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Computer/typing injuries: Keys to prevention
In a practice that lives on frequent typing and computer use, repetitive strain injuries pose an occupational hazard. These painful injuries can dampen quality of life and disable you or a staff member.
The best way to deal with repetitive strain injuries is to avoid them. Here are some simple precautions.
How repetitive strain injuries happen
Repetitive strain injuries result from repeated physical movements. Symptoms vary, but include tightness, stiffness, soreness, or burning in the hands, wrists, fingers, and/or elbows. Tingling, coldness, or numbness in these joints may also occur. Persons with such injuries might be awoken at night by the pain, or they may lose strength and coordination and become clumsy. Pain after a few seconds of typing may signal a repetitive strain injury, as can moderate wrist pain after typing a lengthy document.
Computer typing and mouse use require repeated movements that strain or damage tendons, nerves, and muscles in the hands, arms, wrists, shoulders, and neck. A touch typist who can type fast without looking at the keyboard is at higher risk of repetitive strain injuries than a slower typist who “hunts and pecks” at keys, because slower typing does not cause as much strain.
Today’s medicolegal climate, however, demands that clinicians keep legible (ie, electronic) records, which means additional typing and clicking for you and your staff.
What is worse, computers often are placed in spots for which they were not designed, making mouse and keyboard work awkward and physically taxing. This is particularly true in older hospitals, where charting areas typically were designed for writing but not typing.
Prevention strategies
Harvard RSI Action, a Harvard University student group dedicated to repetitive strain injury education and prevention, offers the following advice:Text-entry solutions: which ‘type’ is right for you ?” Psyber Psychiatry, February 2003). Do not type if you cannot do so for more than 10 minutes without pain.1
Voice recognition software not only processes text but can also be used for Web browsing, launching applications, sending e-mail, and completing forms. But although this technology has improved dramatically in recent years, it is not yet 100% accurate or integrated into all computer applications used by physicians. Popular voice recognition programs include Scansoft Dragon Naturally Speaking and IBM ViaVoice.
Related resources
Typing Injury Frequently Asked Questions. http://www.tifaq.com
Disclosure
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of CURRENT PSYCHIATRY.
In a practice that lives on frequent typing and computer use, repetitive strain injuries pose an occupational hazard. These painful injuries can dampen quality of life and disable you or a staff member.
The best way to deal with repetitive strain injuries is to avoid them. Here are some simple precautions.
How repetitive strain injuries happen
Repetitive strain injuries result from repeated physical movements. Symptoms vary, but include tightness, stiffness, soreness, or burning in the hands, wrists, fingers, and/or elbows. Tingling, coldness, or numbness in these joints may also occur. Persons with such injuries might be awoken at night by the pain, or they may lose strength and coordination and become clumsy. Pain after a few seconds of typing may signal a repetitive strain injury, as can moderate wrist pain after typing a lengthy document.
Computer typing and mouse use require repeated movements that strain or damage tendons, nerves, and muscles in the hands, arms, wrists, shoulders, and neck. A touch typist who can type fast without looking at the keyboard is at higher risk of repetitive strain injuries than a slower typist who “hunts and pecks” at keys, because slower typing does not cause as much strain.
Today’s medicolegal climate, however, demands that clinicians keep legible (ie, electronic) records, which means additional typing and clicking for you and your staff.
What is worse, computers often are placed in spots for which they were not designed, making mouse and keyboard work awkward and physically taxing. This is particularly true in older hospitals, where charting areas typically were designed for writing but not typing.
Prevention strategies
Harvard RSI Action, a Harvard University student group dedicated to repetitive strain injury education and prevention, offers the following advice:Text-entry solutions: which ‘type’ is right for you ?” Psyber Psychiatry, February 2003). Do not type if you cannot do so for more than 10 minutes without pain.1
Voice recognition software not only processes text but can also be used for Web browsing, launching applications, sending e-mail, and completing forms. But although this technology has improved dramatically in recent years, it is not yet 100% accurate or integrated into all computer applications used by physicians. Popular voice recognition programs include Scansoft Dragon Naturally Speaking and IBM ViaVoice.
Related resources
Typing Injury Frequently Asked Questions. http://www.tifaq.com
Disclosure
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of CURRENT PSYCHIATRY.
In a practice that lives on frequent typing and computer use, repetitive strain injuries pose an occupational hazard. These painful injuries can dampen quality of life and disable you or a staff member.
