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Edward J. Khantzian, MD

Dr. Khantzian is clinical professor of psychiatry at Harvard Medical School at Cambridge Hospital in Boston and associate chief of psychiatry at Tewksbury Hospital in Massachusetts.

Disclosure: Dr. Khantzian is on the speaker’s bureau for Janssen.

Please direct all correspondence to: Edward J. Khantzian, MD, 10-12 Phoenix Row, Haverhill, MA 01832; Tel: 978-372-0240; Fax: 978-372-8749; E-mail:

Focus Points

The self-medication hypothesis includes the core aspects that addictive substances relieve psychological suffering and that there is a significant degree of psychopharmacologic specificity in a person’s drug of choice.

Dually diagnosed patients self-medicate painful feeling states which predominate with their psychiatric condition.

Adopting an overarching concept of addictions as a self-regulation disorder helps to explain why many individuals who suffer do not self-medicate their distress, and why others persist with their drug use despite the suffering it causes.


The self-medication hypothesis (SMH) is derived from clinical work with patients who have substance use disorders (SUDs). There are two core aspects of the SMH, namely that substances of abuse relieve human psychological suffering in susceptible individuals and that there is a considerable degree of psychopharmacologic specificity in an individual’s preferred drug. Substances of abuse can relieve a wide range of painful feelings associated with psychiatric illness, thus making patients with a psychiatric disorder more susceptible to SUDs. Those patients who are dually diagnosed with psychiatric illness and SUDs become dependent on a particular class of drugs to relieve the painful affects that predominate with their psychiatric disorder. An appreciation of self-medication factors in dually diagnosed patients has important implications for targeting and treating the distress these patients experience.


Addictive vulnerability is intimately tied to human psychological distress. The self-medication hypothesis (SMH) suggests that at the heart of addictive disorders is suffering, not the seeking of pleasure, reward, or self destruction, as prominent theories have proposed.1 Nowhere is this more evident than in the patient who endures a comorbid psychiatric disorder, the so-called dually diagnosed patient. There is a growing body of evidence from clinical and epidemiologic studies indicating that a significant relationship exists between substance use disorders (SUDs) and psychiatric disorders, and there is a growing preponderance of evidence suggesting that co-occurring psychiatric disorders are etiologically related to and predate SUDs.2-6 This article reviews basic aspects of the SMH of SUDs and considers how it applies to the dilemmas of patients who suffer with psychiatric disorders.

The Self-Medication Hypothesis: Definition

There are two important aspects of the SMH: (1) Individuals use, abuse, and become dependent upon substances because they relieve states of distress; and (2) there is a considerable degree of psychopharmacologic specificity in an individual’s preferred drug. Individuals do not choose to become alcoholic or dependent on opiates, cocaine, or other drugs. Rather, in the course of experimenting with different drugs, a person susceptible to addiction discovers that a particular drug relieves, ameliorates, or changes different painful affect (ie, feeling) states and becomes a favored drug. This second aspect of the SMH has been more difficult to prove empirically,4 but it is uncanny how often patients will verify it by responding when asked, “What is King Drug for you?” A corollary to this “discovery,” depending upon varying feelings which might predominate in the person, is that a drug may be experienced as aversive. For example, an agitated or enraged person will experience cocaine as disorganizing and threatening. An important point here is that addictive drugs are not universally appealing.

Commonly Abused Drugs

The SMH?is based primarily on clinical observations derived from a psychodynamic perspective utilized by investigators dating to the early 1970s. Terms such as “drug-of-choice,”7 “preferential use of drugs,”8 and “self-selection”9 were coined to describe how individuals found certain drugs appealing, contributing to the articulation of the SMH.10 As summarized in a recent update of the SMH,11 the following outlines the main action and appeal of the most commonly abused drugs.


Besides their general calming and “normalizing” effect, opiates attenuate intense, rageful, and violent affect. They counter the internally fragmenting and disorganizing effects of rage and the externally threatening and disruptive aspects of such effects on interpersonal relations.

Central Nervous System Depressants

Short-acting depressants with rapid onset of action (eg, alcohol, barbiturates, benzodiazepines) have their appeal because they are good “ego solvents.” That is, they act on those parts of the self that are cut off from self and others by rigid defenses. These are defenses which produce feelings of isolation, emptiness and related tense/anxious states, and mask fears of closeness and dependency. Although they are not good antidepressants, alcohol and related drugs create the illusion of relief because they temporarily soften the rigid defenses and ameliorate states of isolation and emptiness that predispose to depression.


Stimulants act as augmentors for hypomanic, high-energy individuals as well as those with atypical bipolar disorder. They also appeal to people who are de-energized and bored, and to those who suffer from depression, often of a subclinical variety. In addition, stimulants, including cocaine, can act paradoxically to calm and counteract hyperactivity, emotional lability, and inattention in persons with attention-deficit/ hyperactivity disorder (ADHD).10 In the case of dually diagnosed patients, individuals employ stimulants to counter the cognitive dulling and sedating effects of neuroleptics.


Marijuana has both stimulating and sedating properties. There is relatively little in the literature to describe how and why this drug becomes compelling. Presumably, either the sedating or stimulating properties can be the basis of its appeal. Ned Hallowell, MD, an authority on ADHD, has indicated that marijuana is very appealing to patients with this condition (verbal communication). It would appear that both the sedating and stimulating (acting paradoxically) actions help to counter the restlessness and emotional lability associated with ADHD.

SUDs and Self-Regulation: Relationship to the SMH

Beyond enduring pain and distress, which addictive drugs initially relieve, substance abusers suffer because they have difficulties regulating their self-esteem, relationships, and, especially, their self-care. Adopting an overarching concept of SUDs as self-regulation disorder is necessary because it helps address some of the main criticisms of the SMH; namely, that many individuals suffer with distress but do not become addicted and that there is likely more suffering as a consequence of substance use and abuse as there is relief.

A detailed review of this aspect of the SMH is beyond the scope of this article. More detailed descriptions of self-regulation vulnerabilities in SUDs1,11-13 indicate that it is the combination of contributing factors, such as self-esteem and interpersonal issues, interacting with necessary factors, such as affect and self-care deficits, that makes it more likely that an individual will succumb to addictive disorders. The concept of SUDs as self-regulation disorder also helps to explain how wittingly and unwittingly substance abusers perpetuate their suffering as a means to understand and control it. That is, the operative changes from the relief of suffering to the control of suffering. Another unfortunate consequence of continued substance abuse is that it further exacerbates and perpetuates self-regulation deficits.

Psychiatric Disorders, Self-Regulation, and Human Psychological Suffering

As with SUDs, it can be debated whether psychiatric illness is adaptive or maladaptive. There is an old basic psychodynamic assumption that every psychological problem represents a solution. That is, such problems represent ways to cope with troublesome feelings and external reality. In fact, a recent review of depression bears modern testimony to the persistent usefulness of this paradigm.14 Depression can serve as a coping device just as much as reliance on substances can.

Much of what is presented in this review is based on clinical narrative material—an approach that is more dimensional, dynamic, and derived from a process method of understanding patients’ problems. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Revised15 adopts a categorical and symptom approach to organize symptoms and diagnose psychiatric illness. Each approach has advantages and disadvantages. For the purposes of this review, it can be argued that a diagnostic/categorical approach runs the risk of missing the considerable human suffering associated with psychiatric illness. More particularly, each psychiatric illness we encounter is associated with specific painful affect states that predominate.

Psychiatric disorders, like SUDs, are associated with considerable pain and dysfunction due to self-regulation problems entailing regulation of emotions, self-esteem, relationships, and self-care. It is little wonder then that there is a disproportionately greater degree of substance abuse and dependence among patients with psychiatric illness.5,6 Patients who are dually diagnosed discover that in the short-term, substances relieve, ameliorate, or help control emotional and behavioral dysregulation associated with their psychiatric disorder.

A Case Study

The following case vignette demonstrates a person’s discovery that substances of abuse can serve to counter or relieve painful emotional states rooted in traumatic life experiences. It also detail the often immense suffering that results, some of which may not so readily lend itself to psychiatric classification.

Donald is a 35-year-old recently unemployed, divorced father of three. He was admitted to a public psychiatric hospital after several suicide attempts and after a failure to respond to treatment for long-standing depression. Divorce and the loss of his job loomed large as precipitants for his depression and the persistence of suicidal ideation and attempts. The patient had a history of heavy substance abuse starting in his mid-adolescent years until he received a medical discharge from the Army in his early twenties. Subsequent to leaving the military, he had achieved a protracted period of controlled alcohol use but resumed heavy drinking after discovering his wife’s infidelity 4 years prior. The recent progressive and heavy use of alcohol became a major factor in deteriorating work performance and, ultimately, termination of his employment.

Consultation was requested for the patient to determine if alcohol use was his only substance abuse problem. The interviewer was able to establish sufficiently good contact and trust to consider the information obtained in his evaluation to be credible and believable. Donald reported a remarkable background in terms of a significant abuse history (physical, sexual, and verbal) dating back to infancy and continuing into early adolescence. There was an uncanny interweaving of his personal abuse history with his use and misuse of addictive substances, wherein with little prompting he revealed how various substances acted as antidotes to the suffering his trauma had engendered. His history was also remarkable in that his substance abuse also dated back to early childhood. The description of his personal abuse experience was impressive for the brutal content, but chilling in the matter-of-fact way he recounted it. He claimed remembering that his biological father, also an alcoholic, regularly fondled him and sexually forced himself on him. He said it stopped only with father’s sudden death when he was 3 years of age. His lot was not much better (from age 5 into his teens) at the hands of his stepfather who constantly demeaned him and regularly beat him with his belt buckle, sometimes to discipline him, but at other times, seemingly for no apparent reason.

At the time of his evaluation Donald was receiving oxycodone 60 mg/day for degenerative arthritis of his right hip. A detailed inquiry into his use of substances revealed that his parents laughed when he accidentally became intoxicated at 3 years of age after consuming an alcoholic beverage that had been left lying around the house. He began to experiment with alcohol, marijuana, psychedelics, and psychostimulants by 15 years of age. By his late teens he was using alcohol heavily and had been using heroin intermittently for several years. He recalled feeling “exhilarated” when he first tried free-base cocaine; heroin had a calming and soothing effect, especially on his irritability and rage, which he vividly recalled. He said it made all of his constant inner discomfort disappear. Surprisingly, he made little or no connection to the analgesic and calming effect he had obtained from the oxycodone that had recently been prescribed for his hip pain during his current admission to the hospital. Alcohol, in obliterating doses, was used in a similar fashion to the heroin as a less expensive alternative to calm inner states of apprehension, dysphoria, and feelings of violence. His continuous inner distress, which he admittedly linked to his traumatic history, was expressed endlessly in both physical and emotional ways. He had experienced more than the average young man’s share of somatic symptoms and reactions. The extent of his hip pain was both verified and questioned by several orthopedic consultants. Prior to his hospitalization, atrial fibrillation, which precipitated when feeling stressed, required cardioversion. A range of gastrointestinal complaints was not uncommon.

As extreme and unbelievable as Donald’s case sounds, it is not uncommon and typifies the lifelong dilemmas of patients with psychiatric illness and SUDs. The patient meets criteria for personality disorder with borderline and narcissistic features, major depression, posttraumatic stress disorder, and somatoform disorder. He made it clear that psychological and physical pain and suffering were constants in his life, taking subtle and overt forms. As with other trauma patients, his sleep hours were also invaded by distressing flashbacks and reenactments of his life of traumatic experiences. Such experience associated with infantile trauma has been referred to as “endless suffering” (Henry Krystal, MD, verbal communication). Unfortunately, the persistent and extreme suffering Krystal refers to, is often missed in individuals like Donald as a consequence of off-putting personality characteristics.

As was the case with Donald, it is not uncommon to hear how the stories of substance use and abuse interact with patients’ inner emotional suffering and provide temporary surcease from their distress. This case also typifies the tragic repetitions that occur into adulthood in disrupted relationships and work history. The human tragedy of cases like Donald’s gets lost on the terrain of debates about diagnoses, their believability, and the stigmatization of “drug abuse.” In fact, what is begged here is a measure of empathy for the patients’ suffering and their need to resort to drug solutions and other misbehaviors that are too often confusing, off-putting, and self-defeating.

Psychopathology, Affect States, and Self-Medication: A Sampling


It is important to stress once again that the SMH is about self-medicating painful affects and not disorders/diagnoses, which may be subsyndromal. As Donald’s case exemplifies, depression has many faces. There are depressions in which anger predominates; in other cases, agitations, anxiety, or psychomotor retardation are the most prominent features of a person’s depression. Substances of abuse and their actions interact with a range of affects that can be associated with depression.11

Analgesic Opiates

Analgesic opiates calm, mute, and contain angry rageful affects. This is especially evident with bipolar mood disorders and its variants. In fact, it is probably true that subclinical variants of bipolar conditions and the dysphoria associated with them are frequently driving forces compelling the reliance on addictive drugs to relieve associated distress.


Depressant drugs, such as benzodiazepines, barbiturates, and the lead candidate alcohol, have a biphasic action depending on dose. In high or obliterating doses, alcohol attenuates a range of intense feelings that often accompany depression, including agitation, anger, and irritability. In low to moderate (ie, releasing) doses, depressants can relieve states of anxiety or tension associated with depression.


Stimulant drugs are activating and energizing and more often are experienced as a magical elixir countering the debilitating anhedonia of depression. They are also welcomed by many hypomanic individuals as augmenting drugs that heighten the euphoria such patients enjoy.10

Anxiety Disorders

As with so many psychiatric disorders, anxiety disorders are more often related or linked to the personality organization of the person who suffers from them. Individuals subject to anxiety disorders tend to be tense, “tightly wrapped,” isolative, and cut-off from others.


In low to moderate doses, depressants act as unwrapping and connecting agents—an effect that helps people truly experience their feelings and connect to others in ways which they ordinarily cannot.


Stimulants can have a similar effect but on a different basis; ie, the activating properties of a drug such as cocaine can help such individuals break through their inhibitions where they ordinarily would not.


Presumably, the general muting action of opiates can quiet anxiety, but based on clinical experience, most such individuals do not become hooked on opiates.

Schizophrenic Disorders

In the case of schizophrenic disorders, an individual’s drug-of-choice and the way they use the drug is more complex. Each class of drugs is adopted differentially, depending on the particular symptoms that dominate or alternate in these conditions.

In reviewing the appeal of various addictive drugs for patients who suffer with schizophrenic disorders, it is important to distinguish between positive and negative symptoms associated with schizophrenia. Positive symptoms (paranoia, delusions, aggression, hallucinations, agitation, etc.) are usually appeased by drugs that have a calming effect. However, negative symptoms (alogia, affective flattening, anhedonia, asociality, apathy, attentional impairments) are probably significantly more important in determining reliance on addictive substances among schizophrenic patients than positive symptoms, especially if dependence on nicotine is taken into account.11 This is partially the result of the fact that negative symptoms are the residual aftermath of the more acute phase of schizophrenia when the patient is apt to be too disorganized to obtain or use substances of abuse. It also is the case that there is enormous suffering associated with negative symptoms, often not immediately apparent, that causes patients to resort to substances for relief of their suffering, even if it is only transient.

Analgesic Opiates

Positive symptoms presumably would be attenuated by analgesic opiates because of the drugs’ calming and organizing action, especially with the accompanying rage and aggressivity associated with schizophrenia. However, with some rare exceptions where heroin is readily and easily available, schizophrenic patients are unable to obtain opiates because their disorganized condition in most instances makes them unable to negotiate the hazards to obtain opiates. However, alcohol is readily attainable by such patients, and is extensively abused by schizophrenic patients.


In obliterating doses, alcohol attenuates the voices, delusions, agitation, and anger for schizophrenic patients. As one patient put it, “I can dismiss them (the voices) and not be so distressed by them.” Low to moderate doses of alcohol counter the negative symptoms of asociality in such patients. A case in point, Albanese and colleagues16 published case material showing that when negative symptoms of patients, especially their inability to express their feelings and socialize, were relieved by the atypical neuroleptic clozapine, there was a corresponding decrease in patients’ unrelenting reversion to alcohol use.


There is a disproportionate abuse of stimulants among patients suffering with schizophrenia.17,18 This might be surprising given the psychotogenic properties of stimulants. However, there is evidence indicating that schizophrenic patients find relief from their anhedonia and other negative symptoms through the activating properties of stimulants, including nicotine.11 They also use stimulants to alleviate the sedating properties of neuroleptics.

Posttraumatic Stress Disorder

There is a complex biphasic nature to affect experience in patients suffering with posttraumatic stress disorder (PTSD); they are subject to either emotional flooding and thus overwhelmed with painful affect, or they experience affective numbing which is deadening or confusing. Both extremes are painful and debilitating. Not surprisingly, there is a disproportionate incidence of SUDs among individuals suffering with PTSD.1,11 When experiencing or flooded with intense emotions such as rage, agitation, or fragmentation, PTSD victims might experience opiates or obliterating doses of alcohol as potent antidotes to such unsettling and powerful affects. This is not an uncommon reaction in Vietnam veterans or borderline patients, for example. Conversely, in the case of affective numbing when PTSD patients feel closed down or emotionally dead, low to moderate doses of alcohol often provide release from the sense of restriction and being “cut off” from the rest of the world. Finally, PTSD patients likely discover marked relief from the negative symptoms of anhedonia, apathy, and affective flattening accompanying PTSD when they experiment with or use cocaine. This is just one more example of how the hook gets set with addictive drugs in the context of emotional distress and suffering.


A patient’s drug of choice can be a meaningful clue to the painful emotions with which he or she suffers and can compel drug dependence in susceptible individuals. In the case of dually diagnosed patients, the patient’s psychiatric illness might signal the particular drug with which they might be self-medicating. Such a perspective might also guide the clinician to identify and target what painful feelings might predominate, and how and why such affects might make a particular drug compelling. Finally, a self-medication perspective on substance use and abuse among dually-diagnosed patients can serve as a preeminent guide to treatment, psychotherapeutically and psychopharmacologically. PP


1. Khantzian EJ. Treating Addiction as a Human Process. Northvale, NJ: Jason Aronson; 1999.

2. Khantzian EJ, Dodes L, Brehm N. Determinants and perpetuators of substance abuse: psychodynamics. In: Lowinson JH, Ruiz P, Millman RB, Langrod JG, eds. Substance Abuse: A Comprehensive Textbook. 4th ed. Baltimore, MD: Williams and Wilkins. In Press.

3. Albanese MJ. The self-medication hypothesis: epidemiology, clinical findings and implications. Psychiatric Times. 2003;4:57-64.

4. Albanese MJ. The self-medication hypothesis: theory and content. Psychiatric Times. 2003;3:42-44.

5. Regier DA, Farmer MD, Ral DS, et al. Comorbidity of mental disorders with alcohol and other drugs: results from the epidemiologic catchment area (ECA) study. JAMA. 1990;264:2511-2518.

6. Kessler RC, Crum RM, Warner LA, et al. Lifetime co-occurrence of DSM-III-R alcohol abuse and dependence with other psychiatric disorders in the nation comorbidity survey. Arch Gen Psychiatry.1997; 54:313-321.

7. Weider H, Kaplan E. Drug use in adolescents. Psychoanal Study Child. 1969;24:399-431.

8. Milkman H, Frosch WA. On the preferential abuse of heroin and amphetamine. J Nerv Ment Dis. 1973;156:242-248.

9. Khantzian EJ. Self-selection and progression in drug dependence. Psychiatry Digest. 1975;10:19-22.

10. Khantzian EJ. The self-medication hypothesis of addictive disorders: focus on heroin and cocaine dependence. Am J Psychiatry. 1985;142:1259-1264.

11. Khantzian EJ. The self-medication hypothesis of substance use disorders: A reconsideration and recent applications. Harv Rev Psychiatry. 1997;4:231-244.

12. Khantzian EJ. Self regulation and self-medication factors in alcoholism and the addictions: similarities and differences. In: M. Galanter, ed. Recent Developments in Alcoholism. New York, NY: Plenum; 1990:255-271.

13. Khantzian EJ. Self-regulation vulnerabilities in substance abusers: treatment implications. In: Dowling S, ed. The Psychology and Treatment of Addictive Behaviors. Madison, Conn: International Universities Press; 1995:17-41.

14. Nesse RM. Is depression an adaptation? Arch Gen Psychiatry. 2000;57:14-20.

15. Diagnostic and Statistical Manual of Mental Disorders. 4th ed-rev. Washington, DC: American Psychiatric Association; 2000.

16. Albanese MJ, Khantzian EJ, Murphy SI, Green AI. Decreased substance use in chronically psychotic patients treated with clozapine. Am J Psychiatry. 1994;151:780-781.

17. Brady K, Anton R, Ballenger JC, Lydiard RB, Adinoff B, Selander J. Cocaine abuse among schizophrenic patients. Am J Psychiatry. 1990;147:1164-1167.

18. Schneier FR, Siris SG. A review of psychoactive substance use and abuse in schizophrenia: patterns of drug choice. J Nerv Ment Dis. 1987;175:641-652.


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Methadone Treatment and Recovery
for Opioid Dependence

Janice F. Kauffman, RN, MPH, CAS

Ms. Kauffman is assistant professor of psychiatry in the Department of Psychiatry at Cambridge Hospital in Cambridge, Massachusetts, director of Addiction Psychiatry Service at Brigham and Women’s Hospital in Boston, and director of Substance Abuse Treatment Services at the North Charles Foundation, Inc., in Somerville.

Disclosure: The author reports no financial, academic, or other support of this work.

