosis in this chapter.
As already noted, the intensity and duration of acute manifestations of stimulant intoxication correlate generally with the rate of rise and the height of peak blood levels reflected in brain concentrations. Acute intoxication with stimulants resembles hypomania or a manic state. In low doses, the libido is stimulated and sexual performance is enhanced. In high doses, spontaneous ejaculation and orgasm can occur. With increasing doses, poor judgment, indiscretions, sexual acting-out, and other bizarre behaviors or mental alterations are more likely to be seen. Acute stimulant intoxication can result in seizures, confusion, dystonias, respiratory depression, chest pain, or cardiac arrhythmias (Gold and Miller, 1997) (see Figure 5-4).
Acute MA intoxication, unless delirium or psychosis is present, seldom comes to medical attention. Most cocaine users who come to an ER with drug-related complaints have not used the drug for several hours, and peak plasma levels have already subsided, especially if the cocaine was injected or smoked (Rowbotham, 1993).
Uncomplicated intoxication requires only observation and monitoring in a subdued environment until symptoms subside over several hours. General measures include monitoring of vital signs for rising pulse rate, temperature, or blood pressure; providing a quiet and cool environment that helps to diminish agitation and overreaction to external stimuli; and close observation. Physical exertion and an overheated room can potentiate adverse effects because stimulants affect the body's heat-regulating mechanism at the same time that blood vessel constriction conserves heat. Although verbal reassurance is usually sufficient for quieting the patient, indications that agitation is escalating and moving toward paranoia and potential psychosis, with increasing risk for violence, may warrant pharmacological intervention. Fast-acting benzodiazepines such as lorazepam (Ativan) or diazepam (Valium) are useful for calming an anxious, agitated patient (Ellinwood, 1975; Weis, 1997).
Toxic, fatal, or subfatal syndromes are seldom seen in chronic, high-dose, intravenous stimulant users, probably because tolerance develops rapidly. Most stimulant overdose fatalities occur in neophytes or persons who accidentally ingest large amounts, such as "bodypackers" or children (Ellinwood, 1975). (Bodypackers are individuals who have swallowed waterproof packets filled with cocaine, usually in South America, in an attempt to clear U.S. customs undetected and then pass the packets through the gastrointestinal tract.) It should be noted, however, that the toxic dose for stimulants has enormous variability and appears to be idiosyncratic and unpredictable, without a known relationship to body weight. Hence, the amount of cocaine or MA used is not a reliable predictor of the reaction (Weis, 1997).
The symptoms of a sublethal stimulant overdose may include dizziness, tremor, irritability, confusion, hostility, hallucinations, panic, headache, skin flushing, chest pain, palpitations, cardiac arrhythmias, hypertension, vomiting, cramps, and excessive sweating. High doses of stimulants may cause high fever, cardiac arrhythmias and arrest, irregular breathing, seizures, and stroke. Agitated states characterized by increased aggressiveness or psychotic features may also occur with intoxication, particularly for MA (Weis, 1997). The development of hyperpyrexia (excessively high fever), severe hypertension, convulsions, and cardiovascular collapse signal a life-threatening situation (Ellinwood, 1975).
Lethal doses of stimulants--administered to laboratory dogs by injection or observed in bodypackers when ingested packets leak or break--produce a predictable sequence of events culminating in generalized convulsions and death. Heart rate, blood pressure, cardiac output, and body temperature rise rapidly, and a toxic delirium is observed before generalized and terminal seizures begin (Ellinwood, 1975; Rowbotham, 1993; Wetli, 1993).
Stimulant users who present with life-threatening medical conditions and toxic drug levels should be treated with standard life-saving techniques that respond to the presenting symptoms (Weis, 1997). Acute neurological symptoms such as seizures or rapidly elevating vital signs require immediate intervention. Nondrug causes of any symptoms should be carefully ruled out, and the patient should also be evaluated for multiple substance use. Stimulant overdose patients should be hospitalized, especially if treatment is threatened by polysubstance use (Gold, 1997).
No specific antidotes or antagonists to stimulant overdose are available--unlike naloxone (Narcan) for opiates and the benzodiazepine antagonist flumazenil (Romazicon). However, the following procedures are suggested:
Use standard treatments for arrhythmias, including phenytoin. Atrial arrhythmias that do not respond to cooling and sedation may require cautious use of calcium channel blockers or mixed alpha-/beta-adrenergic blockers such as verapamil (Calan), esmolol (Brevibloc), and labetalol (Goldfrank and Hoffman, 1993). Lidocaine may be contraindicated for ventricular arrhythmias that begin immediately after cocaine use as a response to catecholamine excess but is appropriate for ventricular arrhythmias that indicate an ischemic myocardium. Sodium bicarbonate has proven useful for cocaine-induced wide-complex arrhythmias (Goldfrank and Hoffman, 1993). Also note that management of acute psychiatric manifestations of cocaine intoxication by sedation appears to have a salutary effect on emerging cardiovascular complications.
In general, phenothiazines, especially chlorpromazine (Thorazine, Mellerial), are contraindicated because these drugs lower the seizure threshold (Gold, 1997). Haloperidol (Haldol) has not proven efficacious in preclinical studies in protecting against cocaine-induced seizures or fatalities, but it may have utility for MA-induced psychoses. The serious difficulties encountered in using haloperidol for sedative-hypnotic withdrawal in humans when agitation and hyperthermia are present may also apply to its use for acutely agitated or psychotic stimulant users who already have deficits in thermoregulatory control. Haloperidol may precipitate or exacerbate acute dystonic reactions associated with cocaine use (Goldfrank and Hoffman, 1993).
A characteristic withdrawal-type syndrome usually develops within hours to days after cessation of prolonged and heavy stimulant use. The symptoms can follow long-term use or much shorter binges. Although "cocaine blues" were described as early as the turn of the century (Gawin and Kleber, 1986), more recent investigators note that stimulant withdrawal is much less definitive than withdrawal from opiates or alcohol and has not been so well studied (Lago and Kosten, 1994; West and Gossop, 1994). (See Figure 5-5 for some common signs of stimulant withdrawal.)
Some clinicians distinguish between stimulant withdrawal symptoms following a several-day binge and complaints that characterize withdrawal after more chronic high-dose use. Stimulant users who have binged for 2 to 3 days are dysphoric, exhausted, and sleep for 24 to 48 hours. Cocaine users in this category commonly use alcohol, marijuana, benzodiazepines, or heroin with cocaine to reduce irritability. Following more chronic and regular stimulant use, withdrawal symptoms that subside over 2 to 4 days include dysphoria, irritability, difficulty sleeping, and intense dreaming (CSAT, 1995d).
Other clinicians emphasize differences in severity between withdrawal from cocaine and withdrawal from MA. A substantial number of persons with cocaine dependence have no clinically evident withdrawal symptoms. For the minority of cocaine users who do complain, symptoms begin within hours to days of the last dose, the crash lasts for 3 to 4 days, withdrawal persists from 1 to 10 weeks, with waxing and waning of the drug craving. The mood state of the cocaine user may return to normal after several days to a month.
Withdrawal symptoms seem to be most severe in the initial days following cessation of use (Cornish and O'Brien, 1996; Gold and Miller, 1997). Although there are no physical manifestations of a withdrawal syndrome when MA use is stopped, there are several symptoms that occur when a chronic user stops taking the drug (National Institute on Drug Abuse [NIDA], 1998a). Symptoms begin 12 to 24 hours after binge use is terminated and may persist for 1 to 2 weeks. The client initially feels depressed and anxious, with an intense craving for MA.
This phase is followed by fatigue and sleepiness, although this may be mixed with insomnia. Upon awakening after prolonged sleep, the client may be very hungry, and there may be persisting anhedonia and dysphoria. Other symptoms include paranoia and aggression. Depression appears to be more severe and prolonged following MA use and is correlated with duration of use and size of the doses (Gold and Miller, 1997; Gawin and Ellinwood, 1988).
Stimulant withdrawal is not medically life threatening and, unlike alcohol or barbiturate withdrawal, does not require pharmaceutical intervention. Although no consistent physiological disruptions requiring gradual withdrawal have been observed, some medications may be used to attenuate symptoms and provide support.
The greatest risk from the distinctive stimulant abstinence syndrome is of doing harm to self or others. Because withdrawal-related dysphoria and depression can be particularly severe in stimulant users, risk of suicide is intensified, and sensitive management is essential. Cocaine-induced depression usually dissipates fairly rapidly--in a matter of hours. The depression is agitated and often related to actual situations resulting from drug use (e.g., the client is disturbed that all of his money has been "blown" on the cocaine binge or that interpersonal relationships are jeopardized by his continuing drug dependence).
However, withdrawal-associated depression following high-dose MA use is more prolonged. During the tweaking phase of withdrawal, the high-dose MA user begins a rocky, jittery reaction characterized by agitated paranoia, extreme frustration, and the return of intense drug cravings. Suicidal ideation may be high, and violence is easily provoked.
Tweaking effects after persistent bingeing on ice are particularly dangerous. Clients may misinterpret caretakers' gestures and turn against them. Restraints and sedation in a secure facility may be necessary. Although stress reduction techniques and other approaches to preventing harm should be used standardly, medical personnel can also use benzodiazepines (e.g., diazepam) to control agitation and tachycardia (see further discussion of violence as a special issue).
For clients with preexisting diagnosed or unrecognized clinical depression, cocaine worsens symptomatology. These individuals are most likely to experience deepening dysphoria and/or paranoia after cocaine use. Treatment with selective serotonin reuptake inhibitors (SSRIs) may be of use (Gold, 1997).
Continuing agitation and persistent inability to fall asleep during the tweaking stage may also be treated symptomatically by using the antidepressant trazodone (Desyrel), whose dopaminergic properties help to sedate the client. Benadryl is also used for its sedating properties and for its effects on the dermatologic problems that often accompany MA use (e.g., itching and hypersensitivity of the skin). However, caution should be exercised in using any medications with high abuse/dependence potential. In general, prescriptions should not be written for use outside the treatment facility because use or resale of these drugs is very tempting to this population.
After the tweaking stage, MA abstainers usually "crash" and sleep several days at a time, depending on the dose and duration of the binge. This hypersomnolence may interfere with assessment of mental status and potential for dangerous behavior. Hence, clients should be evaluated immediately after wakening from this prolonged sleep for persisting dysphoria and other psychiatric symptoms of anxiety and depression (Weis, 1997). During this hypersomnolent state, and until sleep deprivation is overcome, active participation in therapy or followup of a referral to a treatment program by stimulant users is not a realistic expectation.
Drug craving during stimulant withdrawal has been treated with a variety of medications (e.g., bromocriptine, amantadine) without demonstrated efficacy in alleviating symptoms, getting clients "clean," or preventing relapse.
"Cocaine dreams" may occur during this period or as late as 8 or 9 months after termination of stimulant use during a protracted abstinence phase. They usually entail vivid recall of actually using and experiencing the high. The client may actually sweat and experience other symptoms of intoxication while dreaming. These intense dreams, which may sometimes contain vignettes in which the drug user loses or drops a supply or refuses to smoke crack/ice, can be used therapeutically to convince clients that they are making progress in treatment by making a subconscious choice not to use. Otherwise, the dreams may enhance drug cravings and intensify a vulnerability for relapse. These dreams are primarily experienced by users of injected cocaine/MA and smoked crack or ice.
Because stimulant users frequently self-medicate withdrawal symptoms with alcohol, benzodiazepines, or opiates, there may be symptoms of withdrawal from these drugs if they have been used continuously or at high doses. These require specific management and titration of substitute doses or other means of alleviating symptoms.
Although fatalities from stimulant overdose or acute myocardial infarction following administration of cocaine by inexperienced users have been documented, and other medical and psychiatric complications have been observed at all dose levels and routes of administration among naive users, the majority of serious stimulant-induced medical and psychological complications follows chronic, high-dose use.