The best way to deal with repetitive strain injuries is to avoid them. Here are some simple precautions.
How repetitive strain injuries happen
Repetitive strain injuries result from repeated physical movements. Symptoms vary, but include tightness, stiffness, soreness, or burning in the hands, wrists, fingers, and/or elbows. Tingling, coldness, or numbness in these joints may also occur. Persons with such injuries might be awoken at night by the pain, or they may lose strength and coordination and become clumsy. Pain after a few seconds of typing may signal a repetitive strain injury, as can moderate wrist pain after typing a lengthy document.
Computer typing and mouse use require repeated movements that strain or damage tendons, nerves, and muscles in the hands, arms, wrists, shoulders, and neck. A touch typist who can type fast without looking at the keyboard is at higher risk of repetitive strain injuries than a slower typist who “hunts and pecks” at keys, because slower typing does not cause as much strain.
Today’s medicolegal climate, however, demands that clinicians keep legible (ie, electronic) records, which means additional typing and clicking for you and your staff.
What is worse, computers often are placed in spots for which they were not designed, making mouse and keyboard work awkward and physically taxing. This is particularly true in older hospitals, where charting areas typically were designed for writing but not typing.
Prevention strategies
Harvard RSI Action, a Harvard University student group dedicated to repetitive strain injury education and prevention, offers the following advice:Text-entry solutions: which ‘type’ is right for you ?” Psyber Psychiatry, February 2003). Do not type if you cannot do so for more than 10 minutes without pain.1
Voice recognition software not only processes text but can also be used for Web browsing, launching applications, sending e-mail, and completing forms. But although this technology has improved dramatically in recent years, it is not yet 100% accurate or integrated into all computer applications used by physicians. Popular voice recognition programs include Scansoft Dragon Naturally Speaking and IBM ViaVoice.
Related resources
Typing Injury Frequently Asked Questions. http://www.tifaq.com
Disclosure
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of CURRENT PSYCHIATRY.
‘Truth serum’ soothes patients with conversion disorder
Conversion disorders result from stress expressed as a physical symptom. Extreme psychological stress after a death, loss, or trauma can manifest as weakness, paralysis, blindness, deafness, or mutism.
Intravenous amobarbital (Amytal)—so-called “truth serum”—is highly effective for extreme conversion symptoms without psychogenic seizures.1 Clinicians who are not skilled in hypnosis might consider amobarbital after ruling out a neurologic or organic cause.
USING AMOBARBITAL
Amobarbital—100 to 500 mg for adults, 25 to 50 mg for children—is given slowly over 10 to 15 minutes and usually works rapidly. Stop the IV as soon as an effect is noticed or the patient starts feeling drowsy.
Other side effects include disinhibition, which may help the patient overcome his or her stress. Amobarbital is contraindicated during pregnancy and in patients with:
- pulmonary disease, as it may slow respiration
- porphyria, an iron metabolism disorder that can be exacerbated with barbiturate use.2
When interviewing a patient before amobarbital treatment, I focus solely on symptom relief. Follow-up psychotherapy can then help the patient understand what caused the stress.
CASE 1: BLINDING VISION
Mr. A, age 25, was hospitalized after complaining he was “blind.” Neurologic and medical examination and brain CT showed no abnormalities. History revealed that Mr. A had a hemorrhoid and was curious about how it looked. He was startled upon seeing the hemorrhoid, after which he had trouble seeing.
The psychiatrist gave amobarbital, 300 mg IV over 30 minutes. Fifteen minutes into the medication, Mr. A began to see shadows, leaves, then people. After another 15 minutes, his sight was normal. He was discharged that day; psychiatric follow-up was arranged.
CASE 2: ON THE SIDELINES
Joey, age 9, was admitted to the pediatric unit after developing acute paralysis. Neurologic and medical work-ups, including CT, were negative.
When I visited him, Joey told me that he was anxious about going to school. I gave him amobarbital, 25 mg over 15 minutes. Then, because he told me he is a football fan, I had Joey imagine that he was a pro quarterback. Within minutes Joey was jogging up and down the hallway. He was discharged; outpatient psychiatric follow-up was scheduled.
1. Sadock BJ, Sadock VA. Kaplan and Sadock’s synopsis of psychiatry: behavioral sciences/clinical psychiatry (9th ed). Baltimore, MD: Lippincott Williams and Wilkins 2002;649-50.