Please direct all correspondence to: Janice F. Kauffman, RN, Department of Psychiatry, Cambridge Hospital, 260 Beacon St, Somerville, MA 02143; Tel: 617-661-5700; Fax: 617-868-4840; E-mail:

Focus Points

Methadone treatment developed as a response to increasing problems with opioid dependence and ineffective approaches to the problem.

Methadone’s pharmacologic properties make it more efficacious than other, shorter-acting opioids.

For a variety of reasons, methadone treatment remains controversial.

Methadone is provided within a comprehensive treatment system.


Unlike any other medical treatment, methadone pharmacotherapy for the treatment of opioid dependence is still controversial despite 40 years of scientific work demonstrating its efficacy. Negative attitudes toward people with opioid dependence have been developing since the Civil War, and have become associated with methadone treatment. The stigma is partly attributable to the criminal behavior of some people with opiate dependence, but also results from factors such as poor education of the treatment community. This article briefly reviews the history of opioid dependence in the United States, the search for solutions, and the development of methadone. It considers the pharmacologic properties of methadone and how these relate to its efficacy. The article also reviews the elements of a comprehensive methadone maintenance program and factors to be considered in selecting patients.


Since the Civil War, opioid use and dependence has been a focus of attention for the medical community, society, and policy makers. Opinions about both the etiology of the problem and the efficacy of methadone treatment remain controversial despite the knowledge gained from scientific research, outcome data of treatment interventions, and clinical experience.1 Opioid dependence is one of the few illnesses for which public opinion overshadows scientific knowledge. Americans exhibit ambivalence about addictive disorders and their treatments. Although it is “in vogue” today to be addicted to something, it is clear that some addictions, such as shopping, food, movies, relationships, and even alcohol, are more acceptable than others, such as cocaine, ecstasy, heroin, and oxycodone HCl.Furthermore, some pharmacologic treatments, such as naltrexone or disulfiram, which deter alcohol- and opiate-dependent patients from relapsing, are more acceptable than pharmacologic treatments, such as methadone, which is perceived as maintaining addiction. The act of prescribing a synthetic morphine-like drug to patients with opioid dependence magnifies societal biases. This is particularly highlighted when the history of opioid dependence and efficacy of methadone maintenance treatment is examined.

History of Opioid Dependence: Reflecting the Views and Understanding of Addiction

The history of opioid dependence is rich and informative. Concerns about opioid addiction in the United States first emerged after the Civil War when narcotic drugs (opiates) were prescribed to alleviate acute and chronic pain, discomforts, and stress.2 The prototypical opiate misusers in the late 19th century were the upper- and upper-middle class white women who had been prescribed them for disorders such as menstrual pain and “female troubles,” and disabled and wounded veterans seeking pain management.3 By the turn of the 20th century, 300,000 people were opiate-dependent.3-5 In general, the medical community treated such people with tolerance and empathy.

At the same time, American society viewed opium use as socially unacceptable. Around the turn of the century, many Europeans immigrated to the US and the population of opioid users began to change. Many opioid users during this time were young, destitute men living impoverished lives in overcrowded tenements and ghettos. They had been using opioids since their adolescent or early adult years and often resorted to illicit activities to support their dependence. Society viewed these immigrants with social, religious, and political disdain.4 After World War II, many Europeans moved out of the northern and western cities to the suburbs, and were replaced by African Americans, Chinese, and Hispanics, who brought with them their culture, customs, and addictions. Class and ethnic biases merged with dissonance and fear, and opiate addiction became a threat, empathy evaporated, and negative attitudes toward opioid users prevailed.5,6

The Federal government attempted to resolve the problem with regulations such as the Harrison Narcotics Act in 1914, which prohibited physicians from prescribing opiates to treat or maintain “addicts.”3 For the most part, the medical community did not challenge the view that addiction was not a disease and that addicts were not patients. As a result, opiate-dispensing clinics were closed precipitously, crime increased, and in 1929 Congress established the US Public Health Service Hospital in Lexington, Kentucky, to incarcerate opiate addicts, either voluntarily or involuntarily, to allay fears about addiction-related crime.3,5,7,8 Interventions were expensive and unsuccessful. People with opioid dependence were detoxified in prison hospitals and offered social, psychological, and psychiatric services. However, a study following 1,912 inmates for at least 1 year, and some as long as 4.5 years, reported that 93% relapsed.3,5 Similarly, a follow-up on 453 inmates found that 97% relapsed in 6 months to 5 years.3,5

In response to the increasing number of heroin users, heroin-related crimes and deaths, the increase in needle-related hepatitis, overcrowded jails, and lack of effective treatment for heroin dependence, the American Medical Association (AMA) and American Bar Association (ABA) recommended that outpatient facilities prescribe opiates for maintenance (1958). Not long afterward, President Kennedy’s Advisory Commission on Narcotic and Drug Abuse recommended research to determine the effectiveness of dispensing narcotics to addicts.3

In 1962 Vincent Dole, MD, a specialist in metabolism at Rockefeller University, was appointed chair of the Narcotics Committee of the Health Research Council of New York City. He received a grant from the Health Research Council to establish a research unit to study the scientific, public health, and social ramifications of opioid maintenance. At the same time, Dole became interested in an article by Marie Nyswander, MD, a psychiatrist, which reflected the latter’s work with addicts at the US Public Health Service Hospital, and in her private practice in East Harlem, New York. She believed that many heroin addicts could function as productive citizens if maintained on opiates.3,5 Dole invited Nyswander and Mary Jean Kreek, MD, a young clinical investigator completing her internal medicine training in neuroendocrinology, to join his research team.

The new team initially administered low-dose morphine to opioid-addicted patients every 4–6 hours. Although these patients did not suffer withdrawal symptoms, they remained apathetic, sedated, and preoccupied with drugs. In addition, in order to maintain a steady state, they had to increase the dose as the patients experienced tolerance.9-11 Although this intervention provided medication access, unadulterated drugs, and clean syringes, it was not a satisfactory solution since it did not help patients improve their social functioning.

In 1964, with the advent of technology that could measure blood concentration of opiates and assess duration of action, methadone, with a long half-life, was administered to patients who had been maintained on morphine. The investigators discovered that methadone doses of 80–120 mg/dayallowed patients to achieve normal social function without drug craving. The patients also did not experience euphoric, tranquilizing, or analgesic effects. In addition, taken orally, methadone was safe and had minimal side effects.10-12 Finally, it was effective for patients tolerant to all opioid drugs, and blocked the euphoric and tranquilizing effects of short-term opioids when patients injected them on their own.

Methadone Meets the Challenges of Opioid Dependence

Several hypotheses have attempted to explain the chronic relapsing nature of opioid dependence. Kolb13 postulated that those who responded to the euphoric effects, which was considered an atypical response, had psychopathology. He also hypothesized that psychopathology was the basis for initial experimentation, initial euphoria, and continued use. Others believed that those who responded positively to opiates had an endorphin deficiency that was corrected by exogenous opiates.14 Repeated use created permanent dysfunction in the endogenous endorphin system, so that normal mood modulation and functioning required continued opioid pharmacotherapy.15 Thus, methadone can be understood as a corrective agent for the brain dysfunction related to chronic relapsing opioid dependence.

The implications for individual patients, public health, and public safety have been enormous. Methadone has reduced the severity of addiction and virulent drug use by allowing a dependent person to maintain an acceptable level of medical and social functioning.16 Methadone maintenance has resulted in a reduction in the spread of needle-borne disease, such as hepatitis, human immunodeficiency virus, and acquired immunodeficiency syndrome.17-20 Furthermore, methadone maintenance patients use fewer costly emergency healthcare resources, attending to their health needs in a less episodic and crisis-oriented fashion.16 With methadone, more former addicts attain and maintain employment and provide for their families. In addition, methadone is associated with a reduction in drug-related crime.21-24

The positive effects of methadone maintenance treatment do not result from the medication ingestion alone, as the treatment of any addictive disorder requires significant lifestyle change. Treatment involves adequate assessment and ongoing attention to the medical, psychological, social, environmental, cultural, and behavioral components of the patient’s life. Methadone without psychosocial treatment is not an effective treatment.25 This is the case for many medical disorders. For example, insulin and antihypertensive medications alone do not successfully treat diabetes and high blood pressure. Comprehensive treatment involves diet, exercise, and lifestyle change. Successful substance abuse treatment involves compliance and change toward a drug/alcohol-free lifestyle. Many patients require treatment for other substance-related problems as well as co-occurring psychiatric disorders, such as depression and anxiety. Therefore, successful treatment for opioid dependence involves addressing the same issues as treatment for patients with addictions involving alcohol, benzodiazepines, cocaine, and other substance- or nonsubstance-related addictive disorders (eg, gambling); it requires both professional interventions and recovery support.

Controversy Surrounding Methadone Maintenance Treatment

Despite the positive results associated with methadone treatment, and its use within well-designed treatment settings, the drug remains a controversial treatment modality.26 Even though science has demonstrated genetic predisposition to and brain changes following substance use, addiction, and especially opiate dependence, some still consider them to be moral weaknesses rather than medical problems. This view gained strength after enactment of the laws prohibiting the prescription of opiates for the treatment of opiate dependence. Criminal behavior increased and individuals with opioid dependence were considered not only morally weak, but criminals as well. Thus, the notion of giving opiate-dependent patients an opioid for the treatment of their addiction was considered heresy. As a result, despite the science, the outcome data, and the anecdotal reports of so many patients receiving methadone treatment, many continued to hold as much distaste for the treatment as for the addiction.27,28

The reasons for negative beliefs are multifold.29,30 Due to a lack of education and accurate information about methadone as a medication, many clinicians are fearful and mistrusting of the medication and the patients taking it. For healthcare professionals, addictions training is limited, and few certification and licensing bodies address opiate dependence and methadone treatment in their qualifying examinations. Other prescribing specialists are angry from past personal or professional negative experiences. Furthermore, there are clinicians whose treatment philosophy does not permit a treatment that they believe is not based on abstinence. For example, many believe that patients on methadone are “just getting high” or are “substituting one drug for another.” They are under the impression that heroin addicts are “bad characters” and that prescribing opioids is not an acceptable way to treat the addiction. Unfortunately, this view has received support from revelations about some unscrupulous methadone programs.

One reason for the negative beliefs lies with the patients themselves. Like patients with other substance use disorders, some opioid-dependent patients abuse alcohol and other drugs, and do not comply completely with the requirement for abstinence. However, relapse is part of the course of any addictive disorder. The treatment of substance dependence has many of the same compliance problems as treatment of obesity, diabetes, hypertension, and asthma.31

Challenging the Controversy: How Methadone Really Works

Methadone is very different from heroin, morphine, and other short-acting opiates. Patients using short-acting opiates (eg, heroin) are never stable; they experience fluctuating “highs” and “lows.” They are listless, unmotivated to improve their lives, and more focused on drug access, drug effect, and the relief of withdrawal, than on the tasks of recovery.32 Dole and colleagues9 demonstrated this when they tried treating heroin addicts with short-acting opiates.

The goals of methadone maintenance treatment are very straightforward. Methadone is a long-acting synthetic opioid that provides stability for 24–36 hours when orally administered for the treatment of opioid dependence. The pharmacokinetics and neurobiology of methadone treatment are beyond the scope of this article, but understanding the different actions of short and long-acting opiates is important to the careful prescription of this medication.33 When administered daily in adequate doses, methadone prevents or reduces drug craving, prevents or reduces signs and symptoms of opiate withdrawal, prevents relapse to the use of opiates, and restores the patient to the normal physiological functions disrupted by repeated short-acting opiate use.34

For many patients methadone maintenance is a long-term treatment. For some, methadone pharmacotherapy may be lifelong. Most importantly, the length of time in treatment should be individually determined and not predetermined by artificial timeframes. Research studies consistently report that the length of time in treatment is positively correlated with successful outcomes.35,36 For example, when patients are precipitously forced to withdraw from the methadone, relapse rates are as high as 82% after a 12-month abstinence period.24

Patients who have demonstrated that they meet the benchmarks of recovery may be considered for medically supervised withdrawal. These benchmarks include no alcohol or drug abuse; a stable living, social, or employment situation; no evidence of illicit activity; psychiatric and medical stability; developing a circle of friends and associates outside of the drug culture; and a system of drug-free support. A patient who reaches these goals might be appropriate for withdrawal from methadone. However, the most important variable is that they are highly motivated to recover. Even with motivation, some patients are unable to remain opiate-free without continued pharmacotherapy. This is likely related to significant changes in brain chemistry rather than to patient failure.

Methadone Maintenance: Where, When, and How

When considering methadone maintenance for an opioid-dependent patient it is important to consider several issues, mostly that the patient desires treatment. Admission to a methadone maintenance program is a commitment to a highly structured treatment intervention. It involves daily medication, urine toxicology screening, and regular attendance to a combination of individual, group, and perhaps family treatment.

Methadone maintenance treatment is most appropriate for the patient with a history of chronic relapse. The patient who has tried and failed other interventions such as inpatient and/or outpatient detoxification, residential treatment, and day treatment is a good candidate for methadone maintenance. Some patients report that they are unable to function without opiates. This may suggest that they are struggling with a biochemical disorder that needs long-term opioid pharmacotherapy to attain and maintain stability.11,15

Like other substance-dependent patients, those on methadone maintenance may have problems with alcohol or other drugs.37-39 In fact, intoxication with other substances may be misconstrued as intoxication from methadone. Thus, these other substance use problems and comorbid psychiatric and medical conditions must be addressed as well. Untreated problems affect the outcomes of the other disorders. At times, patients may require a more intensive level of care, such as the safety and structure of inpatient detoxification or residential care, to fully address environmental and social needs.40 Unfortunately, when a methadone-maintained patient needs inpatient detoxification or residential treatment, access is often denied by the addictions treatment community itself, because of resistance to methadone treatment. Consequently, a patient must give up a medication that stabilizes opioid dependence in order to get treatment for alcoholism or sedative dependence. Clearly, there is room for improvement in integrating methadone maintenance into other substance dependence treatment settings.


Despite studies demonstrating its efficacy, methadone maintenance treatment for people with opioid dependence is not fully embraced by either the treatment community or society. The findings of scientific studies are overshadowed by negative perceptions, which are determined partly by lack of education, divergent treatment philosophies, the behavior of some people with opioid dependence, and other factors. However, for sound pharmacologic reasons, methadone is an effective treatment for opioid dependence. When delivered within a comprehensive treatment program to the right patients, methadone results in improved outcomes on a variety of measures. Physicians owe it to their patients to make this treatment modality available and to better integrate it into other forms of treatment. PP


1. Kreek MJ, Vocci FJ. History and current status of opioid maintenance treatments: blending conference session. J Subst Abuse Treat. 2002;23:93-105.

2. White WL. Slaying the Dragon: the History of Addiction Treatment and Recovery in America. Bloomington, IL: Chestnut Health Systems/ Lighthouse Institute; 1998.

3. Brecher EM. Licit and illicit drugs. In: Consumer Union Report on Narcotics, Stimulants, Depressants, Inhalants, Hallucinogens, and Marijuana. Boston, MA: Little, Brown and Company; 1972.

4. Courtwright DT. Forces of Habit: Drugs and the Making of the Modern World. Cambridge, MA: Harvard University Press; 2001.

5. Courtwright DT, Joseph H, Des Jarlais D. Addicts Who Survived: an Oral History of Narcotic Use in America, 1923-1965. Knoxville, TN: University of Tennessee Press; 1989.

6. Courtwright DT. Dark Paradise. Opiate Addiction in America Before 1940. Cambridge, MA: Harvard University Press; 1982.

7. Cooper JR. Methadone treatment in the United States. In: Awni A, Westmermeyer J, eds. Methadone in the Management of Opioid Dependence: Programs and Policies Around the World. Geneva, Switzerland: World Health Organization; 1988.

8. Gewirtz PD. Notes and comments: Methadone maintenance of heroin addicts. The Yale Law Journal. 1969;78:1175-1211.

9. Dole VP, Nyswander ME, Kreek MJ. Narcotic blockade. Arch Int Med. 1966;118:304-309.

10. Dole VP. Addictive behavior. Scientific American. 1980;243:138-154.

11. Dole VP. Implications of methadone maintenance for theories of narcotic addiction. JAMA. 1988;260:3025-3029.

12. Kreek MJ. Medical safety and side effects of methadone in tolerant individuals. JAMA. 1973; 223:665-668.

13. Kolb L. Pleasure and deterioration from narcotic addiction. Mental Hygiene. 1925;9:699-724.

14. Gold MS, Pottash AC, Sweeney D, et al. Antimanic, antidepressant, and antipanic effects of opiates clinical, neuroanatomical and biochemical evidence. In: Verebey K, ed. Opioids in Mental Illness: Theories, Clinical Observations, and Treatment Possibilities. New York, NY: Academy of Sciences; 1982:141-150.

15. Dole VP, Nyswander ME. Heroin addiction: metabolic disease. Arch Int Med. 1967;120:19-24.

16.California Drug and Alcohol Treatment Assessment (CALDATA): Evaluating Recovery Services: General Report. Sacramento, Calif: State of California Department of Alcohol and Drug Program; 1994.

17. Truman B, Brown JS. HIV infection among intravenous drug use (IVDU) in NYC. Poster presented at: 5th International Conference on AIDS; June 1989; Montreal, Canada.

18. Novick DM, Joseph H, Croxson EA, et al. Absence of antibody to human immunodeficiency virus in long-term, socially rehabilitated methadone maintenance patients. Arch Int Med. 1990;150:97-99.

19. Metzger DS, Woody GE, McLellan AT, et al. Human immunodeficiency virus seroconversion among intravenous drug users in- and out-treatment: An 18-month prospective follow-up. J Acquir Immune Defic Syndr. 1993;6:1049-1056.

20. Ball JC, Lange WR, Myers CP, et al. Reducing the risk of AIDS through methadone maintenance treatment. J Health Soc Behav. 1988;29:214-226.

21. Anglin MD, McGlothlin WH.Methadone maintenance in California: a decade’s experience. In: Brill L, Winick C. eds. The Yearbook of Substance Use and Abuse. New York, NY: Human Services Press; 1985:3.

22. Anglin MD, Powers KI. Methadone treatment and legal supervision: individual and behavioral effects on the behavior of narcotic addicts.
J Appl Behav Sci. 1991;27:515-531.

23. Anglin MD, Speckart GR, Booth MW, Ryan TM. Consequences and costs of shutting off methadone. Addict Behav. 1989;14:307-326.

24. Ball JC, Ross A. The Effectiveness of Methadone Maintenance Treatment: Patients, Programs, Services, and Outcomes. New York, NY: Springer-Verlag; 1991.

25. McLellan AT, Arndt IO, Mertzger DS, Woody GE, O’Brien CP. The Effects of psychosocial services in substance abuse treatment. JAMA. 1993;269:1953-1959.

26. Courtwright DT. The prepared mind: Marie Nyswander, methadone maintenance, and the metabolic theory of addiction.Addiction. 1997;92:257-265.

27. Brown BS, Benn GJ, Jansen DR. Staff and client attitudes towards methadone maintenance. Int J Addict. 1975;72:247-255.

28. Sutker PB, Allain AN, Smith CJ, Cohen GH. Addict descriptions of therapeutic Community, multimodality and methadone maintenance treatment clients and staff. J Consult Clin Psychol. 1978;46:508-517.

29. Institute of Medicine. The Development of Medications for the Treatment of Opiate and Cocaine Addictions: Issues for the Government and Private Sector. Washington, DC: National Academy Press;1995.

30. Institute of Medicine. Dispelling the Myths About Addiction: Strategies to Increase Understanding and Strengthening Research. Washington, DC: National Academy Press; 1997.

31. McLellan AT, Lewis DC, O’Brien CP, Kleber HD. Drug dependence, a chronic medical illness: Implications for treatment, insurance, and outcomes evaluation. JAMA. 2002;284:1690-1695.

32. Hentoff N. A Doctor Among Addicts. New York, NY: Rand McNally & Company; 1968.

33. Kosten TR, George TP. The neurobiology of opioid dependence: implications for treatment. Research Reviews. Science and Practice Perspectives. 2002;7:13-20.

34. Kreek MJ. Rational for maintenance pharmacotherapy of opiate dependence. In: O’Brien, CP, Jaffe, JH, eds. Addictive States. New York, NY: Raven Press, Ltd.; 1992:205-230.

35. Simpson D, Joe GW, Dansereau DF, Chatham LR. Strategies for improving methadone treatment process and outcomes. J Drug Issues. 1997;27:239-260.

36. Simpson D, Joe DW, Rowan-Szal G. Drug abuse treatment retention and process effects on follow-up outcome. Drug Alcohol Depend. 1997;47:227-235.

37. Hubbard RL, Marsden ME, Rachal JV, et al. Drug Abuse Treatment: A National Study of Effectiveness. Chapel Hill, NC: University of North Carolina Press; 1989.

38. Avants SK, Margolin A, Kosten TR. Cocaine abuse in methadone maintenance programs: integrating pharmacotherapy with psychosocial interventions. J Psychoactive Drugs. 1994;26:137-146.

39. Fairbanks JA, Dunteman GH, Condelli WS. Do methadone patients substitute other drugs for heroin? Predicting substance abuse at 1-year follow-up. Am J Drug Alcohol Abuse. 1993;19:465-474.

40. Mee-Lee D, Shulman GD, Fishman M, Gastfriend DR, Griffith GH, eds. ASAM Patient Criteria for the Treatment of Substance Related Disorders. 2nd ed-rev (ASAM PTC-2r). Chevy Chase, MD:American Society of Addiction Medicine, Inc; 2001.


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Edgar P. Nace, MD
Primary Psychiatry. 2003;10(9):65-72

Dr. Nace is clinical professor of psychiatry in the Department of Psychiatry at the University of Texas Southwestern Medical Center in Dallas.

Disclosure: The author reports no financial, academic, or other support of this work.

Disclaimer: The 12 steps, 12 traditions, and 12 promises are reprinted with permission of Alcoholics Anonymous (AA) World Services, Inc. Permission to reprint this material does not mean that AA has reviewed or approved the contents of this publication, nor that AA agrees with the views expressed herein. AA is a program of recovery from alcoholism. Use of the 12 steps and 12 traditions in connection with programs and activities which are patterned after AA but which address other problems does not imply otherwise.

Please direct all correspondence to: Edgar P. Nace, MD, 7777 Forest Lane, #B413, Dallas, TX 75230; Tel: 972-566-6282; Fax: 972-566-3857; E-mail:


Focus Points

Alcoholics Anonymous (AA) is a fellowship that utilizes a 12-step program to assist individuals in achieving abstinence from alcohol.

Participation in AA, in addition to addressing alcohol use, promotes psychological maturity and spiritual growth.

Physicians who understand the benefits of AA will be able to assist patients in joining the AA program.


Alcoholics Anonymous (AA) is a major community resource with which physicians should be familiar. Knowledge and understanding of AA will enable primary care physicians to effectively motivate their problem-drinking patients to participate in AA. It is prudent to recommend AA to any patient with alcohol abuse or dependence. There are no consistent data to suggest who may or may not respond to AA, and, therefore, anyone with a desire to stop drinking is a reasonable candidate for AA membership. Facts about AA, its structure, and process, are briefly described.


Primary care physicians commonly encounter health-impairing behaviors in their patients. Alcoholism is one such behavior and is often a challenge for the practitioner. Physician acceptance of this challenge can lead to improved helath of patients.1 Behavior change is typically incremental and a physician’s attention to the desired change can accelerate the patient’s movement through the following well-recognized stages2:

Precontemplation. This is the stage in which the patient is not considering changes in behavior or is unaware of a need for change.

Contemplation. This is the stage wherein the patient realizes a change is desirable but is ambivalent or uncommitted to making the change.

Determination. During this stage, the patient makes a decision to change behavior.

Action. This stage promotes a particular strategy for producing the change, eg, disulfiram is used to prevent alcohol use, bupropion is taken to help eliminate smoking, exercise is begun as part of weight reduction.

Maintenance. This is the stage during which the patient continues the strategies which effect change. The stage usually requires at least 6 months of the continued behavior change.

Relapse. The adverse behavior is re-initiated in this stage. At this point the individual is counseled to resume the action and maintenance stages.

In order to be successful in guiding the patient in this process of behavior change, the physician will need to have available “tools.” These tools may be pharmacologic treatment, knowledge of specific effective strategies (eg, throw away cigarettes and any smoking-related paraphernalia; remove all alcohol from the house), or, the capacity to direct the patient to community resources.

This article describes Alcoholics Anonymous (AA), a prime community resource for physicians to help the change process in patients with substance use disorders, ie, those with alcohol or drug dependence. The structure of AA, the process of AA participation, and how or why it works, will be described. AA is presented as the generic 12-step program. The information presented about AA can be applied to other 12-step programs such as Narcotics Anonymous, Cocaine Anonymous, and Gamblers Anonymous.

Structure of Alcoholics Anonymous

Founded in 1935, AA has 97,000 groups worldwide.3 It is a fellowship open to anyone who wants to do something positive about their drinking problem. One need not consider oneself an alcoholic in order to participate in AA and there are no age limits, educational requirements, or fees. The only requirement for membership is a desire to stop drinking. Meetings typically last 1 hour and may be speaker meetings during which members tell about their experiences with drinking, what happened to make them want to stop drinking, and how they feel now that they are not drinking. Another meeting format is discussion, during which a member leads a discussion on a topic related to recovery, such as gratitude. In step meetings, the discussion focuses on one of the “12 steps” of AA. Meetings may be open or closed. Closed meetings are for AA members or prospective members only, whereas open meetings include nonalcoholics as well.

The program of AA consists of studying and following the 12 steps (Table 1). AA groups adhere to the “12 traditions” of AA (Table 2). By working the 12 steps and following the 12 traditions,4 AA members can expect to obtain the “12 promises” (Table 3). There are several things that AA is against, such as soliciting members, providing initial motivation for recovery, or participating in or sponsoring research (Table 4).5

The Growth of Alcoholics Anonymous

AA was founded by Bob Smith, MD, a surgeon from Akron, Ohio, and Bill Wilson, an alcoholic from New York City. The birth date of AA is given as June 10, 1935, the day Smith had his last drink. Two and a half years later, “Dr. Bob” and “Bill W” estimated that, as a result of their combined efforts, there was a total of only 40 sober recovering alcoholics in their respective cities. Most alcoholics who were contacted were not maintaining sobriety nor had any interest in Dr. Bob or Bill W’s ideas.6 However, the co-founders knew they were onto something and continued the efforts of carrying hope, strength, and experience to other alcoholics. After 4 years, membership was estimated to be about 100, and by the end of 1941, there were 8,000 members. By 1968, 170,000 members were estimated.7 In spite of early periods of discouragement, the growth of AA has been phenomenal and continues today, exceeding 1 million in membership worldwide.

Affiliation With Alcoholics Anonymous

The 2001 AA General Services Office survey3 reported that 32% of AA newcomers were referred by treatment facilities, 33% were attracted to AA by an AA member, and 33% reported being self-motivated to seek AA.

A study from Great Britain reported that 65% of general practitioners believed that AA had something to offer beyond what could be obtained through medical efforts.8 The 2001 General Services Survey3 reported that 38% of members were referred to AA by a healthcare professional and that 73% of member’s physicians are aware that they are attending AA.

Once an individual begins attending AA meetings, what are the chances that he or she will continue? Estimates from AA General Services Office surveys indicate that only 50% of those who start AA remain for more than 3 months. In a review of AA affiliation,9 approximately 20% of problem drinkers referred to AA were found to attend regularly. In a 4-year follow-up of alcoholism treatment,10 27% of those who had ever gone to AA reported attendance at AA the month prior to follow-up, and of those who reported attending AA regularly, 39% had attended a meeting during the month prior to follow-up. In a review of the literature,10 dropout rates from AA varied from 68% before 10 meetings were attended to 88% by 1 year after discharge. A recent follow-up study of an outpatient program found that a majority of patients were attending AA 6 months after discharge.11 The latter study plus data from the 2001 AA Survey3 indicate an emerging trend—that counseling or other related treatments seem to be influencing AA affiliation; 74% of AA members who received such treatment reported that it played an important part in their seeking help with AA.

The dropout problem raises the question of who is likely to make a stable affiliation with AA. Early research on this problem12,13 suggests that those who join AA are middle-class, guilt-ridden, sociable, cognitively rigid, and socially stable. They are also more likely to be chronic alcoholics or loss-of-control drinkers and to have more alcohol-related problems. A comprehensive recent review of the affiliation process fails to support earlier findings. Emrick10 compared variables used to distinguish between stable and unstable affiliations and found that 64% bear no relationship, 29% show a positive relationship favoring AA affiliation, and only 7% bear a negative relationship to AA affiliation. This leads to the conclusion that most alcoholics have the possibility of making an affiliation with AA. Only those whose goal is not to abstain from alcohol would be seen as exceptions. Currently, it is best to accept that a patient’s affiliation with AA is unpredictable, which again emphasizes the importance of recommending AA to all possible members.

Effectiveness of Alcoholics Anonymous

Efforts have been made to assess the effectiveness of AA attendance. Measurement of outcome typically is limited to abstinence or lack of abstinence from alcohol. In studies of AA from the 1940s to the early 1970s,14 sampling difficulties and other methodological problems were prominent. Nevertheless, the findings indicated that thousands of AA members had achieved sobriety through AA. In a study of 393 AA members, it was determined that 70% of those who stayed sober for 1 year would still be sober at 2 years, and that 90% of those sober at 2 years would remain sober at 3 years.14 In two early studies of AA, sobriety of >2 years’ duration was found in 46% of those sampled.15,16

A review of survey studies10 found that 35% to 40% of respondents reported abstinence of <1 year, with 26% to 40% reporting abstinence of 1–5 years, and 20% to 30% having been sober for 5 years. Overall, 47% to 62% of active AA members had 1 year of continuous sobriety. The 1989 AA General Services Office survey consisting of 9,994 responses from a mailing of 12,000 reported an average sobriety length of 50 months. The 2001 survey reported the average sobriety of members to be 84 months with 18% sober >5 years and 30% sober <1 year.

AA involvement has been found to correlate favorably with a variety of outcome measures. Those patients who attend AA before, during, or after a treatment experience have a more favorable outcome in regard to drinking.10 In the few studies available that assess the outcome on other variables, AA involvement is associated with a more stable social adjustment, more active religious life, internal locus of control, and better employment adjustment.10 Increased ethical concern for others, an increased sense of well-being, and increasing dependence on a spiritual “higher power” with less dependence on others have also been described.17 Finally, there is a positive relationship between outcome and extent of AA participation.10 Outcome is more favorable for those who attend more than one meeting per week and for those who have a sponsor, sponsor others, lead meetings, and work steps 6 through 12 after completing a treatment program.

The Dynamics of Alcoholics Anonymous

The reasons for AA’s effectiveness may be as varied as the individuals involved. At the most basic level, the program works because one follows the 12 steps. It may be that these deceptively simple steps provide a concrete, tangible course of action; they may trigger cognitive processes previously unformed, unfocused, or abandoned and they may encapsulate powerful dynamics capable of having an impact on craving, conditioning, and character. The AA program revolves around the 12 steps, and most members would offer the common-sense explanation that working the steps keeps them sober.18

Additional explanations for AA’s effectiveness include strengthening self-control, decreasing pathological narcissism, empathetic understanding of alcoholics, and spiritual growth. The latter processes are not mutually exclusive and most likely impact a given AA member differently.

Strengthening of Self-Control

Mack19 and Khantzian and Mack20 refer to an aspect of the ego (or self) concerned with choosing, deciding, and directing the personality. Self-governance, or more simply, self-control, encompasses a group of functions in the ego system that provides the individual with a sense of being and a sense of power to be in charge of oneself. The concept of self-control implies a sharing of control with others, and, indeed, indicates that survival and sense of personal value require interdependent participation in social structures.

The alcoholic has lost control over alcohol, and in turn, his or life has become unmanageable. AA recognizes the powerlessness of the individual in the face of the drive to drink and provides a counterforce to the drive to drink through caring and supportive interaction with others. The social aspects of group process operating in AA strengthen the individual’s capacity for self-control by “borrowing” such capacity from fellowship with AA members, the group process, and the acceptance of a higher power. In the most simple terms, the alcoholic learns to substitute people for alcohol.

Khantzian and Mack20 further implicate ego functions in the etiology of and recovery from alcoholism. They view the alcoholic as having certain ego functions that have poorly developed. One such ego disability observed in alcoholics and other addicts is a diminished capacity to recognize, regulate, and tolerate affect. Feelings may seem unmanageable and, therefore, threatening. The ability to describe how one feels may be lacking. The individual, who feels overwhelmed, confused, or painfully uncomfortable with emotion, is subject to develop pseudoindependent personality traits that serve to defend one from painful feelings.21 Such defenses constitute, in part, the defects of character that the AA step program seeks to remove. Thus AA, through the working of the steps (particularly 6, 7, and 11), challenges the past faulty coping strategies of the alcoholic through its recognition that failure to do so will lead one back to drinking.

Another ego function that may be deficient in substance-abusing individuals is that of self-care. This capacity involves reality testing, judgment, anticipation of consequences, and impulse control. AA may strengthen the self-care capacity of the individual by offering self-soothing slogans (eg, “easy does it,” “one day at a time,” “live and let live”) and by providing a caring milieu that the alcoholic gradually identifies with, internalizes, and uses to modulate his or her behavior.

Decreasing Pathological Narcissism

In addition to the specific ego dysfunctions mentioned earlier, Khantzian and Mack20 emphasize the importance of pathological narcissism in substance abusers. Strands of pathological narcissism that may be observed in alcoholics and other addicts include the belief that they can take care of problems themselves, that they are self-sufficient, and that they are able to retain the necessary control over alcohol as well as other areas of their lives. Further, alcohol induces a feeling of personal power and adequacy.22 The person vulnerable to alcoholism or drug addiction may enter adult life wounded by empathic failures in being parented and therefore may retain archaic narcissistic tendencies, such as grandiosity (including self-sufficiency), an overvaluation or devaluation of others, and a reliance on external sources to feel complete.23 An adult burdened by these narcissistic themes is doomed to continuous disappointment in self and others. Depression, anxiety, guilt, and shame can be expected. It is a short step to the discovery of relief from such emotional pain through alcohol. In addition, alcohol’s pharmacologic restoration of a feeling of personal power22 reinforces the original pathological narcissism.24

Cogent to the theme of narcissism are the 12 steps. Step 1, acknowledging powerlessness and loss of control, is the sine qua non, an essential element or condition,of recovery. Without the recognition and acceptance of one’s loss of control, recovery is postponed. Brown25 places particular emphasis on the alcoholic’s need to accept loss of control (ie, accept steps 1 and 2), for such acceptance is considered the nucleus of one’s identity as an alcoholic from which the stages of recovery may unfold. A reading of the steps makes clear how they offer a healthy alternative to pathological expressions of personality. Humility, powerlessness, consideration of others, the need for self-examination, and service are clearly put forth, not as abstract ideals, but as tools to ward off a return to the insanity of alcoholism.

An Empathic Understanding of the Alcoholic

As Bean26 describes, AA has “accomplished a shift from a society-centered view of alcoholism to an abuser-centered one.” AA provides the alcoholic with a protected environment. After years of feeling debased and worthless, the alcoholic is offered an environment free from the conventional view of drunken behavior. The alcoholic discovers that his or her experience is of value and even interesting to others. Further, the alcoholic’s experiences may be useful to someone else, and others thank him or her for sharing it. As Bean explains, “This idea, that a person’s experience is of value, is gratifying to anyone and is especially heady stuff to the chronically self-deprecating alcoholic.”27

Along with the shift in how alcoholism is viewed, AA provides a shift in what is expected of the alcoholic. First, the alcoholic is not asked to admit that he or she is an alcoholic. AA simply asks that one have a sincere desire to stop drinking. There is no effort to point out the error of one’s ways or the evils of alcohol. In fact, the attraction of alcohol and the pleasure of alcohol are openly acknowledged but linked with the statement that “we could not handle it.” The alcoholic who comes to AA is not asked to change, only to listen, identify, and keep coming back. The style of interpersonal contact is nonthreatening. Last names are not given, attendance is not taken, the setting is casual, and humor and friendliness abound. Nevertheless, the meeting is serious. Each member conveys that there is a lot to lose, regardless of how much has actually been lost, but also that there is much to gain in sobriety. Sobriety is the focus, and remains so, unvaryingly. Relapses or “slips” do not represent a failure on the part of the alcoholic or of AA. Rather, slips are further demonstration of the power of alcohol and, therefore, the necessity of AA as a counterforce.

As the alcoholic advances in recovery, self-esteem is protected by abstinence but threatened by remorse over the past. AA techniques to handle this aspect of recovery are:

• When one makes the decision not to drink, encourage that they repent, reform, and build from the wreckage of the past.

• Place blame on the illness, not the alcoholic.

• Avoid censure.

• Reward good behavior by dispensing 30-day, 60-day, 90-day, or
1 year “chips” as milestones in sobriety are achieved.

• Allow expression of low self-esteem in nondestructive ways rather than by drinking.

AA does not ask the alcoholic to get a job, be a better family member, or become more responsible. Sobriety is the goal from which other desirable efforts may emerge. The “depressurization” techniques of AA (“one day at a time,” “keep it simple,” etc.) and the social dimension (sharing “experiences, strength, and hope”) are critical components of the AA experience.

Spiritual Growth

An essential insight of AA for the alcoholic is its recognition and acceptance that one is “not-God.”6 This refers to the necessity for the alcoholic to accept personal limitation. Step 1 of AA communicates to the alcoholic: “We admitted we were powerless over alcohol and that our lives had become unmanageable.” The acceptance of personal limitation—a condition of existence for all—is a life-or-death matter for the alcoholic. In teaching that the first drink gets the alcoholic drunk, AA proclaims that the alcoholic does not have a drinking limit, rather the alcoholic is limited.28 To experience limitation is tantamount to experiencing shame. As painful as the shame is, it is a feeling pivotal to recovery. Acceptance of shame distinguishes the alcoholic who, in Tiebout’s29 terms, complies rather than surrenders. Compliance is motivated by guilt, is superficial, and is ultimately useless to extended recovery. Surrender involves recognition of powerlessness (and the feeling associated with feeling limited or of having fallen short). Through surrender the alcoholic becomes open to the healing forces within AA. The AA program treats shame by enabling the alcoholic to accept his or her need for others, by promoting the acceptance of others as they are (“live and let live”), and by valuing and reinforcing traits of honesty, sharing, and caring.

Spirituality rarely is referred to in medical treatment but is a dimension of the AA program and understood by those who work and live the 12 steps. The spirituality of the AA program may be understood as a series of overlapping themes:

Release. This refers to the “chains being broken”—freedom from the compulsion to drink. The experience of release is a powerful and welcoming event for the alcoholic and seems to occur naturally or to be given rather than achieved.

Gratitude. Gratitude may flow from the feeling of release and includes an awareness of what we have, for example, the gift of life. According to Kurtz,30 the words “think” and “thank” share a common derivation. Thinking leads to remembrance (eg, as the AA speaker tells his or her story), and from remembrance an attitude of thankfulness (gratitude) may be experienced (eg, gratitude that one is now sober).

Humility. Humility conveys the attitude that it is acceptable to be limited, to be simply human. The alcoholic’s awareness of powerlessness over alcohol engenders humility.

Tolerance. Tolerance of differences and limitations fosters the serenity often experienced by AA members.

Recently, Emmonds31 empirically demonstrated that goals, especially those of spiritual striving and those with religious significance, seem to promote personality integration and assist in resolving the pernicious effect of conflict on mental and physical health. AA provides goals for the alcoholic; not only the goal and “promises” of sobriety, but the goals of understanding, embracing, and following the 12 steps.

In addition to the spiritual themes mentioned earlier, an additional spiritual dimension, forgiveness, may be significant. The seeking of forgiveness is implied, not directly expressed, in the 12 steps. For example, steps 6 and 7 (Table 1) ask God to remove defects of character and remove shortcomings. The behavior of AA members toward newcomers (welcoming, accepting, friendly, caring) communicates forgiveness. Forgiveness is neither asked for nor offered at AA. The word itself may or may not be heard at AA meetings, but its meaning pervades the transactions of the meetings. For example, Bean writes32:

Alcoholics know how deeply and painfully ashamed and guilty other alcoholics are about their drinking, how they lie and minimize it, and how this reinforces their sense of worthlessness. The discovery that others have committed what they thought was their own uniquely unforgivable crime brings longed-for solace. Speakers repeatedly report their sense of relief when they first come to AA. They had no further need for dissembling and fear. Here they were among their own kind and were accepted.

Forgiveness may be a precondition for the dynamic forces described in this chapter to be operative. For example, forgiveness precedes hope. Hope is necessarily very tenuous for a newcomer to AA and requires a future orientation—an orientation minimized by AA’s emphasis on “one day at a time.” Forgiveness is experienced in a moment and may be the foundation for a growing sense of hope. Abandoning narcissistic defenses, strengthening the capacity for self-control, and accepting “powerlessness” over alcohol all may be contingent on feeling forgiven or feeling capable of being forgiven. To be forgiven and to feel forgiven implies being accepted, a common description of the AA experience. The experience of shame28 as a pivotal affect and the treatment of shame in AA may become possible only if preceded by a sense of being forgiven.

Limitations of Alcoholics Anonymous

While the average AA participant is white, male (67%), and an average of 46 years of age, AA does attract a young female population as well. Eleven percent of members are 30 years of age3 and 33% are women.3 Adoption of the AA program by minorities has been slower to occur. Yet, most urban areas have several meetings with a predominantly black or Hispanic population. African-American affiliation with AA is growing stronger and may exceed white affiliation on some variables.33

Psychiatric comorbidity may impede AA affiliation for some alcoholics. Personality disorders of the schizoid, avoidant, or paranoid type may not adapt well to the interaction and emotionality of AA meetings. At times, a patient on medication is thrown into conflict by AA members who may advise against the use of any drugs. AA does not hold opinions on psychotropic medications, but occasionally an AA member may inappropriately influence a fellow member who requires specific psychiatric treatment. For example, an alcoholic persuaded to discontinue lithium or neuroleptics may relapse into psychosis at great personal expense. As more alcoholics are reaching AA through rehabilitation programs, AA’s familiarity with and understanding of individual needs may be increased, and the AA member under psychiatric treatment will be less likely to experience conflict and inappropriate advice.

Recommendations for AA should not be limited to certain alcoholics. AA generally seems to accommodate a wide variety of personalities and backgrounds. On a case-by-case basis, social or psychodynamic factors may deter the efficacy of AA utilization, but that can be ascertained on an individual basis only, not by currently available data.

Specific limitations to the AA method have been summarized by Bean12 and include that AA is seen by some as rigid, superficial, inspirational, fanatical, stigmatizing, and focusing only on alcohol. The rigidity is more likely to lie in individual members than the AA program itself. Questioning and intellectualizing are discouraged, but this seems more a means to hold back the ever-present threat of denial. The criticism of superficiality is appropriate if one’s goals are to unravel the complex etiologies of alcoholism or to understand the dynamics of behavior change. AA, however, focuses on abstaining from drinking. It is inspirational rather than reflective, but again, the alcoholic who is early in recovery cannot be expected to obtain or use insight. Morale is of critical concern, and the emotional pitch of AA strikes a respondent chord in the demoralized. Unfortunately, fanaticism or zealotry may form part of the operation of AA loyalty. Such members are repellent to some newcomers, who may feel that their emotional needs are not understood or validated. Some charismatic AA members convert many alcoholics but alienate others. Finally, there may still be a stigma associated with attending AA. However, if there is, it is less so than in past, since acclaim for AA is easily found in popular literature and the media. At the least, any stigma attached to the AA program would be substantially less than that of chronic drunkenness.


By gaining an understanding of this 12-step program the clinician will be prepared to motivate and advocate AA to his or her alcoholic patients. This understanding is gained best by attending AA meetings, discussing AA with experienced members, and reading widely, including the AA literature as well as professional writings on AA. From this effort the physician can inform each patient appropriately of the advantages of AA affiliation. PP


1. Fleming MF, Barry KL, Manuell LB, et al. Brief physician advice for problem drinkers. JAMA. 1997;13:1039-1045.

2. Prochaska JO, Diclemente LL. Transtheoretical therapy: toward a more integrated model of change. Psychotherapy. 1982;19:276-288.

3. Alcoholics Anonymous 2001 Membership Survey. New York, NY: AA World Services; 2002.

4. Twelve Steps, Twelve Traditions. New York, NY: AA World Services; 1978.

5. Information on Alcoholics Anonymous. New York, NY: AA World Services; 1988.

6. Kurtz E. Not-God: a History of Alcoholics Anonymous. Center City, MN: Hazelden; 1979.

7. About AA: A Newsletter for Professional Men and Women. New York, NY: AA?World Services; 1984.

8. Henry S, Robinson D. Understanding Alcoholics Anonymous. Lancet. 1978;2:372-375.

9. Ogborne AC, Glaser FB. Characteristics of affiliates of Alcoholics Anonymous. J Stud Alcohol. 1981;42:661-675.

10. Emrick C. Alcoholics Anonymous: affiliation processes and effectiveness as treatment. Alcoholism (NY). 1987;11:416-423.

11. Thomassen L. AA utilization after introduction to treatment. Subst Use Misuse. 2002;37:239-253.

12. Bean MH. Alcoholics Anonymous: AA. Psychiatr Ann. 1975;5:3-64.

13. Boscarino J. Factors related to “stable” and “unstable” affiliation with Alcoholics Anonymous. Int J Addict. 1980;15:839-848.

14. Leach B, Norris JL. Factors in the development of Alcoholics Anonymous (AA). In: Kissin B, Begleiter H, eds. The Biology of Alcoholism: Treatment and Rehabilitation of the Chronic Alcoholic. New York, NY: Plenum Press; 1977:441-543.

15. Bailey MB, Leach B. Alcoholics Anonymous: Pathway to Recovery: a Study of 1058 Members of the AA Fellowship in New York City. New York, NY: National Council on Alcoholism; 1965.

16. Edwards G, Hensman C, Haukes A, et al. Alcoholics Anonymous: the anatomy of a self-help group. Soc Psychiatry. 1967;1:195.

17. Eckhardt W. Alcoholic values and Alcoholics Anonymous. Q J Stud Alcohol. 1967;28:277-288.

18. Alcoholics Anonymous. 2nd ed. New York, NY: AA World Services; 1955.

19. Mack JE. Alcoholism, AA, the governance of the self. In: Bean MH, Zinberg NE, eds. Dynamic Approaches to the Understanding and Treatment of Alcoholism. New York, NY: The Free Press; 1981.

20. Khantzian EJ, Mack JE. Alcoholics Anonymous and contemporary psychodynamic theory. In: Galanter M, ed. Recent Developments in Alcoholism. New York, NY: Plenum Press; 1989.

21. Wurmser L. Psychoanalytic considerations of the etiology of compulsive drug use. J Am Psychoanal Assoc. 1974;22:820-843.

22. McClelland DC, Davis WN, Kelin R, et al. The Drinking Man. New York, NY: The Free Press; 1972.

23. Kohut H. The Restoration of the Self. New York, NY: International Universities Press; 1977.

24. Nace EP. The Treatment of Alcoholism. New York, NY: Brunner/Mazel; 1987.

25. Brown S. Treating the Alcoholic: a Developmental Model of Recovery. New York, NY: John Wiley; 1985.

26. Bean MH. Alcoholics Anonymous: AA. Psychiatr Ann. 1975;5:6.

27. Bean MH. Alcoholics Anonymous: AA. Psychiatr Ann. 1975;5:23.

28. Kurtz E. Shame and Guilt: Characteristics of the Dependency Cycle. Center City, MN: Hazelden Foundation; 1981.

29. Tiebout HM. Surrender versus compliance in therapy. Q J Stud Alcohol. 1953;14:58-68.

30. Kurtz E. Alcoholics Anonymous and spirituality. Workshop presented by Green Oaks Psychiatric Hospital; June 9, 1989; Dallas, TX.

31. Emmonds RA. The Psychology of Ultimate Concerns: Motivation and Spirituality in Personality. New York, NY: The Guilford Press; 1999.

32. Bean MH. Alcoholics Anonymous: AA. Psychiatr Ann. 1975;5:27.

33. Kastutas LA, Weisner, C, Lee M, et al. Alcoholics Anonymous affiliation at treatment intakes among white and black Americans. J Stud Alcohol. 1999;60:810-816.


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Norman Sussman, MD, DFAPA, and Laurence Westreich, MD

Dr. Sussman is the editor of Primary Psychiatry and clinical professor of psychiatry in the Department of Psychiatry at the New York University School of Medicine in New York City.

Dr. Westreich is clinical associate professor in the Division of Alcoholism and Drug Abuse in the Department of Psychiatry at New York University School of Medicine.

Disclosure: Dr Westreich is on the speaker’s bureau for Odyssey, and Pfizer.

Please direct all correspondence to: Norman Sussman, MD, DFAPA, Department of Psychiatry, New York University School of Medicine, 150 East 58th St., 27th Floor, New York, NY 10155; Tel: 212-588-9722; Fax: 212-588-9721; E-mail:


Focus Points

In the United States, marijuana is perceived as innocuous and commonly used, which presents problems for the clinician encouraging abstinence in an addicted patient.

Signs and symptoms of marijuana withdrawal include irritability, restlessness, depression, anxiety, impaired sleep, nausea, aggression, sweating, and rhinorhea.

Treatment of marijuana withdrawal should include acknowledgment of the difficulty in stopping marijuana use, referral to support and counseling, aggressive pharmacologic treatment of withdrawal effects, and aggressive pharmacologic treatment of any underlying psychopathology.


Knowledge that a patient with a psychiatric disorder is a chronic marijuana smoker presents the clinician with a dilemma: should the patient be treated even with ongoing use of marijuana or should the patient be advised to stop smoking? Although these decisions are made on a case-by-case basis, it would be helpful if some basic guidelines could be developed for treatment decisions in these cases. This article reviews some of the findings from recent research and combines it with the clinical experience of the authors in order to provide some help in understanding the difficulties patients have in discontinuing marijuana and of the ways in which continued use may complicate efforts to treat the underlying psychiatric disorder.


Marijuana is the most commonly used illicit drug in the United States.1 Thus, it is likely that many patients who visit their physicians for routine physical examinations or for treatment of medical problems are smokers of marijuana. It is not known how often patients spontaneously report information about the use of marijuana or how often physicians specifically elicit information about it from their patients. What happens if a marijuana user is diagnosed with depression, anxiety, or another psychiatric disorder? What should the physician recommend about continuing or discontinuing the use of marijuana?

There is a remarkable lack of research literature and clinical guidelines about how to use psychotropic agents in patients who are regular users of marijuana. Indeed, considering the pervasive use of marijuana and the widespread perception of many users, remarkably little has been written about the potential impact of regular use on the course of psychiatric disorders. Physicians may feel challenged about how to advise daily marijuana smokers when treating them with psychotropic drugs, and what the nature and impact of marijuana discontinuation may be in the context of psychiatric treatment.

Marijuana is typically regarded as a relatively innocuous substance. There is even considerable popular sentiment that marijuana and hashish should be legalized. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Text-Revision2 does not include chronic use of cannabis as a disorder. Thus, suggestions by a psychiatrist that chronic marijuana use may interfere with treatment, or that use may be contributing to mood, anxiety, or cognitive symptoms are often dismissed as being judgmental.

Daily marijuana use often results in dependence. In the US, 7.4% of adults and 14.4% of adolescents who used cannabis met diagnostic criteria for dependence within the year.3 A common dilemma is distinguishing between a causal and coincidental relationship. Thus, if there is an association between marijuana use and psychiatric disorder or a specific syndrome, it is not always obvious whether or not the use of marijuana is the cause of the problem. For example, according to data from the National Longitudinal Study of Adolescent Health, marijuana use by adolescents is among the six risk factors for suicide attempts.4

Given the pervasiveness of cannabis use, and its status as a recreational drug, as opposed to a “hard” drug, physicians may encounter patients who are both depressed and regular marijuana users. In this clinical context, a number of questions arise:

• How should treating clinicians address the ongoing use of marijuana if treatment for depression is started?

• Should patients be told to stop smoking?

• If patients are told to stop smoking, is it reasonable to expect that they will be compliant?

• Does use of marijuana while being treated with antidepressant interfere with the effectiveness of the medication?

• What is known about marijuana withdrawal syndrome?

• How can withdrawal be managed?

• Does marijuana increase the risk of mental disorders?

• Does chronic marijuana use represent self-medication?

• Can mental disorders be treated effectively in the face of chronic marijuana use?

This review offers guidance to clinicians who may encounter the dilemma of treating depression in marijuana smokers.

Relationship Between Marijuana and Mental Health

Studies have shown that substance abuse, primarily involving alcohol, marijuana, and cocaine, is common among persons with mental disorders.5 While some studies have found little or no association between marijuana use and poor mental health, others have shown that marijuana users are at increased risk for symptoms of poor mental health.6 It has been argued that marijuana use causes mental disorder and that it represents an attempt to self-medicate.

Epidemiological evidence of a possible causal role of marijuana use in the development of major depressive disorder (MDD) suggests that the risk of a first MDD episode is moderately associated with the frequency of marijuana use and with more advanced stages of marijuana use.7 Compared to those who never use marijuana, even nondependent marijuana users have a 1.6 times greater risk of MDD.7 In addition, one study8 found that continuous heavy use of marijuana can induce psychotic disorder that can be distinguished from cannabis intoxication.

Prenatal Marijuana Exposure

Marijuana is the illicit drug most commonly used by pregnant women. The human placenta is a target for cannabinoids. Marijuana use during pregnancy has been found to affect placental clearance of serotonin through the serotonin transporter.9 There are data suggesting that prenatal exposure is associated with behavior problems beginning at 10 years of age.10

Impact of Marijuana Use at an Early Age

Use is more prevalent among adolescents and younger adults.11 Perhaps the most consistent and most robust finding across the board was the relationship between age of first marijuana and later depression and schizophrenia. A study of the association of marijuana use and adult symptomatology6 found that use of marijuana at an early age appeared to be an important determinant of later mental health outcomes. Use of marijuana at 16 years of age was found to have an effect on later depression.6 This effect negatively impacted educational attainment, employment, marital status, use of alcohol and tobacco, and likelihood of marijuana use as an adult. Depressed adolescents report more frequent use of marijuana, tobacco, and cocaine than nondepressed peers.12

Some findings point to differences in the causal direction of mental disorders based on age. For example, McGee and colleagues13 found that marijuana use among adolescents was the result of a primary mental disorder, while among young adults the use of cannabis seemed to lead to mental disorder. If correct, these findings would suggest that marijuana abuse among adolescents might signal the presence of a primary psychiatric disorder.

Amotivational Effects

Chronic marijuana use has consistently been linked with an amotivational syndrome. Symptoms include apathy, loss of productivity, difficulty in carrying out long-term plans, lethargy, depression, inability to concentrate, and inability to sustain attention.14 These amotivational effects are often additive to the effects of another, freestanding, mental illness. For example, the lethargy and passivity associated with depression can be exacerbated by the misguided use of marijuana as an attempt to self-medicate dysphoria. In addition, subtle effects of marijuana are often missed in the relatively high-functioning individual. For the student or professional with a very high intellectual capacity, steady marijuana use may degrade performance by 20% to 30%, a loss of potential undetectable to the outside world. In this circumstance, only confrontation by a skilled clinician can elicit an attempt at abstinence and a real examination of the benefits of not smoking marijuana.

Marijuana Use for Coping

Marijuana appears to be ineffective when used as a method of coping, the so-called avoidance coping. Indeed, marijuana users who smoke in order to cope are more depressed than others despite their use of the drug. Green and Ritter6 found that current marijuana use does not appear to have a positive association with depression unless a person uses it to cope with problems.


The neuropharmacology of marijuana is relatively poorly understood.15 Does marijuana actually produce physiological effects that underlie the development of psychiatric disorders?

The cannabinoid receptor type 1 (CB1) is highly concentrated in dopamine modulate areas of the brain associated with schizophrenia, and some evidence points to a link between specific genetic polymorphisms in these areas and schizophrenia.16 In an editorial, Rey and Tennant17 point out that marijuana use among young people has become as common, or more common, than smoking cigarettes in some countries. Despite the best efforts of agencies like the Office of National Drug Control Policy (ONDCP), marijuana use is considered relatively benign and socially acceptable in the US, and in many jurisdictions has minor or nonexistent legal consequences. However, there has been little research into the best treatment for those who use marijuana. As with other addictions, moral issues associated with a recommendation for abstinence should be put aside in favor of more practical problems with marijuana use in the psychiatric patient. Although the anxious individual may not identify marijuana as contributing cause for the anxiety, and may even perceive marijuana as a treatment for anxiety, the adept clinician can point out that marijuana functions as a central nervous system depressant and hallucinogenic agent. Like alcohol, marijuana may initially relieve anxiety, but as time passes both substances worsen anxiety and pose risks for addiction and further maladaptive use. This empathic teaching approach is more likely to yield good results from the marijuana-using individual than a punitive or angry approach.

Marijuana is more socially acceptable than other recreational drugs and there is considerable pressure to legalize it. Thus, a better understanding of how chronic marijuana use affects the development and management of mental disorders is warranted.

Marijuana Withdrawal

There are few references to marijuana withdrawal in the literature. The lifetime prevalence of marijuana dependence is the highest of all illicit drugs in the US.18 Some chronic users experience extreme difficulty in discontinuing use. Most discussions characterize discontinuation symptoms as being mildly distressing.

Symptoms of Withdrawal

Only in the past few years have studies begun to appear that define a marijuana withdrawal syndrome. Evidence suggests that while marijuana may lack many of the intense physiological symptoms and life-threatening reactions that accompany discontinuation of other drugs of abuse, the manifestations of its cessation after long-term use may be sufficiently distressing to cause difficulty with discontinuing the drug. Users may find that the rapid emergence of withdrawal symptoms leads them to start smoking again. Regular heavy use of marijuana is associated with the development of tolerance to some psychoactive and some cardiovascular effects, such as tachycardia and hypotension.19

Rat studies20at Virginia Commonwealth University in Richmond found that the administration of a marijuana (cannabinoid) receptor antagonist (SR 141716A) following the administration of chronic tetrahydrocannabinolproduces ptosis, “wet dog shakes,” facial rubbing (interpreted as signs of withdrawal), retropulsion, ear twitching, chewing, licking, and arching of the back. Overall, the animals appeared hyperactive and disorganized.

A summary of symptoms of withdrawal after daily use based on studies from several research centers are listed in the accompanying Table.3,21,22

It has generally been thought that the duration of withdrawal symptoms last only a few days. However, a Harvard University study22 found that symptoms often last for at least 4 weeks. Withdrawal symptoms were more pronounced during the first 10 days after marijuana cessation.

Acknowledgment of Difficulty in Stopping Marijuana Use

As with cocaine withdrawal, the absence of a definitive treatment modality should not lead to ignoring the syndrome itself. By understanding the patient’s reluctance to stop marijuana use as real and mostly biologically based, the clinician can encourage abstinence by using available psychopharmacologic remedies and encouraging emotional support from therapists, family, friends, and peer-led self-help groups, such as Alcoholics Anonymous.

Aggressive Psychopharmacologic Treatment of Withdrawal Effects

There is no clearly established pharmacologic treatment for cannabis dependence and no agent proven to mitigate withdrawal symptoms. Naltrexone, an opioid antagonist, failed to show evidence for efficacy in the treatment of compulsive marijuana use.15 A small study at the New York State Psychiatric Institute in New York City found that the antidepressant nefazodone attenuated some symptoms of marijuana withdrawal.23 The drug reduced ratings of anxiety and muscle pain, but not irritability. In a separate study, the investigators found that the antidepressant bupropion increased the severity of withdrawal symptoms compared to the placebo maintenance group,3 but that it worsened mood.

Insomnia associated with marijuana withdrawal can be treated with soporifics such as zolpidem or the antidepressant trazodone. The patient should be told that these drugs will be only partial remedies, but will likely “take the edge off” the withdrawal syndrome. Often, these sorts of therapeutic maneuvers by the clinician foster a strong therapeutic alliance because the withdrawing patient is reassured that his or her discomfort is being recognized, understood, and treated as well as possible.

Among patients with schizophrenic and schizoaffective disorders, clozapine has been shown to facilitate abstinence from marijuana, but has not been studied for any antiwithdrawal properties.5 Remarkably, a search found no citations of benzodiazepines, such as alprazolam or clonazepam, in the use of withdrawal reduction.

Cui and colleagues18 reported that systemic infusion of lithium suppressed the cannabinoid withdrawal syndrome in rats. The animals were treated chronically with the cannabinoid agonist HU210 and then injected with the cannabinoid antagonist AM281 to provoke withdrawal symptoms. Lithium blocked all the withdrawal symptoms. Caution is recommended in giving too much clinical significance to these results as they were derived from an animal study, but they do suggest a possible avenue of further research. It is of interest that the researchers found evidence that lithium may have protected against withdrawal effects through release of oxytocin from the pituitary gland. To test whether the observed effects were in fact mediated through an oxytocinergic mechanism, they administered high-dose oxytocin. It was found that the exogenous oxytocin, like lithium, blocked the cannabinoid withdrawal syndrome. As mentioned by Uvnas-Moberg and colleagues,24 “There is both clinical and laboratory evidence to suggest a role for oxytocin as an endogenous antidepressant/anxiolytic hormone.” Several classes of drugs that increase plasma oxytocin levels are also effective anxiolytics.

Aggressive Psychopharmacologic Treatment of Underlying Psychopathology

An early and forceful attempt to treat underlying psychopathology reassures the patient that his or her discomfort is understood and will be treated. For example, a depressed patient may complain that only marijuana relieves persistent dysphoria. In this case, prescription of an antidepressant during the time that marijuana withdrawal is being attempted will elicit the earliest possible therapeutic response, while reinforcing the idea that the beneficial effects of marijuana will be replaced by the effects of a medication, without the side effects of marijuana. The clinician should specifically inform the patient that psychotropic medication is less likely to work under the condition of continued marijuana use. That is, ideally, no medication can allow the addict to continue using marijuana without a potentially negative impact on efficacy. At some point, after therapeutic trials of different medications have failed, the need for cessation of marijuana use becomes the foremost issue in ongoing treatment.


The consequences of occasional marijuana use are not known. Marijuana use is not necessarily impairing to its users. Many patients occasionally smoke marijuana recreationally without discernable adverse impact on their emotional state and cognitive performance. Many successful musicians, artists, and writers report that marijuana increases their creativity. Cancer patients undergoing chemotherapy use marijuana to suppress treatment-associated nausea.

Despite the benefits of marijuana use in some patients, the continued use of the drug may be problematic in adolescents and chronic adult users for whom marijuana is associated with a mental disorder. In terms of evidence-based medicine, the clinical implications of regular marijuana use by patients who are being treated for psychiatric disorders has not been systematically studied. Yet, based on clinical experience, it is clear that marijuana use interferes with performance in many areas of life, such as work, school, and family relationships. There is also sufficient evidence to suggest that regular use of marijuana can induce or exacerbate symptoms in the mentally ill person, regardless of the acuteness or chronicity of use. Because of this, continued use of cannabis may constitute a causal or perpetuating factor in the disorder, and should be discontinued if only to ascertain if the symptoms remit. It is analogous to a patient who is unsuccessfully treated for panic attacks, yet who drinks several cups of coffee a day. Eliminating the coffee often alleviates the anxiety symptoms, or permits medications to work. However, cessation of caffeine use may result in a withdrawal syndrome that can be anticipated.

Because discontinuation of chronic cannabis use can result not only in craving, but also in clinically significant psychiatric and physiological withdrawal symptoms, continued abstinence is problematic for many patients. Even though treatment should be attempted while marijuana smoking continues, it should be clearly stated that successful treatment may not be possible in these circumstances. If several trials of medications fail and smoking cannot be stopped, hospitalization for detoxification may be necessary. Since most medical insurance companies do not cover cannabis addiction, hospitalization should be based on the severity of the disorder and its resistance to treatment. PP


1. Johnston D. National Survey Results on Drug Use From the Monitoring the Future Study, 1975-1998, Vol I: Secondary School Students (DHHS Publication No. NIH 99-4660). Rockville, MD: US Department of Health and Human Services; 1999.

2. Diagnostic and Statistical Manual of Mental Disorders. 4th ed, text-rev. Washington, DC: American Psychiatric Association; 2000.

3. Haney M, Ward AS, Comer SD, Hart CL, Foltin RW, Fischman MW. Bupropion worsens mood during marijuana withdrawal. Psychopharmacology (Berl). 2001;155:171-179.

4. Borowsky IW, Ireland M, Resnick MD. Adolescent suicide attempts: risks and protectors. Pediatrics. 2001;107:485-493.

5. Zimmet SH, Strous RD, Burgess ES, Kohnstam AB, Green AI. Effects of clozapine on substance use in patients with schizophrenia and schizoaffective disorder: a retrospective survey. J Clin Psychopharmacol. 2000;20:94-98.

6. Green BE, Ritter C. Marijuana use and depression. J Health Soc Behav. 2000;41:40-49.

7. Chen CY, Wagner FA, Anthony JC. Marijuana use and the risk of major depressive episode. Epidemiological evidence from the United States National Comorbidity Study. Soc Psychiatr Epidemiol. 2002;37:199-206.

8. Nunez LA, Gurpegui M. Cannabis-induced psychosis: a cross-sectional comparison with acute schizophrenia. Acta Psychiatr Scand. 2002:105:173-178.

9. Kenney SP, Kekuda R, Prasad PD, Leibach FH, Devoe LD, Ganapathy V. Cannabinoid receptors and their role in the regulation of the serotonin transporter in human placenta. Am J Obstet Gynecol. 1999;181:491-497.

10. Goldschmidt L, Day NL, Richardson GA. Effects of prenatal marijuana exposure on child behavior problems at age 10. Neurotoxicol Teratol. 2000;22:325-336.

11. National Household Survey. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2000.

12. Field T, Diego M, Sanders C. Adolescent depression and risk factors. Adolescence. 2001;36:491-498.

13. McGee R, Williams S, Poulton R, Moffitt T.
A longitudinal study of caanabis use and mental health from adolescence to early adulthood.
Addiction. 2000;95:491-503.

14. Cherek DR, Lane SD, Dougherty DM. Possible amotivational effects following marijuana smoking under laboratory conditions. Exp Clin Psychopharmacol. 2002;10:26-38.

15. Wachtel SR, de Wit H. Naltrexone does not block the subjective effects of oral Delta(9)-tetrahydrocannabinol in humans. Drugs Alcohol Deprend. 2000;59:251-260.

16. Leroy S, Griffon N, Bourdel MC, Olie JP, Poirier MF, Krebs MO. Schizophrenia and the cannabinoid receptor type 1 (CB1): association study using a single-base polymorphism in coding exon 1. Am J Med Genet. 2001;105:749-752.

17. Rey JM, Tennant CC. Cannabis and mental health: More evidence establishes clear link between use of cannabis and psychiatric illness [editorial]. BMJ. 2002;325:1183-1184.

18. Cui SS, Bowen RC, Gu GB, Hannesson DK, Yu PH, Zhang X. Prevention of cannabinoid withdrawal syndrome by lithium: involvement of oxytocinergic neuronal activation. J Neurosci. 2001;21:9867-9876.

19. Cohen S. The 94-day cannabis study. Ann N Y Acad Sci. 1976;282:211-215.

20. Aceto MD, Scates SM, Lowe JA, Martin BR. Dependence on delta 9-tetrahydrocannabinol: studies on precipitated and abrupt withdrawal. J Pharmacol Exp Ther. 1996;3:1290-1295.

21. Budney AJ, Hughes JR, Moore BA, Novy PL. Marijuana abstinence effects in marijuana smokers maintained in their home environment. Arch Gen Psychiatry. 2001;58:917-924.

22. Kouri EM, Pope HG Jr. Abstinence symptoms during withdrawal from chronic marijuana use. Exp Clin Psychopharmacol. 2000;8:483-492.

23. Haney M, Hart CL, Ward AS, Foltin RW. Nefazodone decreases anxiety during marijuana withdrawal in humans. Psychopharmacology (Berl). 2003;2:157-165.

24. Uvnas-Moberg K, Bjokstrand E, Hillgaart V, Ahlenius S. Oxytocin as a possible mediator of SSRI-induced antidepressant effects. Psychopharmacol (Berl). 1999;142:95-101.


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Treatment Considerations in
Patients With Addictions

Mark J. Albanese, MD, and Howard J. Shaffer, PhD

Dr. Albanese is medical director of addictions at the Cambridge Health Alliance in Cambridge, Massachusetts. He is also advanced fellow in addictions studies in the Division on Addictions and assistant clinical professor of psychiatry in the Department of Psychiatry at Harvard Medical School in Boston.

Dr. Shaffer is director of the Division on Addictions and associate professor of psychology in the Department of Psychiatry at Harvard Medical School.

Disclosure: Dr. Albanese was supported by the Arcadia Charitable Trust and has received research grants from Eli Lilly and Janssen.

Please direct all correspondence to: Mark J. Albanese, MD, Medical Director, Addictions, Cambridge Health Alliance, 26 Central St, Somerville, MA 02143; Tel: 617-591-6020; Fax: 617-591-6054; E-mail:




While many elect to recover from addictive disorders on their own, others choose clinical care. Treatment can occur in a variety of settings and represents an array of clinical modalities. A combination of modalities, such as pharmacologic and psychosocial interventions, yields the most favorable treatment outcomes. Nonspecific treatment factors (eg, empathy and countertransference) also considerably influence treatment outcomes. The treatment process is enhanced when clinicians match clinical interventions with patients’ motivation for change and their stage of addiction or recovery. More research is needed to elucidate the effects of different treatment interventions on long-term outcomes.


Addictive disorders are among the most prevalent biobehavioral conditions in the United States. The National Comorbidity Survey estimates that among the US population between 18 and 54 years of age, the 1-year prevalence of alcohol use and drug use disorders is approximately 10% and 4%, respectively.1 Similarly, the Epidemiologic Catchment Area study estimates the 1-year prevalence of these disorders to be 9% and 4%, respectively. The prevalence of these disorders is even higher among people with a psychiatric illness.1-5 Between 11% and 18% of community members diagnosed with a clinically significant substance abuse or dependence disorder seek treatment from nonspecialty general medical or health systems resources; another 11% seek treatment from the specialty mental health and addiction services sector.1 The good news is that effective treatments for addictions are available. For example, methadone maintenance treatment for opioid dependence is associated with decreased heroin and cocaine use, reduced criminal behavior, and a lower rate of human immunodeficiency virus (HIV) seroconversion.6-13

Although treatment for addiction is efficacious and cost effective, many clinicians do not understand the tenets of such care. This article reviews some principles and components of addiction treatment, as well as factors that often influence treatment outcomes. The natural history of addiction and how it relates to treatment efforts is examined, illustrating the importance of coordinating clinical activities with a patient’s place in the recovery process. Finally, the course of addiction using a stage-change perspective that integrates a variety of theoretical views is discussed.14-16

About Recovery: Addiction is Reversible

Treatment is just one of several pathways to allaying addictive behaviors. Considerable evidence indicates that many addictions (eg, drinking, gambling, smoking, drug use) can resolve without formal treatment.17-27 Similarly, assisted recovery need not always involve clinicians; self-help fellowships, such as Alcoholics Anonymous (AA), are also an option.

Unassisted or “Natural” Recovery

Conventional wisdom has assumed that there are only two ways out of any addiction—treatment or death. However, since Winick24 first described “maturing out” of narcotic use, the idea of recovery from addiction without treatment has caught the attention of many clinical investigators. Research suggests that recovery from addiction without treatment is more common than previously expected.17,20,27 Those who experience unassisted recovery tend to have milder forms of their disorder and fewer coexisting problems that complicate the recovery process.

Assisted Recovery

Not everyone can effectively evoke natural recovery processes. Consequently, many people who might revise their behavior without treatment17-20 seek treatment and recovery through clinical pathways; the majority of these treatment seekers access clinicians who are not addiction specialists. The following principles of treatment will assist clinicians of every specialty in helping patients with addictive disorders.

Treatment Settings

Treatment can take place in diverse settings, with various levels of containment. At one end of the spectrum is treatment within a correctional facility. At the other end is treatment that occurs in a patient’s home (eg, outpatient detoxification), workplace (eg, employee assistance programs), or church basement (eg, AA meeting). In between, the range of settings includes hospital inpatient units, residential facilities (eg, group homes and therapeutic communities), hospital partial care, day treatment programs, community mental health centers, and addiction treatment centers.

Treatment Strategies: Addiction as a Syndrome

Addictive disorders have a variety of characteristics that require treatment. Addiction is a syndrome with common and unique elements. The common attributes, such as anxiety and depression, are shared with other mental disorders. The unique elements, such as increasing the amount of drug used to get the same psychoactive effect as experienced with lesser dosages, are exclusive to substance use disorders. Like other syndromes (eg, acquired immunodeficiency syndrome), addiction has many treatment targets and it responds best to a comprehensive biopsychosocial approach.8 For example, clinicians can combine medications and various forms of psychotherapy and counseling to address a range of problems (eg, biologic, cognitive, behavioral). Each of these treatments is available in short-term and longer-term configurations. These various treatment elements are both additive and interactive, a circumstance necessary to deal with the multidimensional nature of addictive disorders.

For patients with psychiatric comorbidity, integrating addiction care with biopsychosocial treatment produces better outcomes. For example, McClellan and colleagues8 controlled the methadone dosage for opiate abusers to 60–90 mg/day and randomized them to one of three levels of psychosocial treatment for 6 months: methadone alone (ie, minimum methadone services [MMS]); methadone plus counseling (ie, standard methadone services [SMS]); and methadone plus counseling and on-site medical, psychiatric, employment, and family therapy (ie, enhanced methadone services [EMS]). Although MMS subjects exhibited reductions in opiate use, 69% of them met criteria for protective transfer to SMS (ie, eight consecutive weekly urines positive for heroin or cocaine, or three or more medical/psychiatric emergencies). This was significantly different from the SMS subjects (41%) and EMS subjects (19%) who met these criteria. End-of-treatment outcomes revealed that the SMS group showed significantly more and greater improvements than did the MMS group, and the EMS group showed significantly better outcomes than did the SMS group. MMS subjects who had been protectively transferred to SMS showed significant reductions in opiate and cocaine use within 4 weeks.

Components of Treatment

The following sections examine some of the components of a biopsychosocial approach to addictions treatment.


Pharmacologic agents can be one component of a comprehensive treatment plan. Agonists are used as substitutes for substances of abuse during detoxification or maintenance treatment. For example, methadone may be used as a substitute for heroin and nicotine patches for cigarettes. Antagonists or partial agonists compete with substances of abuse, preventing psychoactive substances from interacting at the nerve cell receptors where they exert their effects. For example, naltrexone is an antagonist and buprenorphine a partial agonist of heroin at the brain’s opioid receptors.

Aversive agents cause an unpleasant effect if a person ingests an addictive substance while taking medication for treatment of addiction to that substance. Disulfiram, for example, prevents the complete metabolism of alcohol, resulting in the accumulation of an unpleasant metabolite. Anticraving agents decrease craving for a substance. Naltrexone works at least partially via this mechanism to decrease alcohol ingestion. Agents for comorbid disorders are also frequently prescribed. Among these drugs are agents for medical problems (eg, HIV medications) and psychiatric disorders (eg, antidepressants). Of note, some psychopharmacologic agents can address both the addiction and the psychiatric disorder. For example, some antidepressants improve both the depression and alcohol problem,28 and some of the newer antipsychotic medications alleviate both the psychotic symptoms and the substance use.29

Pharmacotherapy is probably underutilized in patients with addiction. One likely reason is patient ambivalence. For example, patients with two or more stigmatizing mental illnesses (eg, dual or multiple diagnoses) frequently will not take prescribed medication in order to convince themselves that they do not have an illness. Consider a common refrain from our substance-abusing patients: “I might be an addict, but I’m not crazy, doc.” Conversely, for some patients, the grass is greener in another diagnostic category. For example, consider the patient with alcoholism who believes that the real (ie, only) problem is underlying depression, which he or she is self-medicating with alcohol, or the patient with schizophrenia who is convinced that it is cocaine use that is causing the psychotic symptoms.

Clinicians experience ambivalence in a variety of forms. Physicians worry that treating substance-abusing patients with medications enables addiction. Consequently, treatment providers are often reluctant to prescribe psychoactive medication for people with drug use disorders. They believe they are exchanging one type of chemical dependence for another. In the authors’ experience, these beliefs represent countertransference, providing the treatment provider with a rationalization for limiting the clinical relationship.

Of note, patients with addictions can be more sensitive to medication side effects. Frequently, the side effects resemble the uncomfortable feelings experienced during intoxication or withdrawal. For example, the stimulating side effect of an antidepressant could be reminiscent of the psychomotor agitation or anxiety that emerges during alcohol withdrawal. Weiss and colleagues30 recently reported that side effects were the most common reason for lithium noncompliance in substance-abusing patients with bipolar disorder. Physicians should start patients on low doses, and then increase the dose very gradually to therapeutic levels; it is sometimes useful to aim for a lower-than-usual maintenance dose. Alternatively, it is sometimes necessary to use more than one medication in especially refractory dual-diagnosis patients.31-33 Finally, given the potential serious adverse consequences of addictions (eg, suicide and violence) and the relative safety of most medications, the safer treatment course is to err on the side of more liberal use of appropriate medication.

As discussed later, matching treatment to client is crucial. In terms of pharmacology, some studies34 have suggested that different subgroups of patients with alcoholism exhibit distinct responses to selective serotonin reuptake inhibitors (eg, citalopram, fluoxetine), and other data suggest that men and women respond differently to these medications.35

Psychosocial Treatment

There is a considerable range of psychosocial treatment modalities for patients with substance use disorders. These modalities include individual, couples, family, network, vocational, and group therapy. Furthermore, there are a variety of treatment approaches within these modalities. For example, treatments can be psychoeducational, cognitive, behavioral, or psychodynamic. Some observers might include self-help programs (eg, AA or Gamblers Anonymous) among psychosocial treatments. However, these programs are fellowships and should not be considered formal treatments, although they can be very therapeutic.

As noted, when pharmacologic interventions are combined with psychosocial treatments, clinical outcomes improve. In general, however, studies have not demonstrated the superiority of one psychosocial approach compared with others. For example, in the Harvard Cocaine Recovery Project, cocaine-dependent individuals received either one of two group treatments or no group modality. Both recovery training and self-help (ie, a cognitive-behavioral approach) and modified dynamic group therapy (MDGT) (ie, a psychodynamic approach) were similarly more effective than treatment without a group modality.36 Similarly, Project Match found, for the most part, that people with alcohol disorders showed improvement whether they received coping skills, motivational enhancement therapy, or 12-step facilitation (TSF) therapy.37 Despite the observation that participants in Project Match improved regardless of treatment type, as with pharmacologic treatments, there is some support for matching psychosocial interventions.

In the outpatient arm of the trial there was a matching effect for one specified contrast of the psychiatric severity hypothesis. Although the original conceptualization of this hypothesis was that individuals high in psychopathology would have better drinking outcomes with cognitive-behavioral therapy (CBT) rather than TSF, results indicated that there was no reliable difference in the outcome of high psychopathology subjects. On the other hand, subjects without psychopathology had significantly more abstinence in 7 of the 12 follow-up months when treated with TSF rather than CBT. On average, the TSF advantage over CBT was approximately 4 more abstinent days per month.37

Just as one theory of addiction does not necessarily preclude other theories, one psychosocial treatment approach does not preclude others. For example, the authors have developed both an inpatient state hospital dual-diagnosis treatment program and an outpatient substance abuse treatment program that include a variety of groups (eg, relapse prevention, AA and Narcotics Anonymous, and MDGT) that are available for clinicians to suggest according to patient needs identified during a comprehensive clinical evaluation.

Factors That Influence Treatment Outcomes

Nonspecific Factors

Nonspecific or common factors account for a considerable amount of treatment outcome.38,39 Hubble and colleagues38 suggest that nonspecific treatment factors include the extratherapeutic attributes that patients bring with them to treatment (eg, education, family support); the relationship factors expressed by the treatment provider (eg, empathy, caring, warmth); and the hope, expectancies, and placebo effects that are often associated with the start of treatment. Therapist training and experience, as well as opportunities for relapse prevention, can also influence treatment outcomes. Thus, the unique effects of particular treatment programs might be easily mistaken for nonspecific effects that accompany all programs.

A full discussion of the nonspecific factors that influence treatment outcome is beyond the scope of this article. However, there are many useful resources for readers interested in the factors common to successful treatment.38-49 Recognizing nonspecific treatment effects holds the potential to maximize specific treatment benefits. Nonspecific treatment factors also can contribute to poorer outcomes, such as when the relationship between clinician and patient is less than optimal. Arguably the most important adverse relationship factor expressed by the treatment provider is countertransference hate.42,45

Countertransference and Countertransference Hate

People have a tendency to feel congratulatory when someone reveals good news, for example, that he or she is getting married, entering a detoxification facility, or abstaining from gambling. In contrast, a revelation of bad news, such as impending divorce, often stimulates sympathetic feelings. Such responses in a clinician represent countertransference. Weiner stated the following50:        

When a therapist feels or acts toward a patient in ways that are neither part of the real relationship, rationally justified by the circumstances, nor part of the working alliance, appropriate to the terms of the treatment contract, he is manifesting countertransference.                  

Rather than expressing either congratulations or sympathy, a more effective clinical posture would be to ask, “When did you decide?” “How did you decide?” or “What is that going to be like for you?” Congratulations might leave relapsing patients in a difficult position: if they share their difficulties with their therapist in the future, there is a risk that they might disappoint the treatment provider. This type of situation can limit what patients are willing to disclose to their therapist.45

Countertransference can influence not only patient behavior, but also therapist behavior. When patients experience ambivalence about changing their addictive behavior patterns, treatment providers often get frustrated, angry, and perhaps even malevolent.45 Maltsberger and Buie42 suggest that clinical hate and rage comprise three primary elements: malice, aversion, and a mixture of these two emotions. Malicious impulses stimulate a disgust that can make patients seem loathsome (eg, disgust about patients who are self-indulgent). Under these circumstances, patients can become the object of punishment. However, Maltsberger and Buie42 are quick to note that malicious impulses are less dangerous than aversive tendencies because malice allows clinicians to maintain a clinical relationship with a patient whether he or she is abominated or loathed. Aversive impulses, by contrast, tempt the therapist to abandon the patient. Finally, unbearable malicious impulses often stimulate aversive actions. Malicious impulses are more painful to clinicians than the tendency to avoid.42 Therefore, when patients stimulate malevolent impulses, clinicians tend to avoid having to confront or continue working with these individuals. Clinicians need to be aware of these tendencies in order not to drive patients from treatment.

The Course of Addiction

Stage-change concepts have emerged as an important force in the treatment of addictive behaviors.14,16,45,47,51-55 Stage-change theory suggests that an evaluation of a person’s readiness to change and determination of that person’s stage of change are important steps to formulating appropriately matching treatment strategies.47 Motivational enhancement techniques16,47,56-58 can facilitate this process and guide intervention strategies.

Initiation and Positive Consequences

Initiation marks a patient’s first involvement with an object or activity. When this early experience is positive, the relationship with the object of interest is reinforced and tends to continue. For some, this relationship becomes excessive and leads to adverse consequences.

Emergence of Adverse Consequences

Before patients seek treatment, they often experience various problems and have little awareness that their excessive behavior pattern is the primary cause of these difficulties. At this stage, patients are not considering a behavioral change. Their drinking, drugging, or gambling is still viewed as a positive experience. When people experience both positive and negative feelings about an object or activity, they are ambivalent. This ambivalence can become painful and lead to denial. Consequently, the first major clinical challenge is to enhance awareness of consequences and overcome resistance to change. In many cases, inviting or engaging someone struggling with addiction into treatment is the focus of clinical efforts because family members, not the person with the addiction, typically initiate contact with treatment providers.

Psychoeducation can help to start the change process. For example, clinicians can engage family members, providing them with information about addictive disorders and describing the continuum of associated problems. This activity might not include the patient, because he or she might not be very interested in treatment. Family members should be instructed to review the educational materials and take care of themselves. They should not share their treatment discussions with the patient, rather they should simply invite the patient to participate in the next session. This circumstance encourages patients to examine their own behavior patterns, risky situations, and impact on others without alienating or coercing them to participate in treatment. Too often, coercion by the family or treater leads to maliciousness, aversion, and ultimately abandonment. Each of these experiences holds significant risk for the already vulnerable person who is struggling with an addictive disorder.

Once patients’ curiosity and ambivalent feelings emerge, clinicians should request that they self-monitor the behavior in question (eg, drinking, drugging, gambling) and document any urges toward the object of their interest. This evidence can provide the foundation for future efforts at evaluation and treatment planning. Patients then have the opportunity to compare their perception of their experience and how it changes over time. In addition, they can compare their view with that of others. They also have the opportunity to assess the impact of their behavior on their life objectives. During this part of treatment, patients should also be questioned about what their addiction does for them, not just what it is doing to them. By exploring patients’ perception of the benefits and advantages of addiction for them, clinicians are in a better position to develop realistic treatment plans that consider alternative behavior patterns that can fulfill as many of the same addiction objectives as possible without having to engage in the addictive behavior. Taken together, these early treatment activities exercise the ambivalence associated with behavior change and gently diminish denial and resistance.58

Awareness of Adverse Consequences

As patients begin to recognize addictive behavior as the primary cause of their problems, they begin to consider the possibility of addressing these issues. The major clinical challenge is to address patients’ ambivalence about whether they wish to alter their addictive behavior pattern and deal with the associated problems. The primary approach to stimulating the desire to change is to acknowledge that addiction provides positive benefits as well as negative consequences. The clinician must acknowledge that modifying the pattern of behavior that caused problems will require relinquishing some current activities. A decision balance exercise that explores the pluses and minuses of maintaining the behavior and the gains and losses of changing is the major vehicle for resolving the ambivalence about the value of curbing addictive behaviors. A seminal event such as ending a relationship, losing a job, or experiencing a health crisis, referred to as a turning point, often marks the patient’s decision to change.

Turning Points and an Orientation to Change

Once patients accept the notion that changes are necessary and worthwhile, the major challenge is to help them see the array of recovery alternatives. Making choices is central, and the key treatment activity is planning. Therapists’ efforts focus on goal setting and planning for treatment and life changes. Together, the patient and clinicians explore therapeutic options and appropriate action steps, such as the type of treatment setting, program philosophy, level of care, kind and variety of therapeutic modalities, group or individual format, professional profile, and cost. Treatment matching is an important principle. Treatment success is often linked to honoring the person’s preferences and validating the acceptability of the person’s choices.

Active Quitting: Taking Action for Change

When ready to change, the major theme is active learning. The clinical strategy focuses on encouraging patients to initiate a range of new alternative behaviors based on the acquisition of new knowledge, insight, attitudes, and skills. This is the beginning of psychologic detoxification and restoration. Identifying and substituting a different leisure activity for the time spent gambling is an important component of a healthy recovery. The introduction of support fellowships (eg, AA or Gamblers Anonymous) and more involvement in spiritually enriching experiences also can be highly beneficial. However, though clinicians can suggest these support systems, almost any that a recovering person chooses holds potential to be helpful.

Relapse Prevention and Change Maintenance

To achieve enduring treatment goals, the clinical focus must gradually shift to practice the new competencies that will sustain a balanced, healthy lifestyle. Adult learning theory recognizes that developing and mastering new behaviors requires training and repetition. Relapses can and often do occur; because this is a common part of recovery from addictive behavior patterns, clinicians need to pay particular attention to situational risk and negative effect as critical relapse triggers.59-62

In sum, clinicians have relatively specific tasks at different phases of treatment. For example, during the early stages of treatment, clinicians should raise doubt about the effectiveness of addiction to achieve personal goals. Once patients consider changing, clinicians must exercise ambivalence and stimulate motivation to change by identifying reasons to change and risks of the status quo. Once ready to change, patients will need help choosing the best plan. Once there is an agreed-upon plan, clinicians need to teach the patient skills that support change and prevent relapse. Finally, once a patient has made changes, clinicians must help him or her practice these new behaviors and reframe relapse as an ongoing learning process.63 Observers often incorrectly think that changes occur in a linear and progressive fashion. In reality, changing addiction is a recursive process with many opportunities to revisit earlier struggles; these turns provide the opportunity to practice the tasks of recovery necessary to grow as a person and rebuild one’s life.16,47,55

Considering Treatment Efficacy and Outcomes

Currently, there is limited information about long-term effectiveness with all treatment approaches. Clinicians should evaluate addiction treatment outcomes as they do cancer treatments, using 5-year follow-up rates. Similarly, while recovery is best understood as “one day at a time” by patients, the scientific evaluation of recovery should determine how patients have progressed over a 5-year follow-up period. Anything less than this time frame can be misleading, as treatments can provide short-term gains that do not last. Similarly, short-term gains should not lead to the false belief that all risk of relapse is over. As we have noted, because syndromes are multidimensional, these disorders typically do not respond favorably to a single treatment modality—either during the active change phase of treatment or during the relapse prevention phase.


Treatments for addictions are composed of both common and specific factors. These treatments, which have evolved from a variety of theoretical approaches, can be provided in many different settings. Frequently, outcomes are improved when clinicians combine interventions within a comprehensive treatment plan. The stage-change concept, which helps us to appreciate the natural history of addiction, underscores the importance of matching appropriate interventions with patients based on where they are in the process of addiction and recovery. Future research will clarify issues such as how to best match specific treatments with individual patients in order to enhance long-term outcomes. PP


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Elspeth Cameron Ritchie, MD

Primary Psychiatry. 2003;10(8):43-48


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Harish K. Malhotra, MD, Nancy B. Isenberg, MD, and Louis Barash, PhD

Primary Psychiatry. 2003;10(8):74-76


Dr. Malhotra is clinical assistant professor of psychiatry at the University of Medicine and Dentistry of New Jersey (UMDNJ) in Newark, NJ, and an attending in the Department of Psychiatry at Overlook Hospital in Summit, New Jersey. Dr. Isenberg is a specialist in behavioral neurology and neuropsychiatry in the New Jersey Neuroscience Institute at JFK Medical Center in Edison. Dr. Barash is co-principal investigator in the Department of Microbiology and Microbial Genetics at UMDNJ.

Disclosure: Dr. Malhotra is on the speaker’s bureau of AstraZeneca, Eli Lilly, and Bristol-Myers Squibb; Dr. Isenberg is on the speaker’s bureau of Janssen, Novartis, and Pfizer.

Please direct all correspondence to: Harish K. Malhotra, MD, Department of Psychiatry, Overlook Hospital, 33 Overlook Rd, Suite 212, Summit, NJ 07901; Tel: 908-273-6164; Fax: 908-277-1439; E-mail:


Focus Points

It is recommended that whenever there are associated soft neurological symptoms and signs in a case of psychosis, medical causes should be considered in the etiology of the presenting psychosis.

Longitudinal progression of a psychosis can uncover previously hidden aspects of the disease.

Neurodegenerative disorders may become evident as psychiatric syndromes at different stages of life.



Niemann-Pick disease is a neurometabolic genetic disorder. Types A and B reflect a primary and severe acid sphingomyelinase (ASM) deficiency. The ASM enzyme is ordinarily found in lysosomes and is required to metabolize the lipid, sphingomyelin. If ASM is absent or not functioning properly, sphingomyelin cannot be metabolized properly and is accumulated within the cell, eventually causing cell death and the malfunction of major organ systems. Niemann-Pick type A (neurovisceral) is a severe neurological disease in infants, which generally leads to death by 2–3 years of age. Infants with Niemann-Pick disease type A have extremely low levels of ASM (generally <5% of normal). Niemann-Pick disease type B (visceral) generally has little or no neurological involvement and patients may survive into adulthood. Type B has higher levels of ASM (perhaps 10% to 60% of normal). Type A and B are both diagnosed by measuring the ASM activity in white blood cells.

Niemann-Pick disease type C (NPC) is a lipid storage disease that can present in infants, children, or adults. The classic presentation occurs in middle to late childhood with the insidious onset of ataxia, vertical supranuclear gaze palsy (VSGP), dementia, and liver and lung failure. Dystonia and seizures are common. Dysarthria and dysphagia become disabling, making oral feeding impossible. Types C and D are characterized by secondary and variable sphingomyelinase alterations.1-8 The diagnosis of NPC is assay for the deficiency, which shows impaired ability of cultured fibroblasts to esterify exogenously supplied cholesterol, and positive filipin staining. Types C1 and D are indistinguishable except for the occurrence of type D in patients of Nova Scotian Acadian ancestry.

Symptoms mimicking schizophrenia can present in many conditions.4 We describe a patient who carried a diagnosis of schizophrenia for 14 years requiring psychiatric hospitalizations. He was subsequently diagnosed with NPC. The characteristic features of adult-onset NPC and the obstacles to early diagnosis are presented here.


Case Study

Psychiatric History

J.S., a single caucasian male, was 32 years of age in 1999 when his case was reviewed. His psychiatric history dated back to 18 years of age. J.S. had been diagnosed as learning disabled and perceptually impaired, and had completed high school through special classes. At the onset of his illness, J.S. believed that people were changing into bears, dancing around him, and trying to scare him. From July 1996 through August 1997, he was hospitalized for psychiatric treatment three times. During those hospitalizations J.S. presented with bruises on his face, mumbling, and an inability to explain what happened to him. J.S. was casually attired, disheveled, nonspontaneous, incoherent, loud, and threatening. His speech was described as irrelevant. His mood was anxious and his affect was constricted. His behavior was destructive and required seclusion. J.S. showed grossly impaired judgment, loose association, tangential thinking, and no insight. He was unable to give goal-oriented answers. J.S. admitted to “buzzing noises” in his ears. His sensorium was clear, but he was unable to name recent or past dates. He showed no signs of suicidal or homicidal ideas.

During another hospital admission J.S. was described as having auditory hallucinations, paranoid delusions, low frustration toleration, intrusiveness, poor speech communication, and difficulty following directions. J.S. was evaluated by a speech therapist and was found to have dysarthric speech. During that hospitalization, J.S. was diagnosed as having schizophrenia chronic undifferentiated type, polysubstance dependence, borderline intellectual functioning, phonological disorder, and mixed expressive language disorder.


Personal and Family History

Family history revealed that J.S.’s father was a 64-year-old electrician and his mother was a 58-year-old secretary who had been adopted. His mother suffered from a history of alcoholism, and the paternal side of family had a history of mental illness.

Personal history revealed that J.S. was a full-term baby, delivered by induction of labor. He had a poor APGAR score (measure of respiration, heart action, muscle tone, skin color, and reflexe adequacy in a newborn) and spoke and walked late. J.S. had suffered some traumatic experiences: he had been raped in 1995 (the rapist was apprehended and convicted). In addition, he had been a victim of a bus accident from which he sustained a head injury, but details were not available. He had a history of arrest for drug possession. He worked in Union County Vocational Rehabilitation as a cook and was on supplemental social security income. He lived in a group home.


Clinical Presentation

The first author (H.K.M.) had been treating J.S. for the last 2 years in a day program for the chronically mentally ill. In January 1999, H.K.M. noted that the patient complained of repeated falls, difficulty with balance, and difficulty controlling eye movements. Hence a referral was made to the second author (N.B.I.), a neurologist.

The patient was examined by N.B.I. on February 10, 1999, who noted the patient had a history of poor balance and was prone to falling, especially when attempting to climb stairs. Moreover, his balance had worsened over the last 2 years. J.S. had falling incidents almost daily and had difficulty rising from a chair and climbing or descending stairs. J.S. denied light-headedness, vertigo, akathisia, stiffness, dystonia, motor weakness, or auditory/visual hallucinations in the interval prior to the examinations. He also denied having any recent change in his speech, but said that he had problems with slurring of his speech for as long as he could remember.

N.B.I. noted that J.S. was taking divalproex 250 mg PO QID, thiothixene 5 mg QAM and 10 mg QHS, and benztropine 4 mg/day in divided doses.


Neurological Examinations

Neurological examinations revealed that J.S. was sitting comfortably in the chair without adventitious movements. His blood pressure was 100/70 mm Hg (mercury) when seated, with a pulse of 70, which was regular. He was alert. J.S.’s attention and concentration were easily distracted, but he was able to repeat six digits forward and four digits backward. When asked to say the months backward, he repeated them forward. J.S. was unable to spell “world” backward. On memory functions, J.S. was oriented to self, time, and place. He was able to immediately encode three words on the first try, and to recall three words at 5–10 minutes without any cues. His fund of knowledge was poor and he was unable to name the current president. His recollection of the king’s story (a one-paragraph story used to assess comprehension of narrative) was with poor details and lack of assimilation of the gestalt. His visual spatial memory showed that he was able to encode three objects on the first try and recall all three at 5 and 10 minutes as well. He had very good recall of lurid details of a movie he had seen the previous evening.

Language functioning showed that spontaneous speech was fluent without paraphasic errors, but with prominent lingual dysarthria. J.S. was able to follow simple commands (left/right, multi-step, and cross mid-line). Repetition was intact, as was naming both high- and low-frequency words. Reading was intact. When asked to write any sentence, he wrote, “I am smart.” Calculations were impaired with mistakes on simple subtractions, as well as making changes.

J.S. had no evidence of dyspraxia or apraxia. Visuospatial construction showed that pentagons were well constructed, while a cube gave some difficulty. Frontal executive function examination showed that his clock drawing demonstrated very poor organization, and writing of consecutive numbers up to fifteen. J.S. was able to make the clock hands say 10 minutes after two o’clock without difficulty.

Ramparts demonstrated stimulus-bound behavior and J.S.’s multiple loops demonstrated closing in, as well as perseverance. He was unable to learn the Luria hand sequence (frontal lobe evaluation where examiner asks patient to repeat the hand sequence fist, chop, flat) in less than five repetitions, and was unable to perform go/no/go (frontal lobe evaluation where examiner asks patient “When I tap my hand once, you tap twice; when I tap twice, do not tap at all”). Fluency was impaired for both semantic, as well as phonemic cues. Similarities were concrete. J.S. also had slowness noted on execution of movements and perseverance.

On examination of his cranial nerves, J.S.’s pupils were equally round and reactive to light and accommodation. His discs were bilaterally sharp. Visual fields were full. J.S. had a vertical supranuclear gaze palsy, which was most pronounced on downward gaze. He had absent optokinetic nystagmus in the vertical direction with a symmetrical intact vestibulo-ocular response. There was slight hypomimia with a symmetrical slow smile. The remainder of his cranial nerves, including hearing, was intact. No orobuccal or lingual dyskinesia were noted. Motor examination showed normal bulk, mildly increased tone with slight rigidity, and cog-wheeling bilaterally. Rapid alternating movements were clumsy and slowed, more on the right than on the left.

Sensory examination showed that J.S. was intact to all four modalities, including joint position sense, vibration, pinprick, and light touch. No axial rigidity was noted. Finger-to-nose and heel-to-shin was intact and without evidence of dysmetria. His reflexes were three plus throughout, with toes upgoing bilaterally. Glabellar and snout reflexes were present. J.S. had a wide-based gait. He was able to arise from a chair only with prominent retropulsion. He was able to walk on his toes and heels, exhibiting mildly reduced arm swing. The Romberg test was negative although he had a very prominent retropulsion. (Romberg test: patient stands with eyes open and then closed with feet approximated; sign is positive if closing eyes increases unsteadiness, indicating loss of proprioceptive control).

Magnetic resonance imaging was reviewed with a neuroradiologist and was thought to be most consistent with perinatal insult with mildly increased signal in T-2 in the periventricular region. Laboratory values were notable for normal ceruloplasmin, copper, complete blood count, SMAC (basic chemistry profile), vitamin B12 level, hexoscamidase-A levels and serum acanthocytes. Laboratory data was noted for a cholesterol count of 144, which was low. Vitamin E (α-tocopherol portion) was slightly low as well. In addition, fibroblast culture was notable for an abnormal cholesterol esterification, which was depressed by over 20%, confirming the diagnosis of NPC (Figures 1, 2, and 3).


J.S. had a constellation of signs and symptoms of ataxia and VSGP, which may be suggestive of NPC. Other possible causes of VSGP and dysarthria supranuclear gaze palsy include spinocerebellar degeneration, progressive supranuclear gaze palsy, ataxia, Huntington’s disease, and Parkinson’s disease, all of which were unlikely to be present in J.S. given his absence of the other commonly associated signs. A β-lipoproteinemia or vitamin E deficiency is also unlikely to be responsible for the symptoms, due to the absence of peripheral neuropathy. Although vitamin B12 deficiency could also present with psychosis, the absence of weakness, anterior and posterior columnar dysfunction, or peripheral neuropathy, further made this diagnosis unlikely as well. A blood smear for acanthocytes for β-lipoproteinemia was negative.

Cholesterol esterification and fibroblast assays may be abnormal and low in familial hypercholesterolemia, hyperlipidemia type 2, Wolman’s disease, and mucolipidosis type 2 and 3. The patient’s low peripheral cholesterol, however, was inconsistent with the initial two diagnoses, namely, hyperlipidemia type 2 and 3, and Wolman’s disease. Also, J.S. did not have any of the phenotypic features of mucolipidosis, which were disorders present in early childhood.

His life-long diagnoses of schizophrenia chronic undifferentiated type, borderline intellectual functioning, phonological disorder, and mixed expressive language disorder all could be explained by the slowly developing neurological disorder NPC which took 14 years to become severe enough to be correctly diagnosed. The new diagnosis of psychiatric disorder due to medical condition of NPC would not change the pharmacologic management but would help guide the future planning.

The final impression was that this 32-year-old gentleman, with a prior diagnosis of schizophrenia, showed disinhibition, frontal executive dysfunction, dementia, supranuclear vertical gaze palsy, dysarthria, and ataxia. All of them were slowly progressive with fibroblast culture abnormal for cholesterol esterification. The clinical picture was consistent with the diagnosis of NPC. It is recommended that whenever there are associated soft neurological symptoms and signs in a case of psychosis, medical causes should be considered in the etiology of the presenting psychosis.  PP



1. Shulman LM, Nobel DJ, Weiner WJ. Psychosis as the initial manifestation of adult-onset Niemann-Pick Disease Type C. Neurology. 1995;45:1739-1749.

2. Fox JT, Jr, Kane FJ, Jr. Niemann-Picks disease manifesting as schizophrenia. Dis Nerv Sys. 1967;28:194.

3. Cummings JL. Organic delusions: phenomenology, anatomical correlations and review. Br J Psychiatry. 1985;146:184-197.

4. Lanska DJ, Lanska MJ. Niemann-Picks disease type C in a middle-aged woman. Neurology. 1993;43:1435-1436.

5. Dunn HC, Sweeney VP. Progressive supranuclear palsy in an unusual juvenile variant of Niemann-Picks disease. Neurology. 1971;21:442.

6. Cobcroft R. Images in haematology: type C Niemann-Pick disease. Br J Haematology. 2000;111:718.

7. Imrie J. Isolated splenomegaly as the presenting feature of Niemann-Pick disease type C. Arch Dis Child. 2001;84:427-429.

8. Vanier MT. Lipid changes in Niemann-Pick disease type C brain: personal experiences and review of the literature. Neurochemical Res.1999;24:481-489.


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John Zajecka, MD, and Corey Goldstein, MD

Primary Psychiatry. 2003;10(8):60-65


Dr. Friedman is executive directorat the National Center for Posttraumatic Stress Disorder at the Veteran’s Affairs Medical and Regional Office Center in White River Junction,  Vermont, and professor of psychiatry in the Department of Psychiatry and Pharmacology at Dartmouth Medical School, in Hanover, NH.

Disclosure: Dr. Friedman is on the PTSD Scientific Advisory Boards for GlaxoSmithKline and Pfizer.

Please direct all correspondence to: Matthew J. Friedman, MD, PhD, National Center for PTSD (116D), VA Medical & Regional Office Center, 215 North Main St, White River Junction, VT 05009; Tel: 802-296-5132; Fax: 802-296-5135; E-mail:


Focus Points

The empirical evidence on efficacy of psychotropic medications in the treatment of posttraumatic stress disorder (PTSD) symptoms are reviewed.

A general approach to pharmacotherapy for PTSD is presented.

Potential adverse side effects associated with medication treatment
are reviewed.



What are the best medications for posttraumatic stress disorder (PTSD)? The selective serotonin reuptake inhibitors (SSRIs) paroxetine and sertraline have received Food and Drug Administration approval for the treatment of PTSD due to efficacy shown in clinical trials. Although research with other classes of medications has been less extensive, there is currently a fair amount of preliminary information to guide clinician choices for PTSD treatment. This review considers the following classes of medications: SSRIs, newer antidepressants, monoamine oxidase inhibitors, tricyclic antidepressants, antiadrenergics, anticonvulsants, benzodiazepines, and conventional and atypical antipsychotics. At this time, SSRIs are recommended as first-line treatments for PTSD. Evidence favoring other medications is mixed. Current data suggests that there is no indication for prescribing either benzodiazepines or conventional antipsychotic agents for PTSD.


Psychopharmacologic Management of PTSD

Since its introduction as a formal diagnosis in 19801, posttraumatic stress disorder (PTSD) has been shown to have a lifetime prevalence of 8% in the United States,2 with a much higher prevalence in countries affected by civil war, genocide, forced migration, and terrorism.3 Furthermore, evidence continues to accumulate indicating that in addition to its public health significance as a prevalent psychiatric disorder, PTSD is a risk factor for many medical illnesses.4

The last decade has been marked by an increase in clinical trials on both pharmacologic and psychosocial treatments for PTSD, culminating in a practice guideline developed by the International Society for Traumatic Stress Studies (ISTSS).5 It is an exciting time to consider psychopharmacologic management of PTSD. Two medications, paroxetine and sertraline, both selective serotonin reuptake inhibitors (SSRIs), have already received Food and Drug Administration approval for the treatment of PTSD. Other candidate medications are being tested in multi-site treatment trials. Expanding our knowledge of biological alterations associated with PTSD promises to open the way for the developing and testing of new compounds and our growing understanding of the normal human response to traumatic stress has begun to generate interest in pharmacologic interventions for acutely traumatized individuals.6-8

In addition to a number of recent reviews on pharmacotherapy for adults and children,9 practice guidelines are currently being developed by the American Psychiatric Association and jointly by the US Departments of Veterans Affairs and Defense. These will update the first practice guidelines developed by ISTSS which recommend SSRIs as first-line treatments and other antidepressants as second-rank medications for PTSD.10

This article will review results from clinical trials on pharmacotherapy for PTSD in order to equip practitioners with the latest evidence-based information on the relative efficacy of medications currently used in psychiatric practice.


Results From Clinical Trials

Selective Serotonin Reuptake Inhibitors

Sertraline and paroxetine have received FDA approval for the treatment of PTSD based on positive findings in large multisite trials.11-14 These agents offer many benefits (Table).15 They are broad spectrum medications which ameliorate symptoms from all three PTSD symptom clusters as defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV)16: re-experiencing, avoidant/numbing, and hyperarousal symptoms. They also have proven efficacy against other major DSM-IV psychiatric disorders that are frequently comorbid with PTSD, such as depression, panic disorder, social phobia, and obsessive-compulsive disorder. Sertraline and paroxetine also appear to promote reduction of clinically significant symptoms that are often associated with PTSD, such as suicidal, aggressive, and impulsive behavior. Finally, as with all SSRIs, their side-effect profile is relatively benign compared to other medications. A large multisite trial and smaller open trials with fluoxetine indicate that SSRIs are very effective for PTSD.17 Research with the SSRI citalopram indicates that the drug is effective in children with PTSD.18 Open clinical trials with fluvoxamine have also shown favorable results.9



Although second-generation antidepressants are very popular with clinicians, they have not been tested extensively in PTSD and there are no randomized clinical trials supporting their effectiveness. The best evidence from open trials supports the use of nefazodone, which, similar to SSRIs, promotes serotonergic actions.10,19 Nefazodone is also less likely to cause insomnia or sexual dysfunction than SSRIs. Trazodone, which has limited efficacy as a stand-alone treatment, has proven very useful as augmentation therapy with SSRIs. Through its serotonergic action it is synergistic with SSRIs while its sedating properties make it a useful bedtime medication that antagonizes SSRI-induced insomnia.10

Other second-generation antidepressants, such as venlafaxine and bupropion, cannot be recommended at this time because there is very little data demonstrating their efficacy in PTSD. Because PTSD is often comorbid with major depression and as venlafaxine and bupropion are both effective antidepressants with relatively benign side-effect profiles, some clinicians automatically favor them over older agents despite the fact that both monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs) have proven efficacy in PTSD whereas venlafaxine and bupropion have not.


Monoamine Oxidase Inhibitors

Despite one very successful randomized clinical trial with phenelzine20 and a quantitative review suggesting that MAOIs produce moderate-to-good global improvement and reduction of reexperiencing symptoms for PTSD patients,21 these compounds have received little experimental attention since 1990. This lack of attention is probably due to clinician concerns about potentially serious side effects, lack of interest by pharmaceutical companies, and hopes that safer selective MAO-A inhibitors will enjoy wider use.

Certainly, MAOIs are contraindicated for patients who cannot adhere to tyramine-free diets, for patients who cannot abstain from alcohol or many illicit drugs, and for patients prescribed SSRIs, central nervous system (CNS) stimulants, decongestants, or meperidine. Despite this, there remain many patients who might benefit from MAOIs when clinical trials with SSRIs have failed. Before initiating phenelzine treatment, patients should be completely weaned from other antidepressants for at least 7 days (or 5 weeks if they had been taking fluoxetine). In addition to their usefulness in PTSD, MAOIs have proven efficacy in depression and panic disorder.


Tricyclic Antidepressants

TCAs are old-fashioned, but potent antidepressants, which, like MAOIs, have not been tested in recent years. The milder side-effect profile of SSRIs and other second-generation antidepressants has undoubtedly contributed to the relative neglect of TCAs, which were once a mainstay of psychopharmacotherapy. Two randomized clinical trials with veterans showed that imipramine and amitriptyline, respectively, produced global improvement and reduced reexperiencing symptoms in veteran subjects20,22 although a third trial with desipramine was negative.23 In the one head-to-head comparison between imipramine and phenelzine, the MAOI was more effective although the TCA was still superior to placebo.20 Side effects associated with TCAs are well-known and can often be managed successfully, but sometimes are the cause of noncompliance or discontinuation. One clear advantage of TCAs and MAOIs over newer antidepressants is their lower cost, which may be a crucial consideration for some patients.


Antiadrenergic Agents

One of the earliest and best established findings in PTSD research is the excessive adrenergic reactivity among patients with the disorder.24 Despite this robust experimental finding, and despite open trials dating back to 1984,10 antiadrenergic medications have been largely neglected until recently. All of the agents listed in the Table are safe medications that have been used for many years in treating cardiovascular disease, especially hypertension and cardiac arrhythmias. Although all agents listed achieve the end result of reduced adrenergic activity, they do it via three different mechanisms of action: Propranolol is a postsynaptic β-adrenergic antagonist; prazosin is a postsynaptic α1 receptor antagonist; and clonidine and guanfacine are presynaptic α2-receptor agonists which reduce the amount of norepinephrine released into the synaptic cleft.

The best research on this class of agents has focused on prazosin, which has produced marked reduction in traumatic nightmares, improved sleep, and global improvement among veterans with PTSD.25 Propranolol has been tested in sexually and/or physically abused children with chronic PTSD and produced significant reduction in reexperiencing and arousal symptoms.26 Because of laboratory research suggesting that propranolol might reduce sympathetic arousal and the encoding of highly charged emotional memories during the immediate aftermath of a traumatic event,27,28 propranolol was administered prospectively to emergency room patients to see whether it might prevent the later development of PTSD. Although the trend toward lower rates of PTSD was nonsignificant 3 months later, patients who had received an acute 10-day course of propranolol exhibited significantly less sympathetic nervous system hyper-reactivity at the 3-month follow-up assessment.29

Clonidine and guanfacine are especially interesting agents because of laboratory evidence that disinhibition of adrenergic neurons with the α2-adrenergic antagonist yohimbine, produces panic attacks, dissociative symptoms, and PTSD flashbacks among combat veterans with this disorder.24 Since both clonidine and guanfacine directly oppose the actions of yohimbine, there is a rationale to suggest that they might be especially effective clinically for patients in whom dissociation and flashbacks figure prominently. While there are a number of clinical trials currently exploring this possibility, it is merely speculation at this point.

Clonidine has also been used successfully with Southeast Asian refugees with PTSD both as a supplement to antidepressant treatment or by itself. Indeed, it has been reported that in many cases, these refugees prefer clonidine to any other medication and can be maintained for years on clonidine alone.30



An important neurobiological model for PTSD is that certain brain nuclei become sensitized or “kindled” following exposure to traumatic events. Such a model which led to the successful use of carbamazepine and valproate in the treatment of bipolar affective disorder has also been proposed for PTSD.31,32 Unfortunately, there have been no randomized trials with either anticonvulsant involving PTSD patients, although promising open trials with both medications have been reported.10 As shown in the Table, both agents have effectively reduced hyperarousal symptoms. Carbamazepine appears to reduce reexperiencing and aggressive symptoms while valproate has been more effective in reducing avoidant/numbing symptoms. Both of these medications have many potential side effects and are not always well tolerated by patients. The major concerns with carbamazepine are neurological symptoms, hyponatremia, and bone marrow suppression resulting in leukopenia. Valproate is teratogenic and contraindicated for women who plan to become pregnant, since its disruption of fetal development occurs early in the first trimester. Therefore, it is best to discontinue this medication before pregnancy begins. Impaired liver function and thrombocytopenia may also occur with valproate. In short, the complexities of clinical management with these effective anticonvulsants have shifted current attention to newer agents (eg, gabapentin, lamotrigine, and topiramate) which have yet to be tested systematically with PTSD patients.



Although lithium’s properties are well established both as an antikindling agent and as an effective agent for recurrent affective disorders, it has received little attention as a treatment for PTSD. Indeed, with the exception of two small series of open-label case reports published approximately 20 years ago,33 there has been no systematic investigation of lithium with respect to PTSD. In the aforementioned clinical trials, lithium reportedly reduced autonomic arousal, irritability, aggression, anxiety, insomnia, alcohol consumption, and capacity to cope with stress. Due to lack of research in PTSD, lithium cannot be recommended as treatment for PTSD at this time.



Because of their proven efficacy as anxiolytics, benzodiazepines are often prescribed for PTSD. This is unfortunate because studies with alprazolam and clonazepam indicate that these agents have no proven efficacy against core PTSD symptoms,10,34 while there are many more effective nonbenzodiazepine agents available. In PTSD, benzodiazepines can be expected to improve sleep and reduce general anxiety but not to have any salutary impact on the syndrome itself. Furthermore, there are potential risks of prescribing these agents because they may exacerbate depressive symptoms, produce CNS depression, or be problematic for patients with past or present alcohol/drug misuse. In addition, alprazolam may produce rebound anxiety, which is poorly tolerated by PTSD patients.


Antipsychotic Agents

When PTSD first burst upon the clinical scene in the 1970s with Vietnam veterans seeking treatment at VA hospitals, many conventional antipsychotic agents were prescribed to ameliorate intense hyperarousal, hypervigilance, dissociative symptoms, aggressivity, and re-experiencing symptoms. It is now understood that these PTSD symptoms have a very different pathophysiology than psychotic disorders and that there are much more effective treatments available. In addition, the many side effects, especially extrapyramidal symptoms, make these agents a poor choice for PTSD treatment. Conventional antipsychotics are not recommended for PTSD patients.10

In contrast, atypical antipsychotic agents, which have potent pharmacologic actions, have a less toxic side-effect profile. Although there are very little data from clinical trials, preliminary studies with atypical antipsychotics suggest that they may be effective agents for PTSD global improvement, selective action on DSM-IV?B (intrusive recollections), C (avoidant/numbness), or D (hyperarousal) symptoms, and on aggressive behavior.10 Atypical agents may have a unique niche as augmentation treatment for partial responders to SSRIs or other first- or second-line agents, especially for patients with intense hypervigilance/paranoia, agitation, dissociation, or brief psychotic reactions associated with their PTSD.35 As for side effects, all atypicals may produce weight gain and olanzapine treatment has been linked to the onset of type II diabetes mellitus.


A General Approach to Pharmacotherapy

Pharmacotherapy is only one of several treatment options for PTSD patients, especially in view of the great success of cognitive-behavioral therapy (CBT).36 Medication may be a good choice when patient acceptability of such an approach is high, when comorbid conditions are present that are responsive to pharmacotherapy (eg, depression, panic disorder, social phobia, and obsessive-compulsive disorder), or when CBT treatment is unavailable.9

At this time, SSRIs must be considered first-line treatment for PTSD. For patients who exhibit a partial response to SSRIs, one should consider continuation or augmentation.37 A recent trial with sertraline showed that approximately half of all patients who failed to exhibit a successful clinical response after 12 weeks of sertraline treatment, did respond when SSRI treatment was extended for another 24 weeks.38 Practically speaking, clinicians and patients will usually be reluctant to stick with an ineffective medication for 36 weeks, as in this experiment. Therefore, augmentation strategies seem to make sense. Here are a few suggestions based on clinical experience and pharmacologic estimates, rather than on hard evidence:16

Excessively aroused, hyperreactive, or dissociating patients might be helped by augmentation with an antiadrenergic agent; labile, impulsive, and/or aggressive patients might benefit from augmentation with an anticonvulsant; and fearful, hypervigilent, paranoid, and psychotic patients might benefit from an atypical antipsychotic.



SSRIs are first-line treatments for PTSD?due to their broad spectrum effects against all PTSD symptom clusters, their efficacy against many comorbid disorders, and their effectiveness against associated symptoms, such as impulsivity, aggression, and suicidal thoughts.9,10 Patients who cannot tolerate SSRIs or who show no improvement might benefit from MAOIs, TCAs, or the antidepressant nefazodone. (Venlafaxine and bupropion cannot be recommended because they have not been tested systematically in clinical trials).16 Evidence favoring the use of these agents is not as compelling as for SSRIs because many fewer subjects have been tested at this point.

There is a strong rationale from laboratory research to consider antiadrenergic agents and it is hoped that more extensive testing will establish their usefulness for PTSD patients. In addition, despite suggestive theoretical considerations and clinical findings, there is only a small amount of evidence to support the use of carbamazepine or valproate with PTSD patients. Research with other anticonvulsants is at a preliminary stage.

Benzodiazepines cannot be recommended for PTSD patients as they do not appear to have efficacy against core PTSD symptoms. In addition, neither conventional antipsychotics nor lithium can be recommended for PTSD patients. Preliminary results suggest, however, that atypical antipsychotics may be useful, especially to augment treatment with first- or second-line medications, although much more research is needed.

Although we have just scratched the surface in our search for effective agents for PTSD, different pharmacologic agents will surface as potential treatments for PTSD as we learn more about the pathophysiology of the disorder. Some agents, such as corticotropin-releasing factor antagonists and substance P antagonists, are beginning to be tested while others are still on the drawing board.We can all look forward to exciting future developments in the treatment of PTSD.  PP



1. Diagnostic and Statistical manual of Mental Disorders. 3rd ed. Washington, DC: American Psychiatric Association; 1980.

2. Kessler DC, Sonnega A, Bromet G, Hughes M, Nelson CB. Posttraumatic stress disorder in the national comorbidity survey. Arch Gen Psychiatry. 1995;52:1048-1060.

3. de Jong JTVM, Komproe IH, van Ommern M, et al. Lifetime events and posttraumatic stress disorder in 4 postconflict settings. JAMA. 2001;286:555-562.

4. Somatic Consequences of Exposure to Extreme Stress. Schnurr PP, Green B, eds. Washington, DC: American Psychological Association. In press.

5. Effective Treatments for Posttraumatic Stress Disorder: Practice Guidelines from the International Society for Traumatic Stress Studies. Foa EB, Keane TM, Friedman MJ, eds. New York, NY: Guilford; 2000.

6. Friedman MJ. Future pharmacotherapy for PTSD: prevention and treatment. Psychiatr Clin North Am. 2002;25:1-15.

7. Morgan CA, Krystal JH, Southwick SM. Toward early pharmacological posttraumatic stress intervention. Biol Psychiatry. In press.

8. Pine DS. Developmental psychobiology and response to threats: relevance to trauma in children and adolescents. Biol Psychiatry. In press.

9. Friedman MJ, Donnelly CL, Mellman TA. Pharmacotherapy for PTSD. Psychiatr Ann. 2003;33:57-62.

10. Friedman MJ, Davidson JRT, Mellman TA, Southwick SM. Guidelines for pharmacotherapy and position paper on practice guidelines. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for Post-traumatic Stress Disorder: Practice Guidelines from the International Society for Traumatic Stress Studies. New York, NY: Guilford; 2000:84-105.

11. Brady K, Pearlstein T, Asnis GM, et al. Efficacy and safety of sertraline treatment of posttraumatic stress disorder. JAMA. 2000;283:1837-1844.

12. Davidson JRT, Rothbaum BO, van der Kolk BA, et al. Multicenter, double-blind comparison of sertraline and placebo in the treatment of posttraumatic stress disorder. Arch Gen Psychiatry. 2001;58:485-492.

13. Marshall RD, Beebe KL, Oldham M, Zaninelli R. Efficacy and safety of paroxetine treatment for chronic PTSD: a fixed-dose-placebo-controlled study. Am J Psychiatry. 2001;158:1982-1988.

14. Tucker P, Zaninelli R, Yehuda R, Ruggiero L, Dillingham K, Pitts CD. Paroxetine in the treatment of chronic posttraumatic stress disorder: results of a placebo-controlled, flexible-dosage trial. J Clin Psychiatry. 2001;62:860-868.

15. Friedman MJ. Post-traumatic Stress Disorder. Kansas City, MO: Compact Clinicals; 2001.

16. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.

17. Martenyi F, Brown EB, Zhang H, Prakash A, Koke SC. Fluoxetine versus placebo in posttraumatic stress disorder. J Clin Psychiatry. 2002;63:199-206.

18. Seedat S, Lockhat R, Kaminer D, Zungu-Dirwayi N, Stein DJ. An open trial of citalopram in adolescents with post-traumatic stress disorder. Int Clin Psychopharmacol. 2001;16:21-25.

19. Bryant RA, Friedman MJ. Medication and non-medication treatments of posttraumatic stress disorder. Curr Opin Psychiatry. 2001;14:119-123.

20. Kosten TR, Frank JB, Dan E, McDougle CJ, Giller EL. Pharmacotherapy for post-traumatic stress disorder using phenelzine or imipramine. J Nerv Ment Dis. 1991;179:366-370.

21. Southwick SM, Yehuda R, Giller EL, Charney DS. Use of tricyclics and monoamine oxidase inhibitors in the treatment of PTSD: a quantitative review. In: Murburg MM, ed. Catecholamine Function in Post-traumatic Stress Disorder: Emerging Concepts. Washington, DC: American Psychiatric Press; 1994:293-305.

22. Davidson J, Kudler H, Smith R, et al. Treatment of post-traumatic stress disorder with amitriptyline and placebo. Arch Gen Psychiatry. 1990;47:259-266.

23. Reist C, Kauffman CD, Haier RJ, et al. controlled trial of desipramine in 18 men with post-traumatic stress disorder. Am J Psychiatry. 1989;146:513-516.

24. Southwick SM, Paige SR, Morgan CA, et al. Adrenergic and serotonergic abnormalities in PTSD: catecholamines and serotonin. Semin Clin Neuropsychiatry. 1999;4:242-248.

25. Raskind MA, Peskind ER, Kanter ED, et al. Prazosin reduces nightmares and other PTSD symptoms in combat veterans: a placebo-controlled study. Am J Psychiatry. In press.

26. Famularo R, Kinscherff R, Fenton T. Propranolol treatment for childhood posttraumatic stress disorder, acute type. Am J Dis Child. 1988;142:1244-1247.

27. Bryant RA, Harvey AG, Guthrie RM, Moulds ML. A prospective study of psychophysiological arousal, acute stress disorder and posttraumatic stress disorder. J Abnorm Psychol. 2000;109:341-344.

28. Shalev AY, Sahart T, Freedman S, et al. A prospective study of heart rate response following trauma and the subsequent development of posttraumatic stress disorder. Arch Gen Psychiatry. 1998;55:553-559.

29. Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry. 2002;51:189-192.

30. Kinzie JD, Friedman MJ. Psychopharmacology for refugee and asylum seeker patients. In: JP Wilson, B Drozdek, eds. Broken Spirits: The Treatment of Asylum Seekers and Refugees with PTSD. New York, NY: Brunner-Routledge Press. In press.

31. Post RM, Weiss SRB, Li H, et al. Sensitization components of posttraumatic stress disorder; implications for therapeutics. Semin Clin Neuropsychiatry. 1999;4:282-294.

32. Post RM, Weiss SRB, Smith MA. Sensitization and kindling: implications for the evolving neural substrate of PTSD. In: MJ Friedman, DS Charney, AY Deutch, eds. Neurobiological and Clinical Consequences of Stress: From Normal Adaptation to Post-traumatic Stress Disorder. Philadelphia, PA: Lippincott-Raven; 1995:135-147.

33. Friedman MJ, Southwick SM. Towards pharmacotherapy for post-traumatic stress disorder. In: Friedman MJ, Charney DS, Deutch AY, eds. Neurobiological and Clinical Consequences of Stress: From Normal Adaptation to Post-Traumatic Stress Disorder. Philadelphia, PA: Lippincott-Raven; 1995:465-481.

34. Braun P, Greenberg D, Dasberg H, Lerer B. Core symptoms of posttraumatic stress disorder unimproved by alprazolam treatment. J Clin Psychiatry. 1990;51:236-238.

35. Monnelly EP, Ciraulo DA, Knapp C, Keane T. Low dose risperidone as adjunctive therapy for irritable aggression in posttraumatic stress disorder. J Clin Psychhopharmacol. 1999;19:377-378.

36. Rothbaum BO, Meadows EA, Resick P, Foy DW. Cognitive-behavioral therapy. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for Post-traumatic Stress Disorder: Practice Guidelines from the International Society for Traumatic Stress Studies. New York, NY: Guilford; 2000:60-83.

37. Shalev AY, Friedman MJ, Foa EB, Keane TM. Integration and summary. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for PTSD: Practice Guidelines from the International Society for Traumatic Stress Studies. New York, NY: Guilford; 2000:359-379.

38. Lonborg PD, Hegel MT, Goldstein S, et al. Sertraline treatment of posttraumatic stress disorder: results of weeks of open-label continuation treatment. J Clin Psychiatry. 2001;62:325-331.


Dr. Ruzek is associate director of education, Mr. Young is disaster services coordinator, and Dr. Walser is psychologist at the National Center for Posttraumatic Stress Disorder and Veteran’s Affairs Palo Alto Health Care System in Menlo Park, California.

Disclosure: The authors report no financial, academic, or other support of this work.

Please direct all correspondence to: Josef I. Ruzek, PhD, National Center for Posttraumatic Stress Disorder, Education and Clinical Laboratory Division, VA Palo Alto Health Care System, 795 Willow Rd, CA 94025; Tel: 650-493-5000; Fax: 650-617-2769; E-mail:


Focus Points

Group treatment of posttraumatic stress disorder (PTSD) can enable helpful comparison with other trauma sufferers and may promote the recognition of the “normality” of posttraumatic reactions.

Education groups focus on helping PTSD survivors understand their experience and familiarize themselves with available treatment options; coping skills training focuses on teaching them how to incorporate the support recovery techniques they learn about.

Repeated exposure to distressing aspects of traumatic memories can help reduce the fear and arousal associated with the trauma, correct faulty perceptions of danger, improve perceived self-control of memories and accompanying negative emotions, and strengthen adaptive coping responses under conditions of distress.

Group cognitive therapy focuses on educating patients about the relationships between thoughts and emotions, exploring negative thoughts commonly held by trauma survivors, identifying personal negative beliefs, developing alternative interpretations or judgments, and practicing new thinking.



What are the advantages of using group treatment for individuals diagnosed with posttraumatic stress disorder (PTSD) and other trauma-related problems and what are the goals of the different types of group intervention? As one of the most common modes of posttrauma care, groups can be used to provide support, educate participants about PTSD, teach trauma-related coping skills, or facilitate therapeutic exposure and cognitive restructuring. Although research to date is limited, existing evidence suggests that group therapy may be a potentially effective intervention for PTSD. This article outlines several varieties of group intervention, explores issues related to patient selection, and discusses considerations in establishing and managing group services.



There are several potential advantages to the use of group treatment as a modality in care for trauma survivors with posttraumatic stress disorder (PTSD). First, many trauma survivors feel alone in their experiences. Meeting and sharing with other survivors of a similar trauma can promote a sense of acceptance and belonging. This may be especially useful for those (eg, Vietnam veterans, sexual assault survivors) who encounter negative reactions from others regarding their experience and for whom social alienation may be especially strong. Group treatment enables comparison with other PTSD sufferers and may promote the recognition of the universality of posttraumatic reactions. In addition, they may encourage adaptive functioning through modeling of coping behaviors (eg, self-disclosure) of other survivors. From a provider perspective, group treatment can be cost-efficient in comparison with individual counseling.

Whether these potential benefits of groups render them effective treatments for PTSD is not clear. Very little research has addressed the effectiveness of group treatments for PTSD. In a recent review,1 <20 group psychotherapy outcome studies were located, and only two were randomized-controlled trials. Most existing studies focus on individuals with chronic PTSD, and most have obtained positive treatment outcomes. Evidence, to date, therefore suggests that group treatment is beneficial for those with chronic PTSD, but research in this area is in its infancy and more study is required before the impact of group treatment can be confidently asserted. In particular, there is little research comparing different kinds of group treatments, and no studies comparing group with individual treatment. In addition, little is known about the processes through which group treatments benefit trauma survivors. Despite these limitations of the data, group treatment for PTSD is recommended as “potentially effective” in the International Society for Traumatic Stress Studies (ISTSS) practice guidelines.2

Group interventions for trauma survivors may take many forms. Groups may be used to provide social support, trauma-related education, training in skills for coping with PTSD symptoms and other posttrauma challenges, or opportunity for detailed exploration of traumatic experiences and associated emotions. In the following sections, we review a variety of group alternatives, patient matching considerations, and process issues.


Varieties of Group Treatment for Posttraumatic Stress Disorder 

Group Support

Social support is likely one of the most powerful components of group interventions for PTSD. In fact, some group treatments for PTSD focus primarily on providing social support as the primary active ingredient of therapy. There are many reasons why group support is indicated for trauma survivors with PTSD. Many of those who develop problems following trauma feel different from other people, alone with their distress, or misunderstood by those around them. Often, they doubt whether it is even possible that others can understand what they are experiencing. Trauma survivor support groups, being typically comprised of those who have undergone similar traumatic experiences, are well suited to challenging such perceptions. They may be especially useful in helping survivors address traumas that are difficult to talk about with family and friends (eg, sexual assault), due to perceived social stigma, embarrassment, shame, guilt, or fear of negative reactions from others.3

Some individuals with PTSD become socially isolated, in part because isolation often enables avoidance of trauma reminders and feelings of vulnerability. One effect of this isolation is to cut survivors off from others who might otherwise be of help to them, practically and emotionally. Isolation may enable avoidance of talking about the experience, but this may delay the potentially helpful processing of experience that survivors often require. Support groups provide a useful means to begin reducing social isolation, create an opportunity for contact with others in a safe and structured context, and give help in facing the many ongoing symptoms, stressors, and problems related to the traumatic experience.


Group Education

Education is a component of all treatments for PTSD and may be usefully delivered in a group format. PTSD education is intended to improve understanding and recognition of symptoms, reduce fear and shame about symptoms, and, generally, “normalize” the experience of the survivor. Understanding how PTSD develops can make symptoms seem more predictable and less frightening. Recognizing symptom triggers can help individuals cope more effectively with them. Education should also aim to reduce negative forms of coping with symptoms, such as extreme avoidance or alcohol and drug use. In some settings, education should give participants information to help them better decide whether and when to seek further treatment. When PTSD-related education is provided to individuals as part of their formal PTSD treatment, it is important to give them a clear understanding of how recovery is thought to take place, what will happen in treatment, and, as appropriate, the role of medication.

Education includes didactic presentation of materials, but must be accompanied with active prompting of questions and discussion. Simple educational instruction is limited in its impact on more complex actions important to recovery. Whenever possible, presentation of information should be expanded to include opportunity to observe and practice coping behaviors to increase likelihood of behavior change.


Trauma-Related Coping Skills Training in Groups

Individuals diagnosed with PTSD have difficulty coping with everyday circumstances and problems.4 Patients often report feeling overwhelmed and are steeped in negative emotions such as shame, guilt, anxiety, and depression.5 PTSD symptoms interfere with healthy coping, interpersonal relationships, and role functioning. One main goal of PTSD treatment is to empower the patient to manage personal difficulties, and training in coping skills can foster its achievement.6

Whereas education groups focus on helping survivors understand their experience and know what to do about it, coping skills training focuses on teaching them know how to do the supportive recovery techniques. It relies on a cycle of instruction that includes education, demonstration, rehearsal with feedback and coaching, and repeated practice. Groups include regular between-session task assignments with diary self-monitoring and the real-world practice of skills. Coping skills can include a range of interpersonal and intrapersonal self-management strategies, such as problem-solving, management of distressing trauma-related thoughts, identification and management of personal trauma “triggers,” relaxation and breathing, anger management, assertion, emotional “grounding,” and use of social support. Skills are selected to target adaptive behaviors that may be new for the individual or may be impaired due to PTSD.

Group therapy is a particularly effective way to train patients diagnosed with PTSD in the use of coping skills. Many of their difficulties are associated with maladaptive patterns in relationships that can interfere with coping. Teaching coping skills in the group setting allows individuals to obtain direct feedback from others about their use of skills and their general interpersonal style. Coping skills training has a here-and-now focus and provides useful tools for change in the immediate environment. Active engagement in new coping behaviors that address current problems faced by patients can serve to lessen distress relatively quickly and help the patient to prepare for more intense therapy if needed.


Therapeutic Exposure and Cognitive Restructuring in Groups

The group methods outlined above have not included a detailed in-session exploration of traumatic experiences by participants, nor have they included a detailed review and rethinking of distressing trauma-related beliefs or concerns. However, exposure and cognitive restructuring methods are among the best-validated components of PTSD treatment.2,7 While most of the empirical evidence supporting exposure and cognitive therapy has been derived from examinations of individually-administered care, these treatments can be delivered in groups.

Therapeutic exposure groups include the repeated exploration of traumatic memories as the central treatment component. From a cognitive-behavioral perspective, repeated exposure to distressing aspects of traumatic memories can help reduce the fear and arousal associated with the trauma, and can also help correct faulty perceptions of danger, improve perceived self-control of memories and accompanying negative emotions, and strengthen adaptive coping responses under conditions of distress.6 In “imaginal” exposure, participants verbally recount the details of their experience. This is the primary vehicle for exposure, although it is often supplemented by real-world in vivo exposure to (objectively safe) situations associated with the trauma.

When this therapy is provided in groups, exposure itself is embedded in a range of other group processes and activities. Initial introductory sessions are intended to provide education about PTSD and the treatment process, teach and reinforce basic coping skills, and prepare members for their upcoming task of therapeutic re-experiencing of their traumatic memories. Preparation for exposure is accomplished by setting clear group rules and structure, building group cohesion, discussing realistic expectations for outcome, presenting a clear rationale for exposure treatment, and teaching and supporting coping skills to be consciously employed during and following exposure. After the introductory sessions, trauma scenes are selected and systematic exposure of each member to key individual trauma memories takes place. Finally, relapse prevention and termination sessions focus on helping members consolidate their experiences during exposure, plan for anticipated difficulties, and maintain coping skills.

Compared with individual treatment, the group setting limits the number of traumatic experiences to which an individual may be exposed. Therefore, therapists and group members discuss which traumatic experiences will be explored. Members are encouraged to select scenes that are especially distressing, related to current symptomatology (eg, nightmares), and associated with fear as the predominant affect.

In the group environment, exposure is conducted by focusing upon one member at a time to ensure a minimum of 30 minutes of exposure to important trauma-related reminders, and to prevent cognitive avoidance. In describing their experiences, members are instructed to emphasize their sensory perceptions, thoughts, and emotional reactions that occurred during the event. During recounting of the traumatic experience, the facilitators give minimal directions unless emotional avoidance is occurring; if avoidance is apparent, leaders can ask questions to direct the attention of the survivor to the avoided material. This in-session exposure is supplemented with self-exposure homework. The purpose of the exposure homework is to increase the number of times trauma scenes are re-experienced to ensure that fears are effectively reduced. Typically, cassette recordings of the individual trauma narratives are made, and members are asked to listen to their personal recordings at least once each week, noting distress levels and reporting on coping skills used to manage resultant distress. The goal of the process is to access painful memories but to prevent overwhelming negative emotion.

In order to be considered suitable candidates for this kind of group activity, prospective members should show understanding and acceptance of the rationale for trauma exposure work, willingness to disclose personal traumatic experiences, and ability to establish interpersonal trust with other group members and leaders. Prior group experience and completion of a preparatory course of individual therapy including coping skills training, are very desirable. It is recommended that practitioners not deliver group-administered exposure therapy unless they have received training in the method.

Group treatment can also be used as a vehicle for conducting cognitive restructuring of negative trauma-related beliefs. A range of negative thoughts troubles many trauma survivors, including thoughts of guilt and self-blame, negative views about self (eg, personal weakness) or performance in the traumatic situation, inaccurate concerns about symptoms, problematic views of other people and the world in general, and fears about the future. Group cognitive therapy focuses on educating participants about the relationships between thoughts and emotions, exploring common negative thoughts held by trauma survivors, identifying personal negative beliefs, developing alternative interpretations or judgments, and practicing new thinking. This is a systematic approach that goes well beyond simple discussion of beliefs to include individual assessment, self-monitoring of thoughts, homework assignments, and real-world practice. This kind of cognitive therapy in groups may be less emotionally provocative for participants than exposure therapy, but it may provide significant help to group members.

For more information on this approach, Resick and Schnicke8 incorporate extensive cognitive restructuring and limited exposure therapy in their manual on cognitive-processing therapy. In addition, Young and colleagues9 present a different group-administered combination of exposure and cognitive treatments in the context of disaster-related PTSD.


Manualized Group Treatments for Posttraumatic Stress Disorder and Related Problems

There are few manualized interventions that are specific to the treatment of trauma. There are several manuals that have received scientific support or are under investigation and that can guide the practitioner in effective and practical intervention.

Seeking Safety. Developed by Najavits,5 this manualized group treatment for co-occurring PTSD and substance abuse focuses on trauma-related coping skills training. It is designed to help patients gain control over extreme symptoms, reduce risky behavior, reduce trauma-related distress, and reduce substance use. The manual addresses a wide range of interpersonal, behavioral, and cognitive coping skills that can be used with most trauma survivors (not just those with substance abuse problems).

Acceptance and Commitment Therapy. This manualized treatment that has been shown to be effective with sexual abuse trauma survivors10 and is currently under investigation for use with survivors of war trauma.11 The intervention encourages acceptance of avoided internal experience and commitment to valued action in the service of enhancing life experience. Mindfulness exercises and experiential strategies are used to help the patient take action in the face of difficult emotional and
cognitive reactions.

Cognitive-Processing Therapy. This approach has been manualized for use with rape victims.8 However, the methods outlined can be easily adapted for other PTSD populations.


Matching Practitioners, Patients, and Group Methods

In deciding whether group therapy and what kind of group methods should be offered to trauma survivors, it is necessary that all potential participants be assessed prior to group participation. Practitioners must use clinical judgment in making these determinations because empirically-based criteria for matching individual patients to either group or individual forms of trauma treatment, or to varieties of group intervention, do not presently exist. Rationally-derived indications and contraindications for group therapy have been put forward, and key considerations include ability to establish trust with others and similarity in terms of traumatic experiences to other group members.1 Contraindications include limited cognitive capacity, active psychosis, and active suicidality or homicidality.

One consideration is how recently the survivor has experienced trauma. Group interventions during the acute phase of trauma response are often delivered to survivors of disaster or other events affecting multiple persons. In addition to supporting individual trauma survivors, they may assist with group cohesion and morale in groups whose members have enduring relationships (eg, firefighters, military units). One of the most common group interventions is “psychological debriefing,”12 the term for a family of interventions that involve bringing survivors together soon after a traumatic event to review the facts of what happened, explore thoughts and feelings associated with the event, and provide education. Overall, evidence for the utility of group debriefing is mixed, and methodologically rigorous studies have yet to be conducted. There has been some concern in the field that a single exploration of traumatic experience in a group or individual setting may exacerbate rather than reduce distress in some survivors. ISTSS practice guidelines recommend that the method should be conducted by experienced, well-trained practitioners, should not be mandatory, and should utilize some clinical assessment of potential participants.13 Studies of other group approaches to early intervention14 have yet to be conducted. Certainly, group support, education, and coping skills training constitute reasonable services to offer recent trauma survivors who want them, although their capacity to prevent development of PTSD has not been demonstrated.

In work with those whose trauma exposure occurred in the more distant past, a basic consideration is the degree to which the patient is likely to be able to tolerate the “opening up” of trauma-related emotions. If the patient does not wish to explore traumatic experiences in detail or is in some other way a poor candidate for trauma-focused therapies, or if the practitioner is not trained in managing the detailed exploration of traumatic experiences, potentially helpful treatment elements—education of participants about stress reactions, “normalization” of reactions to trauma, and instruction in coping—can still be delivered in groups.

Group-administered PTSD education and social support groups may be usefully delivered to most trauma survivors and can often be provided by practitioners who are not specialists in PTSD. However, even in such less emotionally provocative group formats, experience in assessing and treating trauma survivors is necessary in preparing the practitioner to respond to emergent issues. Similarly, clinicians who are familiar with coping skills training with other treatment populations can deliver skills-training groups, but basic clinical familiarity with PTSD is necessary.


Group Process Considerations

Evidenced-based reports describing the effectiveness of specific procedural considerations related to the delivery of group treatment for PTSD are lacking. Our clinical experience and the writings of others15-17 suggest some general guidelines. First, there are clear advantages to having two therapists conduct a treatment group for PTSD. While one therapist is presenting material or working more directly with a member, the other therapist can observe the group process and bring others into the discussion.15 This is particularly important in trauma-focused treatment where the account of one group member may trigger an emotional reaction in another. In addition, while group participants are often advised to not leave the group while it is in session, there is often no reasonable way to prevent a member from leaving. A second therapist can either accompany the member who is making his or her way toward the door or consult with the member outside the group room. Having two therapists also allows for postsession (and postgroup) discussions about what took place during the session, what seemed to be effective, what did not work, and what could be done differently the next time. There is the added potential that two therapists bring more clinical skills, experience, and knowledge to the group.

Second, concrete steps should be taken to establish and maintain group identity, cohesion, and trust. Group identity can be fostered by encouraging members to view themselves as survivors who have made a commitment to regaining control of their lives, helping members choose a name for the group, and eventually, if appropriate, encouraging supportive relationships to develop outside the group. Group cohesion and trust are essential to detailed discussions of traumatic experiences and can be achieved through a variety of introductory activities,17 group structures and rules,9 and efforts to maintain active involvement of all group members.

Therapists will need to actively manage relationships between members. When group trauma work addresses existential issues such as dying, exposure to death and horror, social responsibility, fear, and helplessness, group members may at some point “transfer” feelings of hostility toward one another or the group leaders. Group leaders can normalize such reactions and help members explore and understand them. Therapists may themselves also have strong emotional reactions to the issues encountered in trauma groups. It is important that these be anticipated and that group leaders engage in self-monitoring of their responses, take ongoing active coping steps, and seek formal collegial or supervisory support if they find themselves experiencing strong or surprising reactions to the group or its members.

A related responsibility for leaders is to manage difficult group members and those experiencing intense affective reactions. While the need to manage difficult patients is common across treatments and strategies for working with problem patients have been described in the general group literature,18 individuals in treatment for PTSD often have a high levels of irritability, alienation, mistrust, or difficulty in managing anger. When a group member becomes angry or enraged during a session, it is recommended that the leaders quickly intervene to demonstrate that the group remains under their control (thus upholding safety), while validating the survivor’s anger, and giving clear messages about what is permissible in the group (referring to previously established ground-rules).

Finally, it is important in any session to keep an active involvement of all group members. There may be a primary speaker, but routinely encouraging others to speak as well is recommended. When a participant is providing “too much” detail, is tangential, or is monopolizing group time, we recommend that the group leader(s) validate the survivor’s need to talk, while emphasizing the importance of hearing from other members during the limited group time. Depending on the spoken content, a group leader can ask the survivor to “hold that thought” while giving a commitment to later give the survivor more time. When returning, the therapist might say “Tom, you were thoughtful enough to give the floor to Allen. We have a few minutes left and I wanted to get back to you. Can you find a way to briefly tell us what you felt you needed to say, or should we talk after group, or do you want to wait till the next session to share with the group?”



Group treatments for PTSD may offer much of value to the trauma survivor, from emotional and practical support, to education about trauma and its impact, to training in more effective ways of coping. Groups can also be used to deliver therapeutic exposure and cognitive therapy, two of the best-validated forms of PTSD treatment. Selection of group approach must depend on time since traumatization, patient functioning and motivation, targets of treatment, and the experience and skills of the practitioner. Group services for trauma survivors are certain to remain a staple of clinical care. The effectiveness is suggested by clinical experience but requires empirical demonstration.  PP



1. Foy DW, Glynn SM, Schnurr PP, et al. Group therapy. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for PTSD: Practice Guidelines from the International Society for Traumatic Stress Studies. New York, NY: Guilford; 2000:155-175.

2. Foa EB, Keane TM, Friedman MJ. Effective Treatments for PTSD: Practice Guidelines from the International Society for Traumatic Stress Studies. New York, NY: Guilford; 2000.

3. Linehan M. Cognitive-Behavioral Treatment of Borderline Personality Disorder. New York, NY: Guilford; 1993.

4. Herman JL. Trauma and Recovery. New York, NY: Basic Books; 1992.

5. Najavits LM. Seeking Safety: A Treatment manual for PTSD and Substance Abuse. New York, NY: Guilford; 2002.

6. Foy DW, Ruzek JI, Glynn SM, Riney SJ, Gusman FD. Trauma focus group therapy for combat-related PTSD. An update. J Clin Psychology. 2002;58:907-918.

7. Foa EB. Psychological processes related to recovery from a trauma and an effective treatment for PTSD. Ann N Y Acad Sci. 1997;821:410-424.

8. Resick PS, Schnicke MK. Cognitive Processing Therapy for Rape Victims: A Treatment Manual. Newbury Park, Calif.: Sage; 1993.

9. Young BH, Ruzek JI, Ford JD. Cognitive-behavioral group treatment for disaster-related PTSD. In: Young BH, Blake DD, eds. Group Treatments for Post-Traumatic Stress Disorder. Philadelphia, Penn: Taylor & Francis; 1999:149-200.

10. Follette VM. Acceptance and commitment therapy in the treatment of incest survivors: a contextual approach. In: Hayes SC, Jacobson NS, Follette VM, Dougher M, eds. Acceptance and Change: Content and Context in Psychotherapy. Reno, NV: Context Press; 1994.

11. Walser RW, Gregg JA, Westrup D, Rogers D, Loew D. Acceptance and commitment therapy: treatment of complex PTSD. Paper presented at: Annual Meeting of the International Society for Traumatic Stress; November, 2002; Baltimore, MD.

12. Mitchell JT. When disaster strikes. J Emerg Med Serv. 1983;8:36-39.

13. Bisson JI, McFarlane AC, Rose S. Psychological debriefing. In: Foa E, Keane T, Friedman M, eds. Effective Treatments for PTSD: Practice Guidelines From the International Society for Traumatic Stress Studies. New York, NY: Guilford; 2000:39-59.

14. Ruzek JI. Providing “brief education and support” for emergency response workers: An alternative to debriefing. Mil Med. 2002;167(suppl 9):73-75.

15. Chard KM, Resick PA, Weertz JJ. Group treatment of sexual assault survivors. In: Young BH, Blake DD, eds. Group Treatments for Post-Traumatic Stress Disorder. Philadelphia, Penn: Taylor & Francis; 1999:35-50.

16. Harney PA, Harvey MR. Group psychotherapy: An overview. In: Young BH, Blake DD, eds. Group Treatments for Post-Traumatic Stress Disorder. Philadelphia, Penn: Taylor & Francis; 1999:1-14.

17. Zaidi LY. Group treatment for adult survivors of childhood sexual abuse. In: Young BH, Blake DD, eds. Group Treatments for Post-Traumatic Stress Disorder. Philadelphia, Penn: Taylor & Francis; 1999:201-220.

18. Yalom ID. Theory and Practice of Group Psychotherapy. 4th ed. New York, NY: Basic Books; 1995.