Because tolerance develops rapidly to the subjective and cardiovascular effects of stimulants, the specification of complications following chronic use is complex (Rowbotham, 1993). However, cocaine toxicity affects nearly every organ system, with the most dramatic changes found in the cardiovascular system, the brain, the liver, and the pulmonary system (Majewska, 1996). Although there are some minor differences between the sequelae of chronic MA and cocaine use, the incidence of such side effects as chest pain, seizures, paranoid reactions, and suicidal thoughts is about the same for both drugs. Chronic MA users appear to have more headaches, severe depression, and hallucinations than counterpart cocaine users, but the evidence from community samples is not definitive (CSAT, 1997).
Figure 5-6 summarizes some of the more common symptoms and potentially serious complaints presented by chronic stimulant users. The following section contains a detailed description of stimulant-induced medical and psychiatric complications with limited comments about management of these conditions. Schrank specifies more detailed ER procedures for responding to some of the more frequently seen complications (Schrank, 1993). Figure 5-7 shows the distinctive indicators of chronic MA use and chronic cocaine use.
Cardiotoxicity stemming from catecholamine excess is observed in both cocaine and MA users. Although the cardiac effects are more profound for MA users because this drug results in even greater elevation of catecholamines than cocaine, the incidence of fatalities following myocardial infarction has been less frequent until the recent increase in inhaling (smoking) or injecting MA (Cho, 1990; Cook et al., 1993; CSAT, 1997).
Stimulants, especially cocaine, have been linked to virtually every form of heart disease, including different forms of arrhythmias, coronary vasospasm, myocardial ischemia, myocardial infarction, and cardiomyopathy (Cornish and O'Brien, 1996; Gold, 1997). Case reports of fatalities from myocardial infarction and tachyarrhythmias document their occurrence at all dose levels and routes of administration in otherwise healthy young adults without the usual coronary risk factors, but preexisting coronary artery disease can exacerbate the response and increase the likelihood of sudden death, as can hyperthermia and agitation (Ellinwood and Lee, 1989; Gold, 1997; Schrank, 1993). Tachycardia, hypertension, ruptured blood vessels, arrhythmias, and arteriosclerotic lesions typically precede myocardial ischemia and infarction (Majewska, 1996). With prompt medical intervention, patients generally survive stimulant-induced cardiomyopathy with heart failure (CSAT, 1997). There is some controversy about optimal pharmacologic approaches to treating arrhythmias and other cardiac effects. Lidocaine was previously used but may be contraindicated for ventricular arrhythmias because it lowers the seizure threshold (Goldfrank and Hoffman, 1993). However, certain calcium channel blockers (e.g., Nifedipine, diltiazem, verapamil) seem promising (Gold, 1997; Schrank, 1993).
Cocaine crack smokers frequently seek medical attention for difficulties in breathing (dyspnea) or severe chest pain. This may result from cocaine-induced pulmonary hemorrhage, lung damage, pneumonia, pulmonary edema, asthma, pneumothorax, pneumomediastinum, or pneumopericardium (Cornish and O'Brien, 1996; Gold, 1997). Pulmonary barotrauma may result from spasmic coughing following smoke inhalation or odd mechanisms of drug delivery (mouth-to-mouth inhalation), with sudden increases in airway pressure that result in alveolar rupture and the induction of free air into the pleural cavity, mediastinum, or subcutaneous tissues. The amount of free air is usually small and resolves spontaneously under observation. The possibility of esophageal rupture should be considered in pneumomediastinum if vomiting is present (Schrank, 1993). Cocaine can also cause sudden death by respiratory failure from drug-induced inhibition of the medullary centers in the brain (Gold, 1997).
Tracheobronchitis with cough is a frequent accompaniment of crack smoking, as are lobar and nonlobar pneumonias. Bronchospasm is another complaint of these smokers, usually in clients with a history of asthma (Schrank, 1993). Crack lung is a new syndrome that manifests with symptoms of pneumonia--severe chest pains and breathing problems with high fever--but no substantiating lung X-ray evidence. The condition does not respond to standard treatment, although anti-inflammatory drugs may relieve symptoms. Clients with crack lung may suffer from oxygen starvation or loss of blood with potentially fatal results (Gold, 1997).
Pulmonary edema has been observed in both cocaine and MA fatalities and attributed variously to deep inhalation aggravation of preexisting conditions (Nestor et al., 1989) and granulomas formed in response to adulterants added to the drugs (CSAT, 1997). Chronic obstructive lung disease in MA users is thought to result from thrombosis of small pulmonary vessels with gradual reduction of pulmonary vascular bed, pulmonary fibrosis, and granuloma formation (CSAT, 1997).
An increasing amount of research has recently focused on neurological impairments apparently resulting from high-dose and chronic use of stimulants, particularly by more rapid routes of administration. Some of the more devastating cerebrovascular consequences of cocaine and MA use have been known for years--seizures, ischemic strokes, and subarachnoid and intracerebral hemorrhages. Other neurological complications include optic neuropathy, global brain ischemia, and edema following myocardial infarction. Newer brain-imaging techniques now demonstrate various degrees of previously undetected and unsuspected cerebral atrophy and brain lesions in many chronic cocaine users (Cornish and O'Brien, 1996; Schrank, 1993; Majewska, 1996).
Seizures are a well-known complication of cocaine use, occurring almost immediately after any of the more rapid delivery routes, but not always dose-related. Chronic use may sensitize (kindle) an individual's response, but this is not definitively proven (Daras, 1996; Gold, 1997). Most cocaine-induced seizures are of short duration and leave no residual effects, although prolonged seizures can be catastrophic (see earlier references under overdose management) (Schrank, 1993; Cornish and O'Brien, 1996).
Cerebral hemorrhage and ischemic strokes are relatively rare events for stimulant users but occur more frequently with users of crack and ice. At least half of those who suffer brain hemorrhages have such underlying abnormalities as arteriovenous malformations and cerebral aneurysms. Stimulant-induced hypertension probably leads to rupture of these abnormalities that will also require surgical intervention to correct. Cocaine-induced hypertension and vasospasm seem to be associated with other cases.
The toxic role of simultaneous alcohol and cocaine use that produces cocaethylene (see later discussion) is also under investigation (Schrank, 1993; Daras, 1996). Another unresolved issue is whether CNS vasculitis is a causal factor; MA-induced necrotizing vasculitis has been documented since 1970 (Miller et al., 1993). Cocaine-using clients who complain of headache while intoxicated should be evaluated for possible intracranial hemorrhage (Ellinwood and Lee, 1989; Daras, 1996).
The recently documented neurological deficiencies found in chronic cocaine users, particularly in the basal ganglia and frontal cortex, are similar to those found in a variety of neurological/psychiatric disorders, including bipolar disorder, schizophrenia, and frontal lobe degeneration from seizures, stroke, or injury that is accompanied by dementia, apathy, depression, and social disinhibition (Majewska, 1996). Animal studies have confirmed similar enduring, possibly permanent, CNS changes, associated with repeated high doses of MA. Neurotoxicity at an early age may predispose stimulant users to premature onset of movement disorders such as Parkinson's disease and other dystonic or choreoathetoid disorders involving undulating, involuntary, whole body movements that may appear at the end of a prolonged binge in chronic users and are not related to use of neuroleptic medications (CSAT, 1997; Gold and Miller, 1997).
An array of cognitive deficits is also observed in cocaine and other stimulant users that also characterizes brain aging and dementia and may indicate premature brain aging or possible cerebral atrophy in these drug-dependent individuals. These include problems in attention, concentration, problem-solving, abstraction, arithmetic performance, new learning, and short-term memory (Majewska, 1996; Cornish and O'Brien, 1996; Gold, 1997). Unfortunately, many of the studies documenting these deficits lack adequate data on respondents' premorbid performance (Daras, 1996).
Cocaine and MA may be direct muscle toxins because acute rhabdomyolysis--a condition that destroys skeletal muscle--has been diagnosed in users who did not have any of the previously associated risk factors (i.e., hyperthermia, agitation, seizures, hypotension, toxic delirium or coma, or acute renal failure). Muscle necrosis may occur after any route of drug administration, and the presence of rhabdomyolysis should be considered in stimulant-intoxicated clients, particularly those complaining of myalgia or muscle tenderness. One study found that one-fourth of clients presenting with cocaine-related complaints had evidence of mild, usually asymptomatic, rhabdomyolysis--defined as elevated creatine kinase levels that were five times higher than normal (Goldfrank and Hoffman, 1993; Schrank, 1993).
Although mild cases of rhabdomyolysis may not lead to renal complications, renal insult and failure is a distinct possibility for patients with concomitant hyperthermia, seizures, delirium, or coma (Schrank, 1993). Renal failure from rhabdomyolysis has been reported as an outcome of cocaine and MA use (Scandling and Spital, 1982). Accompanying hepatic damage is rare and probably an idiosyncratic response (CSAT, 1997).
Abdominal pain, nausea, and vomiting are experienced by some stimulant users, probably indicating mild intestinal ischemia. Severe bowel infarction with elevated white blood cell counts, metabolic acidosis, and shock have also been observed. Occasionally, severe abdominal pain, bowel obstruction, or sudden onset of seizures are indicative of leakage or rupture of packets of cocaine ingested by "bodypackers" (Schrank, 1993). Another observed syndrome, "cocaine colitis," manifests as abdominal pain along with diarrhea and bloody stools, probably indicating diffuse gastrointestinal hemorrhage and tissue necrosis (Goldfrank and Hoffman, 1993).
As already noted, intravenous injection of cocaine or MA is associated with a variety of infectious diseases. Unsterile paraphernalia are particularly likely to result in blood-borne transmission of HIV/AIDS and hepatitis B, C, and D. Associated malnutrition in chronic users further lowers resistance to infection. Injection cocaine users are at greater risk of infectious endocarditis than other parenteral drug users (Daras, 1996).
Disinhibition and the initial aphrodisiac effects of stimulants are associated with participation in high-risk and unprotected sexual activity. Vigorous and prolonged sexual activity or anal intercourse is likely to damage tissues or protective condoms and thereby increase the likelihood of transmitting sexually contracted diseases (Cornish and O'Brien, 1996).
Use of stimulants by pregnant women has been related to poor obstetrical outcomes and adverse effects for the developing fetus, the newborn and the older child. An increased incidence of preecalmpsia, spontaneous abortions, and abruptio placentae has been observed among cocaine-using pregnant women. Toxic effects also result in fetal cerebral infarctions as well as low birth weight for gestational age and small head circumference. Recent studies in several separate locations have found similar rates of these complications in MA- and cocaine-using women and their prenatally exposed offspring (CSAT, 1997; Oro and Dixon, 1987).
Newborns exposed to stimulants in the womb may have poor feeding and sleep patterns, tremor, and hypertonia. Difficulties in consoling these "jittery" babies may inhibit close bonding with their mothers and contribute to developmental problems (Gold, 1997). Despite a spate of articles outlining probable behavioral and cognitive deficiencies in prenatally stimulant-exposed children, more recent meta-analyses have only confirmed lower birth weight compared with controls, but no clearly attributable effects on the fetus, infant, or child (Rabin and Little, 1994; Cornish and O'Brien, 1996).
A major problem with most of the earlier studies is that polysubstance use among pregnant women is ubiquitous, so that attribution of prenatal-exposure effects to any single drug is very difficult. Additional methodological confounds were introduced by differences in mothers' nutritional status, prenatal care, socioeconomic level, and trimester of maternal drug use, as well as a failure to account for the impact of the home environment in predicting IQ (CSAT, 1997; Cornish and O'Brien, 1996). Essentially, the long-term effects of maternal stimulant use on offspring are not known.
Chronic, high-dose stimulant use also affects reproductive and sexual functioning in both males and females. Men report gynecomastia (development of breasts), loss of sexual interest, impotence, and difficulty in maintaining an erection or ejaculating. Women have derangements of the menstrual cycle, including amenorrhea and infertility, as well as greater difficulty in achieving orgasm (Gold, 1997). Female stimulant users who have irregular or no menstrual periods often think they cannot get pregnant, although they are not always infertile and can have unwanted pregnancies. Testing for pregnancy and regular use of birth control should be encouraged.
Increased HIV and hepatitis B and C transmission are likely consequences of increased stimulant use, particularly in individuals who inject intravenously and share equipment. Infection with HIV and other infectious diseases is spread among injection drug users primarily through the reuse of contaminated syringes, needles, or other paraphernalia by more than one person. In nearly one-third of Americans infected with HIV, injection drug use is a risk factor, making substance abuse the fastest growing vector for the spread of HIV in the nation (NIDA, 1998a).
Research also indicates that MA and related psychomotor stimulants can increase libido in users, in contrast to opiates, which actually decrease libido. However, long-term cocaine use may be associated with decreased sexual functioning, at least in men (Rawson et al., 1998b). In addition, the use of MA seems to be associated with rougher sex, which may lead to bleeding and abrasions. The combination of injection and sexual risks may result in HIV becoming a greater problem among MA users than among opiate and other substance users, something that already seems to be happening in California (NIDA, 1998a).
Initially described by Young and Scoville in 1938, amphetamine psychosis is a usually brief and spontaneously remitting paranoid state that is frequently accompanied by intense, fear- evoking delusions and hallucinations, but with clear consciousness and a relatively intact formal thought process (Angrist, 1994). Stimulant-induced psychosis occurs while the user is intoxicated, not in withdrawal after drug cessation (Tinklenberg, 1975). The condition is not rare or idiosyncratic, but typically follows chronic, high-dose administration of amphetamines, MA, or cocaine. However, this drug-induced psychosis is more prevalent among amphetamine and MA users than those who use cocaine, probably because the short half-life of cocaine makes it difficult to accumulate and sustain high plasma levels of that drug (Angrist, 1994; King and Ellinwood, 1997). Nonetheless, the condition has been reported after acute intoxication in relatively naive users and occasionally after low doses.
Original reports of the condition described a threshold dose for eliciting a psychotic response as chronic administration of 50 mg amphetamine daily, but at least 10 cases have been documented at lower doses, and there are also case studies of psychotic reactions after a single dose (usually high) or only brief exposure to the drug (Angrist, 1994). Because studies of stimulant users have found a surprising prevalence of coexisting, often premorbid, psychiatric disorders (one-fourth of participantsin one study had preexisting schizophrenia), low doses of stimulants may actually precipitate latent schizophrenia in some users whose psychosis is then mistakenly diagnosed as stimulant-induced (Angrist, 1994).
Several investigators claim that a toxic paranoid reaction or psychosis, usually accompanied by delusions and/or hallucinations, is a probable complication of high-dose MA use. Amphetamine-induced psychosis has been investigated prospectively under experimental conditions in at least two studies involving fewer than 50 clients. Griffith and colleagues successfully elicited psychotic symptoms in 25 of 31 experienced users after high-dose administration of MA and observed that 22 of the 25 were frankly psychotic (Griffith et al., 1972). Bell evoked similar amphetamine-induced psychosis in 11 of 13 subjects (Bell, 1973)--the remaining 2 were found to have preexisting schizophrenia (Angrist, 1994). Surveys of chronic cocaine users in treatment have also found that one-half to two-thirds had paranoid experiences that were not trivial (Angrist, 1994).
However, there are methodological problems with each of the investigative approaches to studying stimulant-induced psychosis that make the findings less than compelling. When this condition is studied prospectively, the drug-experienced volunteers who must be used for ethical reasons have unknown (unobserved) sensitivity and tolerance to stimulants; the numbers are, of necessity, quite small for drawing definitive conclusions, and at least some of the participants have managed to continue drug use, even under rigorous laboratory conditions. Data from case reports have other drawbacks: The premorbid history of drug use and psychiatric status is unknown and may not be accurately reported by respondents (Angrist, 1994; CSAT, 1997).
Some researchers and clinicians describe the development of stimulant-induced psychosis as an evolving process. Panel members depicted MA users as having brief and transient psychotic episodes before a full-blown psychosis emerges after more extensive chronic use. MA users often recognize these early psychotic effects and try to stave them off by self-medicating with alcohol or decreasing drug use. In several articles, Ellinwood and colleagues describe the evolution of MA-induced psychosis as progressively abnormal behaviors--beginning at moderately high doses--with intense feelings of curiosity about the environment and patterns of exploration that result, for example, in examining the punctuation periods in a magazine text for evidence of a secret code (Ellinwood et al., 1973).
This first enthusiasm about "discoveries" moves over time and increasing doses from "watching the world" to feelings of being watched. Behaviors become more fixed and stereotyped, culminating with intense suspiciousness and, in psychotic reactions, paranoid delusions that misinterpret environmental cues. Visual hallucinations may be overreactions to barely glimpsed and recognizable objects in the client's peripheral vision; auditory hallucinations similarly begin with hearing simple noises. In later stages of the psychosis, the client loses all contact with reality and has delusions of persecution. If he is exhausted after a prolonged binge, the hyper-reactivity to stimuli and confusion can lead to panic, sudden violence, even homicide (King and Ellinwood, 1997).
The DSM-IV (American Psychiatric Press, 1994) distinguishes between cocaine intoxication with "perceptual disturbances" and cocaine-induced psychotic disorder with either delusions or hallucinations (depending on which is the prominent feature). In the former, the drug user has intact reality testing and is aware that auditory, visual, or tactile hallucinations are substance-induced, not actual representations of external reality. Another common manifestation, before paranoia is rampant and as deterioration develops, is stereotypy--persistent, repetitive acts such as disassembling and reassembling radios or other small gadgets that seems to offer some relief from agitation and anxiety. Even though the client seems to know that the behavior is meaningless, stopping it results in irritability and frustration (King and Ellinwood, 1997; Tinklenberg, 1975). As chronic, high-dose stimulant consumption continues, most users also withdraw from all social interactions and initiate other bizarre behaviors before the intensive drug use culminates in paranoid reactions or psychosis without any insight into activities.
Symptoms of stimulant-induced toxic psychosis usually abate spontaneously within a week (CSAT, 1997). Hallucinations stop within 24 to 48 hours of abstinence, and paranoia and delusions decrease over the next week to 15 days. The client may sleep after the first 24 hours for as long as 3 days, with extensive dreaming during this phase (Ellinwood, 1975). Clinicians also report that drug-induced psychosis dissipates more quickly for cocaine users--usually in 1 to 3 days--compared with up to 2 to 3 weeks for MA users. Users of ice are reputed to have the most intense and persistent psychoses (Sowder and Beschner, 1993).
Toxic stimulant psychosis can have typical and atypical presentations. Case reviews have established that approximately 80 percent of these psychotic clients experience paranoid delusions; 60 to 70 percent have hallucinations; 12 percent have tactile hallucinations (e.g., cocaine bugs crawling on the skin); olfactory hallucinations are present in fewer than 10 percent; and about 7 percent become disoriented. Hyperactivity and excitation are usually present (Tinklenberg, 1975; Ellinwood, 1975; Angrist, 1994). The client is generally oriented and has intact memory and an appropriate level of consciousness. Clients remember the psychotic episodes with remarkable clarity (Tinklenberg, 1975; Ellinwood, 1975). Thought disorder, if present, is usually mild and transient (CSAT, 1997).
A few clients are confused--usually delirious from high doses to which they have not developed tolerance; bizarre, usually autoerotic, sexual behavior is present in some, and others have destructive outbursts or make unmotivated assaults. One investigator found no differences in symptoms between relatively naive and chronic amphetamine users with psychotic reactions, but others claim that individuals who binge on high doses over a few days have more delusions and disorganized hallucinations and paranoid ideation than chronic users who have more systematic delusions. Intravenous drug administration caused no change in symptoms, but more rapid progression to psychosis (Angrist, 1994; CSAT, 1997).
Several issues pertaining to stimulant-induced psychosis remain unresolved. There is some disagreement about the role of drug sensitization (kindling) in precipitating more frequent toxic psychotic reactions at smaller-than-previously-required doses and sooner after drug use is reinitiated following a period of abstinence. There is also disagreement about the role of sensitization in deepening the depression experienced after withdrawal. The mechanisms for this "reverse tolerance" are not fully understood. Although animal experiments have shown that daily, intermittent dosing with stimulants results in sensitization, studies of amphetamine-induced psychosis in humans have yielded more ambiguous results (CSAT, 1997). However, a 1991 survey by Satel and colleagues of 50 cocaine-dependent clients consecutively admitted to a treatment program found that two-thirds (68 percent) had experienced paranoid psychosis while intoxicated and during the immediate postdrug crash (Satel et al., 1991).
The reported characteristics of this paranoia were consistent with a sensitization process. All of those with a paranoid reaction had, on average, years of binge use before paranoid symptoms gradually emerged. Anxiety gradually intensified during binges before frank paranoid delusions were experienced. Once paranoia emerged, every subsequent binge produced intensified reactions (despite use of anxiolytic street drugs by half of the group to ameliorate paranoid reactions), and the onset of these delusions after starting a run accelerated over time. Half of those who had experienced paranoid psychosis acknowledged engaging in bizarre behavior such as hiding or compulsively "checking up" on things; nearly two-fifths had secured weapons to protect themselves from imagined assailants. This paranoia persisted for an average of 12 hours, with near total resolution in 97 percent of cases before awakening after the postbinge crash (Gawin and Khalsa-Denison, 1996).
Similar results are reported by Brady and colleagues after a 1991 study of another 55 cocaine-dependent clients in treatment--53 percent had experienced cocaine psychosis, most with less drug and increasing frequency over time and with more rapid onset for the majority (Brady et al., 1991). It seems clear that sensitization to the psychosis-inducing effects of cocaine does occur, although the evidence for sensitization with amphetamines is somewhat less clear (Angrist, 1994).
The role of stress or other "triggers" such as alcohol use or insomnia in precipitating the return of psychotic symptoms that were initially induced by stimulants is also controversial.
Some investigators have reported that stress can evoke the return of psychotic symptoms (delusions, hallucinations, paranoia, suicidal thoughts) without further amphetamine or MA use and after long periods of abstinence (NIDA, 1998a; Sowder and Beschner, 1993; Spotts and Spotts, 1980).
However, Angrist questions the accuracy of such reports of spontaneous or stress-induced psychosis following amphetamine psychosis because the reported cases were not carefully monitored with urine toxicologies to rule out continuing substance use or examined for the possibility of simultaneous development of another psychiatric disorder (Angrist, 1994).
The duration of toxic stimulant psychosis is another issue in some dispute. Typically, uncomplicated psychosis induced by stimulants resolves rapidly unless more of the drug is taken. However, several Japanese investigators (i.e., Tatesu, 1964; Nakatani, 1990; Iwanami et al., 1994 [as cited in Angrist, 1994]) have reported persisting psychoses in chronic stimulant users for up to 1 year after abstinence when amphetamine metabolites were no longer present.
Angrist argues that Western investigators do not see prolonged psychoses very frequently, and the persisting psychoses observed in Japan may actually be cases where stimulants precipitated latent schizophrenia (or bipolar disorder), or the disorder was present but undiagnosed before amphetamine use began (Angrist, 1994). He concludes that the potential for amphetamine to cause long-standing psychosis may be a complication for some individuals. This conclusion is, however, unproven because the premorbid state of clients in reported studies has not been known and because continued substance use has not been ruled out by urine toxicology monitoring.
Treatment of the client who presents with toxic stimulant psychosis entails rapid, systematic visual assessment, continued observation and monitoring, and symptom management. All unnecessary stimulation should be reduced, but complete sensory deprivation should be avoided by providing quiet rooms with moderate lighting and sufficient space and insisting on subdued talking without any rapid or unexpected movements. The clinician should reassure the client that the condition is drug-induced and will subside (Tinklenberg, 1975). Restraints may be required initially to gain control of the client, but should be checked frequently to ensure that risk to extremities is minimized, that respiration is not compromised, and that heat loss is not inhibited. Agitation should be controlled promptly by sedation with parenteral benzodiazepines--usually diazepam.
Differential diagnosis of acute confusional states must be instituted immediately. Consideration should be given to the possibility of head injury, intracranial hemorrhage, or thyrotoxicosis. Information from significant others is helpful, and toxicology testing is also useful to confirm a diagnosis (Schrank, 1993).
Acute stimulant-induced psychosis should generally be managed in a hospital psychiatric department or similar facility. Minor psychotic episodes with low-grade symptoms that respond readily to neuroleptic medications may, on some occasions, be managed in a well-staffed, free-standing chemical dependency unit if sufficient personnel with training and experience in treating dual diagnosis are readily available. Urine testing is recommended to confirm a diagnosis of drug-induced psychosis because the syndrome can closely mimic other psychotic disorders such as schizophrenia, hypomania, depression, obsessive-compulsive reactions, or catatonia. However, a negative urine report does not necessarily mean that stimulants were not present (Ellinwood, 1975; Tinklenberg, 1975). The criteria for placement should reflect the persistence of the condition, the competence and training of personnel, and the drug taken. MA users who have accumulated high plasma levels from longer binges and larger doses of stimulants with longer half-lives are particularly prone to violence during psychosis--their paranoia makes them suspicious of attempts to medicate them, they are likely to become aggressive, and they don't comply with medication instructions after release from the hospital.
The criteria for continued hospitalization or inpatient care during psychosis are perceived risk or threats to self and others, as well as elevated vital signs, severe suicidal ideation, persistence of psychological or cognitive impairments beyond the usual time for spontaneous resolution, and severity of any medical problems such as serious heart disease, a history of infarcts, concomitant alcohol, barbiturate or opiate dependence, or diabetes and similar conditions that require careful monitoring (Tinklenberg, 1975). Release should not be considered until the medical crisis is resolved or until the patient has been stabilized psychologically for 24 hours and is able to self-calm without continuing use of neuroleptics. Buspirone hydrochloride (Buspar) is used experimentally in Hawaii to treat low-grade residual psychosis and is anecdotally effective when given in larger than usual doses (over 60 mg). It is relatively safe, although not advisable if the client has a history of benzodiazepine abuse.
A major perceived problem associated with amphetamine/MA abuse is the potential for sudden and intense violence (Miczek and Tidey, 1989). MA has been associated with crime and combative behavior (Sowder and Beschner, 1993). Anecdotal reports by law enforcement officials, psychiatrists, and drug users themselves, as well as some surveys, link stimulants to aggression and unprovoked assaults. Users have committed murders and other violent acts while intoxicated with amphetamines. Nonetheless, the effects of stimulants on aggression and violence are complex and paradoxical. There are sharply differing opinions about the nature and extent of the problem (King and Ellinwood, 1997; Miczek and Tidey, 1989).
In a 1987 review of clinical observations and survey results, Miczek found differing representations of amphetamine effects (Miczek, 1987). Some surveys found that sizeable proportions of prison populations and juvenile delinquents commit crimes of violence while intoxicated by amphetamines, but other studies identified only rare cases and small percentages of juvenile delinquents and hostile persons who were amphetamine users. The reliability of these studies was unfortunately compromised by the lack of matched samples and reliance on verbal self-reports containing questionable information about dose and frequency of drug administration. It may be that intense violent acts are more prominent among chronic high-dose users, but no reports linked amphetamines to a high incidence of excessively violent behavior or other offensive social behavior (Miczek and Tidey, 1989).
Although well-controlled experimental studies of stimulant-associated aggression or violence in humans are scarce, the conclusions are similarly ambivalent. Early studies of cocaine or amphetamines did not focus on this aspect or note any increased aggression as a behavioral side effect. In fact, low doses (10 to 30 mg) of particular stimulants (i.e., Ritalin) have well-known and carefully studied beneficial effects on children 5 to 14 years old who are diagnosed with attention deficit/hyperactivity disorder (AD/HD) which manifests as aggressive, destructive, irritable, hyperactive behavior. Animal studies of mice, rats, squirrels, monkeys, and cats have examined aggression induced by isolation, pain, and brain stimulation in combination with amphetamines, with mixed results.
The most important determinants of aggression and defensive responses seem to be situation, species, prior experience with these behaviors, dosage, and chronicity of the stimulus. For example, a substantial increase in aggressive behavior can be evoked if amphetamines are administered to animals that are repeatedly confronting an intruder. Most importantly, there may be a biphasic dose effect on aggressive behavior in some animals: Aggression can be enhanced at low doses and also at higher doses, up to a point at which stereotypy and social withdrawal interfere (Miczek and Tidey, 1989; King and Ellinwood, 1997).
Other research more clearly confirms the effect of amphetamines on human aggression. A recent Japanese study ascertained that MA users scored higher on tests of verbal and physical aggressiveness and on impulsiveness than either alcoholic or normal control groups (Mukasa, 1990 [cited in Sowder and Beschner, 1993]). An earlier investigator found that participants in a task that enabled them to reward competitors with money or punish them with white noise increased their aggressiveness after 5 and 10 mg doses of amphetamines, whereas caffeine reduced the frequency of this aggressive behavior (Cherek et al., 1986 [cited in King and Ellinwood, 1997]).
Probably the most useful explanation of amphetamine effects on violence is offered by researchers who claim that stimulants do have a specific, but complex association with violent behavior. Chronic, moderate-to-high dose MA use, especially if the drug is injected or used by another rapid route of administration, often results in assaultive behavior and other forms of violence in the context of an interaction of behavioral and psychological effects (e.g., hyperactivity, agitation, emotional lability, and paranoid delusional thinking) combined with personality factors and social environment (King and Ellinwood, 1997). In other words, certain individuals who are regularly using high doses of amphetamine may be prone to intense violence, especially if experiencing paranoid delusions, but it is not known how frequently this occurs or what circumstances/personality characteristics promote this reaction (Miczek and Tidey, 1989).
The Consensus Panel notes that the combination of low impulse control, paranoia, poor judgment, and grandiosity experienced by the chronic MA user, especially during a psychotic or prepsychotic episode, is a natural setup for violence. Similarly, the combination of a long-acting drug and a sustained high--because of MA's ready availability and low cost--results in a more severe/intense withdrawal reaction and accompanying susceptibility toward violence. The tweaker who is ready to crash after bingeing on ice does not need provocation to react aggressively, but confrontation increases the likelihood of a violent reaction.
Because drug-induced psychoses apparently increase the potential for violence in response to perceived persecution and paranoia, sound behavioral management techniques to prevent this negative and dangerous response are essential. The techniques listed in Figure 5-8 have been demonstrated to be useful and should be adopted by ER personnel as well as emergency medical technicians and police.
Stimulant users have a surprising number of co- or preexisting disorders that can make differential diagnosis challenging or complicate treatment. Recently, investigators have become more interested in the implications of premorbid conditions as potential indicators of vulnerability to stimulant dependence. Majewska points out the need for more research to establish the epidemiological relationships between preexisting neurological deficits resulting from genetic, developmental, traumatic, or neurotoxic factors and vulnerability to drug addiction (Majewska, 1996). More specifically, preclinical studies and some surveys seem to indicate that neurological deficits associated with AD/HD, neuroanatomical abnormalities, lead poisoning, alcoholism, posttraumatic brain lesions, and posttraumatic stress disorder (PTSD) may be correlated with increased vulnerability to stimulant addiction. Another investigator (Bauer, 1996) lists another set of conditions or disorders that frequently co-occur with cocaine use disorders and notes that these correlates represent potential confounds to research regarding the sequelae of cocaine abuse and dependence as well as potential risk factors for developing those disorders. These include antisocial personality disorder, depression, other DSM Axis I disorders, polysubstance use, aggression, a family history of alcoholism or other substance use disorders, prescribed psychoactive medications, seizures, head injury, HIV/AIDS, and other major medical problems.
The following sections describe some of the most commonly identified premorbid and co-occurring disorders among stimulant users, with some comments on treatment precautions.
Concomitant use of a variety of other licit and illicit psychoactive substances is a common correlate of stimulant use. These substances are frequently used to attenuate aversive symptoms experienced in the posteuphoric phase of use (Weis, 1997) or may be administered to prolong or counter particular effects of stimulant intoxication. Different combinations of substances are used to titrate mood states or effects (CSAT, 1997).
Cocaine users tend to prefer alcohol, marijuana, or opiates. There is generally less alcohol use but more marijuana use among MA users than cocaine users (CSAT, 1997). Cigarette smoking is almost ubiquitous among stimulant users, usually to relieve perceived stress. Speedballing--simultaneous use of opioids and cocaine or other stimulants--is still prevalent in many places because the combination is perceived to smooth the effects of each drug. Some clients who are taking prescribed neuroleptics for psychiatric problems take stimulants to counteract the sedating properties of these antipsychotic medications (Weis, 1997).
Various reports indicate that 62 to 90 percent of cocaine users concurrently drink alcohol to prolong the high and attenuate unpleasant agitation and sleeplessness that emerge at the end of a binge (Gold, 1997; Gold and Miller, 1997). However, the combination of cocaine and alcohol appears to be particularly dangerous. Researchers have established that cocaethylene, an ethyl ester of benzoylecgonine, is formed in the liver when these two substances are used together and that this metabolite is particularly toxic to the liver. A substance user who combines cocaine and alcohol may experience more intense pleasure from the experience than using either substance alone, but is also exposed to the combined toxicities of cocaine and the even more potent cocaethylene (Gold, 1997; Cornish and O'Brien, 1996). Mendelson and colleagues found that a combination of ingested alcohol and injected MA increased users' perception of intoxication as well as cardiac responses, with potential for more serious cardiovascular consequences (Mendelson et al., 1995). Yamamura and colleagues found the combination aggravated both somatic and mental disorders (Yamamura et al., 1992). Because cocaethylene has a longer half-life (2 hours) than cocaine (38 to 60 minutes), the cumulative and additive effects found in the combination increase the incidence of lethal heart attacks and stroke (18 times higher risk of sudden death than with cocaine alone).
Cocaethylene appears to prolong the duration of cocaine-related increases in blood pressure and, in turn, to increase the likelihood of small vessel intercerebral infarcts. In addition, cocaethylene increases the risk of panic and anxiety attacks that chronic cocaine users experience, especially those that persist for some time. There is some indication that cocaethylene produces greater irritability and more persistent withdrawal complaints (Gold and Miller, 1997). The role of cocaethylene in evoking violence and intensifying agitation is also being investigated (Schrank, 1993).
Concomitant use of benzodiazepines and cocaine to blunt dysphoric effects is also common. This combination may enhance respiratory depression and prolong altered mental states, but decrease risk of seizures--especially if diazepam is taken before cocaine is used (Schrank, 1993).
The popularity of marijuana among stimulant users is explained by its pharmacologic properties. Because marijuana induces vasodilation of nasal mucosa, it attenuates the vasoconstriction of cocaine so that absorption is increased. Smoking marijuana before snorting cocaine decreases the time to peak euphoric effects, decreases dysphoric effects, and increases peak cocaine levels apparently by increasing bioavailability (Gold, 1997).
It is believed that most stimulant users have concurrent psychiatric disorders. A 1991 survey of nearly 300 treatment-seeking cocaine users found that more than 70 percent had a lifetime history of psychiatric disorders such as alcoholism, major depression, bipolar disorder, anhedonia, anxiety, phobias, antisocial personality, and childhood AD/HD (Rounsaville and Carroll, 1991). At least four other earlier studies found similar comorbidity of cocaine with most of these same psychiatric diagnoses in addition to PTSD (Majewska, 1996). As many as half of surveyed cocaine users in treatment have lifetime diagnoses of depression; 20 to 25 percent have cyclic mood disorders; and sizeable percentages of these clients report borderline or antisocial personality, PTSD, or residual AD/HD (Gold, 1997). These psychiatric disorders are more common among stimulant users than in the general population (Weis, 1997).
Identified anxiety, phobias, AD/HD, and antisocial personality disorder typically precede cocaine dependence, whereas alcoholism, depression, and paranoia generally follow stimulant use. Although the symptoms of stimulant-induced psychosis closely mimic those of schizophrenia, and heavy use of cocaine/amphetamines may precipitate latent schizophrenia, the two disorders are not closely correlated (Majewska, 1996). Panic attacks are another correlate of cocaine use. Risk for this problem may increase because of sensitization to cocaine (Gold, 1997).
Differentiating comorbid psychiatric disorders from stimulant-related disorders can be challenging. Acute or chronic stimulant intoxication can elicit symptoms of anxiety that are indistinguishable from phobias, obsessive compulsiveness, panic, and generalized anxiety. The parallels between symptoms of stimulant-induced psychosis and schizophrenia are well known. Withdrawal from stimulants can cause depression that is indistinguishable from major depression from other causes (Gold and Miller, 1997). It can take at least a month of abstinence from all stimulant use to differentiate stimulant-induced dysphoria, depression, paranoia, or anxiety from a true psychiatric disorder.
The prognosis for substance use disorders is worsened by the presence of other untreated psychiatric disorders (or substance use disorders). Clients with comorbid psychiatric and drug dependence disorders need to have both treated; the psychiatric problems usually improve with abstinence. Antidepressant and neuroleptic medications with low anticholinergic and sedative properties are preferred in order to avoid another addiction. Sedative-hypnotics and benzodiazepines must be used with caution in high-risk populations (Gold and Miller, 1997).
Any preexisting acute or chronic physical conditions are also likely to be complicated and exacerbated by the stress of stimulant intoxication and withdrawal. Particularly dangerous coexisting medical conditions include any history of seizures, coronary heart disease, cardiac or thyroid problems, hypertension, or respiratory and pulmonary disease. Hypertension, renal failure, and diabetes mellitus, which are risk factors for stroke, can be exacerbated if cocaine/crack is smoked (Cornish and O'Brien, 1996).
Clients who are already taking medications for other medical conditions may be at special risk if stimulants are mixed with, for example, antidepressants, medications for high blood pressure, or antipsychotics. The effects of such drug interactions may be difficult to predict.
Crack- or MA-using mothers may be identified during prenatal care or in the delivery room through pregnancy or delivery complications, positive urine toxicologies, or acknowledged histories of substance use. Newborns who were exposed to stimulants in utero may manifest neurobehavioral problems that are less obvious and dangerous than those seen in opiate- or alcohol-exposed counterparts. The symptoms of stimulant exposure in newborns are likely to be transient and not require direct intervention. However, the young babies are typically irritable, tremulous, lethargic, emotionally labile, and somnolent. They may have a pronounced startle reaction, CNS instability, and prolonged and inconsolable crying. A few have signs of vascular disruptions and, rarely, congenital malformations, particularly of the heart, gastrointestinal tract, or skeletal system. Risk of sudden infant death syndrome may be heightened slightly.
Management is primarily by close observation in a quiet nursery environment, gentle handling, careful attention to feeding habits, and promoting positive bonding with the mother. More information about assessing, diagnosing, and managing the stimulant-exposed neonate can be found in TIP 5, Improving Treatment for Drug-Exposed Infants (CSAT, 1993).
Patients appearing in hospital emergency departments following mild to severe traumas may be stimulant users who have been involved in fights or accidents of various types. The incidence of broken hands after fighting seems to be particularly high among MA users. TIP 16, Alcohol and Other Drug Screening of Hospitalized Trauma Patients (CSAT, 1995b), provides relevant information regarding how to identify and manage trauma patients with acute or chronic substance use disorders, including stimulant abuse. Several widely used screening instruments that can help hospital personnel determine substance use status of conscious trauma patients are described, as are laboratory tests to determine substance use status of any individual with potential symptoms of substance use, abuse, or dependence.
Diagnosis can be based on established DSM-IV criteria for amphetamine or cocaine abuse/dependence and other listed composites (American Psychiatric Press, 1994). For treatment reimbursement, the diagnosis may also need to reflect criteria according to the International Classification of Diseases (American Medical Association, 1997). Arriving at a diagnosis is simplified by having information available from a relevant and accurate client history, a urine toxicology screen or similar laboratory tests, and clinical observations of physical signs and mental status.
An appropriate substance use history should include the substance(s) and medications used during the last 30 days; the specific substance(s) or combinations typically used with the usual dose, frequency, and route of administration; the duration of use; and the time and amount of last use, as well as when the symptoms or complaints developed and how they have progressed. If the client has been bingeing, a brief description of this and previous episodes is helpful. In addition, the history should include information about any previous seizures, delirium tremens, heart and pulmonary problems, paranoid reactions (with or without delusions and hallucinations), and other serious medical and psychological conditions and psychiatric diagnoses, as well as all current medications the client is taking. Although people with stimulant use disorders are not as likely as those with other types of substance use disorders (i.e., alcoholics) to have a genetic component or familial history, information about other substance abuse or psychiatric problems in the family can be enlightening.
For most patients presenting in an ER, the substance and medical history will, of necessity, be brief and focus on the potential causes for the observed symptoms and complaints and any potential medical or psychological problems that are likely to complicate management and the patient's response. Stabilize the patient medically before trying to take a history and assess potential danger to self or others; beware of exaggeration or dismissal by the patient of his symptoms and condition; and use significant others, whenever possible, to validate his history. In situations where the patient is delirious, psychotic, or unable to respond, information from accompanying friends or significant others about the antecedents of the problem is particularly important. Sometimes, the substance history must await symptomatic management.
The history may be supplemented by a variety of screening instruments constructed to ascertain substance use disorders, although these are not notably reliable if used with acutely psychotic or intoxicated individuals. A number of these screening instruments are described in detail in TIP 16, Alcohol and Other Drug Screening of Hospitalized Trauma Patients (CSAT, 1995b).
A urine screen or toxicology test may be used to identify which substances the client has used recently. This testing is vital to confirm clinicians' personal assessments and observations. Some ERs have bedside or patient-side urine immunoassay testing kits (dipstick tests) that can be used for a quick turnaround without waiting on more formal assays. These can be validated by additional laboratory studies that require 6 to 8 hours or longer for processing in a hospital setting.
The results of either dipstick or Enzyme Multiplied Immunoassay Technique (EMIT) tests are appropriate to use for medical purposes, but cannot be used for criminal prosecution because no chain of custody is established. Alternative techniques for determining substance use are analyses of hair, blood, sweat, or tissue samples. In general, however, urine has become the standard method of determining substance use in an individual, and tests are readily available in the medical setting where other types of testing are not. Urine screens are less expensive than drawing blood samples for testing or other alternatives. Both qualitative and quantitative urine assays are usually needed to verify use and time/amount taken. Repeated assays may be used to track elimination of stimulants from the system if large amounts have been detected.
Because no standard set of substances is tested in a urine substance screen, medical personnel should make certain that assays for suspected substances are included. Also, no toxicology screen can determine with certainty that any particular substance--or any substances at all--was ingested. The detection limitations may be too broad or the specific substance may have been completely metabolized before a urine specimen was collected. A positive report will not necessarily indicate when the substance was last used: Metabolites for some substances are detectable for days or weeks after last use, but take some time after substance administration to be detectable in urine (CSAT, 1995b).
Stimulants can be detected in urine for approximately 24 to 48 hours following use and, maximally, for 3 days after a single dose and 7 to 12 days following repeated high doses (American Psychiatric Press, 1994). Cocaine is excreted more rapidly and is more difficult to detect in urine samples than MA. However, an EMIT test can detect benzoylecgonine, an inactive cocaine metabolite, in urine for up to 72 hours after last ingestion (Weis, 1997). Benzoylecgonine has been found in urine as late as 22 days after last cocaine intoxication in three asymptomatic clients with substantial histories of cocaine use (Goldfrank and Hoffman, 1993). Many prescription and over-the-counter drugs (e.g., diet aids, cold remedies) contain phenylpropanolamine or ephedrine that may yield positive EMIT or RIA tests for amphetamines. A procedure that does not have cross-reactivity to phenylpropanolamine or ephedrine will be needed to confirm that amphetamine was consumed (Hawks and Chiang, 1986).
Data acquired from monitoring vital signs (temperature, blood pressure, pulse rate, respiration rate) can be used to document physical indicators. In addition, observations of physical manifestations listed for acute or chronic users and from the withdrawal stage can be documented. Similarly, a variety of instruments exists to determine mental status, although observational data regarding psychological and mental status may be adequate.
In the diagnostic process, other disorders and conditions with similar or identical presentations must be considered to rule out or include them. As already noted, many stimulant users have coexisting mental illnesses such as bipolar disorders, borderline personality, and so on. Similarly, the cause of a heart attack or seizure must be determined for optimal continuing care and medical management.
Before a differential diagnosis of a coexisting psychiatric disorder (dual diagnosis) can be made, the client must be abstinent for some period of time, at least 3 to 4 weeks. The syndrome and symptoms presented can be treated meanwhile, and a diagnosis of psychotic disorder, not otherwise specified (NOS), can be given. More information regarding the diagnostic process for clients with symptoms that indicate coexisting substance use and mood disorders can be found in TIP 9, Assessment and Treatment of Patients With Coexisting Mental Illness and Alcohol and Other Drug Abuse (CSAT, 1994a).
New forms of brain imaging techniques offer a promising approach for making a differential diagnosis if current research determines that these techniques are useful for distinguishing among drug-induced and other forms of psychosis.
Because the ER may be the stimulant user's first point of contact with the medical system and potential treatment, attention needs to be given to establishing and supporting a continuum of care in which appropriate linkages among all necessary services and programs for substance users are represented. Although the burden of developing and encouraging these linkages among treatment components cannot fall to hospital staff alone, and it would be unrealistic to expect this, cooperation and enlightened self-interest are encouraged. If not hooked up to the treatment system, cocaine and MA users are likely to return repeatedly to the ER and other parts of the hospital for care of more and more serious health and mental health problems. Stimulant abuse/dependence, as all substance use disorders, is a life-long, relapsing condition that requires ongoing management and support.
Hence, treatment programs should take primary responsibility for developing linkages with hospitals, using several approaches. The most exemplary approach--and that most likely to succeed--is to have a substance abuse treatment counselor or trained nurse/social worker visit the hospital and other medical facilities regularly in order to identify, screen, encourage, and follow up clients who have stimulant-related and other substance use problems and need access to the ongoing treatment continuum. A face-to-face visit by an outreach specialist is particularly effective in supporting the crisis-precipitated motivation to enter treatment, especially if the potential client is hospitalized for some length of time. Because a crisis creates an intervention opportunity, clients may be unusually receptive to considering lifestyle alternatives and the need for longer term treatment.
It also may be realistic for hospital staff to hand out a list of available treatment facilities for stimulant use and/or other substance use disorders that is developed and provided by the substance use disorder treatment staff. However, it is not very likely that clients in crisis will follow up the suggested referral, especially if they are in the early stages of crashing (and terribly sleepy) or paranoid.
Some educational literature might also be helpful--particularly regarding withdrawal symptoms, drug-induced psychoses, and medical complications--if the client or a significant other is willing to read it. Because it is imperative for doctors and other medical staff to know about the addiction process in order to understand clients they see everyday, cross-training in the field of substance use disorder treatment is vital for learning about and actively supporting the development and use of linkages and referral mechanisms. It is believed that at least one-fourth of those treated in hospitals has some type of substance use-related problem.
Motivation for change is often difficult to determine in the substance user. Health problems may, however, be the motivation to move the individual from contemplation to action (Prochaska et al., 1992). Health care personnel working with a patient hospitalized for an acute drug episode may capitalize on the fact that the situation was so acute from drug use that he had to be hospitalized.
Hospitals often deal with a population known as "frequent flyers," that is, persons with frequent, revolving admissions to hospital ERs or inpatient hospital beds because of medical or psychiatric complications resulting from their substance use. The financial burdens can be severe for the patient and, in the case of those lacking insurance, the hospital's costs of care may be unrecoverable. A collaborative arrangement between the hospital and a local treatment facility can allow for door-to-door drug treatment.
In obtaining the client's consent for treatment, gathering information from others about his history of substance use, making referrals for continuing care, or seeking reimbursement from insurance carriers, hospital staff must be familiar with the provisions of special Federal and State laws and regulations for protection of clients' confidentiality as set forth in 42 U.S.C. §290dd-2 (1992) and C.F.R. Part 2. Intoxicated or psychotic clients may have diminished capacity for providing informed consent to treatment. If consent is obtained, even temporarily, from a relative, this may be considered a "disclosure of identifying information" and subject to Federal guidelines. In referring a client from a hospital to another treatment program and making an appointment, staff are also making a disclosure and will ordinarily need a written consent form from the client containing specified information (see Figure 5-9).
Special exceptions, however, apply to information needed in a medical emergency that can be provided to medical personnel who need health- or treatment-related facts about a client in order to treat his life-threatening condition. However, the treatment program that is, for example, providing this information to a hospital before transferring the client for emergency care, must document specific data in his record regarding the nature of the emergency, what information was released, the name of the person making the disclosure, and the date and time. Additional information about consent, confidentiality, and other types of communications governed by Federal regulations is presented in TIP 19, Detoxification From Alcohol and Other Drugs, (CSAT, 1995d).
This chapter has two purposes: (1) to provide specific recommendations for treatment tailored to the special needs of each group and (2) to underscore the need for cultural competence in the treatment setting. The second point is crucial to success in treatment for a variety of clients. The Consensus Panel feels strongly that cultural competence in the treatment setting extends beyond racial/ethnic sensitivity to understanding the mores of groups bound together by gender, age, geography, sexual preferences, criminal activity, substance use, and medical and mental illnesses. In addition, treatment providers need to understand the "culture" of their own organization, and determine how it may or may not be welcoming to members of other cultures.
This chapter discusses treatment issues specific to the following groups:
Again, treatment for stimulant use disorders for members of any of these groups must occur against the backdrop of a solid understanding of the needs of the one or multiple groups in which a client may claim membership.
The injecting cocaine user (ICU), like other injecting drug users (IDUs), poses a major public health problem by transmitting HIV and hepatitis. This transmission can occur in several ways. First, ICUs may spread infections by sharing injecting equipment with other IDUs. Second, ICUs may share needles with other populations that have their own independent risk for HIV and hepatitis, such as homosexuals and bisexuals. Third, ICUs may transmit the disease to nonsubstance users through sexual contact.
Stimulant and other substance users make up the estimated 1 to 1.5 million IDUs in the United States. Approximately 85 percent of these IDUs do not receive any drug treatment services on any given day (Lurie and Drucker, 1997). Clearly, IDUs who are not in treatment are at great risk of suffering the many consequences of continued drug injection (Metzger et al., 1993).
The proportion of these IDUs who are ICUs can be best estimated by the National AIDS Demonstration Research (NADR) program, sponsored by the National Institute on Drug Abuse (NIDA). This program has provided the most comprehensive profile of active IDUs not in substance use disorder treatment. In that program 13,475 active IDUs were assessed from 28 sites across the country. The primary injected drugs were heroin (28 percent), cocaine (21 percent), and a combination of heroin and cocaine (35 percent). These estimates appear consistent with some treatment samples. For example, 20 percent of treatment-seeking cocaine users in the Los Angeles area were found to have injected drugs in the preceding year (Khalsa et al., 1992). Moreover, 94 percent of these ICUs reported sharing needles with other users. Together, these data suggest that somewhere between 20 percent and 51 percent (cocaine alone and combined cocaine-heroin users) of IDUs are cocaine users and that these users share injecting equipment that is putting them at risk for HIV, hepatitis, and other diseases.
One factor that may increase risk of infection among ICUs is their pattern of use. Cocaine is frequently used in intermittent cycles of repeated multiple uses known as binges. Indeed, this pattern of use has been confirmed in human laboratory studies (Ward et al., 1997). This pattern often leads to more frequent injections during a binge than are generally observed in heroin-dependent populations. Moreover, injecting cocaine users often share needles with more people then those who report injecting other drugs.
Indeed, this greater frequency of injection during a binge appears to have as its consequence a greater likelihood of HIV infection. The frequent use of cocaine during binges, along with greater likelihood of shared needles, has been demonstrated to cause twice the risk of HIV infection for ICUs than for other IDUs (Chaisson et al., 1989; Anthony et al., 1991), and 1.5 times the risk of crack smokers (Kral et al., 1998).
A variety of interventions has been used to reduce the consequences of injection drug use (for reviews see Des Jarlais and Friedman, 1996; Sorenson, 1991). These interventions are tailored to injection drug users (IDUs) in general, yet the results from this research are more applicable to ICUs. It is important to note that education alone may not be effective in preventing the consequences of injecting drugs, because studies have shown that such programs increase knowledge without changing behavior.
Evidence shows that multicomponent HIV prevention programs, which include instruction on bleach disinfection along with skills training, counseling, and HIV testing, reduce the risk of transmission over time (Institute of Medicine [IOM], 1995). However, these results have not been supported in other studies, which failed to prove the efficacy of bleach disinfection. This may be caused by either ineffective disinfection procedures or inconsistent use of effective ones. The 1995 Report on the Prevention of HIV Infection, sponsored by the Institute of Medicine, recommends that bleach disinfection, when performed according to the guidelines provided by the Centers for Disease Control and Prevention (CDC) and the Center for Substance Abuse Treatment (CSAT), is likely to prevent HIV infection for IDUs who share injecting equipment. The IOM report recommends that IDUs be trained in effective procedures and more research be conducted to identify the simplest effective disinfection procedures. Expanding that view, Des Jarlais and Friedman stated that, as currently implemented, bleach disinfection should not be relied on by HIV prevention programs (Des Jarlais and Friedman, 1996). They suggest, however, that bleach disinfection is more effective than not and should be performed when equipment is shared.
Needle exchange programs have been implemented in a wide variety of circumstances throughout the world (Hurley et al., 1997). The vast majority of studies and reports on needle exchange procedures suggests that they reduce the risk of HIV and hepatitis, and neither lead to more injecting drug use nor create new IDUs (Hurley et al., 1997; IOM, 1995).
Some populations received no noticeable benefit from these programs, however. For example, a drop in HIV infection was not seen in Montreal. One possible reason for this is that Montreal's needle exchange program restricted the number of needles a client could obtain per visit--fewer needles than ICUs typically use in the course of their drug use. Consequently, clients turned to other needle sources, negating the effect of the program.
Although these data tend to support the use of needle exchange programs, no controlled trial has yet to be conducted. The IOM report recommends that communities that desire such programs be permitted to use them. It also recommends that needle exchange be implemented as part of a multicomponent treatment, and that additional research and evaluation be conducted to evaluate the effects of needle exchange programs.
Research has found that men who have sex with men (MSMs) and who abuse alcohol, stimulants, inhalants, and other noninjection street drugs are more likely than non-substance users to engage in unprotected sex and become infected with HIV (Paul et al., 1991, 1993, 1994). Sexual risk-taking among MSMs, like that among the general population, often occurs under the influence of substance use, particularly stimulants. Sexual risk-taking within the context of substance use is hypothesized to occur due to disinhibition effects, learned patterns (especially between stimulant use and certain high-risk sexual practices), low self-esteem, altered perception of risk, lack of assertiveness to negotiate safe practices, and perceived powerlessness (Paul et al., 1993).
Alternatively, sex networks and sexual mixing patterns (Renton et al., 1995) might better explain the higher risk of HIV infection related to substance abuse among MSMs. As suggested by Renton and colleagues, MSM substance users may form tightly defined groups characterized by higher HIV seroprevalence rates, higher sexual mixing, greater injection drug use, and more trading sex for money, food, and drugs. These factors, rather than the suggested links between substance use and high-risk sex, would therefore account for higher HIV risks among MSM substance users. Regardless of which hypothesis better explains the connection between substance abuse and HIV/AIDS among MSMs, HIV/AIDS clearly intertwines with substance abuse. Unfortunately, similar to IDUs, it is estimated that only 10 percent of all MSMs who abuse substances seek therapy at substance use disorder treatment centers. Because of the stigmatization of MSMs, HIV-infected MSM substance users either do not seek treatment at traditional substance use disorder treatment centers, or they remain "closeted" when they do attend treatment.
Outreach strategies for HIV prevention may readily translate to substance use interventions. In addition, there tends to be a stigma against substance users in the gay community, and outreach workers must be prepared to help clients overcome the stigma in order to get into treatment.
Of concern in this population is that any injection drug use, and use of injected methamphetamine (MA) in particular, increases the risk of HIV and/or hepatitis transmission from needles as well as from drug-induced bad judgment, feelings of invulnerability, risky behaviors, and repetitive and prolonged sexual behavior. A study of MA-using gay men in Los Angeles found that 62.5 percent of all participants reported having anal sex without a condom, and 56.3 percent reported having sex with someone who had HIV (Frosch et al., 1996). For counselors and outreach workers, risk assessment, including use analysis focused on how sex fits into the use patterns, is critical. It is important in the assessment process to capture these patterns.
Education of counselors, as well as clients, regarding the particular effects of this class of drugs is extremely important. Recently, there has been some backsliding with regard to injection drug use and sexual behaviors because of the perception that the new AIDS drugs mean a positive diagnosis is no longer automatically a death sentence. Not only does this myth need to be countered, but information on the effects of long-term stimulant use could diminish the attractiveness of MA-enhanced sexual performance. Side effects of long-term use include diminished sexual desire and performance. With ice in particular, clients show decreased ability to achieve orgasm, briefer erection periods, and an increase in impotence. Finally, counselor education needs to ensure lack of bias and sensitivity to the sexual practices of gay men.
Cocaine and heroin are sometimes used together in a practice commonly known as speedballing. Some clients claim that methadone lengthens and mellows the effects of cocaine, presumably attenuating the negative reinforcers associated with cocaine crash (Condelli et al., 1991). Some patients also use alcohol or benzodiazepines or both concurrently with cocaine and heroin to reduce these effects of the cocaine crash, often marked by anxiety, depression, fatigue, and jitteriness. Thus, just as heroin use can increase the likelihood of cocaine dependence, cocaine use can increase the risk of heroin dependence (Dunteman et al., 1992).
Although methadone is very rarely combined with MA, there are some issues in this population of which counselors should be aware: treatment difficulties, medical risks, cocaine use, counselor training, and need for enhanced services.
Stimulant abuse rates among methadone clients vary by program but range from 40 to 60 percent in inner city populations, according to data on positive screens for cocaine. These data suggest that the routes to MA use are established, and further study may be required to determine the extent to which they are used. In addition, data show a very high number of sedative users, including users of benzodiazepines, among methadone clients.
Individuals with co-occurring mental disorders may be defined as those persons with coexisting stimulant use and/or other substance use disorders and any of the following disorders:
It is critical to be aware of the fact that a DSM-IV diagnosis of a mental disorder is different from the mere production of symptoms (American Psychiatric Press, 1994). For example, most stimulant users will enter treatment exhibiting symptoms of depression. Similarly, many MA users will exhibit psychotic symptoms that are quite common in schizophrenics. However, the symptoms of depression are not the same as the psychiatric illness of depression, nor are the psychotic symptoms evidence of schizophrenia. Many of the symptom clusters, commonly associated with specific psychiatric disorders (e.g., depression, anxiety, psychosis, bipolar mood fluctuations, antisocial behavior) are frequently seen during the use of stimulants or during the period of early abstinence.
In fact, many individuals will bring their psychiatric diagnosis into their substance use disorder treatment evaluation. Many stimulant users have sought psychiatric care for their stimulant problems before entering treatment (many individuals apparently feel it is preferable to have a diagnosis of depression or bipolar illness to substance dependence). Therefore, they will contend that they have a psychiatric disorder and require psychiatric care (i.e., medication, psychotherapy) rather than substance use disorder treatment.
It should not be assumed that because an individual has received a previous psychiatric diagnosis, or because she has symptoms typically associated with a psychiatric disorder, that she is necessarily a "dual diagnosis" client. The accurate diagnosis of psychiatric comorbidity among stimulant users requires considerable diagnostic sophistication. It is often necessary to make a provisional diagnosis, which is modified after additional data are collected. For many cocaine users, it is often necessary to have 1 to 2 weeks of cocaine abstinence; for MA users, it is often helpful to have 30 days of abstinence to make an accurate psychiatric diagnosis. Another important element in the diagnosis is to obtain a careful history regarding the historical relationship between the onset of psychiatric symptoms and the substance use history.
Dual diagnosis will often encompass three or more coexisting conditions. Clients who use stimulants may or may not have an underlying psychiatric disorder, and it is often impossible to discern the source of behaviors symptomatic of a psychiatric condition until the client is substance-free. In many cases, a month's abstinence will be required before an accurate psychiatric assessment can be completed. Although treatment of clients with a dual diagnosis can be complex, this population often hits bottom faster and therefore enters treatment more quickly, and often with more motivation, than do clients who use substances without the more serious underlying problems.
Consensus Panel suggestions for treatment interventions for persons with a stimulant use disorder and a coexisting psychiatric disorder are discussed in the sections below.
Symptoms of depression may occur as part of the use of or withdrawal from stimulants. Where possible, it is helpful to wait to treat depression until the client has begun recovery from a substance use disorder, and the Consensus Panel recommends waiting to use medication to treat depressive symptoms if at all feasible. However, if the client is suicidal, hospitalization is the recommended course of action.
Clients with bipolar disorder may be treated in traditional treatment settings if they are well controlled on their medications for the bipolar condition. Use of stimulants can initiate a manic episode. Therefore, medication management is one of the most important issues in treating clients with bipolar disorder.
The diagnosis of antisocial personality disorders (ASP) is directly affected by substance use behavior. For example, many behaviors associated with chronic MA use mimic ASP, including law breaking, aggressiveness, and poor impulse control. Both cocaine use and ASP are associated with violence.
Many clients with ASP are involved with the criminal justice system, so coordination between systems (substance use disorder treatment, mental health, physical health) is important. Generally, men are more likely than women to present with ASP, and men typically use substances at a higher rate. Therefore, programs that are geared toward male clients with ASP and criminal involvement are necessary in a substance use disorder treatment system.
Cocaine use can induce panic disorders, which can act as a trigger for panic attacks even after a client is substance-free. Panic disorders seem to be common for both cocaine and MA users long after they have discontinued using the drug and are often associated with depressions secondary to cocaine withdrawal. Health care providers should exercise extreme care in prescribing benzodiazepines for this disorder, due to their high addiction potential. Cognitive-behavioral techniques to recognize and manage symptoms may be some clinically useful strategies.
Often, women who use ice are at an increased risk of PTSD because of substance-related episodes of domestic violence, sexual assault, and incest.
Recommended treatment approaches include referring clients to sexual assault and incest support groups as quickly as possible. Group counseling should be available in a woman-only format and should include coaching on what to expect from dreams, fears, and sleep disruptions as a result of PTSD and withdrawal from ice. Information on practical tools to combat nightmares such as night lights, herb teas, relaxation techniques, as well as information on relapse triggers, will provide clients with reassurance and skills to get through this period.
Counselors need special training to work with individuals with a co-occurring substance use disorder and PTSD. Issues include relapse triggers, timing of addressing issues in group sessions, and the tools and social skills women need in order to facilitate a successful recovery.
The prevalence of AD/HD in the general population ranges between 3 and 9 percent of adults. In the population of adults with substance use disorders, the prevalence of AD/HD ranges between 1 and 5 percent. However, one study has found that in the population of persons with adult AD/HD 40 percent had co-occurring substance use disorders, generally involving marijuana or alcohol (Biederman et al., 1993, 1995). These substance use disorders were detected when the clients entered treatment for AD/HD.
It is critical to retrieve a clear longitudinal history of both substance use and symptoms of AD/HD prior to completing a diagnosis of co-occurring disorder. Side effects of cocaine use can mirror some symptoms of AD/HD, but they disappear when use ceases. Generally, persons with adult AD/HD had the disease when they were children, although it may not have been diagnosed as such. It is important to include an assessment of childhood symptoms when completing the client's history. The presence of AD/HD symptoms in childhood provides a reliability measure for the presence of the adult disease.
Estimates of the prevalence of substance use disorders in the schizophrenic population range from 30 to 50 percent. Much of this use stems from peer group-seeking behaviors. Using substances is normal, it's what the other people on the streets are doing, and substance use can give persons with schizophrenia the sense of well-being and fitting they otherwise lack.
It is important to treat substance use in clients with schizophrenia immediately in order to allow medication for the mental illness time to take effect. A person with schizophrenia who continues to use cocaine will become fully psychotic, and those who continue to use MA will develop a psychosis indistinguishable from that created by paranoid schizophrenia.
After a stabilization period, treatment for both conditions can occur simultaneously with slight modifications. Modified group counseling may be used to treat substance use disorders. However, groups must be smaller and more controlled than in traditional substance use disorder treatment, and confrontational settings should be avoided. To be effective, each group session should focus on a particular skill or topic.
This section refers to clients who are undergoing treatment for a substance use disorder and who have one or more co-occurring medical disorders. Good clinical practice suggests that, prior to initiation of treatment for a substance use disorder, each client should be given a thorough physical examination. Followup should include contact with the clients and other providers and review of treatment records from them. In addition, treatment providers should be trained in the following:
Finally, it is important to note that linkages between substance use disorder treatment providers and the physicians and specialists who treat the client can improve treatment outcomes for the client.
This section discusses some medical conditions that require particular attention on the part of the substance use disorder treatment provider: epidemiology, diabetes, and HIV/AIDS.
Chapter 5 of this TIP discussed some of the common medical illnesses seen in substance-using populations. Because the stimulant-using population tends to be younger, the medical conditions are not generally as severe as observed in the population of substance users as a whole. For example, because most persons who use stimulants range in age from 25 to 35 years, they do not present with conditions common to middle and old age such as coronary artery disease. Generally, primary medical problems are dental, dermatological, ear, nose, and throat, otitis media, nutritional (very thin clients who either use cocaine, have AIDS, or both), asthma, neurological disorders, seizures, and residual problems from a stroke. Secondary conditions include blood borne diseases, HIV, hepatitis, and sexually transmitted diseases.
Stimulant users in particular present higher rates of thyroid problems, in the form of permanent hyperthyroidism or hypothyroidism. This may be attributed to impure MA, resulting in a chemical, tissue-specific reaction in the thyroid, but more research needs to be performed in this area. For a complete list of the general medical complications of stimulant use, please refer to Chapter 5.
Persons who use stimulants are often at risk for hepatitis, which, due to the ease of global travel, is no longer restricted to Third World countries. The Centers for Disease Control and Prevention (CDC) estimates that 150,000 people in the United States are infected each year by hepatitis A alone. The CDC lists household or sexual contact, sharing of infected needles, and recent international travel as the major known risk factors for transmission of hepatitis A. Hepatitis B virus (HBV) is a more virulent form of the disease and is much more prevalent than HIV, with an estimated 1.2 million Americans currently chronic carriers of HBV. Hepatitis B may develop into a chronic disease (which means lasting more than 6 months) in up to 10 percent of the 200,000 newly infected people each year. If left untreated, the risk of developing cirrhosis (scarring of the liver) and liver cancer is increased in clients with chronic hepatitis B. Treatment programs for stimulant users should include a screening for hepatitis in each client's initial assessment.
Another important initial screening for persons with stimulant use disorders is that for HIV. Clients may be reluctant to undergo an HIV test because they fear the results. However, being diagnosed negative can act as a powerful motivator for stimulant users to comply with treatment more fully, once they no longer fear that they will develop AIDS. Testing negative can also encourage clients to practice preventive measures in other areas of their lives. Testing positive, although discouraging to the client, is an important part of the screening that the treatment provider needs to be aware of. Once the HIV status of the client is known, treatment can be planned that will include a medical component in the substance use disorder recovery program.
However, some special issues remain. One of the critical aspects of providing substance use disorder treatment to persons with HIV or AIDS is the continuing education that providers need regarding the changing and complex array of medication regimens available to this population. In addition, providers should know that clients with HIV/AIDS, armed with these new medicines, are approaching life differently. Now that they know they will live longer, they may return to using substances.
An issue with stimulant use is the increased risk of contracting HIV through the high-risk sexual behavior facilitated by the drug. By and large, clients have grown more aware of the risk of transmission from needles, although this is an area that requires further study. Cocaine users have more opportunities for exposure to HIV than do other stimulant users because they require multiple injections to maintain a high and therefore may run out of needles more quickly and be tempted to share. Bartering sex for drugs is a more likely route to HIV infection than unclean needles for MA users, because MA requires fewer injections.
Treating clients with HIV/AIDS is another area in which program linkages become critical to successful treatment. It is helpful, where possible, to have staff and nurses skilled in each type of treatment situated to provide clients convenient access. Anecdotal data from providers indicate that clients tend to get lost on the way to a referral appointment, and co-locating providers, such as an obstetrician-gynecologist in a methadone clinic, helps to mitigate this problem. For more information on this topic, please refer to Treatment for HIV-Infected Alcohol and Other Drug Abusers (TIP 15) (CSAT, 1995a; revision in press).
A significant amount of crime is committed by substance users, and it is important to carefully assess this population. Many persons in the criminal justice system commit crimes while inhibitions are reduced by substance use, and others steal in order to buy drugs. These types of clients form the target treatment population. Other persons in the criminal justice system simply sell drugs but do not use them, or use drugs but are not addicted to the particular drug they sell. Self-report data indicate that 72 percent of persons in the criminal justice system are substance-dependent. These clients are often extremely complex in terms of case management: One client may have simultaneous involvement in the criminal justice, substance use disorder treatment, and mental health systems. There is little research on the specific issues faced by criminal justice clients with stimulant use disorders.
For more information on this topic, please refer to TIP 12, Combining Substance Abuse Treatment With Intermediate Sanctions for Adults in the Criminal Justice System (CSAT, 1994c); TIP 17, Planning for Alcohol and Other Drug Abuse Treatment for Adults in the Criminal Justice System (CSAT, 1995c); TIP 21, Combining Alcohol and Other Drug Abuse Treatment With Diversion for Juveniles in the Justice System (CSAT, 1995e); TIP 23, Treatment Drug Courts: Integrating Substance Abuse Treatment With Legal Case Processing (CSAT, 1996); and TIP 29, Continuity of Offender Treatment for Substance Use Disorders From Institution to the Community (CSAT, 1998b).
One of the most important issues in developing treatment options for different racial/ethnic groups is to move beyond cultural sensitivity and into cultural competence. Cultural competence is not just an understanding of superficial ethic designations but instead a knowledge of regional and socioeconomic patterns.
Cultural competence is critical for working in the drug treatment field today, because providers need to be culturally sensitive when working with diverse populations. Progressively increasing levels of cultural capacity include:
Cultural sensitivity involves a basic understanding and appreciation of sociocultural factors as these relate to the client's treatment needs and the choice of relevant treatment. Cultural competence involves a greater depth of understanding of the client's needs within the client's cultural context. It also involves greater skills and experiences that allow working with cultural nuances as presented by the client, and the capacity to interpret deeper meanings in the client's thoughts and behaviors. Cultural competence aids in making better treatment decisions because it is based on a more effective matching of the client's needs with the relevant treatment options.
Outreach issues will be specific to the targeted ethnic population, but topics to consider for each include
Many of the above considerations involve slowing down the course of treatment to accommodate racial/ethnic mores. Of concern to the Consensus Panel is the method of payment for this type of care. Managed care is reluctant to fund long-term treatment or treatments that cannot be reduced to billable units.
According to 1990 census data, approximately 25 percent of the U.S. population lives in rural areas. Colorado, Idaho, Montana, New Mexico, North Dakota, Nevada, South Dakota, Utah, and Wyoming have been identified as "frontier States," with at least half of their counties possessing six or fewer persons per square mile. All of these are western States--in which MA use is high.
The National Household Survey, conducted by the Substance Abuse and Mental Health Services Administration (SAMHSA), revealed that large metropolitan areas and rural areas had similar rates for substance use among youths 12 to 17 years old (SAMHSA, 1998). What differed was the specific substances used, not the prevalence of substance usage.
Strict regulatory controls on lawfully manufactured MA limit its diversion from licit to illicit channels. The bulk of MA currently on the streets has been illegally manufactured in clandestine labs. Rural areas are at high risk for being targeted by drug manufacturers and dealers. A rural community offers secluded areas in which to produce illegal drugs and access to major transportation routes for distribution with minimal risk of discovery by law enforcement. Small towns tend to be on major highways and interstates, which facilitates transportation to other regions for sale and distribution. This is a risk factor that many rural and/or frontier communities are unprepared for because they often lack the treatment resources or the community infrastructure, such as police forces trained specifically in dealing with these issues. This can lead to swift and severe problems for ill-prepared communities.
The number of MA treatment facility admissions is highest in the western States where they now surpass cocaine admissions. Primary MA admission rates are beginning to rise in some southern and midwestern States.
In the State of Nevada, (a frontier State), the client data system for 1997 admissions to publicly funded substance use disorder treatment centers reported that of those individuals seeking treatment for substance use disorders, 52 percent were seeking treatment for MA use.
Rural areas face the challenge of providing access to services for clients who may live hundreds of miles away from the nearest treatment provider. An entire day might be spent traveling by car to a service provider, because most rural areas lack public transportation.
Rural areas usually have a fragmented service system and limited resources. The lack of medical and social services in rural areas prohibits any continuum of care or even referral for specialized care. In many rural communities there are no treatment services available. Often only one social service provider is available and is generally overwhelmed by the various needs of the community. Social service agencies in rural areas tend to be multiservice agencies out of necessity.
Rural communities are generally allocated minimal funding for treatment because funding is usually based on population, which results in the provision of minimal services. There are rarely any sources within the community from which to seek additional funding. The lack of adequate funding limits staffing, staff salaries (which contributes to a high staff turnover), and the ability to provide support services such as childcare or transportation in the areas where that support is needed most.
Confidentiality is rare in rural settings. There is no anonymity in a small rural community. Everyone knows everyone and observes each other's comings and goings. Most rural communities' lack of available and appropriate office space leaves treatment providers practicing in whatever space they can find--which often involves little privacy.
Continuing education for treatment providers is nonexistent in most rural areas. Consequently, treatment providers often lack the most current information in the field.
The following are various strategies that can help provide treatment services to rural populations:
Treating stimulant use disorders in women can involve a host of complex issues (including pregnancy, children, domestic abuse, and socioeconomic problems) that can impact diagnosis and treatment of stimulant use disorders. However, although women's use of stimulants has not been well studied, one recent study does point to a gender difference in women's response to cocaine (Lukas et al., 1996). In addition, in recent studies of MA use, the percentage of female MA users appears higher than with samples of cocaine or heroin users (Rawson et al., 1998a).
Although MA use is traditionally associated with males, growing numbers of women are using this class of drug, for reasons ranging from a desire to lose weight to the wish to be a "superwoman" who must self-medicate to get through an overextended day. Data on women who were sexually abused as children suggest they use cocaine as adults in order to "feel better."
There are a number of entry points in the system for women who might not present directly for treatment, including
Two types of barriers must often be addressed concerning outreach to women who use substances, including stimulants. First, internal barriers to seeking treatment for substance use disorders that include guilt, depression, fear of children being taken away, and fear of partners who are using or dealing drugs must be identified and mitigated. Second, external barriers to be examined include lack of accessibility to treatment programs, need for child care, or lack of community-based programs that prevent women from seeking treatment. Often, reducing just one barrier is enough to bring a woman into treatment. For example, treatment programs that provide child care may have higher participation levels than those that do not.
Treatment programs must focus on the physical health of the woman entering treatment. Anecdotal data suggest that women experience more rapid physical deterioration than men from MA and cocaine use, but there is no solid research base to support this observation. Generally, by the time women get into treatment they are sicker than their male counterparts. In addition, women who are not in the workplace may have used the drug for a longer period of time without detection than their working counterparts and will be in worse shape when they do enter treatment.
Treatment programs must also consider the type of stimulant used. Ice, because it is a drug that is often used in family or community settings, exacerbates all of the women's issues described in this section.
Treatment for women should involve a holistic approach, including consideration of the following:
One relapse issue to consider for female clients is the negative impact of long-term MA use on sexual performance--the drug may cause women to lose sexual desire and the ability to achieve orgasm. However, they may also resort to MA or cocaine use, if pressured for sex, in order to get through the experience. In addition, women who return to the community to live, but who are living in a dependent relationship, may need to trade sex for food and shelter. This pressure for sex can lead to a resumption of substance use.
Intensive outpatient programs, which at first glance may appear to be more accessible to women with children, in fact present their own barriers. Programs that require frequent onsite visits but do not provide child care onsite will not enhance compliance with the treatment regime.
Adolescents can present many issues of concern besides their stimulant use. The path to abuse and dependence for this group may start because of general substance and alcohol experimentation, negative peer group or gang exposure, attempts to self-medicate for undiagnosed mental health conditions, poor self image (e.g., the desire to lose weight), the need to fabricate confidence to facilitate criminal activities, or any combination of these and other issues confronting adolescents. Other contributing issues may include anxiety, depression, loneliness, coping with past sexual or physical victimization, homelessness, and teen pregnancy.
The adolescent population is comprised of three subgroups:
A common treatment principle across all subgroups is that, to adolescents, the concept of death is so remote as to render scare tactics useless in pursing lifelong sobriety. However, this population offers hope to treatment providers because adolescents are not yet entrenched in their illness, and if substances can be removed from their lives, they can move on and learn with the rest of their peer group. Although there are many problems inherent in treating this population, the rewards of success can be that much greater.
Although national studies at this time do not show evidence of high usage rates of MA or cocaine, these substances warrant attention for at least two reasons. First, adolescents tend to be multiple substance users, so an increase in use rates reported for other substances and stimulants can be somewhat indicative of trends in use of MA, and second, adolescents tend to use substances that are convenient to obtain; therefore rates of use are likely to be higher in areas with ample availability.
Nationally, the 1996 Monitoring the Future Study revealed an increase in opiate and cocaine use among 8th, 10th, and 12th graders, and teens in particular doubled opiate use (NIDA, 1998b). Amphetamines are not high on the list of drugs, with 2 to 3 percent of adolescent respondents reporting use during the period surveyed.
In terms of regional use by adolescents, problem areas include the West Coast, Midwest, and Hawaii. In California, rates of MA use among adolescents are higher than marijuana use. In Hawaii, data from Adolescent Drug Abuse Diagnosis (ADAD) (treatment programs that receive State funding) show that younger people (11 to 12 years old) are coming into treatment for ice use, indicating an even earlier initiation of gateway drugs leading to ice. In Arizona, although there are no data on the prevalence of MA use among adolescents, the proliferation of labs in both the inner city and all over the region, including home-based labs, suggests higher availability and therefore higher use among youth in this State.
Cultural and socioeconomic factors may also predict use in the adolescent population. In Hawaii, use patterns among Hawaiian and Filipino youth are related to the higher use patterns of their cultural groups as a whole. By contrast, MA use is not yet a big issue among Native American adolescents. MA use by youth is higher in lower middle class and working class neighborhoods, but adolescents from all socioeconomic classes use MA.
Outreach to the adolescent population must focus not only on identifying high-risk youth but must also on identifying the most effective methods to reach them. High-risk youth will often have low motivation, drop out of high school, and show early involvement in low-level criminal activity. Often they have a number of hard to treat psychiatric issues, such as conduct disorder, depression, and AD/HD.
Outreach workers should get to these youths as early as possible. Counselors, teachers, school administrators, and others who work with young adolescents need training to identify behaviors that, if left unaddressed, can contribute to later abuse of substances, including stimulants. Generally, the more problems observed in an adolescent, the more she will be at risk for substance and stimulant abuse and dependence.
Although data are not stimulant-specific, it is useful for persons who work with adolescents to know that very often there is a psychiatric disorder that precedes the substance use disorder. It is important to treat the psychiatric problems in order to prevent self-medication. In addition, this group of adolescents tends to be impulsive, which puts them at higher risk for using substances. Adolescents with depression and conduct disorders are more likely to get involved in substance use than are their counterparts who are not dealing with mental health issues.
Because the public substance use disorder treatment system is often adult-driven, it is hard to know where to refer adolescents for screening and assessment. Often they show up in the juvenile justice system. When adolescents are referred for a discipline problem, it is important to screen for coexisting or underlying mental health and substance use disorders. A number of good screening and assessment tools exist for this purpose--for a list of them, please refer to the upcoming revised TIP, Screening and Assessing Adolescents for Substance Use Disorders. Adults who can serve as referral sources for adolescent substance users include pediatricians, teachers, school nurses, and school psychologists. This mix of professionals is important in order to cast a wide net for detecting adolescent stimulant use disorders.
A cautionary note for counselors new to this population--adolescents often experiment with substances and other risk-taking behaviors without developing dependence. Therefore, it is a mistake to automatically label experimental substance use behavior as a problem or dependence. With this population in particular, it is important not to over identify or label adolescents as substance abusers. (More information on this topic will be available in the revised TIP, Screening and Assessing Adolescents for Substance Use Disorders [CSAT, 1999a].)
Outreach also includes prevention and early intervention efforts. Although prevention efforts should begin earlier, middle school children, 11 to 12 years old, form an ideal target for comprehensive prevention programs. One example includes life skills-training programs for truant youths (a high-risk group whether or not they are using substances). Prevention efforts that take into consideration the influences of culture and family are important to consider. In Hawaii, the police department runs a prevention program for Hawaiian youths that is grounded in the base of the local culture.
Treatment settings and approaches for adolescents include
Programs for adolescents should focus on cessation of use as well as developing the life and educational skills that clients have missed while using substances. Adolescents need more intensity in programming, such as partial hospitalization, or attending treatment after school 5 days per week. It is generally better to avoid mixing adults and youths.
Programs for adolescents should involve the family, even when treatment takes place outside the home. Assessment should determine whether or not the family itself is substance-free. It is also important that assessment and treatment programs for adolescents be developmentally based.
The adolescent population demands heightened attention because of the impact of stimulant and other substance use on this important develop-mental bridge into adulthood. Stimulant use can impede physical, emotional, and mental development.
Adolescents who use ice often move quickly into psychosis. This leads to a problem with differential diagnosis in cases of potential schizophrenia. With ice use, it can be difficult to determine whether psychosis is the result of schizophrenia or whether it was induced by MA use.
Stimulant use, especially of ice, may be a cause of an early onset of anorexia. Adolescents often abuse stimulants both to lose weight and to cope with sexual inhibitions. Dramatic weight loss in this population is a warning sign for MA use. However, physical health issues, other than anorexia and dental problems, are not as prevalent in the adolescent population as they are in the population of adults who use stimulants.
Teenage pregnancy is another concern because of the association of substance use and early sexual activity, compounded by impaired judgment regarding birth control and prevention of sexually transmitted diseases.
A final note on the adolescent population concerns the lack of community resources generally available to this group. Community-based organizations must be tapped, especially for adolescents from minority groups. Prevention of substance use disorders should be a part of the curriculum for professional groups and continuing education for any community member who works with the adolescent population. (More information on this topic will be available in the upcoming, revised TIP, Treatment of Adolescents With Substance Use Disorders [CSAT, 1999b]).