2. Ibid:1018-9
Dr. Newmark is chief, department of psychiatry, Cooper University Hospital, Camden, NJ, and professor of psychiatry, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Camden.
Conversion disorders result from stress expressed as a physical symptom. Extreme psychological stress after a death, loss, or trauma can manifest as weakness, paralysis, blindness, deafness, or mutism.
Intravenous amobarbital (Amytal)—so-called “truth serum”—is highly effective for extreme conversion symptoms without psychogenic seizures.1 Clinicians who are not skilled in hypnosis might consider amobarbital after ruling out a neurologic or organic cause.
USING AMOBARBITAL
Amobarbital—100 to 500 mg for adults, 25 to 50 mg for children—is given slowly over 10 to 15 minutes and usually works rapidly. Stop the IV as soon as an effect is noticed or the patient starts feeling drowsy.
Other side effects include disinhibition, which may help the patient overcome his or her stress. Amobarbital is contraindicated during pregnancy and in patients with:
- pulmonary disease, as it may slow respiration
- porphyria, an iron metabolism disorder that can be exacerbated with barbiturate use.2
When interviewing a patient before amobarbital treatment, I focus solely on symptom relief. Follow-up psychotherapy can then help the patient understand what caused the stress.
CASE 1: BLINDING VISION
Mr. A, age 25, was hospitalized after complaining he was “blind.” Neurologic and medical examination and brain CT showed no abnormalities. History revealed that Mr. A had a hemorrhoid and was curious about how it looked. He was startled upon seeing the hemorrhoid, after which he had trouble seeing.
The psychiatrist gave amobarbital, 300 mg IV over 30 minutes. Fifteen minutes into the medication, Mr. A began to see shadows, leaves, then people. After another 15 minutes, his sight was normal. He was discharged that day; psychiatric follow-up was arranged.
CASE 2: ON THE SIDELINES
Joey, age 9, was admitted to the pediatric unit after developing acute paralysis. Neurologic and medical work-ups, including CT, were negative.
When I visited him, Joey told me that he was anxious about going to school. I gave him amobarbital, 25 mg over 15 minutes. Then, because he told me he is a football fan, I had Joey imagine that he was a pro quarterback. Within minutes Joey was jogging up and down the hallway. He was discharged; outpatient psychiatric follow-up was scheduled.
Conversion disorders result from stress expressed as a physical symptom. Extreme psychological stress after a death, loss, or trauma can manifest as weakness, paralysis, blindness, deafness, or mutism.
Intravenous amobarbital (Amytal)—so-called “truth serum”—is highly effective for extreme conversion symptoms without psychogenic seizures.1 Clinicians who are not skilled in hypnosis might consider amobarbital after ruling out a neurologic or organic cause.
USING AMOBARBITAL
Amobarbital—100 to 500 mg for adults, 25 to 50 mg for children—is given slowly over 10 to 15 minutes and usually works rapidly. Stop the IV as soon as an effect is noticed or the patient starts feeling drowsy.
Other side effects include disinhibition, which may help the patient overcome his or her stress. Amobarbital is contraindicated during pregnancy and in patients with:
- pulmonary disease, as it may slow respiration
- porphyria, an iron metabolism disorder that can be exacerbated with barbiturate use.2
When interviewing a patient before amobarbital treatment, I focus solely on symptom relief. Follow-up psychotherapy can then help the patient understand what caused the stress.
CASE 1: BLINDING VISION
Mr. A, age 25, was hospitalized after complaining he was “blind.” Neurologic and medical examination and brain CT showed no abnormalities. History revealed that Mr. A had a hemorrhoid and was curious about how it looked. He was startled upon seeing the hemorrhoid, after which he had trouble seeing.
The psychiatrist gave amobarbital, 300 mg IV over 30 minutes. Fifteen minutes into the medication, Mr. A began to see shadows, leaves, then people. After another 15 minutes, his sight was normal. He was discharged that day; psychiatric follow-up was arranged.
CASE 2: ON THE SIDELINES
Joey, age 9, was admitted to the pediatric unit after developing acute paralysis. Neurologic and medical work-ups, including CT, were negative.
When I visited him, Joey told me that he was anxious about going to school. I gave him amobarbital, 25 mg over 15 minutes. Then, because he told me he is a football fan, I had Joey imagine that he was a pro quarterback. Within minutes Joey was jogging up and down the hallway. He was discharged; outpatient psychiatric follow-up was scheduled.
1. Sadock BJ, Sadock VA. Kaplan and Sadock’s synopsis of psychiatry: behavioral sciences/clinical psychiatry (9th ed). Baltimore, MD: Lippincott Williams and Wilkins 2002;649-50.
2. Ibid:1018-9
Dr. Newmark is chief, department of psychiatry, Cooper University Hospital, Camden, NJ, and professor of psychiatry, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Camden.
1. Sadock BJ, Sadock VA. Kaplan and Sadock’s synopsis of psychiatry: behavioral sciences/clinical psychiatry (9th ed). Baltimore, MD: Lippincott Williams and Wilkins 2002;649-50.
2. Ibid:1018-9
Dr. Newmark is chief, department of psychiatry, Cooper University Hospital, Camden, NJ, and professor of psychiatry, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Camden.
Suicidal patient jumps from building after protesting hospital discharge
Hudson County (NJ) superior court
A 44-year-old man with bipolar disorder and a history of suicidal behavior was hospitalized after telling the treating psychiatrist he had suicidal thoughts. Approximately 3 weeks later, the psychiatrist informed the patient he would be discharged.
Despite his objections, the patient was discharged 4 days later with the psychiatrist’s approval. This occurred even though the patient was found to be suicidal when he was evaluated that day by an in-hospital social services agency.
Two days later, the patient jumped from a 4-story building and sustained permanent partial paralysis. Subsequent treatments included spinal rod insertion, laminectomy, skin grafts, and 3 months’ rehabilitation.
The patient sued the psychiatrist for negligence for both the discharge and for inadequate medication management. The suit claimed that the prescribed mood stabilizer was dosed below therapeutic serum levels and that the psychiatrist switched the patient’s adjunctive antidepressant too close to his discharge date to determine its efficacy.
- The case was settled for $1 million.
Inappropriate drug therapy blamed for inducing fatal heart failure
Kings County (CA) superior court
A patient with severe mental illness died of congestive heart failure (CHF), and his three minor children argued that their father’s medications caused his death.
The patient’s surgeon and family practitioner observed that he had a history of acute psychosis and was taking haloperidol. He was also being treated for schizophrenia and bipolar disorder and was living in a group home. The patient was diagnosed with diabetes in 1998.
In 2000, a group home staff member observed ankle swelling and foam around the patient’s mouth. The consulting psychiatrist reduced the mood stabilizer dosage. The family physician subsequently saw the patient for complaints of cough, wheeze, dizziness, and foam on the mouth. Neither physician acknowledged the foam.
The patient was found dead the next day. Autopsy showed that he died of drug intoxication; toxicology studies showed that serum levels of two psychotropic medications were elevated.
The plaintiffs argued that the psychiatrist’s mismanagement of the psychotropics led to the patient’s death, and that the family practitioner failed to test for CHF. The psychiatrist argued that the drug levels were necessary to control the patient’s mental illness. The family practitioner questioned the autopsy conclusion and stated that relevant diagnostic studies were not ordered because the patient’s presentation was atypical for CHF.
- The jury settled in the defense’s favor.
Unattended patient sustains brain injury in attempted suicide
Unnamed county (MN) district court
A patient was hospitalized in the psychiatric unit with a diagnosis of major depressive disorder, suicidal ideation, and a defined suicide plan. The hospital psychiatrist ordered a suicide watch.
Three days after admission, hospital staff allowed the patient to use the psychiatric unit’s exercise equipment. When left unsupervised in the exercise room, the patient attempted suicide by hanging. Staff discovered and resuscitated the patient, but the hanging attempt resulted in severe anoxic brain injury, which caused permanent and total disability.
- The case was settled out of court for $2.75 million.
Bipolar teen attacks mother with knife; family blames misdiagnosis
Tarrant County (TX) district court
A 14-year-old boy was being treated in early 2000 by a psychiatric group for depression and hyperactivity, for which he was prescribed methylphenidate and paroxetine. Later that year, he became agitated and attacked his mother with a knife. He was arrested and charged with assault with a deadly weapon.
The plaintiff sued the psychiatrists for failure to diagnose his bipolar condition and showed that prescribing paroxetine without a mood stabilizer is contraindicated in bipolar patients. The defendants argued that the patient did not have bipolar disorder when the medications were prescribed.
- The jury found no negligence. Claims by the plaintiff’s mother were dismissed.
Hudson County (NJ) superior court
A 44-year-old man with bipolar disorder and a history of suicidal behavior was hospitalized after telling the treating psychiatrist he had suicidal thoughts. Approximately 3 weeks later, the psychiatrist informed the patient he would be discharged.
Despite his objections, the patient was discharged 4 days later with the psychiatrist’s approval. This occurred even though the patient was found to be suicidal when he was evaluated that day by an in-hospital social services agency.
Two days later, the patient jumped from a 4-story building and sustained permanent partial paralysis. Subsequent treatments included spinal rod insertion, laminectomy, skin grafts, and 3 months’ rehabilitation.
The patient sued the psychiatrist for negligence for both the discharge and for inadequate medication management. The suit claimed that the prescribed mood stabilizer was dosed below therapeutic serum levels and that the psychiatrist switched the patient’s adjunctive antidepressant too close to his discharge date to determine its efficacy.
- The case was settled for $1 million.
Inappropriate drug therapy blamed for inducing fatal heart failure
Kings County (CA) superior court
A patient with severe mental illness died of congestive heart failure (CHF), and his three minor children argued that their father’s medications caused his death.
The patient’s surgeon and family practitioner observed that he had a history of acute psychosis and was taking haloperidol. He was also being treated for schizophrenia and bipolar disorder and was living in a group home. The patient was diagnosed with diabetes in 1998.
In 2000, a group home staff member observed ankle swelling and foam around the patient’s mouth. The consulting psychiatrist reduced the mood stabilizer dosage. The family physician subsequently saw the patient for complaints of cough, wheeze, dizziness, and foam on the mouth. Neither physician acknowledged the foam.
The patient was found dead the next day. Autopsy showed that he died of drug intoxication; toxicology studies showed that serum levels of two psychotropic medications were elevated.
The plaintiffs argued that the psychiatrist’s mismanagement of the psychotropics led to the patient’s death, and that the family practitioner failed to test for CHF. The psychiatrist argued that the drug levels were necessary to control the patient’s mental illness. The family practitioner questioned the autopsy conclusion and stated that relevant diagnostic studies were not ordered because the patient’s presentation was atypical for CHF.
- The jury settled in the defense’s favor.
Unattended patient sustains brain injury in attempted suicide
Unnamed county (MN) district court
A patient was hospitalized in the psychiatric unit with a diagnosis of major depressive disorder, suicidal ideation, and a defined suicide plan. The hospital psychiatrist ordered a suicide watch.
Three days after admission, hospital staff allowed the patient to use the psychiatric unit’s exercise equipment. When left unsupervised in the exercise room, the patient attempted suicide by hanging. Staff discovered and resuscitated the patient, but the hanging attempt resulted in severe anoxic brain injury, which caused permanent and total disability.
- The case was settled out of court for $2.75 million.
Bipolar teen attacks mother with knife; family blames misdiagnosis
Tarrant County (TX) district court
A 14-year-old boy was being treated in early 2000 by a psychiatric group for depression and hyperactivity, for which he was prescribed methylphenidate and paroxetine. Later that year, he became agitated and attacked his mother with a knife. He was arrested and charged with assault with a deadly weapon.
The plaintiff sued the psychiatrists for failure to diagnose his bipolar condition and showed that prescribing paroxetine without a mood stabilizer is contraindicated in bipolar patients. The defendants argued that the patient did not have bipolar disorder when the medications were prescribed.
- The jury found no negligence. Claims by the plaintiff’s mother were dismissed.
Hudson County (NJ) superior court
A 44-year-old man with bipolar disorder and a history of suicidal behavior was hospitalized after telling the treating psychiatrist he had suicidal thoughts. Approximately 3 weeks later, the psychiatrist informed the patient he would be discharged.
Despite his objections, the patient was discharged 4 days later with the psychiatrist’s approval. This occurred even though the patient was found to be suicidal when he was evaluated that day by an in-hospital social services agency.
Two days later, the patient jumped from a 4-story building and sustained permanent partial paralysis. Subsequent treatments included spinal rod insertion, laminectomy, skin grafts, and 3 months’ rehabilitation.
The patient sued the psychiatrist for negligence for both the discharge and for inadequate medication management. The suit claimed that the prescribed mood stabilizer was dosed below therapeutic serum levels and that the psychiatrist switched the patient’s adjunctive antidepressant too close to his discharge date to determine its efficacy.
- The case was settled for $1 million.
Inappropriate drug therapy blamed for inducing fatal heart failure
Kings County (CA) superior court
A patient with severe mental illness died of congestive heart failure (CHF), and his three minor children argued that their father’s medications caused his death.
The patient’s surgeon and family practitioner observed that he had a history of acute psychosis and was taking haloperidol. He was also being treated for schizophrenia and bipolar disorder and was living in a group home. The patient was diagnosed with diabetes in 1998.
In 2000, a group home staff member observed ankle swelling and foam around the patient’s mouth. The consulting psychiatrist reduced the mood stabilizer dosage. The family physician subsequently saw the patient for complaints of cough, wheeze, dizziness, and foam on the mouth. Neither physician acknowledged the foam.
The patient was found dead the next day. Autopsy showed that he died of drug intoxication; toxicology studies showed that serum levels of two psychotropic medications were elevated.
The plaintiffs argued that the psychiatrist’s mismanagement of the psychotropics led to the patient’s death, and that the family practitioner failed to test for CHF. The psychiatrist argued that the drug levels were necessary to control the patient’s mental illness. The family practitioner questioned the autopsy conclusion and stated that relevant diagnostic studies were not ordered because the patient’s presentation was atypical for CHF.
- The jury settled in the defense’s favor.
Unattended patient sustains brain injury in attempted suicide
Unnamed county (MN) district court
A patient was hospitalized in the psychiatric unit with a diagnosis of major depressive disorder, suicidal ideation, and a defined suicide plan. The hospital psychiatrist ordered a suicide watch.
Three days after admission, hospital staff allowed the patient to use the psychiatric unit’s exercise equipment. When left unsupervised in the exercise room, the patient attempted suicide by hanging. Staff discovered and resuscitated the patient, but the hanging attempt resulted in severe anoxic brain injury, which caused permanent and total disability.
- The case was settled out of court for $2.75 million.
Bipolar teen attacks mother with knife; family blames misdiagnosis
Tarrant County (TX) district court
A 14-year-old boy was being treated in early 2000 by a psychiatric group for depression and hyperactivity, for which he was prescribed methylphenidate and paroxetine. Later that year, he became agitated and attacked his mother with a knife. He was arrested and charged with assault with a deadly weapon.
The plaintiff sued the psychiatrists for failure to diagnose his bipolar condition and showed that prescribing paroxetine without a mood stabilizer is contraindicated in bipolar patients. The defendants argued that the patient did not have bipolar disorder when the medications were prescribed.
- The jury found no negligence. Claims by the plaintiff’s mother were dismissed.
Malpractice: Why do we worry so much?
Psychiatrists seem to worry more than other physicians about malpractice claims, even though other specialists face greater numbers of claims and more-astronomical awards. One source of our anxiety is psychiatry’s difficulty in defining “standard of care.”
Twenty years ago, patients with identical symptoms could receive very different treatments, depending on the treating psychiatrists’ philosophies. Our standard of care is better-defined today, but we still may offer a suicidally depressed patient a broader range of treatments than other specialists offer patients with life-threatening illnesses.
We also worry because of the greater “creativity” personal injury lawyers can use in making claims against us, compared with other specialties. For example, most claims against a diagnostic radiologist are limited to failure to diagnose something. Psychiatrists can be subject to claims for not only failing to diagnose or treat mental disorders but also for failing to restrain patients who harm themselves or to protect people we have never met from harm our patients may cause.
To address these concerns, we obtained permission to abstract malpractice cases of interest to psychiatrists from the newsletter Medical Malpractice Verdicts, Settlements & Experts, published by attorney Lewis L. Laska of Nashville, TN. “Malpractice Verdicts”—featuring brief summaries of selected court decisions—debuts this month.
This new column is designed to help CURRENTPSYCHIATRY readers keep up with case law affecting our specialty and the torts of which we might be accused. Then, at least, we might be able to protect ourselves better and worry a little less.
Psychiatrists seem to worry more than other physicians about malpractice claims, even though other specialists face greater numbers of claims and more-astronomical awards. One source of our anxiety is psychiatry’s difficulty in defining “standard of care.”
Twenty years ago, patients with identical symptoms could receive very different treatments, depending on the treating psychiatrists’ philosophies. Our standard of care is better-defined today, but we still may offer a suicidally depressed patient a broader range of treatments than other specialists offer patients with life-threatening illnesses.
We also worry because of the greater “creativity” personal injury lawyers can use in making claims against us, compared with other specialties. For example, most claims against a diagnostic radiologist are limited to failure to diagnose something. Psychiatrists can be subject to claims for not only failing to diagnose or treat mental disorders but also for failing to restrain patients who harm themselves or to protect people we have never met from harm our patients may cause.
To address these concerns, we obtained permission to abstract malpractice cases of interest to psychiatrists from the newsletter Medical Malpractice Verdicts, Settlements & Experts, published by attorney Lewis L. Laska of Nashville, TN. “Malpractice Verdicts”—featuring brief summaries of selected court decisions—debuts this month.
This new column is designed to help CURRENTPSYCHIATRY readers keep up with case law affecting our specialty and the torts of which we might be accused. Then, at least, we might be able to protect ourselves better and worry a little less.
Psychiatrists seem to worry more than other physicians about malpractice claims, even though other specialists face greater numbers of claims and more-astronomical awards. One source of our anxiety is psychiatry’s difficulty in defining “standard of care.”
Twenty years ago, patients with identical symptoms could receive very different treatments, depending on the treating psychiatrists’ philosophies. Our standard of care is better-defined today, but we still may offer a suicidally depressed patient a broader range of treatments than other specialists offer patients with life-threatening illnesses.
We also worry because of the greater “creativity” personal injury lawyers can use in making claims against us, compared with other specialties. For example, most claims against a diagnostic radiologist are limited to failure to diagnose something. Psychiatrists can be subject to claims for not only failing to diagnose or treat mental disorders but also for failing to restrain patients who harm themselves or to protect people we have never met from harm our patients may cause.
To address these concerns, we obtained permission to abstract malpractice cases of interest to psychiatrists from the newsletter Medical Malpractice Verdicts, Settlements & Experts, published by attorney Lewis L. Laska of Nashville, TN. “Malpractice Verdicts”—featuring brief summaries of selected court decisions—debuts this month.
This new column is designed to help CURRENTPSYCHIATRY readers keep up with case law affecting our specialty and the torts of which we might be accused. Then, at least, we might be able to protect ourselves better and worry a little less.
Using psychotropics safely in patients with HIV/AIDS: Watch for drug-drug interactions with antiretrovirals
Psychiatric patients—especially those with substance abuse disorders—are at high risk for HIV infection, which puts psychiatrists on the AIDS pandemic’s front lines.
In the wake of last month’s International AIDS Conference in Thailand, this article supplements American Psychiatric Association guidelines for managing patients with HIV/AIDS.1 Here is updated information on:
- who is at greatest risk for HIV infection today
- neuropsychiatric side effects of HIV medications
- in-office assessment of HIV-associated cognitive changes
- how to avoid psychotropic/antiretroviral interactions.
HIV and psychiatric patients
Psychiatric patients are among those at highest risk for HIV (Box).2-4 Cournos and McKinnon5 found that HIV seroprevalence among persons with severe mental illness was 4% to 23%compared with 0.4% in the general population.6 They defined severe mental illness as schizophrenia, schizoaffective disorder, major depression, or bipolar disorder accompanied by significant functional impairment, disruption of normal life tasks, periods of hospitalization, and need for psychotropics.
Infection rates varied with HIV geographic concentration, presence of comorbid substance use disorders, age, and ethnicity, but not psychiatric diagnosis. Unsafe sex and drug use (including noninjection) were associated with infection, and women were as likely to be infected as men.
Side effects and interactions
‘Triple therapy.’ Combining three antiretroviral agents—highly-active antiretroviral therapy (HAART) or “triple therapy”—is standard treatment for HIV infection in the United States. Initially, HAART was recommended for all patients with early-stage HIV, even if asymptomatic. This changed as antiretrovirals’ side effects—such as peripheral neuropathy with didanosine— and drug resistance from suboptimal adherence became apparent. Viral resistance develops if patients are <95% adherent to antiretroviral regimens.7
Antiretroviral therapy is usually started when:
- CD4 lymphocyte count is <200 cells/mm3 or abruptly decreasing
- plasma viral load is >55,000 copies/mL or abruptly increasing
- symptomatic AIDS emerges.
Psychiatric side effects. Psychiatric symptoms—such as depression, anxiety, confusion, psychosis, hallucinations, insomnia, and mania—are common side effects of antiretrovirals and other drugs used to treat HIV and its opportunistic infections and cancers (Table 1).8 Two antiretrovirals are of particular interest to psychiatrists:
Efavirenz is a non-nucleoside reverse transcriptase inhibitor that causes vivid dreams, especially when initiated.
AIDS death rates have declined in the United States since antiretroviral therapies were introduced in 1996, but the rate of new HIV infection has not changed.2 An estimated 850,000 to 950,000 Americans have HIV, and 25% do not know it.3
Changing demographics. Some 40,000 new HIV infections occur in the United States each year (70% among men), and one-half of the newly-infected are under age 25. African Americans and Hispanics represent 51% of total AIDS cases in men and 77% in women. From 1998 to 2002—the most recent data available from the Centers for Disease Control and Prevention (CDC)—AIDS incidence steadily decreased among whites and Hispanics but increased among blacks, Asian/Pacific Islanders, and American Indian/Alaska Natives.
Transmission routes. Approximately 60% of men with HIV are infected through male-to-male sex, 25% through IV drug use, and 15% through heterosexual sex. Unprotected anal sex appears to be occurring more frequently in some urban centers, particularly among young men who have sex with men.4 Approximately 75% of women with HIV are infected through heterosexual sex and 25% through IV drug use.
Ritonavir is a protease inhibitor that may inhibit psychotropics metabolized by cytochrome P450 3A4 and 2D6 isoenzymes.
Other HIV medications increase or decrease psychotropic blood levels via inhibition or induction of CYP isoenzymes (Table 2).9 When a patient is taking ritonavir or another protease inhibitor, reduced starting dosages of selective serotonin reuptake inhibitors (SSRIs) may be appropriate. Benzodiazepine dosages may need to be increased because of ritonavir induction of the enzyme glucuronosyltransferase.
Table 1
Psychiatric side effects of common HIV medications
| Drug | Side effects, by frequency |
|---|---|
| Acyclovir | Unknown: hallucination, confusion, thought insertion, insomnia |
| Amphotericin B | >5%: confusion, insomnia, somnolence; 1-5%: agitation, anxiety, depression, hallucination, nervousness, psychosis; Unkown: delirium |
| β-Lactam antibiotics | <1%: insomnia, somnolence, anxiety, nervousness, impaired concentration, confusion, nightmares, hallucination; Unkown: paranoia, mania |
| Trimethoprim/sulfamethoxazole | Unknown: hallucinations, depression, apathy, nervousness |
| Cycloserine Unknown: | psychosis, somnolence, depression, confusion, irritability, anxiety |
| Didanosine | Unknown: nervousness, anxiety, confusion, seizures, insomnia |
| Efavirenz | 13-16%: depression; 8-11%: anxiety; 2-6%: nervousness; >5%: headache, seizures, confusion; <2%: suicidal ideation and behavior, aggression |
| Unknown: | agitation, lability, neurosis, psychosis, insomnia, impaired concentration, somnolence, euphoria, amnesia, hallucination |
| Foscarnet | >5%: depression, confusion, anxiety; 1-5%: insomnia, somnolence, amnesia, nervousness, agitation, aggression, hallucination |
| Interferon-a | 6-19%: depression; 12-16%: irritability; 6-12%: insomnia; 3-8%: impaired concentration; >5%: anxiety: <5%: confusion, mania, aggression, delirium, lability, suicidal ideation, psychosis, personality disorder, alcohol intolerance |
| Isoniazid | Unknown: depression, agitation, hallucination, paranoia, anxiety, psychosis |
| Lamivudine | <11%: insomnia; <9%: mania, depressive disorders, dreams |
| Methotrexate | Unknown: cognitive and mood changes |
| Pentamidine | Unknown: confusion, lability, hallucination; Rare: anxiety, fatigue |
| Procarbazine | Unknown: hallucination, depression, nervousness, apprehension, mania, loss of appetite, insomnia, nightmares, confusion, malaise |
| Quinolones | <1%: somnolence, insomnia; Occasional: agitation, anxiety, depression, panic attacks, confusion, hallucination, aggression, psychosis, paranoia; |
| Rare: | suicidal ideation and suicide (no relationship with drug confirmed) |
| