Current Psychiatry

Psychiatry is the only medical specialty with a longtime nemesis; it’s called “antipsychiatry,” and it has been active for almost 2 centuries. Although psychiatry has evolved into a major scientific and medical discipline, the century-old primitive stage of psychiatric treatments instigated an antagonism toward psychiatry that persists to the present day.

A recent flurry of books critical of psychiatry is evidence of how the antipsychiatry movement is being propagated by journalists and critics whose views of psychiatry are unflattering despite the abundance of scientific advances that are gradually elucidating the causes and treatments of serious mental disorders.

What are the “wrongdoings” of psychiatry that generate the long-standing protests and assaults? The original “sin” of psychiatry appears to be locking up and “abusing” mentally ill patients in asylums, which 2 centuries ago was considered a humane advance to save seriously disabled patients from homelessness, persecution, neglect, victimization, or imprisonment. The deteriorating conditions of “lunatic” asylums in the 19^th and 20^th centuries were blamed on psychiatry, not the poor funding of such institutions in an era of almost complete ignorance about the medical basis of mental illness. Other perceived misdeeds of psychiatry include:

• Medicalizing madness (contradicting the archaic notion that psychosis is a type of behavior, not an illness)
• Drastic measures to control severe mental illness in the pre-pharmacotherapy era, including excessive use of electroconvulsive therapy (ECT), performing lobotomies, or resecting various body parts
• Use of physical and/or chemical restraints for violent or actively suicidal patients
• Serious or intolerable side effects of some antipsychotic medications
• Labeling slaves’ healthy desire to escape from their masters in the 19^th century as an illness (“drapetomania”)
• Regarding psychoanalysis as unscientific and even harmful
• Labeling homosexuality as a mental disorder until American Psychiatric Association members voted it out of DSM-II in 1973
• The arbitrariness of psychiatric diagnoses based on committee-consensus criteria rather than valid and objective scientific evidence and the lack of biomarkers (this is a legitimate complaint but many physiological tests are being developed)
• Psychoactive drugs allegedly are used to control children (antipsychiatry tends to minimize the existence of serious mental illness among children, although childhood physical diseases are readily accepted)
• Psychiatry is a pseudoscience that pathologizes normal variations of human behaviors, thoughts, or emotions
• Psychiatrists are complicit with drug companies and employ drugs of dubious efficacy (eg, antidepressants) or safety (eg, antipsychotics).

Most of the above reasons are exaggerations or attributed to psychiatry during an era of primitive understanding of psychiatric brain disorders. Harmful interventions such as frontal lobotomy—for which its neurosurgeon inventor received the 1949 Nobel Prize in Medicine—were a product of a desperate time when no effective and safe treatments were available. Although regarded as an effective treatment for mood disorders, ECT certainly was abused many decades ago when it was used (without anesthesia) in patients who were unlikely to benefit from it.

David Cooper¹ coined the term “antipsychiatry” in 1967. Years before him, Michel Foucault propagated a paradigm shift that regarded delusions not as madness or illness, but as a behavioral variant or an “anomaly of judgment.”² That antimedicalization movement was supported by the First Church of Christ, Scientist, the legal system, and even the then-new specialty of neurology, plus social workers and “reformers” who criticized mental hospitals for failing to conduct scientific investigations.³

Formerly institutionalized patients such as Clifford Beers⁴ demanded improvements in shabby state hospital conditions more than a century ago and generated antipsychiatry sentiments in other formerly institutionalized persons. Such antipathy was exacerbated by bizarre psychiatrists such as Henry Cotton at Trenton State Hospital in New Jersey, who advocated that removing various body parts (killing or disfiguring patients) improved mental health.⁵

Other ardent antipsychiatrists included French playwright and former asylum patient Antonin Artaud in the 1920s and psychoanalysts Jacques Lacan and Erich Fromm, who authored antipsychiatry writings from a “secular-humanistic” viewpoint. ECT use in the 1930s and frontal leucotomy in the 1940s understandably intensified fear toward psychiatric therapies. When antipsychotic medications were discovered in the 1950s (eventually helping to shut down most asylums), these medications’ neurologic side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) prompted another outcry by antipsychiatry groups, although there was no better alternative to control psychosis.

In the 1950s, a right-wing antipsychiatry movement regarded psychiatry as “subversive, left-wing, anti-American, and communist” because it deprived individuals of their rights. Psychologist Hans Eysenck rejected psychiatric medical approaches in favor of errors in learning as a cause of mental illness (as if learning is not a neurobiologic event).

The 1960s witnessed a surge of antipsychiatry activities by various groups, including prominent psychiatrists such as R.D. Laing, Theodore Lidz, and Silvano Arieti, all of whom argued that psychosis is “understandable” as a method of coping with a “sick society” or due to “schizophrenogenic parents” who inflict damage on their offspring. Thomas Szasz is a prominent psychiatrist who proclaimed mental illness is a myth.⁶ I recall shuddering when he spoke at the University of Rochester during my residency, declaring schizophrenia a myth when I had admitted 3 patients with severe, disabling psychosis earlier that day. I summoned the chutzpah to tell him that in my experience haloperidol surely reduced the symptoms of the so-called “myth”! Szasz collaborated with the Church of Scientology to form the Citizens Commission on Human Rights. Interestingly, Christian Scientists and some fundamental Protestants³ agreed with Szasz’s contention that insanity is a moral, not a medical, issue.

A major impact of the antipsychiatry movement is evident in Italy due to the efforts of Franco Basaglia, an influential “psychiatrist-reformer.” Basaglia was so outraged with the dilapidated and prison-like conditions of mental institutions that he convinced the Italian Parliament to pass a law in 1978⁷ that abruptly dismantled and closed all mental hospitals in Italy. Because of uncontrolled psychosis or mania, many patients who were released ended up in prisons, which had similar or worse repressive conditions as the dismantled asylums. Many chronically hospitalized patients died because of self-neglect or victimization within a few months of their abrupt discharge.

Finally, the antipsychiatry movement aggressively criticizes the pharmaceutical industry’s research, tactics, and influence on psychiatry. Also included in the attacks are academic psychiatrists who conduct FDA clinical trials for new drugs and educate practitioners about the efficacy/safety and indications of new FDA-approved drugs. Although industry research grants are deposited at the investigators’ universities, critics mistakenly assume these psychiatrists personally benefit. The content of all educational programs about psychiatric drugs is strictly restricted to the FDA-approved product label, but critics assume that expert speakers, who are compensated for their time and effort, are promoting the drug rather than educating practitioners about the efficacy, safety, tolerability, and proper use of new medications. Part of the motive for attacking this collaboration is the tenet held by many in the antipsychiatry movement that medications are ineffective, unnecessary, or even dangerous. I wish antipsychiatrists would spend a week on an acute psychiatric unit to witness the need for and benefit from psychotropic medications for psychotic, manic, or depressed patients. Although psychiatric patients experience side effects, they are no worse than those experienced by cancer, arthritis, or diabetes patients.

The antipsychiatry movement is regarded by some as “intellectual halitosis” and by others as a thorn in the side of mainstream psychiatry; most believe that many of its claims are unfair exaggerations based on events and primitive conditions of more than a century ago. However, although irritating and often unfair, antipsychiatry helps keep us honest and rigorous about what we do, motivating us to relentlessly seek better diagnostic models and treatment paradigms. Psychiatry is far more scientific today than it was a century ago, but misperceptions about psychiatry continue to be driven by abuses of the past. The best antidote for antipsychiatry allegations is a combination of personal integrity, scientific progress, and sound evidence-based clinical care.

Psychiatry is the only medical specialty with a longtime nemesis; it’s called “antipsychiatry,” and it has been active for almost 2 centuries. Although psychiatry has evolved into a major scientific and medical discipline, the century-old primitive stage of psychiatric treatments instigated an antagonism toward psychiatry that persists to the present day.

A recent flurry of books critical of psychiatry is evidence of how the antipsychiatry movement is being propagated by journalists and critics whose views of psychiatry are unflattering despite the abundance of scientific advances that are gradually elucidating the causes and treatments of serious mental disorders.

What are the “wrongdoings” of psychiatry that generate the long-standing protests and assaults? The original “sin” of psychiatry appears to be locking up and “abusing” mentally ill patients in asylums, which 2 centuries ago was considered a humane advance to save seriously disabled patients from homelessness, persecution, neglect, victimization, or imprisonment. The deteriorating conditions of “lunatic” asylums in the 19^th and 20^th centuries were blamed on psychiatry, not the poor funding of such institutions in an era of almost complete ignorance about the medical basis of mental illness. Other perceived misdeeds of psychiatry include:

• Medicalizing madness (contradicting the archaic notion that psychosis is a type of behavior, not an illness)
• Drastic measures to control severe mental illness in the pre-pharmacotherapy era, including excessive use of electroconvulsive therapy (ECT), performing lobotomies, or resecting various body parts
• Use of physical and/or chemical restraints for violent or actively suicidal patients
• Serious or intolerable side effects of some antipsychotic medications
• Labeling slaves’ healthy desire to escape from their masters in the 19^th century as an illness (“drapetomania”)
• Regarding psychoanalysis as unscientific and even harmful
• Labeling homosexuality as a mental disorder until American Psychiatric Association members voted it out of DSM-II in 1973
• The arbitrariness of psychiatric diagnoses based on committee-consensus criteria rather than valid and objective scientific evidence and the lack of biomarkers (this is a legitimate complaint but many physiological tests are being developed)
• Psychoactive drugs allegedly are used to control children (antipsychiatry tends to minimize the existence of serious mental illness among children, although childhood physical diseases are readily accepted)
• Psychiatry is a pseudoscience that pathologizes normal variations of human behaviors, thoughts, or emotions
• Psychiatrists are complicit with drug companies and employ drugs of dubious efficacy (eg, antidepressants) or safety (eg, antipsychotics).

Most of the above reasons are exaggerations or attributed to psychiatry during an era of primitive understanding of psychiatric brain disorders. Harmful interventions such as frontal lobotomy—for which its neurosurgeon inventor received the 1949 Nobel Prize in Medicine—were a product of a desperate time when no effective and safe treatments were available. Although regarded as an effective treatment for mood disorders, ECT certainly was abused many decades ago when it was used (without anesthesia) in patients who were unlikely to benefit from it.

David Cooper¹ coined the term “antipsychiatry” in 1967. Years before him, Michel Foucault propagated a paradigm shift that regarded delusions not as madness or illness, but as a behavioral variant or an “anomaly of judgment.”² That antimedicalization movement was supported by the First Church of Christ, Scientist, the legal system, and even the then-new specialty of neurology, plus social workers and “reformers” who criticized mental hospitals for failing to conduct scientific investigations.³

Formerly institutionalized patients such as Clifford Beers⁴ demanded improvements in shabby state hospital conditions more than a century ago and generated antipsychiatry sentiments in other formerly institutionalized persons. Such antipathy was exacerbated by bizarre psychiatrists such as Henry Cotton at Trenton State Hospital in New Jersey, who advocated that removing various body parts (killing or disfiguring patients) improved mental health.⁵

Other ardent antipsychiatrists included French playwright and former asylum patient Antonin Artaud in the 1920s and psychoanalysts Jacques Lacan and Erich Fromm, who authored antipsychiatry writings from a “secular-humanistic” viewpoint. ECT use in the 1930s and frontal leucotomy in the 1940s understandably intensified fear toward psychiatric therapies. When antipsychotic medications were discovered in the 1950s (eventually helping to shut down most asylums), these medications’ neurologic side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) prompted another outcry by antipsychiatry groups, although there was no better alternative to control psychosis.

In the 1950s, a right-wing antipsychiatry movement regarded psychiatry as “subversive, left-wing, anti-American, and communist” because it deprived individuals of their rights. Psychologist Hans Eysenck rejected psychiatric medical approaches in favor of errors in learning as a cause of mental illness (as if learning is not a neurobiologic event).

The 1960s witnessed a surge of antipsychiatry activities by various groups, including prominent psychiatrists such as R.D. Laing, Theodore Lidz, and Silvano Arieti, all of whom argued that psychosis is “understandable” as a method of coping with a “sick society” or due to “schizophrenogenic parents” who inflict damage on their offspring. Thomas Szasz is a prominent psychiatrist who proclaimed mental illness is a myth.⁶ I recall shuddering when he spoke at the University of Rochester during my residency, declaring schizophrenia a myth when I had admitted 3 patients with severe, disabling psychosis earlier that day. I summoned the chutzpah to tell him that in my experience haloperidol surely reduced the symptoms of the so-called “myth”! Szasz collaborated with the Church of Scientology to form the Citizens Commission on Human Rights. Interestingly, Christian Scientists and some fundamental Protestants³ agreed with Szasz’s contention that insanity is a moral, not a medical, issue.

A major impact of the antipsychiatry movement is evident in Italy due to the efforts of Franco Basaglia, an influential “psychiatrist-reformer.” Basaglia was so outraged with the dilapidated and prison-like conditions of mental institutions that he convinced the Italian Parliament to pass a law in 1978⁷ that abruptly dismantled and closed all mental hospitals in Italy. Because of uncontrolled psychosis or mania, many patients who were released ended up in prisons, which had similar or worse repressive conditions as the dismantled asylums. Many chronically hospitalized patients died because of self-neglect or victimization within a few months of their abrupt discharge.

Finally, the antipsychiatry movement aggressively criticizes the pharmaceutical industry’s research, tactics, and influence on psychiatry. Also included in the attacks are academic psychiatrists who conduct FDA clinical trials for new drugs and educate practitioners about the efficacy/safety and indications of new FDA-approved drugs. Although industry research grants are deposited at the investigators’ universities, critics mistakenly assume these psychiatrists personally benefit. The content of all educational programs about psychiatric drugs is strictly restricted to the FDA-approved product label, but critics assume that expert speakers, who are compensated for their time and effort, are promoting the drug rather than educating practitioners about the efficacy, safety, tolerability, and proper use of new medications. Part of the motive for attacking this collaboration is the tenet held by many in the antipsychiatry movement that medications are ineffective, unnecessary, or even dangerous. I wish antipsychiatrists would spend a week on an acute psychiatric unit to witness the need for and benefit from psychotropic medications for psychotic, manic, or depressed patients. Although psychiatric patients experience side effects, they are no worse than those experienced by cancer, arthritis, or diabetes patients.

The antipsychiatry movement is regarded by some as “intellectual halitosis” and by others as a thorn in the side of mainstream psychiatry; most believe that many of its claims are unfair exaggerations based on events and primitive conditions of more than a century ago. However, although irritating and often unfair, antipsychiatry helps keep us honest and rigorous about what we do, motivating us to relentlessly seek better diagnostic models and treatment paradigms. Psychiatry is far more scientific today than it was a century ago, but misperceptions about psychiatry continue to be driven by abuses of the past. The best antidote for antipsychiatry allegations is a combination of personal integrity, scientific progress, and sound evidence-based clinical care.

Psychiatry is the only medical specialty with a longtime nemesis; it’s called “antipsychiatry,” and it has been active for almost 2 centuries. Although psychiatry has evolved into a major scientific and medical discipline, the century-old primitive stage of psychiatric treatments instigated an antagonism toward psychiatry that persists to the present day.

A recent flurry of books critical of psychiatry is evidence of how the antipsychiatry movement is being propagated by journalists and critics whose views of psychiatry are unflattering despite the abundance of scientific advances that are gradually elucidating the causes and treatments of serious mental disorders.

What are the “wrongdoings” of psychiatry that generate the long-standing protests and assaults? The original “sin” of psychiatry appears to be locking up and “abusing” mentally ill patients in asylums, which 2 centuries ago was considered a humane advance to save seriously disabled patients from homelessness, persecution, neglect, victimization, or imprisonment. The deteriorating conditions of “lunatic” asylums in the 19^th and 20^th centuries were blamed on psychiatry, not the poor funding of such institutions in an era of almost complete ignorance about the medical basis of mental illness. Other perceived misdeeds of psychiatry include:

• Medicalizing madness (contradicting the archaic notion that psychosis is a type of behavior, not an illness)
• Drastic measures to control severe mental illness in the pre-pharmacotherapy era, including excessive use of electroconvulsive therapy (ECT), performing lobotomies, or resecting various body parts
• Use of physical and/or chemical restraints for violent or actively suicidal patients
• Serious or intolerable side effects of some antipsychotic medications
• Labeling slaves’ healthy desire to escape from their masters in the 19^th century as an illness (“drapetomania”)
• Regarding psychoanalysis as unscientific and even harmful
• Labeling homosexuality as a mental disorder until American Psychiatric Association members voted it out of DSM-II in 1973
• The arbitrariness of psychiatric diagnoses based on committee-consensus criteria rather than valid and objective scientific evidence and the lack of biomarkers (this is a legitimate complaint but many physiological tests are being developed)
• Psychoactive drugs allegedly are used to control children (antipsychiatry tends to minimize the existence of serious mental illness among children, although childhood physical diseases are readily accepted)
• Psychiatry is a pseudoscience that pathologizes normal variations of human behaviors, thoughts, or emotions
• Psychiatrists are complicit with drug companies and employ drugs of dubious efficacy (eg, antidepressants) or safety (eg, antipsychotics).

Most of the above reasons are exaggerations or attributed to psychiatry during an era of primitive understanding of psychiatric brain disorders. Harmful interventions such as frontal lobotomy—for which its neurosurgeon inventor received the 1949 Nobel Prize in Medicine—were a product of a desperate time when no effective and safe treatments were available. Although regarded as an effective treatment for mood disorders, ECT certainly was abused many decades ago when it was used (without anesthesia) in patients who were unlikely to benefit from it.

David Cooper¹ coined the term “antipsychiatry” in 1967. Years before him, Michel Foucault propagated a paradigm shift that regarded delusions not as madness or illness, but as a behavioral variant or an “anomaly of judgment.”² That antimedicalization movement was supported by the First Church of Christ, Scientist, the legal system, and even the then-new specialty of neurology, plus social workers and “reformers” who criticized mental hospitals for failing to conduct scientific investigations.³

Formerly institutionalized patients such as Clifford Beers⁴ demanded improvements in shabby state hospital conditions more than a century ago and generated antipsychiatry sentiments in other formerly institutionalized persons. Such antipathy was exacerbated by bizarre psychiatrists such as Henry Cotton at Trenton State Hospital in New Jersey, who advocated that removing various body parts (killing or disfiguring patients) improved mental health.⁵

Other ardent antipsychiatrists included French playwright and former asylum patient Antonin Artaud in the 1920s and psychoanalysts Jacques Lacan and Erich Fromm, who authored antipsychiatry writings from a “secular-humanistic” viewpoint. ECT use in the 1930s and frontal leucotomy in the 1940s understandably intensified fear toward psychiatric therapies. When antipsychotic medications were discovered in the 1950s (eventually helping to shut down most asylums), these medications’ neurologic side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) prompted another outcry by antipsychiatry groups, although there was no better alternative to control psychosis.

In the 1950s, a right-wing antipsychiatry movement regarded psychiatry as “subversive, left-wing, anti-American, and communist” because it deprived individuals of their rights. Psychologist Hans Eysenck rejected psychiatric medical approaches in favor of errors in learning as a cause of mental illness (as if learning is not a neurobiologic event).

The 1960s witnessed a surge of antipsychiatry activities by various groups, including prominent psychiatrists such as R.D. Laing, Theodore Lidz, and Silvano Arieti, all of whom argued that psychosis is “understandable” as a method of coping with a “sick society” or due to “schizophrenogenic parents” who inflict damage on their offspring. Thomas Szasz is a prominent psychiatrist who proclaimed mental illness is a myth.⁶ I recall shuddering when he spoke at the University of Rochester during my residency, declaring schizophrenia a myth when I had admitted 3 patients with severe, disabling psychosis earlier that day. I summoned the chutzpah to tell him that in my experience haloperidol surely reduced the symptoms of the so-called “myth”! Szasz collaborated with the Church of Scientology to form the Citizens Commission on Human Rights. Interestingly, Christian Scientists and some fundamental Protestants³ agreed with Szasz’s contention that insanity is a moral, not a medical, issue.

A major impact of the antipsychiatry movement is evident in Italy due to the efforts of Franco Basaglia, an influential “psychiatrist-reformer.” Basaglia was so outraged with the dilapidated and prison-like conditions of mental institutions that he convinced the Italian Parliament to pass a law in 1978⁷ that abruptly dismantled and closed all mental hospitals in Italy. Because of uncontrolled psychosis or mania, many patients who were released ended up in prisons, which had similar or worse repressive conditions as the dismantled asylums. Many chronically hospitalized patients died because of self-neglect or victimization within a few months of their abrupt discharge.

Finally, the antipsychiatry movement aggressively criticizes the pharmaceutical industry’s research, tactics, and influence on psychiatry. Also included in the attacks are academic psychiatrists who conduct FDA clinical trials for new drugs and educate practitioners about the efficacy/safety and indications of new FDA-approved drugs. Although industry research grants are deposited at the investigators’ universities, critics mistakenly assume these psychiatrists personally benefit. The content of all educational programs about psychiatric drugs is strictly restricted to the FDA-approved product label, but critics assume that expert speakers, who are compensated for their time and effort, are promoting the drug rather than educating practitioners about the efficacy, safety, tolerability, and proper use of new medications. Part of the motive for attacking this collaboration is the tenet held by many in the antipsychiatry movement that medications are ineffective, unnecessary, or even dangerous. I wish antipsychiatrists would spend a week on an acute psychiatric unit to witness the need for and benefit from psychotropic medications for psychotic, manic, or depressed patients. Although psychiatric patients experience side effects, they are no worse than those experienced by cancer, arthritis, or diabetes patients.

The antipsychiatry movement is regarded by some as “intellectual halitosis” and by others as a thorn in the side of mainstream psychiatry; most believe that many of its claims are unfair exaggerations based on events and primitive conditions of more than a century ago. However, although irritating and often unfair, antipsychiatry helps keep us honest and rigorous about what we do, motivating us to relentlessly seek better diagnostic models and treatment paradigms. Psychiatry is far more scientific today than it was a century ago, but misperceptions about psychiatry continue to be driven by abuses of the past. The best antidote for antipsychiatry allegations is a combination of personal integrity, scientific progress, and sound evidence-based clinical care.

CASE: Space traveler

Mr. O, age 69, is a patient at a long-term psychiatric hospital. He has a 56-year psychiatric history, a current diagnosis of schizoaffective disorder, and suffered a torn rotator cuff approximately 5 years ago. His medication regimen is haloperidol decanoate, 100 mg IM every month, duloxetine, 60 mg/d, and naproxen, as needed for chronic pain.

He frequently lies on the floor. Attendants urge him to get up and join groups or sit with other patients but he complains of pain and soon finds another spot on the floor to use as a bed.

Eight months earlier, a homeless shelter sent Mr. O to the emergency room (ER) because he tried to eat a dollar bill and a sock. In the ER he was inattentive, with loose associations and bizarre delusions; he believed he was on a spaceship. Mr. O was admitted to the hospital, where clinicians noted that his behavior remained bizarre and he complained of insomnia. They also noted a history of setting fires, which complicated discharge planning and contributed to their decision to transfer him to our psychiatric facility for longer-term care.

During our initial interview, Mr. O readily picks himself off the floor. His responses are logical and direct but abrupt and unelaborated. His first and most vehement complaint is pain. Zolpidem, he says, is the only treatment that helps.

He says he began using zolpidem approximately 5 years ago because pain from a shoulder injury kept him awake at night. When he could not obtain the drug by prescription, he bought it on the street. One day when living in the homeless shelter, he took 30 or 40 mg of zolpidem, then “blacked out” and awoke in the ER.

His first experience with psychiatric treatment was the result of problems getting along with his single mother because of “petty things” such as shooting off a BB gun in their apartment, he says. As a teenager he was sent to a boarding school; as a young adult, to a psychiatric hospital. After his release he returned to his mother’s apartment. He worked steadily for 20 years before he obtained Social Security benefits, and then worked intermittently “off the books” until approximately 15 years ago. Mr. O lived with his mother until her death 17 years earlier, and then in her apartment alone until a fire, which he set accidentally by smoking in bed after taking zolpidem, forced him to leave 3 years ago. He says, “My whole life was in that place.” He was admitted to a psychiatric hospital for an unknown reason, which was his first psychiatric admission in 40 years. After he was released from the hospital, Mr. O lived in various homeless shelters and adult homes until his current hospitalization.

The author’s observations

An effective and well-tolerated drug with a reputation for rarely being abused, zolpidem is widely prescribed as a hypnotic. Zolpidem and benzodiazepines have different chemical structures but both act at the GABA_A receptor and have comparable behavioral effects.¹ The reported incidence of zolpidem abuse is much lower than the reported rate of benzodiazepine abuse when used for sleep²; however, abuse, dependence, and withdrawal have been reported.^2-4 Zolpidem abuse seems to be more common among patients with a history of abusing other substances or a history of psychiatric illness.² A French study⁴ found that abusers fell into 2 groups. The younger group (median age 35) used higher doses—a median of 300 mg/d—and took zolpidem in the daytime to achieve euphoria. A second, older group (median age 42) used lower doses—a median of 200 mg/d—at nighttime to sleep.

There are few reports of delirium and symptoms such as visual hallucinations and distortions associated with zolpidem use.^5,6 These reactions have occurred in persons without a history of psychosis. They usually are associated with doses ≥10 mg.

In the ER Mr. O showed a disturbance in consciousness with inability to focus attention and a perceptual disturbance (he believed he was in a spaceship) that developed over hours to days. He met criteria for delirium, possibly caused by zolpidem, but his presentation also could have been attributable to an underlying psychiatric disorder.

ER and inpatient psychiatrists noted Mr. O was intoxicated with zolpidem when the shelter brought him to the ER, but both groups diagnosed schizoaffective disorder and treated him with antipsychotics. They saw his >50-year psychiatric history as evidence of an underlying, long-standing condition such as schizoaffective illness.

However, features of Mr. O’s illness are not typical of a chronic psychotic illness. He recalls psychiatric hospitalizations in his youth and recently, but not for the 40 years in between. Mr. O says he has never experienced auditory hallucinations. For these reasons, our treatment team obtains old medical records to investigate his early history (Table).

Table

Mr. O’s clinical course

HISTORY: Destructive and defiant

Mr. O’s mother reported that he had been a nervous, restless child who would scream and yell at the slightest provocation. At age 10 he became wantonly destructive. His mother bought him an expensive toy that he destroyed after a short time; he asked for another toy, which he also destroyed. When such behavior became more frequent, she took him to a city hospital, where he was treated for 6 weeks and released at age 13. He was sent to a boarding school but soon was expelled for drinking and selling beer.

Mr. O was admitted to long-term psychiatric facilities 6 times in the next 10 years, from the late 1950s to the late 1960s. He was first admitted at age 17 for temper tantrums during which he fired an air rifle and smashed windows in the home he shared with his mother. During examination he had no delusions or hallucinations but did have flat affect and a hostile attitude. Doctors documented that almost all his tantrums were as a result of interactions with his mother.

Records from this psychiatric admission state that Mr. O showed no unusual distractibility, “psychotic trends,” or paranoid thinking. After approximately 6 months in the hospital he was discharged home with the diagnosis of primary behavior disorder, simple adult maladjustment. Mr. O, who was age 18 at the time, and his mother were eager for him to complete high school and learn auto mechanics.

Nine months later, he returned to the psychiatric facility because of excessive drinking and inability to secure employment, according to his records. In the hospital, he was productive and reliable. When he was discharged home 3 months later, doctors wrote that his determination to stop drinking was firmly fixed. They encouraged Mr. O to complete high school as a night student and find employment during the day. His mother was delighted with his improvement.

A third admission, less than 2 months later, occurred after he broke a window during an argument with his mother. He had a job but quit. After 5 months he was discharged with the same diagnosis of primary behavior disorder, but his mother would not let him back in her home. He was referred to the social service department to be placed on welfare.

A year later, Mr. O had trouble managing his welfare allotment and moved repeatedly. He said he returned to the psychiatric hospital because his welfare payments had been discontinued. During this admission, doctors noted “psychopathic” symptoms; Mr. O was defiant and resented authority and regular work. Mr. O eloped from the hospital several times and brought beer into the building. After 18 months he was discharged with the same diagnosis, with plans to apply for welfare. He was not prescribed medication.

Mr. O’s fifth admission came nearly 2 years later after his mother complained that he stole from her home and carried a weapon. In the hospital he was described as manageable and without overt psychotic symptoms. When he was discharged a little more than a year after being admitted, doctors wrote that he was a psychopath who had a history of drinking, stealing, and delinquent tendencies as a teenager. His diagnosis remained primary behavior disorder.

A year after this discharge, Mr. O was arrested for causing serious property damage when he was intoxicated on alcohol. Subsequently he was readmitted.

After a few months in the hospital, Mr. O changed. He developed a silly laugh, loose associations, irrelevant and incoherent speech, and a belief that hospital staff were against him. Although Mr. O denied auditory hallucinations, a psychiatrist wrote that he seemed to be experiencing hallucinations and prescribed chlorpromazine. The next day Mr. O slashed his arms and legs in several places, requiring many sutures. His diagnosis was changed to psychosis with psychopathic personality. However, within a few months, psychiatrists determined that Mr. O had recovered, so they stopped chlorpromazine. Months later, clinicians wrote that Mr. O was idle most of the time, neat, clean, and not involved in arguments with other patients. He was discharged after 1 month in the hospital.

Over the years, psychiatrists had differing opinions about Mr. O’s diagnosis. One noted that his mental illness was characterized by emotional instability and poor judgment. He had impulsive reactions without regard for others, rapid mood swings, irritability, and depression with transient paranoia. Another clinician detected evidence of schizoid personality disorder because Mr. O did not experience hallucinations or a gross thought disorder, but did have rambling, circumstantial, autistic (unrealistic), and ambivalent thought content. Another psychiatrist wrote Mr. O best fit in the category of psychosis with psychopathic personality, which was his diagnosis at discharge from his sixth hospitalization.

The author’s observations

Mr. O’s old medical records revealed the diagnostic thinking and treatment practices of a past era. They did not demonstrate that Mr. O met current criteria for schizophrenia or schizoaffective disorder, although he may have had a brief psychotic episode. Because there was little support for a diagnosis of schizoaffective illness and haloperidol use, we stopped the drug but continued duloxetine for chronic pain. It was clear that he has a substance use disorder and perhaps met criteria for antisocial personality disorder.

OUTCOME: Further explanations

Approximately 2 months after stopping haloperidol, Mr. O is more spontaneous, logical, and relevant. He does not have delusions or hallucinations. Despite further attempts at pain management with physical therapy and increased doses of duloxetine, he still complains of pain. We do not prescribe zolpidem.

Mr. O is unwilling to discuss the incident more than 40 years ago when he cut his arms and legs except to say, “That’s the past. My life wasn’t so good at that time.” When we ask why he had been a client of Adult Protective Services 5 years before he was burned out of his apartment, he admitted that he was 21 months in arrears in his rent. “I used to do this thing called crack,” he explains. He was discharged to an adult home with a prescription for duloxetine after he promised to never smoke in his room again.

Related Resource

• Aggarwal A, Sharma DD. Zolpidem withdrawal delirium: a case report. J Neuropsychiatry Clin Neurosci. 2010;22(4):451.

Drug Brand Names

• Chlorpromazine • Thorazine
• Clozapine • Clozaril
• Duloxetine • Cymbalta
• Haloperidol decanoate • Haloperidol decanoate
• Haloperidol • Haldol
• Naproxen • Naproxyn, Aleve, others
• Zolpidem • Ambien

Disclosure

The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Space traveler

Mr. O, age 69, is a patient at a long-term psychiatric hospital. He has a 56-year psychiatric history, a current diagnosis of schizoaffective disorder, and suffered a torn rotator cuff approximately 5 years ago. His medication regimen is haloperidol decanoate, 100 mg IM every month, duloxetine, 60 mg/d, and naproxen, as needed for chronic pain.

He frequently lies on the floor. Attendants urge him to get up and join groups or sit with other patients but he complains of pain and soon finds another spot on the floor to use as a bed.

Eight months earlier, a homeless shelter sent Mr. O to the emergency room (ER) because he tried to eat a dollar bill and a sock. In the ER he was inattentive, with loose associations and bizarre delusions; he believed he was on a spaceship. Mr. O was admitted to the hospital, where clinicians noted that his behavior remained bizarre and he complained of insomnia. They also noted a history of setting fires, which complicated discharge planning and contributed to their decision to transfer him to our psychiatric facility for longer-term care.

During our initial interview, Mr. O readily picks himself off the floor. His responses are logical and direct but abrupt and unelaborated. His first and most vehement complaint is pain. Zolpidem, he says, is the only treatment that helps.

He says he began using zolpidem approximately 5 years ago because pain from a shoulder injury kept him awake at night. When he could not obtain the drug by prescription, he bought it on the street. One day when living in the homeless shelter, he took 30 or 40 mg of zolpidem, then “blacked out” and awoke in the ER.

His first experience with psychiatric treatment was the result of problems getting along with his single mother because of “petty things” such as shooting off a BB gun in their apartment, he says. As a teenager he was sent to a boarding school; as a young adult, to a psychiatric hospital. After his release he returned to his mother’s apartment. He worked steadily for 20 years before he obtained Social Security benefits, and then worked intermittently “off the books” until approximately 15 years ago. Mr. O lived with his mother until her death 17 years earlier, and then in her apartment alone until a fire, which he set accidentally by smoking in bed after taking zolpidem, forced him to leave 3 years ago. He says, “My whole life was in that place.” He was admitted to a psychiatric hospital for an unknown reason, which was his first psychiatric admission in 40 years. After he was released from the hospital, Mr. O lived in various homeless shelters and adult homes until his current hospitalization.

The author’s observations

An effective and well-tolerated drug with a reputation for rarely being abused, zolpidem is widely prescribed as a hypnotic. Zolpidem and benzodiazepines have different chemical structures but both act at the GABA_A receptor and have comparable behavioral effects.¹ The reported incidence of zolpidem abuse is much lower than the reported rate of benzodiazepine abuse when used for sleep²; however, abuse, dependence, and withdrawal have been reported.^2-4 Zolpidem abuse seems to be more common among patients with a history of abusing other substances or a history of psychiatric illness.² A French study⁴ found that abusers fell into 2 groups. The younger group (median age 35) used higher doses—a median of 300 mg/d—and took zolpidem in the daytime to achieve euphoria. A second, older group (median age 42) used lower doses—a median of 200 mg/d—at nighttime to sleep.

There are few reports of delirium and symptoms such as visual hallucinations and distortions associated with zolpidem use.^5,6 These reactions have occurred in persons without a history of psychosis. They usually are associated with doses ≥10 mg.

In the ER Mr. O showed a disturbance in consciousness with inability to focus attention and a perceptual disturbance (he believed he was in a spaceship) that developed over hours to days. He met criteria for delirium, possibly caused by zolpidem, but his presentation also could have been attributable to an underlying psychiatric disorder.

ER and inpatient psychiatrists noted Mr. O was intoxicated with zolpidem when the shelter brought him to the ER, but both groups diagnosed schizoaffective disorder and treated him with antipsychotics. They saw his >50-year psychiatric history as evidence of an underlying, long-standing condition such as schizoaffective illness.

However, features of Mr. O’s illness are not typical of a chronic psychotic illness. He recalls psychiatric hospitalizations in his youth and recently, but not for the 40 years in between. Mr. O says he has never experienced auditory hallucinations. For these reasons, our treatment team obtains old medical records to investigate his early history (Table).

Table

Mr. O’s clinical course

HISTORY: Destructive and defiant

Mr. O’s mother reported that he had been a nervous, restless child who would scream and yell at the slightest provocation. At age 10 he became wantonly destructive. His mother bought him an expensive toy that he destroyed after a short time; he asked for another toy, which he also destroyed. When such behavior became more frequent, she took him to a city hospital, where he was treated for 6 weeks and released at age 13. He was sent to a boarding school but soon was expelled for drinking and selling beer.

Mr. O was admitted to long-term psychiatric facilities 6 times in the next 10 years, from the late 1950s to the late 1960s. He was first admitted at age 17 for temper tantrums during which he fired an air rifle and smashed windows in the home he shared with his mother. During examination he had no delusions or hallucinations but did have flat affect and a hostile attitude. Doctors documented that almost all his tantrums were as a result of interactions with his mother.

Records from this psychiatric admission state that Mr. O showed no unusual distractibility, “psychotic trends,” or paranoid thinking. After approximately 6 months in the hospital he was discharged home with the diagnosis of primary behavior disorder, simple adult maladjustment. Mr. O, who was age 18 at the time, and his mother were eager for him to complete high school and learn auto mechanics.

Nine months later, he returned to the psychiatric facility because of excessive drinking and inability to secure employment, according to his records. In the hospital, he was productive and reliable. When he was discharged home 3 months later, doctors wrote that his determination to stop drinking was firmly fixed. They encouraged Mr. O to complete high school as a night student and find employment during the day. His mother was delighted with his improvement.

A third admission, less than 2 months later, occurred after he broke a window during an argument with his mother. He had a job but quit. After 5 months he was discharged with the same diagnosis of primary behavior disorder, but his mother would not let him back in her home. He was referred to the social service department to be placed on welfare.

A year later, Mr. O had trouble managing his welfare allotment and moved repeatedly. He said he returned to the psychiatric hospital because his welfare payments had been discontinued. During this admission, doctors noted “psychopathic” symptoms; Mr. O was defiant and resented authority and regular work. Mr. O eloped from the hospital several times and brought beer into the building. After 18 months he was discharged with the same diagnosis, with plans to apply for welfare. He was not prescribed medication.

Mr. O’s fifth admission came nearly 2 years later after his mother complained that he stole from her home and carried a weapon. In the hospital he was described as manageable and without overt psychotic symptoms. When he was discharged a little more than a year after being admitted, doctors wrote that he was a psychopath who had a history of drinking, stealing, and delinquent tendencies as a teenager. His diagnosis remained primary behavior disorder.

A year after this discharge, Mr. O was arrested for causing serious property damage when he was intoxicated on alcohol. Subsequently he was readmitted.

After a few months in the hospital, Mr. O changed. He developed a silly laugh, loose associations, irrelevant and incoherent speech, and a belief that hospital staff were against him. Although Mr. O denied auditory hallucinations, a psychiatrist wrote that he seemed to be experiencing hallucinations and prescribed chlorpromazine. The next day Mr. O slashed his arms and legs in several places, requiring many sutures. His diagnosis was changed to psychosis with psychopathic personality. However, within a few months, psychiatrists determined that Mr. O had recovered, so they stopped chlorpromazine. Months later, clinicians wrote that Mr. O was idle most of the time, neat, clean, and not involved in arguments with other patients. He was discharged after 1 month in the hospital.

Over the years, psychiatrists had differing opinions about Mr. O’s diagnosis. One noted that his mental illness was characterized by emotional instability and poor judgment. He had impulsive reactions without regard for others, rapid mood swings, irritability, and depression with transient paranoia. Another clinician detected evidence of schizoid personality disorder because Mr. O did not experience hallucinations or a gross thought disorder, but did have rambling, circumstantial, autistic (unrealistic), and ambivalent thought content. Another psychiatrist wrote Mr. O best fit in the category of psychosis with psychopathic personality, which was his diagnosis at discharge from his sixth hospitalization.

The author’s observations

Mr. O’s old medical records revealed the diagnostic thinking and treatment practices of a past era. They did not demonstrate that Mr. O met current criteria for schizophrenia or schizoaffective disorder, although he may have had a brief psychotic episode. Because there was little support for a diagnosis of schizoaffective illness and haloperidol use, we stopped the drug but continued duloxetine for chronic pain. It was clear that he has a substance use disorder and perhaps met criteria for antisocial personality disorder.

OUTCOME: Further explanations

Approximately 2 months after stopping haloperidol, Mr. O is more spontaneous, logical, and relevant. He does not have delusions or hallucinations. Despite further attempts at pain management with physical therapy and increased doses of duloxetine, he still complains of pain. We do not prescribe zolpidem.

Mr. O is unwilling to discuss the incident more than 40 years ago when he cut his arms and legs except to say, “That’s the past. My life wasn’t so good at that time.” When we ask why he had been a client of Adult Protective Services 5 years before he was burned out of his apartment, he admitted that he was 21 months in arrears in his rent. “I used to do this thing called crack,” he explains. He was discharged to an adult home with a prescription for duloxetine after he promised to never smoke in his room again.

Related Resource

• Aggarwal A, Sharma DD. Zolpidem withdrawal delirium: a case report. J Neuropsychiatry Clin Neurosci. 2010;22(4):451.

Drug Brand Names

• Chlorpromazine • Thorazine
• Clozapine • Clozaril
• Duloxetine • Cymbalta
• Haloperidol decanoate • Haloperidol decanoate
• Haloperidol • Haldol
• Naproxen • Naproxyn, Aleve, others
• Zolpidem • Ambien

Disclosure

The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Space traveler

Mr. O, age 69, is a patient at a long-term psychiatric hospital. He has a 56-year psychiatric history, a current diagnosis of schizoaffective disorder, and suffered a torn rotator cuff approximately 5 years ago. His medication regimen is haloperidol decanoate, 100 mg IM every month, duloxetine, 60 mg/d, and naproxen, as needed for chronic pain.

He frequently lies on the floor. Attendants urge him to get up and join groups or sit with other patients but he complains of pain and soon finds another spot on the floor to use as a bed.

Eight months earlier, a homeless shelter sent Mr. O to the emergency room (ER) because he tried to eat a dollar bill and a sock. In the ER he was inattentive, with loose associations and bizarre delusions; he believed he was on a spaceship. Mr. O was admitted to the hospital, where clinicians noted that his behavior remained bizarre and he complained of insomnia. They also noted a history of setting fires, which complicated discharge planning and contributed to their decision to transfer him to our psychiatric facility for longer-term care.

During our initial interview, Mr. O readily picks himself off the floor. His responses are logical and direct but abrupt and unelaborated. His first and most vehement complaint is pain. Zolpidem, he says, is the only treatment that helps.

He says he began using zolpidem approximately 5 years ago because pain from a shoulder injury kept him awake at night. When he could not obtain the drug by prescription, he bought it on the street. One day when living in the homeless shelter, he took 30 or 40 mg of zolpidem, then “blacked out” and awoke in the ER.

His first experience with psychiatric treatment was the result of problems getting along with his single mother because of “petty things” such as shooting off a BB gun in their apartment, he says. As a teenager he was sent to a boarding school; as a young adult, to a psychiatric hospital. After his release he returned to his mother’s apartment. He worked steadily for 20 years before he obtained Social Security benefits, and then worked intermittently “off the books” until approximately 15 years ago. Mr. O lived with his mother until her death 17 years earlier, and then in her apartment alone until a fire, which he set accidentally by smoking in bed after taking zolpidem, forced him to leave 3 years ago. He says, “My whole life was in that place.” He was admitted to a psychiatric hospital for an unknown reason, which was his first psychiatric admission in 40 years. After he was released from the hospital, Mr. O lived in various homeless shelters and adult homes until his current hospitalization.

The author’s observations

An effective and well-tolerated drug with a reputation for rarely being abused, zolpidem is widely prescribed as a hypnotic. Zolpidem and benzodiazepines have different chemical structures but both act at the GABA_A receptor and have comparable behavioral effects.¹ The reported incidence of zolpidem abuse is much lower than the reported rate of benzodiazepine abuse when used for sleep²; however, abuse, dependence, and withdrawal have been reported.^2-4 Zolpidem abuse seems to be more common among patients with a history of abusing other substances or a history of psychiatric illness.² A French study⁴ found that abusers fell into 2 groups. The younger group (median age 35) used higher doses—a median of 300 mg/d—and took zolpidem in the daytime to achieve euphoria. A second, older group (median age 42) used lower doses—a median of 200 mg/d—at nighttime to sleep.

There are few reports of delirium and symptoms such as visual hallucinations and distortions associated with zolpidem use.^5,6 These reactions have occurred in persons without a history of psychosis. They usually are associated with doses ≥10 mg.

In the ER Mr. O showed a disturbance in consciousness with inability to focus attention and a perceptual disturbance (he believed he was in a spaceship) that developed over hours to days. He met criteria for delirium, possibly caused by zolpidem, but his presentation also could have been attributable to an underlying psychiatric disorder.

ER and inpatient psychiatrists noted Mr. O was intoxicated with zolpidem when the shelter brought him to the ER, but both groups diagnosed schizoaffective disorder and treated him with antipsychotics. They saw his >50-year psychiatric history as evidence of an underlying, long-standing condition such as schizoaffective illness.

However, features of Mr. O’s illness are not typical of a chronic psychotic illness. He recalls psychiatric hospitalizations in his youth and recently, but not for the 40 years in between. Mr. O says he has never experienced auditory hallucinations. For these reasons, our treatment team obtains old medical records to investigate his early history (Table).

Table

Mr. O’s clinical course

HISTORY: Destructive and defiant

Mr. O’s mother reported that he had been a nervous, restless child who would scream and yell at the slightest provocation. At age 10 he became wantonly destructive. His mother bought him an expensive toy that he destroyed after a short time; he asked for another toy, which he also destroyed. When such behavior became more frequent, she took him to a city hospital, where he was treated for 6 weeks and released at age 13. He was sent to a boarding school but soon was expelled for drinking and selling beer.

Mr. O was admitted to long-term psychiatric facilities 6 times in the next 10 years, from the late 1950s to the late 1960s. He was first admitted at age 17 for temper tantrums during which he fired an air rifle and smashed windows in the home he shared with his mother. During examination he had no delusions or hallucinations but did have flat affect and a hostile attitude. Doctors documented that almost all his tantrums were as a result of interactions with his mother.

Records from this psychiatric admission state that Mr. O showed no unusual distractibility, “psychotic trends,” or paranoid thinking. After approximately 6 months in the hospital he was discharged home with the diagnosis of primary behavior disorder, simple adult maladjustment. Mr. O, who was age 18 at the time, and his mother were eager for him to complete high school and learn auto mechanics.

Nine months later, he returned to the psychiatric facility because of excessive drinking and inability to secure employment, according to his records. In the hospital, he was productive and reliable. When he was discharged home 3 months later, doctors wrote that his determination to stop drinking was firmly fixed. They encouraged Mr. O to complete high school as a night student and find employment during the day. His mother was delighted with his improvement.

A third admission, less than 2 months later, occurred after he broke a window during an argument with his mother. He had a job but quit. After 5 months he was discharged with the same diagnosis of primary behavior disorder, but his mother would not let him back in her home. He was referred to the social service department to be placed on welfare.

A year later, Mr. O had trouble managing his welfare allotment and moved repeatedly. He said he returned to the psychiatric hospital because his welfare payments had been discontinued. During this admission, doctors noted “psychopathic” symptoms; Mr. O was defiant and resented authority and regular work. Mr. O eloped from the hospital several times and brought beer into the building. After 18 months he was discharged with the same diagnosis, with plans to apply for welfare. He was not prescribed medication.

Mr. O’s fifth admission came nearly 2 years later after his mother complained that he stole from her home and carried a weapon. In the hospital he was described as manageable and without overt psychotic symptoms. When he was discharged a little more than a year after being admitted, doctors wrote that he was a psychopath who had a history of drinking, stealing, and delinquent tendencies as a teenager. His diagnosis remained primary behavior disorder.

A year after this discharge, Mr. O was arrested for causing serious property damage when he was intoxicated on alcohol. Subsequently he was readmitted.

After a few months in the hospital, Mr. O changed. He developed a silly laugh, loose associations, irrelevant and incoherent speech, and a belief that hospital staff were against him. Although Mr. O denied auditory hallucinations, a psychiatrist wrote that he seemed to be experiencing hallucinations and prescribed chlorpromazine. The next day Mr. O slashed his arms and legs in several places, requiring many sutures. His diagnosis was changed to psychosis with psychopathic personality. However, within a few months, psychiatrists determined that Mr. O had recovered, so they stopped chlorpromazine. Months later, clinicians wrote that Mr. O was idle most of the time, neat, clean, and not involved in arguments with other patients. He was discharged after 1 month in the hospital.

Over the years, psychiatrists had differing opinions about Mr. O’s diagnosis. One noted that his mental illness was characterized by emotional instability and poor judgment. He had impulsive reactions without regard for others, rapid mood swings, irritability, and depression with transient paranoia. Another clinician detected evidence of schizoid personality disorder because Mr. O did not experience hallucinations or a gross thought disorder, but did have rambling, circumstantial, autistic (unrealistic), and ambivalent thought content. Another psychiatrist wrote Mr. O best fit in the category of psychosis with psychopathic personality, which was his diagnosis at discharge from his sixth hospitalization.

The author’s observations

Mr. O’s old medical records revealed the diagnostic thinking and treatment practices of a past era. They did not demonstrate that Mr. O met current criteria for schizophrenia or schizoaffective disorder, although he may have had a brief psychotic episode. Because there was little support for a diagnosis of schizoaffective illness and haloperidol use, we stopped the drug but continued duloxetine for chronic pain. It was clear that he has a substance use disorder and perhaps met criteria for antisocial personality disorder.

OUTCOME: Further explanations

Approximately 2 months after stopping haloperidol, Mr. O is more spontaneous, logical, and relevant. He does not have delusions or hallucinations. Despite further attempts at pain management with physical therapy and increased doses of duloxetine, he still complains of pain. We do not prescribe zolpidem.

Mr. O is unwilling to discuss the incident more than 40 years ago when he cut his arms and legs except to say, “That’s the past. My life wasn’t so good at that time.” When we ask why he had been a client of Adult Protective Services 5 years before he was burned out of his apartment, he admitted that he was 21 months in arrears in his rent. “I used to do this thing called crack,” he explains. He was discharged to an adult home with a prescription for duloxetine after he promised to never smoke in his room again.

Related Resource

• Aggarwal A, Sharma DD. Zolpidem withdrawal delirium: a case report. J Neuropsychiatry Clin Neurosci. 2010;22(4):451.

Drug Brand Names

• Chlorpromazine • Thorazine
• Clozapine • Clozaril
• Duloxetine • Cymbalta
• Haloperidol decanoate • Haloperidol decanoate
• Haloperidol • Haldol
• Naproxen • Naproxyn, Aleve, others
• Zolpidem • Ambien

Disclosure

The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Caffeine belongs to the xanthine chemical group and its stimulant effects are the result of its competitive antagonism on adenosine receptors A1 and A2A in the CNS. Caffeine also slows the rate of dopamine reuptake and increases glutamate release, which theoretically could cause neuropsychiatric symptoms.1,2 Toxicity ranges have been recorded at 150 to 200 mg/kg. Increased psychotic features in schizophrenia patients have been reported at doses as low as 10 mg/kg.1 Earlier studies of caffeine use in patients with psychotic disorders reveal induction in thought disorders, social withdrawal, and euphoric activation3; however, these results have been variable.1

The American Association of Poison Control Centers reported 4,600 caffeine-related calls in 2005; one-half of which involved patients age <19.⁴ For a list of the caffeine content of 20 popular drinks, see the Table.

TABLE

Caffeine content of 20 popular drinks^a

Caffeine-induced psychosis?

My team recently treated a woman with prodromal psychotic symptoms for whom ingesting a high dose of caffeine precipitated a psychotic break.

Ms. P, age 19, presented to our Naval outpatient psychiatry clinic reporting a decline in her ability to organize her thoughts over the past 6 months. She said at times she experienced visual hallucinations and feeling that she was being followed but no one was there. Ms. P also stated she felt other people were talking about her and described ideas of reference. She described her prodrome as an unrelenting and existential interest in the number 33.

The patient drank 4 cups of coffee each day, plus an additional 3 to 4 cups of coffee and 2 to 3 Monster energy drinks on days she was on duty. Ms. P was ingesting approximately 21 to 22 mg/kg/d of caffeine. Basic lab and radiographic work were unremarkable. We asked her to reduce or discontinue her use of caffeinated beverages and return for follow-up in 1 to 2 weeks.

When Ms. P returned 2 weeks later, she said she had reduced her caffeine intake to a periodic cup of coffee or Monster drink. She reported improved sleep quality and quantity; moreover, she experienced a substantial decline in thought disruptions and paranoid thought patterns. However, over the next 4 weeks Ms. P’s reality testing gradually deteriorated, so we prescribed ziprasidone, 20 mg/d, which dissipated her perceptual disturbances. Ms. P tolerated the low-dose antipsychotic and medically retired from military service.

Disclosure

Dr. Whiting reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

Caffeine belongs to the xanthine chemical group and its stimulant effects are the result of its competitive antagonism on adenosine receptors A1 and A2A in the CNS. Caffeine also slows the rate of dopamine reuptake and increases glutamate release, which theoretically could cause neuropsychiatric symptoms.1,2 Toxicity ranges have been recorded at 150 to 200 mg/kg. Increased psychotic features in schizophrenia patients have been reported at doses as low as 10 mg/kg.1 Earlier studies of caffeine use in patients with psychotic disorders reveal induction in thought disorders, social withdrawal, and euphoric activation3; however, these results have been variable.1

The American Association of Poison Control Centers reported 4,600 caffeine-related calls in 2005; one-half of which involved patients age <19.⁴ For a list of the caffeine content of 20 popular drinks, see the Table.

TABLE

Caffeine content of 20 popular drinks^a

Caffeine-induced psychosis?

My team recently treated a woman with prodromal psychotic symptoms for whom ingesting a high dose of caffeine precipitated a psychotic break.

Ms. P, age 19, presented to our Naval outpatient psychiatry clinic reporting a decline in her ability to organize her thoughts over the past 6 months. She said at times she experienced visual hallucinations and feeling that she was being followed but no one was there. Ms. P also stated she felt other people were talking about her and described ideas of reference. She described her prodrome as an unrelenting and existential interest in the number 33.

The patient drank 4 cups of coffee each day, plus an additional 3 to 4 cups of coffee and 2 to 3 Monster energy drinks on days she was on duty. Ms. P was ingesting approximately 21 to 22 mg/kg/d of caffeine. Basic lab and radiographic work were unremarkable. We asked her to reduce or discontinue her use of caffeinated beverages and return for follow-up in 1 to 2 weeks.

When Ms. P returned 2 weeks later, she said she had reduced her caffeine intake to a periodic cup of coffee or Monster drink. She reported improved sleep quality and quantity; moreover, she experienced a substantial decline in thought disruptions and paranoid thought patterns. However, over the next 4 weeks Ms. P’s reality testing gradually deteriorated, so we prescribed ziprasidone, 20 mg/d, which dissipated her perceptual disturbances. Ms. P tolerated the low-dose antipsychotic and medically retired from military service.

Disclosure

Dr. Whiting reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

Caffeine belongs to the xanthine chemical group and its stimulant effects are the result of its competitive antagonism on adenosine receptors A1 and A2A in the CNS. Caffeine also slows the rate of dopamine reuptake and increases glutamate release, which theoretically could cause neuropsychiatric symptoms.1,2 Toxicity ranges have been recorded at 150 to 200 mg/kg. Increased psychotic features in schizophrenia patients have been reported at doses as low as 10 mg/kg.1 Earlier studies of caffeine use in patients with psychotic disorders reveal induction in thought disorders, social withdrawal, and euphoric activation3; however, these results have been variable.1

The American Association of Poison Control Centers reported 4,600 caffeine-related calls in 2005; one-half of which involved patients age <19.⁴ For a list of the caffeine content of 20 popular drinks, see the Table.

TABLE

Caffeine content of 20 popular drinks^a

Caffeine-induced psychosis?

My team recently treated a woman with prodromal psychotic symptoms for whom ingesting a high dose of caffeine precipitated a psychotic break.

Ms. P, age 19, presented to our Naval outpatient psychiatry clinic reporting a decline in her ability to organize her thoughts over the past 6 months. She said at times she experienced visual hallucinations and feeling that she was being followed but no one was there. Ms. P also stated she felt other people were talking about her and described ideas of reference. She described her prodrome as an unrelenting and existential interest in the number 33.

The patient drank 4 cups of coffee each day, plus an additional 3 to 4 cups of coffee and 2 to 3 Monster energy drinks on days she was on duty. Ms. P was ingesting approximately 21 to 22 mg/kg/d of caffeine. Basic lab and radiographic work were unremarkable. We asked her to reduce or discontinue her use of caffeinated beverages and return for follow-up in 1 to 2 weeks.

When Ms. P returned 2 weeks later, she said she had reduced her caffeine intake to a periodic cup of coffee or Monster drink. She reported improved sleep quality and quantity; moreover, she experienced a substantial decline in thought disruptions and paranoid thought patterns. However, over the next 4 weeks Ms. P’s reality testing gradually deteriorated, so we prescribed ziprasidone, 20 mg/d, which dissipated her perceptual disturbances. Ms. P tolerated the low-dose antipsychotic and medically retired from military service.

Disclosure

Dr. Whiting reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

Ms. B, age 29, has bipolar disorder that is stabilized by valproate, 1,250 mg/d. After 1 month of treatment, she shows scalp hair loss. She takes no other medications and is distressed because she had never experienced such copious hair loss. Ms. B’s blood valproate level is at a therapeutic level. She wants to know if the hair loss will be permanent and what she can do to stop it.

Up to 28% of patients who take valproate suffer temporary alopecia.^1,2 In most cases, hair loss is associated with long-term valproate pharmacotherapy. Hair loss appears to be dose-related² and may be more common in women than in men. Usually patients will report gradual but steady hair loss, commonly beginning 2 to 6 months after initiating treatment.³ Complete hair loss is rare and new hair growth typically begins approximately 2 to 3 months after alopecia onset.

Valproate can cause telogen effluvium, a non-scarring form of alopecia that occurs by precipitating the follicles into a premature rest phase. Other medications that may cause this type of hair loss include desipramine, imipramine, selective serotonin reuptake inhibitors, dopaminergics, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors, and cimetidine, as well as withdrawal from minoxidil, oral contraceptives, sulfasalazine, and antithyroid medicines.³

Advising patients

In addition to reducing a patient’s valproate dosage when clinically feasible, you can suggest pharmacologic and lifestyle changes to help patients minimize hair loss:

1. Recommend a biotin supplement. Valproate can cause biotin deficiency and may lead to low serum and liver tissue biotinidase enzyme⁴; a major clinical manifestation of biotin deficiency is alopecia.

2. Tell patients to avoid taking valproate during meals to prevent its chelating effect on food. The chelating effect of valproate makes metals that facilitate hair growth, such as zinc and selenium, unavailable for absorption.⁵

3. Recommend zinc and selenium supplements, which can help stop further hair loss and regenerate hair.⁵

4. Suggest practical advice for hair care, including using soft brushes and mild shampoos and avoiding dyes, heated curlers, and hair dryers.

5. Consider minoxidil therapy. However, this is an expensive option and there are no cases documenting its use for alopecia caused by mood stabilizers.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Ms. B, age 29, has bipolar disorder that is stabilized by valproate, 1,250 mg/d. After 1 month of treatment, she shows scalp hair loss. She takes no other medications and is distressed because she had never experienced such copious hair loss. Ms. B’s blood valproate level is at a therapeutic level. She wants to know if the hair loss will be permanent and what she can do to stop it.

Up to 28% of patients who take valproate suffer temporary alopecia.^1,2 In most cases, hair loss is associated with long-term valproate pharmacotherapy. Hair loss appears to be dose-related² and may be more common in women than in men. Usually patients will report gradual but steady hair loss, commonly beginning 2 to 6 months after initiating treatment.³ Complete hair loss is rare and new hair growth typically begins approximately 2 to 3 months after alopecia onset.

Valproate can cause telogen effluvium, a non-scarring form of alopecia that occurs by precipitating the follicles into a premature rest phase. Other medications that may cause this type of hair loss include desipramine, imipramine, selective serotonin reuptake inhibitors, dopaminergics, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors, and cimetidine, as well as withdrawal from minoxidil, oral contraceptives, sulfasalazine, and antithyroid medicines.³

Advising patients

In addition to reducing a patient’s valproate dosage when clinically feasible, you can suggest pharmacologic and lifestyle changes to help patients minimize hair loss:

1. Recommend a biotin supplement. Valproate can cause biotin deficiency and may lead to low serum and liver tissue biotinidase enzyme⁴; a major clinical manifestation of biotin deficiency is alopecia.

2. Tell patients to avoid taking valproate during meals to prevent its chelating effect on food. The chelating effect of valproate makes metals that facilitate hair growth, such as zinc and selenium, unavailable for absorption.⁵

3. Recommend zinc and selenium supplements, which can help stop further hair loss and regenerate hair.⁵

4. Suggest practical advice for hair care, including using soft brushes and mild shampoos and avoiding dyes, heated curlers, and hair dryers.

5. Consider minoxidil therapy. However, this is an expensive option and there are no cases documenting its use for alopecia caused by mood stabilizers.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Ms. B, age 29, has bipolar disorder that is stabilized by valproate, 1,250 mg/d. After 1 month of treatment, she shows scalp hair loss. She takes no other medications and is distressed because she had never experienced such copious hair loss. Ms. B’s blood valproate level is at a therapeutic level. She wants to know if the hair loss will be permanent and what she can do to stop it.

Up to 28% of patients who take valproate suffer temporary alopecia.^1,2 In most cases, hair loss is associated with long-term valproate pharmacotherapy. Hair loss appears to be dose-related² and may be more common in women than in men. Usually patients will report gradual but steady hair loss, commonly beginning 2 to 6 months after initiating treatment.³ Complete hair loss is rare and new hair growth typically begins approximately 2 to 3 months after alopecia onset.

Valproate can cause telogen effluvium, a non-scarring form of alopecia that occurs by precipitating the follicles into a premature rest phase. Other medications that may cause this type of hair loss include desipramine, imipramine, selective serotonin reuptake inhibitors, dopaminergics, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors, and cimetidine, as well as withdrawal from minoxidil, oral contraceptives, sulfasalazine, and antithyroid medicines.³

Advising patients

In addition to reducing a patient’s valproate dosage when clinically feasible, you can suggest pharmacologic and lifestyle changes to help patients minimize hair loss:

1. Recommend a biotin supplement. Valproate can cause biotin deficiency and may lead to low serum and liver tissue biotinidase enzyme⁴; a major clinical manifestation of biotin deficiency is alopecia.

2. Tell patients to avoid taking valproate during meals to prevent its chelating effect on food. The chelating effect of valproate makes metals that facilitate hair growth, such as zinc and selenium, unavailable for absorption.⁵

3. Recommend zinc and selenium supplements, which can help stop further hair loss and regenerate hair.⁵

4. Suggest practical advice for hair care, including using soft brushes and mild shampoos and avoiding dyes, heated curlers, and hair dryers.

5. Consider minoxidil therapy. However, this is an expensive option and there are no cases documenting its use for alopecia caused by mood stabilizers.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

I read and enjoyed Dr. Nasrallah’s excellent summary of schizophrenia symptoms in “The primary and secondary symptoms of schizophrenia: Current and future management” (Current Psychiatry, supplement to September 2011, p. S5-S9).

I have a suggestion to add to the list of secondary negative symptoms based only on my observations: demoralization caused by repeated failures in all dimensions—self, interpersonal, social, and industrial. I have seen demoralization in schizophrenia patients manifest as low self-esteem, hopelessness, apathy, and self reproach.

Robert A. Williams, MD
Biological Psychiatry Institute, Ltd.
Phoenix, AZ

I read and enjoyed Dr. Nasrallah’s excellent summary of schizophrenia symptoms in “The primary and secondary symptoms of schizophrenia: Current and future management” (Current Psychiatry, supplement to September 2011, p. S5-S9).

I have a suggestion to add to the list of secondary negative symptoms based only on my observations: demoralization caused by repeated failures in all dimensions—self, interpersonal, social, and industrial. I have seen demoralization in schizophrenia patients manifest as low self-esteem, hopelessness, apathy, and self reproach.

Robert A. Williams, MD
Biological Psychiatry Institute, Ltd.
Phoenix, AZ

I read and enjoyed Dr. Nasrallah’s excellent summary of schizophrenia symptoms in “The primary and secondary symptoms of schizophrenia: Current and future management” (Current Psychiatry, supplement to September 2011, p. S5-S9).

I have a suggestion to add to the list of secondary negative symptoms based only on my observations: demoralization caused by repeated failures in all dimensions—self, interpersonal, social, and industrial. I have seen demoralization in schizophrenia patients manifest as low self-esteem, hopelessness, apathy, and self reproach.

Robert A. Williams, MD
Biological Psychiatry Institute, Ltd.
Phoenix, AZ

We agree with Drs. Meraj and Poje in “Capacity assessment: A fundamental skill” (Current Psychiatry, September 2011, p. 72-73) that clinical judgment often is used in addition to or in lieu of quantitative scales when evaluating medical decision-making capacity. We further agree that the formulation by Appelbaum1 is invaluable in such cases.

However, we disagree with the authors’ emphasis on “ability to retain information” as 1 of 4 criteria for decision-making, because long-term declarative memory is irrelevant to a patient’s ability to reason from stable values and preferences.

We use the mnemonic CURA to recall Appelbaum’s criteria: the patient must Communicate a choice; Understand relevant facts; Reason about information; and, importantly, Appreciate the consequences.

We add that the stringency for demonstrating decision-making capacity should increase with greater consequences of the patient’s choice. A clinician may judge a patient to have capacity to consent to low-risk diagnostics, and then the same clinician might appropriately judge that patient lacks capacity to refuse life-saving treatment. A useful model is a “sliding scale” of capacity evaluation,² wherein the threshold for a given decision is proportional to the likely outcome at stake.

Timothy Kreider, MD, PhD
Psychiatry Resident
University of Pennsylvania
Philadelphia, PA

Rashi Aggarwal, MD
Assistant Professor
Department of Psychiatry
New Jersey Medical School
Newark, NJ

References

1. Appelbaum PS. Clinical practice. Assessment of patients’ competence to consent to treatment. N Engl J Med. 2007;357(18):1834-1840.

2. Drane JF. Competency to give an informed consent. A model for making clinical assessments. JAMA. 1984;252(7):925-927.

The authors respond

Thank you for your letter. We emphasize that memory deficits should be implicated in any condition that negatively affects capacity (eg, delirium, dementia). Memory would be beneficial to a patient undergoing capacity evaluation.

For example, consider a 70-year-old male with a history of dementia who is admitted to the neurology service with delirium and refuses a procedure in the evening despite frequent reassurance. The next morning the same patient doesn’t remember seeing you and denies refusing the procedure. His decision-making is greatly affected by fluctuating cognition and memory.

Another scenario would be a patient with such a significant impairment in short-term memory that she is unable to follow the basis of the argument. How could a patient unable to recall the basis of an argument be entrusted to make an intelligent decision?

We argue that memory should be taken in account in these evaluations. Although we agree in principle with the comments made by Drs. Kreider and Aggarwal, it is important to make capacity evaluations on a case-by-case basis and our article presents basic principles to help guide a typical clinician making those assessments.

Adeel Meraj, MD
Third-Year Psychiatry Resident
University of Kansas Medical Center
Kansas City, KS

Albert Poje, PhD
Assistant Professor of Psychology
Department of Psychiatry and Behavioral Sciences
University of Kansas Medical Center
Kansas City, KS

We agree with Drs. Meraj and Poje in “Capacity assessment: A fundamental skill” (Current Psychiatry, September 2011, p. 72-73) that clinical judgment often is used in addition to or in lieu of quantitative scales when evaluating medical decision-making capacity. We further agree that the formulation by Appelbaum1 is invaluable in such cases.

However, we disagree with the authors’ emphasis on “ability to retain information” as 1 of 4 criteria for decision-making, because long-term declarative memory is irrelevant to a patient’s ability to reason from stable values and preferences.

We use the mnemonic CURA to recall Appelbaum’s criteria: the patient must Communicate a choice; Understand relevant facts; Reason about information; and, importantly, Appreciate the consequences.

We add that the stringency for demonstrating decision-making capacity should increase with greater consequences of the patient’s choice. A clinician may judge a patient to have capacity to consent to low-risk diagnostics, and then the same clinician might appropriately judge that patient lacks capacity to refuse life-saving treatment. A useful model is a “sliding scale” of capacity evaluation,² wherein the threshold for a given decision is proportional to the likely outcome at stake.

Timothy Kreider, MD, PhD
Psychiatry Resident
University of Pennsylvania
Philadelphia, PA

Rashi Aggarwal, MD
Assistant Professor
Department of Psychiatry
New Jersey Medical School
Newark, NJ

References

1. Appelbaum PS. Clinical practice. Assessment of patients’ competence to consent to treatment. N Engl J Med. 2007;357(18):1834-1840.

2. Drane JF. Competency to give an informed consent. A model for making clinical assessments. JAMA. 1984;252(7):925-927.

The authors respond

Thank you for your letter. We emphasize that memory deficits should be implicated in any condition that negatively affects capacity (eg, delirium, dementia). Memory would be beneficial to a patient undergoing capacity evaluation.

For example, consider a 70-year-old male with a history of dementia who is admitted to the neurology service with delirium and refuses a procedure in the evening despite frequent reassurance. The next morning the same patient doesn’t remember seeing you and denies refusing the procedure. His decision-making is greatly affected by fluctuating cognition and memory.

Another scenario would be a patient with such a significant impairment in short-term memory that she is unable to follow the basis of the argument. How could a patient unable to recall the basis of an argument be entrusted to make an intelligent decision?

We argue that memory should be taken in account in these evaluations. Although we agree in principle with the comments made by Drs. Kreider and Aggarwal, it is important to make capacity evaluations on a case-by-case basis and our article presents basic principles to help guide a typical clinician making those assessments.

Adeel Meraj, MD
Third-Year Psychiatry Resident
University of Kansas Medical Center
Kansas City, KS

Albert Poje, PhD
Assistant Professor of Psychology
Department of Psychiatry and Behavioral Sciences
University of Kansas Medical Center
Kansas City, KS

We agree with Drs. Meraj and Poje in “Capacity assessment: A fundamental skill” (Current Psychiatry, September 2011, p. 72-73) that clinical judgment often is used in addition to or in lieu of quantitative scales when evaluating medical decision-making capacity. We further agree that the formulation by Appelbaum1 is invaluable in such cases.

However, we disagree with the authors’ emphasis on “ability to retain information” as 1 of 4 criteria for decision-making, because long-term declarative memory is irrelevant to a patient’s ability to reason from stable values and preferences.

We use the mnemonic CURA to recall Appelbaum’s criteria: the patient must Communicate a choice; Understand relevant facts; Reason about information; and, importantly, Appreciate the consequences.

We add that the stringency for demonstrating decision-making capacity should increase with greater consequences of the patient’s choice. A clinician may judge a patient to have capacity to consent to low-risk diagnostics, and then the same clinician might appropriately judge that patient lacks capacity to refuse life-saving treatment. A useful model is a “sliding scale” of capacity evaluation,² wherein the threshold for a given decision is proportional to the likely outcome at stake.

Timothy Kreider, MD, PhD
Psychiatry Resident
University of Pennsylvania
Philadelphia, PA

Rashi Aggarwal, MD
Assistant Professor
Department of Psychiatry
New Jersey Medical School
Newark, NJ

References

1. Appelbaum PS. Clinical practice. Assessment of patients’ competence to consent to treatment. N Engl J Med. 2007;357(18):1834-1840.

2. Drane JF. Competency to give an informed consent. A model for making clinical assessments. JAMA. 1984;252(7):925-927.

The authors respond

Thank you for your letter. We emphasize that memory deficits should be implicated in any condition that negatively affects capacity (eg, delirium, dementia). Memory would be beneficial to a patient undergoing capacity evaluation.

For example, consider a 70-year-old male with a history of dementia who is admitted to the neurology service with delirium and refuses a procedure in the evening despite frequent reassurance. The next morning the same patient doesn’t remember seeing you and denies refusing the procedure. His decision-making is greatly affected by fluctuating cognition and memory.

Another scenario would be a patient with such a significant impairment in short-term memory that she is unable to follow the basis of the argument. How could a patient unable to recall the basis of an argument be entrusted to make an intelligent decision?

We argue that memory should be taken in account in these evaluations. Although we agree in principle with the comments made by Drs. Kreider and Aggarwal, it is important to make capacity evaluations on a case-by-case basis and our article presents basic principles to help guide a typical clinician making those assessments.

Adeel Meraj, MD
Third-Year Psychiatry Resident
University of Kansas Medical Center
Kansas City, KS

Albert Poje, PhD
Assistant Professor of Psychology
Department of Psychiatry and Behavioral Sciences
University of Kansas Medical Center
Kansas City, KS

Discuss this article at www.facebook.com/CurrentPsychiatry

Assessing capacity

We agree with Drs. Meraj and Poje in “Capacity assessment: A fundamental skill” (Current Psychiatry, September 2011, p. 72-73) that clinical judgment often is used in addition to or in lieu of quantitative scales when evaluating medical decision-making capacity. We further agree that the formulation by Appelbaum^{The primary and secondary symptoms of schizophrenia: Current and future management” (Current Psychiatry, supplement to September 2011, p. S5-S9).}

I have a suggestion to add to the list of secondary negative symptoms based only on my observations: demoralization caused by repeated failures in all dimensions—self, interpersonal, social, and industrial. I have seen demoralization in schizophrenia patients manifest as low self-esteem, hopelessness, apathy, and self reproach.

Robert A. Williams, MD
Biological Psychiatry Institute, Ltd.
Phoenix, AZ

Discuss this article at www.facebook.com/CurrentPsychiatry

Assessing capacity

We agree with Drs. Meraj and Poje in “Capacity assessment: A fundamental skill” (Current Psychiatry, September 2011, p. 72-73) that clinical judgment often is used in addition to or in lieu of quantitative scales when evaluating medical decision-making capacity. We further agree that the formulation by Appelbaum^{The primary and secondary symptoms of schizophrenia: Current and future management” (Current Psychiatry, supplement to September 2011, p. S5-S9).}

I have a suggestion to add to the list of secondary negative symptoms based only on my observations: demoralization caused by repeated failures in all dimensions—self, interpersonal, social, and industrial. I have seen demoralization in schizophrenia patients manifest as low self-esteem, hopelessness, apathy, and self reproach.

Robert A. Williams, MD
Biological Psychiatry Institute, Ltd.
Phoenix, AZ

Discuss this article at www.facebook.com/CurrentPsychiatry

Assessing capacity

We agree with Drs. Meraj and Poje in “Capacity assessment: A fundamental skill” (Current Psychiatry, September 2011, p. 72-73) that clinical judgment often is used in addition to or in lieu of quantitative scales when evaluating medical decision-making capacity. We further agree that the formulation by Appelbaum^{The primary and secondary symptoms of schizophrenia: Current and future management” (Current Psychiatry, supplement to September 2011, p. S5-S9).}

I have a suggestion to add to the list of secondary negative symptoms based only on my observations: demoralization caused by repeated failures in all dimensions—self, interpersonal, social, and industrial. I have seen demoralization in schizophrenia patients manifest as low self-esteem, hopelessness, apathy, and self reproach.

Robert A. Williams, MD
Biological Psychiatry Institute, Ltd.
Phoenix, AZ

Alcohol dependence is not an acute illness. Progression from alcohol use to dependence typically takes years, and alcohol dependence is a chronic illness with symptom severity that increases over time.1,2 As the level of alcohol intake increases, the probability of developing an alcohol use disorder, cirrhosis, seizures, cancer, hypertension, stroke, and injuries significantly increases.3,4 Most alcohol-related harm occurs in high-risk drinkers who do not meet DSM-IV-TR criteria for an alcohol use disorder.5,6

Clinicians therefore have an opportunity to intervene at early stages of alcohol use to help prevent progression to dependence and reduce harm. The concept of a continuum from low-to high-risk alcohol use is replacing the disease-oriented model that focuses on identifying and treating individuals who meet DSM-IV-TR criteria for alcohol use disorders (Figure 1).^4,7 Efforts to provide screening and intervention earlier in the disease course have:

• mainly been carried out in the primary care setting
• been aimed at nontreatment-seeking, nondependent individuals
• led to recommendations for safe alcohol consumption limits.^8-10

One of the largest outreach efforts is a federally funded screening, brief intervention, referral to treatment (SBIRT) program established in 17 states that targets hospital emergency rooms, community health centers, and trauma centers.¹¹

Although research on the use of brief interventions for problem drinking in psychiatric settings is limited,^12-15 psychiatrists can employ these strategies, even during a brief medication management visit.

Figure 1: Recommended treatment based on type of alcohol use

NIAAA: National Institute on Alcohol Abuse and Alcoholism
Source: References 7,16

How much is too much?

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) recommends men age <65 drink no more than 4 drinks/day and no more than 14 drinks/week and women of any age and men age ≥65 drink no more than 3 drinks/day and no more than 7 drinks/week.¹⁶ A standard drink is defined as 14 grams of absolute ethanol (12 ounces of beer, 5 ounces of wine, or 1.5 ounces of distilled spirits). Drinking above these levels is likely to result in harm and is defined as hazardous or at-risk use.^10,17,18 Harmful use is alcohol consumption that has resulted in adverse mental or physical effects.^10,17,18 We use “problem drinking” to describe both at-risk and harmful use as alcohol intake that exceeds NIAAA-recommended limits but does not meet DSM-IV-TR criteria for an alcohol use disorder.

In the United States, approximately 20% of the population exceeds NIAAA recommended alcohol intake guidelines without meeting criteria for an alcohol use disorder.¹⁸ Problem drinkers have an increased risk of developing an alcohol use disorder, nicotine dependence, liver disease, financial problems, marital disruptions, injuries, and driver’s license suspensions.^4-6,19

Problem drinking is common in psychiatric populations and may lead to difficulties beyond those experienced in the general population.^20,21 For example, problem drinking in individuals with bipolar disorder is associated with reduced medication compliance, greater functional impairment, and possibly more suicide attempts.^22,23 Even moderate alcohol use below the NIAAA-recommend levels may increase symptom severity in patients with bipolar disorder.^22,23

Interviewing techniques

Interventions to identify and treat problem drinkers have focused on the primary care setting because these physicians often are the only medical professionals problem drinkers encounter.^8-10 The style of counseling is based on motivational interviewing. Providers use therapeutic empathy, describe risk, deal with ambivalence and resistance, assess motivation to change, emphasize patient responsibility and self-efficacy, and provide a menu of specific strategies to reduce alcohol use. However, unlike standard motivational interviewing, in brief interventions, providers use clear, directive advice to reduce alcohol consumption in the context of the medical provider role. Brief interventions also draw on cognitive-behavioral therapy and general education strategies utilizing contracting, goal setting, and written materials such as self-help manuals.²⁴

Clinicians’ time demands have driven an effort to make interventions for problem drinkers efficient and time-limited. A single short intervention (5 to 15 minutes) can be effective, but 2 to 4 sessions of 5 to 15 minutes each seems to be more effective.^8,10 The emphasis is on increasing a patient’s insight and awareness of risk to prompt him or her to establish and manage a goal to reduce alcohol intake. As opposed to abstinence, which is commonly recommended for patients with alcohol use disorders, reducing intake typically is encouraged for problem drinkers.^9,10,16,18 For patients who use alcohol over the recommended limits and also meet criteria for an alcohol use disorder, clinicians can deliver a brief intervention, but should recommend abstinence from drinking and provide referral for further treatment.^9,10,16,18

Compared with controls, problem drinkers who receive a brief intervention are twice as likely to moderate their drinking at 6 to 12 months²⁵ and significantly reduce alcohol intake by approximately 4 drinks per week at follow-ups of 12 months or more.^8,10,26 In addition, providing brief interventions significantly decreases the proportion of individuals whose alcohol intake exceeds recommended levels.¹⁰ A meta-analysis and a systemic review indicate brief interventions for problem drinkers reduce morbidity and mortality resulting from motor vehicle crashes, falls, suicide attempts, domestic violence, assaults, and child abuse.^5,27

A brief intervention

Screening and brief intervention guidelines suggest a standard approach for assessing and managing problem drinking and alcohol use disorders.^7,16 This approach can be described by the “5 As of intervention” (Table 1),¹⁰ which is one way to summarize the different brief intervention strategies described in the literature.^{7,9,10,16-18,28-30}

Ask. Asking a question about any alcohol use is a simple way to initiate a conversation about the topic (“Do you sometimes drink beer, wine, or other alcoholic beverages?”). Incorporating questions about alcohol consumption into inquiries about other health habits (eg, smoking, exercise) may decrease patients’ defensiveness. If your patient reports using alcohol, follow up by screening for ≥5 drinks a day for men or ≥4 drinks a day for women (“In the past year, how many times have you had 5 or more drinks a day?”). Use at this level ≥1 times a year indicates a positive screen that provides good sensitivity and specificity for detecting problem drinking and alcohol use disorders.¹⁸ Then ask about weekly alcohol intake (“On average, how many days a week do you have an alcoholic drink?” “On a typical drinking day how many drinks do you have?”). Presenting a chart that describes what constitutes a standard drink—available from the NIAAA (see Related Resources)—may be helpful.

You also can use additional questions from the CAGE screening test (Table 2).³¹ In clinics with a more formal screening protocol, patients may be asked to complete a written self-report such as the Alcohol Use Disorders Identification Test (AUDIT). This 10-question survey covers domains of alcohol consumption, drinking behavior, and alcohol-related problems.^17,18 If your patient is a problem drinker, further assessment could determine if he or she has an alcohol use disorder.

Advise. Provide feedback about your patient’s drinking and its consequences along with clear recommendations in an empathic, nonconfrontational manner (“You’re drinking more than is medically safe; I strongly recommend you cut down”). Comparing your patient’s drinking pattern to population norms may be helpful (“Less than 20% of people drink a much as you”).^7,16 When possible, tie the consequences of the patient’s drinking to his or her current physical, mental, family, social, and legal concerns. Convey your concerns empathically, as a medical provider providing health recommendations (“As your doctor, I am concerned about how much you drink and how it is affecting your health”). However, to respect patient autonomy, give a medical recommendation, rather than a directive (“As your doctor, I feel I should tell you” rather than “You should”). Finally, express a clear message of your willingness to help.

Assess your patient’s readiness to change (“Given what we’ve talked about, are you willing to consider making changes in your drinking?”). Showing the links between alcohol use and personal consequences may improve patient engagement (“If you keep drinking at your current levels, do you think your goal of improving your grades will be easier, harder, or no different?”).²⁸ If your patient is willing to make a change, negotiate a patient-specific goal, such as reducing drinking to within the recommended limits, using alcohol only a few days a week instead of every day, or abstaining for a defined period. If the patient is not willing to change, restate your concern regarding his or her health-related consequences and your willingness to help.

Assist. After you’ve negotiated a goal with your patient, discuss a treatment plan to help the patient achieve the goal. This should include steps the patient will take to reduce or quit drinking. Consider offering handouts on standard drink sizes, alcohol-associated harms, and strategies for cutting down or abstaining (eg, pacing use, spacing drinks by including nonalcoholic beverages, plans to handle urges, using alcohol money for other items), and calendars for tracking drinking (ie, a drinking diary). Help your patient identify situations where he or she is likely to have difficulty achieving the goal and strategies for avoiding or managing such situations. Ask patients to identify a family member or friend who can help them. Refer patients who have an alcohol use disorder to addiction treatment.

For patients who are not willing to change, discuss the perceived benefits of continued drinking vs reducing or stopping drinking to encourage them to reflect on their alcohol use patterns. Discuss any potential barriers to change. Keep in mind ambivalence and reluctance to change drinking patterns are common and many patients are unaware of the risks of their alcohol use. This discussion may lead patients to contemplate change later.

Arrange. Schedule a follow-up appointment to reinforce the treatment plan with further support, feedback, and assistance in setting, achieving, and maintaining realistic goals. Consider a follow-up phone call 2 weeks after the brief intervention to check on progress and a follow-up appointment in 1 month. Clinical staff may have the opportunity to e-mail or text message patients to check on progress between face-to-face visits. At the follow-up appointment, ask if your patient was able to meet and sustain the drinking goal. If so, support continued adherence, renegotiate drinking goals if indicated, and encourage follow-up with at least annual rescreening. When patients are unable to meet their treatment goals, acknowledge that change is difficult, encourage any positive changes, and address barriers to reaching the goal. Reemphasize your willingness to help, reevaluate the diagnosis, treatment plan, and goals, and schedule close follow-up. Consider engaging significant others in the treatment process.

Table 1

Brief interventions: ‘5As’ to address alcohol use

Table 2

CAGE questionnaire to detect alcohol use disorders

Use in psychiatric practice

Problem drinking may not be adequately addressed in psychiatric settings. In a survey of problem drinkers identified in the general population, only 64% discussed their drinking during a mental health visit and only 40% received counseling about their alcohol use from their mental health provider.³² In a study of 200 psychiatric inpatients, 49% exhibited problem drinking as measured by AUDIT, but only 27% of patients had alcohol use recorded in their medical record.³³ In addition, routine use of screening tools such as CAGE or AUDIT appears to be low in many psychiatric settings even though research has shown that tools such as AUDIT or computerized screening may be effective for identifying problem drinking in psychiatric outpatient settings.^20,21,34

Several small studies support the efficacy of brief interventions for problem drinking in psychiatric settings. A study in a psychiatric emergency service found patients with either schizophrenia/bipolar disorder or depression/anxiety decreased their drinking by about 7 drinks a week over 6 months after a brief intervention.¹⁵ This study was small and the decrease in alcohol intake was not significant within the 2 population groups (P = .10 for schizophrenia/bipolar disorder, n = 34, P = .05 for depression/anxiety, n = 53); however, there was a significant decrease for all patients with follow-up (P = .0096, N = 55).¹⁵ In another study, psychiatric inpatients with problem drinking who received a brief motivational intervention demonstrated a statistically significant reduction in alcohol consumption at 6 months compared with patients who received only an information packet,¹³ but health-related outcomes at 5 years did not differ between the 2 groups.¹⁴ Finally, in a study of 344 nonpsychotic psychiatric outpatients with problem drinking, one-half of those who received a brief telephone intervention reduced their drinking to non-hazardous levels at a 6-month follow-up (intervention 43.8%, control 27.7%).¹²

Related Resources

• National Institute on Alcohol Abuse and Alcoholism. www.niaaa.nih.gov.
• Saunders JB, Aasland OG, Babor TF, et al. Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons with Harmful Alcohol Consumption—II. Addiction. 1993;88(6):791-804.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Alcohol dependence is not an acute illness. Progression from alcohol use to dependence typically takes years, and alcohol dependence is a chronic illness with symptom severity that increases over time.1,2 As the level of alcohol intake increases, the probability of developing an alcohol use disorder, cirrhosis, seizures, cancer, hypertension, stroke, and injuries significantly increases.3,4 Most alcohol-related harm occurs in high-risk drinkers who do not meet DSM-IV-TR criteria for an alcohol use disorder.5,6

Clinicians therefore have an opportunity to intervene at early stages of alcohol use to help prevent progression to dependence and reduce harm. The concept of a continuum from low-to high-risk alcohol use is replacing the disease-oriented model that focuses on identifying and treating individuals who meet DSM-IV-TR criteria for alcohol use disorders (Figure 1).^4,7 Efforts to provide screening and intervention earlier in the disease course have:

• mainly been carried out in the primary care setting
• been aimed at nontreatment-seeking, nondependent individuals
• led to recommendations for safe alcohol consumption limits.^8-10

One of the largest outreach efforts is a federally funded screening, brief intervention, referral to treatment (SBIRT) program established in 17 states that targets hospital emergency rooms, community health centers, and trauma centers.¹¹

Although research on the use of brief interventions for problem drinking in psychiatric settings is limited,^12-15 psychiatrists can employ these strategies, even during a brief medication management visit.

Figure 1: Recommended treatment based on type of alcohol use

NIAAA: National Institute on Alcohol Abuse and Alcoholism
Source: References 7,16

How much is too much?

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) recommends men age <65 drink no more than 4 drinks/day and no more than 14 drinks/week and women of any age and men age ≥65 drink no more than 3 drinks/day and no more than 7 drinks/week.¹⁶ A standard drink is defined as 14 grams of absolute ethanol (12 ounces of beer, 5 ounces of wine, or 1.5 ounces of distilled spirits). Drinking above these levels is likely to result in harm and is defined as hazardous or at-risk use.^10,17,18 Harmful use is alcohol consumption that has resulted in adverse mental or physical effects.^10,17,18 We use “problem drinking” to describe both at-risk and harmful use as alcohol intake that exceeds NIAAA-recommended limits but does not meet DSM-IV-TR criteria for an alcohol use disorder.

In the United States, approximately 20% of the population exceeds NIAAA recommended alcohol intake guidelines without meeting criteria for an alcohol use disorder.¹⁸ Problem drinkers have an increased risk of developing an alcohol use disorder, nicotine dependence, liver disease, financial problems, marital disruptions, injuries, and driver’s license suspensions.^4-6,19

Problem drinking is common in psychiatric populations and may lead to difficulties beyond those experienced in the general population.^20,21 For example, problem drinking in individuals with bipolar disorder is associated with reduced medication compliance, greater functional impairment, and possibly more suicide attempts.^22,23 Even moderate alcohol use below the NIAAA-recommend levels may increase symptom severity in patients with bipolar disorder.^22,23

Interviewing techniques

Interventions to identify and treat problem drinkers have focused on the primary care setting because these physicians often are the only medical professionals problem drinkers encounter.^8-10 The style of counseling is based on motivational interviewing. Providers use therapeutic empathy, describe risk, deal with ambivalence and resistance, assess motivation to change, emphasize patient responsibility and self-efficacy, and provide a menu of specific strategies to reduce alcohol use. However, unlike standard motivational interviewing, in brief interventions, providers use clear, directive advice to reduce alcohol consumption in the context of the medical provider role. Brief interventions also draw on cognitive-behavioral therapy and general education strategies utilizing contracting, goal setting, and written materials such as self-help manuals.²⁴

Clinicians’ time demands have driven an effort to make interventions for problem drinkers efficient and time-limited. A single short intervention (5 to 15 minutes) can be effective, but 2 to 4 sessions of 5 to 15 minutes each seems to be more effective.^8,10 The emphasis is on increasing a patient’s insight and awareness of risk to prompt him or her to establish and manage a goal to reduce alcohol intake. As opposed to abstinence, which is commonly recommended for patients with alcohol use disorders, reducing intake typically is encouraged for problem drinkers.^9,10,16,18 For patients who use alcohol over the recommended limits and also meet criteria for an alcohol use disorder, clinicians can deliver a brief intervention, but should recommend abstinence from drinking and provide referral for further treatment.^9,10,16,18

Compared with controls, problem drinkers who receive a brief intervention are twice as likely to moderate their drinking at 6 to 12 months²⁵ and significantly reduce alcohol intake by approximately 4 drinks per week at follow-ups of 12 months or more.^8,10,26 In addition, providing brief interventions significantly decreases the proportion of individuals whose alcohol intake exceeds recommended levels.¹⁰ A meta-analysis and a systemic review indicate brief interventions for problem drinkers reduce morbidity and mortality resulting from motor vehicle crashes, falls, suicide attempts, domestic violence, assaults, and child abuse.^5,27

A brief intervention

Screening and brief intervention guidelines suggest a standard approach for assessing and managing problem drinking and alcohol use disorders.^7,16 This approach can be described by the “5 As of intervention” (Table 1),¹⁰ which is one way to summarize the different brief intervention strategies described in the literature.^{7,9,10,16-18,28-30}

Ask. Asking a question about any alcohol use is a simple way to initiate a conversation about the topic (“Do you sometimes drink beer, wine, or other alcoholic beverages?”). Incorporating questions about alcohol consumption into inquiries about other health habits (eg, smoking, exercise) may decrease patients’ defensiveness. If your patient reports using alcohol, follow up by screening for ≥5 drinks a day for men or ≥4 drinks a day for women (“In the past year, how many times have you had 5 or more drinks a day?”). Use at this level ≥1 times a year indicates a positive screen that provides good sensitivity and specificity for detecting problem drinking and alcohol use disorders.¹⁸ Then ask about weekly alcohol intake (“On average, how many days a week do you have an alcoholic drink?” “On a typical drinking day how many drinks do you have?”). Presenting a chart that describes what constitutes a standard drink—available from the NIAAA (see Related Resources)—may be helpful.

You also can use additional questions from the CAGE screening test (Table 2).³¹ In clinics with a more formal screening protocol, patients may be asked to complete a written self-report such as the Alcohol Use Disorders Identification Test (AUDIT). This 10-question survey covers domains of alcohol consumption, drinking behavior, and alcohol-related problems.^17,18 If your patient is a problem drinker, further assessment could determine if he or she has an alcohol use disorder.

Advise. Provide feedback about your patient’s drinking and its consequences along with clear recommendations in an empathic, nonconfrontational manner (“You’re drinking more than is medically safe; I strongly recommend you cut down”). Comparing your patient’s drinking pattern to population norms may be helpful (“Less than 20% of people drink a much as you”).^7,16 When possible, tie the consequences of the patient’s drinking to his or her current physical, mental, family, social, and legal concerns. Convey your concerns empathically, as a medical provider providing health recommendations (“As your doctor, I am concerned about how much you drink and how it is affecting your health”). However, to respect patient autonomy, give a medical recommendation, rather than a directive (“As your doctor, I feel I should tell you” rather than “You should”). Finally, express a clear message of your willingness to help.

Assess your patient’s readiness to change (“Given what we’ve talked about, are you willing to consider making changes in your drinking?”). Showing the links between alcohol use and personal consequences may improve patient engagement (“If you keep drinking at your current levels, do you think your goal of improving your grades will be easier, harder, or no different?”).²⁸ If your patient is willing to make a change, negotiate a patient-specific goal, such as reducing drinking to within the recommended limits, using alcohol only a few days a week instead of every day, or abstaining for a defined period. If the patient is not willing to change, restate your concern regarding his or her health-related consequences and your willingness to help.

Assist. After you’ve negotiated a goal with your patient, discuss a treatment plan to help the patient achieve the goal. This should include steps the patient will take to reduce or quit drinking. Consider offering handouts on standard drink sizes, alcohol-associated harms, and strategies for cutting down or abstaining (eg, pacing use, spacing drinks by including nonalcoholic beverages, plans to handle urges, using alcohol money for other items), and calendars for tracking drinking (ie, a drinking diary). Help your patient identify situations where he or she is likely to have difficulty achieving the goal and strategies for avoiding or managing such situations. Ask patients to identify a family member or friend who can help them. Refer patients who have an alcohol use disorder to addiction treatment.

For patients who are not willing to change, discuss the perceived benefits of continued drinking vs reducing or stopping drinking to encourage them to reflect on their alcohol use patterns. Discuss any potential barriers to change. Keep in mind ambivalence and reluctance to change drinking patterns are common and many patients are unaware of the risks of their alcohol use. This discussion may lead patients to contemplate change later.

Arrange. Schedule a follow-up appointment to reinforce the treatment plan with further support, feedback, and assistance in setting, achieving, and maintaining realistic goals. Consider a follow-up phone call 2 weeks after the brief intervention to check on progress and a follow-up appointment in 1 month. Clinical staff may have the opportunity to e-mail or text message patients to check on progress between face-to-face visits. At the follow-up appointment, ask if your patient was able to meet and sustain the drinking goal. If so, support continued adherence, renegotiate drinking goals if indicated, and encourage follow-up with at least annual rescreening. When patients are unable to meet their treatment goals, acknowledge that change is difficult, encourage any positive changes, and address barriers to reaching the goal. Reemphasize your willingness to help, reevaluate the diagnosis, treatment plan, and goals, and schedule close follow-up. Consider engaging significant others in the treatment process.

Table 1

Brief interventions: ‘5As’ to address alcohol use

Table 2

CAGE questionnaire to detect alcohol use disorders

Use in psychiatric practice

Problem drinking may not be adequately addressed in psychiatric settings. In a survey of problem drinkers identified in the general population, only 64% discussed their drinking during a mental health visit and only 40% received counseling about their alcohol use from their mental health provider.³² In a study of 200 psychiatric inpatients, 49% exhibited problem drinking as measured by AUDIT, but only 27% of patients had alcohol use recorded in their medical record.³³ In addition, routine use of screening tools such as CAGE or AUDIT appears to be low in many psychiatric settings even though research has shown that tools such as AUDIT or computerized screening may be effective for identifying problem drinking in psychiatric outpatient settings.^20,21,34

Several small studies support the efficacy of brief interventions for problem drinking in psychiatric settings. A study in a psychiatric emergency service found patients with either schizophrenia/bipolar disorder or depression/anxiety decreased their drinking by about 7 drinks a week over 6 months after a brief intervention.¹⁵ This study was small and the decrease in alcohol intake was not significant within the 2 population groups (P = .10 for schizophrenia/bipolar disorder, n = 34, P = .05 for depression/anxiety, n = 53); however, there was a significant decrease for all patients with follow-up (P = .0096, N = 55).¹⁵ In another study, psychiatric inpatients with problem drinking who received a brief motivational intervention demonstrated a statistically significant reduction in alcohol consumption at 6 months compared with patients who received only an information packet,¹³ but health-related outcomes at 5 years did not differ between the 2 groups.¹⁴ Finally, in a study of 344 nonpsychotic psychiatric outpatients with problem drinking, one-half of those who received a brief telephone intervention reduced their drinking to non-hazardous levels at a 6-month follow-up (intervention 43.8%, control 27.7%).¹²

Related Resources

• National Institute on Alcohol Abuse and Alcoholism. www.niaaa.nih.gov.
• Saunders JB, Aasland OG, Babor TF, et al. Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons with Harmful Alcohol Consumption—II. Addiction. 1993;88(6):791-804.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Alcohol dependence is not an acute illness. Progression from alcohol use to dependence typically takes years, and alcohol dependence is a chronic illness with symptom severity that increases over time.1,2 As the level of alcohol intake increases, the probability of developing an alcohol use disorder, cirrhosis, seizures, cancer, hypertension, stroke, and injuries significantly increases.3,4 Most alcohol-related harm occurs in high-risk drinkers who do not meet DSM-IV-TR criteria for an alcohol use disorder.5,6

Clinicians therefore have an opportunity to intervene at early stages of alcohol use to help prevent progression to dependence and reduce harm. The concept of a continuum from low-to high-risk alcohol use is replacing the disease-oriented model that focuses on identifying and treating individuals who meet DSM-IV-TR criteria for alcohol use disorders (Figure 1).^4,7 Efforts to provide screening and intervention earlier in the disease course have:

• mainly been carried out in the primary care setting
• been aimed at nontreatment-seeking, nondependent individuals
• led to recommendations for safe alcohol consumption limits.^8-10

One of the largest outreach efforts is a federally funded screening, brief intervention, referral to treatment (SBIRT) program established in 17 states that targets hospital emergency rooms, community health centers, and trauma centers.¹¹

Although research on the use of brief interventions for problem drinking in psychiatric settings is limited,^12-15 psychiatrists can employ these strategies, even during a brief medication management visit.

Figure 1: Recommended treatment based on type of alcohol use

NIAAA: National Institute on Alcohol Abuse and Alcoholism
Source: References 7,16

How much is too much?

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) recommends men age <65 drink no more than 4 drinks/day and no more than 14 drinks/week and women of any age and men age ≥65 drink no more than 3 drinks/day and no more than 7 drinks/week.¹⁶ A standard drink is defined as 14 grams of absolute ethanol (12 ounces of beer, 5 ounces of wine, or 1.5 ounces of distilled spirits). Drinking above these levels is likely to result in harm and is defined as hazardous or at-risk use.^10,17,18 Harmful use is alcohol consumption that has resulted in adverse mental or physical effects.^10,17,18 We use “problem drinking” to describe both at-risk and harmful use as alcohol intake that exceeds NIAAA-recommended limits but does not meet DSM-IV-TR criteria for an alcohol use disorder.

In the United States, approximately 20% of the population exceeds NIAAA recommended alcohol intake guidelines without meeting criteria for an alcohol use disorder.¹⁸ Problem drinkers have an increased risk of developing an alcohol use disorder, nicotine dependence, liver disease, financial problems, marital disruptions, injuries, and driver’s license suspensions.^4-6,19

Problem drinking is common in psychiatric populations and may lead to difficulties beyond those experienced in the general population.^20,21 For example, problem drinking in individuals with bipolar disorder is associated with reduced medication compliance, greater functional impairment, and possibly more suicide attempts.^22,23 Even moderate alcohol use below the NIAAA-recommend levels may increase symptom severity in patients with bipolar disorder.^22,23

Interviewing techniques

Interventions to identify and treat problem drinkers have focused on the primary care setting because these physicians often are the only medical professionals problem drinkers encounter.^8-10 The style of counseling is based on motivational interviewing. Providers use therapeutic empathy, describe risk, deal with ambivalence and resistance, assess motivation to change, emphasize patient responsibility and self-efficacy, and provide a menu of specific strategies to reduce alcohol use. However, unlike standard motivational interviewing, in brief interventions, providers use clear, directive advice to reduce alcohol consumption in the context of the medical provider role. Brief interventions also draw on cognitive-behavioral therapy and general education strategies utilizing contracting, goal setting, and written materials such as self-help manuals.²⁴

Clinicians’ time demands have driven an effort to make interventions for problem drinkers efficient and time-limited. A single short intervention (5 to 15 minutes) can be effective, but 2 to 4 sessions of 5 to 15 minutes each seems to be more effective.^8,10 The emphasis is on increasing a patient’s insight and awareness of risk to prompt him or her to establish and manage a goal to reduce alcohol intake. As opposed to abstinence, which is commonly recommended for patients with alcohol use disorders, reducing intake typically is encouraged for problem drinkers.^9,10,16,18 For patients who use alcohol over the recommended limits and also meet criteria for an alcohol use disorder, clinicians can deliver a brief intervention, but should recommend abstinence from drinking and provide referral for further treatment.^9,10,16,18

Compared with controls, problem drinkers who receive a brief intervention are twice as likely to moderate their drinking at 6 to 12 months²⁵ and significantly reduce alcohol intake by approximately 4 drinks per week at follow-ups of 12 months or more.^8,10,26 In addition, providing brief interventions significantly decreases the proportion of individuals whose alcohol intake exceeds recommended levels.¹⁰ A meta-analysis and a systemic review indicate brief interventions for problem drinkers reduce morbidity and mortality resulting from motor vehicle crashes, falls, suicide attempts, domestic violence, assaults, and child abuse.^5,27

A brief intervention

Screening and brief intervention guidelines suggest a standard approach for assessing and managing problem drinking and alcohol use disorders.^7,16 This approach can be described by the “5 As of intervention” (Table 1),¹⁰ which is one way to summarize the different brief intervention strategies described in the literature.^{7,9,10,16-18,28-30}

Ask. Asking a question about any alcohol use is a simple way to initiate a conversation about the topic (“Do you sometimes drink beer, wine, or other alcoholic beverages?”). Incorporating questions about alcohol consumption into inquiries about other health habits (eg, smoking, exercise) may decrease patients’ defensiveness. If your patient reports using alcohol, follow up by screening for ≥5 drinks a day for men or ≥4 drinks a day for women (“In the past year, how many times have you had 5 or more drinks a day?”). Use at this level ≥1 times a year indicates a positive screen that provides good sensitivity and specificity for detecting problem drinking and alcohol use disorders.¹⁸ Then ask about weekly alcohol intake (“On average, how many days a week do you have an alcoholic drink?” “On a typical drinking day how many drinks do you have?”). Presenting a chart that describes what constitutes a standard drink—available from the NIAAA (see Related Resources)—may be helpful.

You also can use additional questions from the CAGE screening test (Table 2).³¹ In clinics with a more formal screening protocol, patients may be asked to complete a written self-report such as the Alcohol Use Disorders Identification Test (AUDIT). This 10-question survey covers domains of alcohol consumption, drinking behavior, and alcohol-related problems.^17,18 If your patient is a problem drinker, further assessment could determine if he or she has an alcohol use disorder.

Advise. Provide feedback about your patient’s drinking and its consequences along with clear recommendations in an empathic, nonconfrontational manner (“You’re drinking more than is medically safe; I strongly recommend you cut down”). Comparing your patient’s drinking pattern to population norms may be helpful (“Less than 20% of people drink a much as you”).^7,16 When possible, tie the consequences of the patient’s drinking to his or her current physical, mental, family, social, and legal concerns. Convey your concerns empathically, as a medical provider providing health recommendations (“As your doctor, I am concerned about how much you drink and how it is affecting your health”). However, to respect patient autonomy, give a medical recommendation, rather than a directive (“As your doctor, I feel I should tell you” rather than “You should”). Finally, express a clear message of your willingness to help.

Assess your patient’s readiness to change (“Given what we’ve talked about, are you willing to consider making changes in your drinking?”). Showing the links between alcohol use and personal consequences may improve patient engagement (“If you keep drinking at your current levels, do you think your goal of improving your grades will be easier, harder, or no different?”).²⁸ If your patient is willing to make a change, negotiate a patient-specific goal, such as reducing drinking to within the recommended limits, using alcohol only a few days a week instead of every day, or abstaining for a defined period. If the patient is not willing to change, restate your concern regarding his or her health-related consequences and your willingness to help.

Assist. After you’ve negotiated a goal with your patient, discuss a treatment plan to help the patient achieve the goal. This should include steps the patient will take to reduce or quit drinking. Consider offering handouts on standard drink sizes, alcohol-associated harms, and strategies for cutting down or abstaining (eg, pacing use, spacing drinks by including nonalcoholic beverages, plans to handle urges, using alcohol money for other items), and calendars for tracking drinking (ie, a drinking diary). Help your patient identify situations where he or she is likely to have difficulty achieving the goal and strategies for avoiding or managing such situations. Ask patients to identify a family member or friend who can help them. Refer patients who have an alcohol use disorder to addiction treatment.

For patients who are not willing to change, discuss the perceived benefits of continued drinking vs reducing or stopping drinking to encourage them to reflect on their alcohol use patterns. Discuss any potential barriers to change. Keep in mind ambivalence and reluctance to change drinking patterns are common and many patients are unaware of the risks of their alcohol use. This discussion may lead patients to contemplate change later.

Arrange. Schedule a follow-up appointment to reinforce the treatment plan with further support, feedback, and assistance in setting, achieving, and maintaining realistic goals. Consider a follow-up phone call 2 weeks after the brief intervention to check on progress and a follow-up appointment in 1 month. Clinical staff may have the opportunity to e-mail or text message patients to check on progress between face-to-face visits. At the follow-up appointment, ask if your patient was able to meet and sustain the drinking goal. If so, support continued adherence, renegotiate drinking goals if indicated, and encourage follow-up with at least annual rescreening. When patients are unable to meet their treatment goals, acknowledge that change is difficult, encourage any positive changes, and address barriers to reaching the goal. Reemphasize your willingness to help, reevaluate the diagnosis, treatment plan, and goals, and schedule close follow-up. Consider engaging significant others in the treatment process.

Table 1

Brief interventions: ‘5As’ to address alcohol use

Table 2

CAGE questionnaire to detect alcohol use disorders

Use in psychiatric practice

Problem drinking may not be adequately addressed in psychiatric settings. In a survey of problem drinkers identified in the general population, only 64% discussed their drinking during a mental health visit and only 40% received counseling about their alcohol use from their mental health provider.³² In a study of 200 psychiatric inpatients, 49% exhibited problem drinking as measured by AUDIT, but only 27% of patients had alcohol use recorded in their medical record.³³ In addition, routine use of screening tools such as CAGE or AUDIT appears to be low in many psychiatric settings even though research has shown that tools such as AUDIT or computerized screening may be effective for identifying problem drinking in psychiatric outpatient settings.^20,21,34

Several small studies support the efficacy of brief interventions for problem drinking in psychiatric settings. A study in a psychiatric emergency service found patients with either schizophrenia/bipolar disorder or depression/anxiety decreased their drinking by about 7 drinks a week over 6 months after a brief intervention.¹⁵ This study was small and the decrease in alcohol intake was not significant within the 2 population groups (P = .10 for schizophrenia/bipolar disorder, n = 34, P = .05 for depression/anxiety, n = 53); however, there was a significant decrease for all patients with follow-up (P = .0096, N = 55).¹⁵ In another study, psychiatric inpatients with problem drinking who received a brief motivational intervention demonstrated a statistically significant reduction in alcohol consumption at 6 months compared with patients who received only an information packet,¹³ but health-related outcomes at 5 years did not differ between the 2 groups.¹⁴ Finally, in a study of 344 nonpsychotic psychiatric outpatients with problem drinking, one-half of those who received a brief telephone intervention reduced their drinking to non-hazardous levels at a 6-month follow-up (intervention 43.8%, control 27.7%).¹²

Related Resources

• National Institute on Alcohol Abuse and Alcoholism. www.niaaa.nih.gov.
• Saunders JB, Aasland OG, Babor TF, et al. Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons with Harmful Alcohol Consumption—II. Addiction. 1993;88(6):791-804.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.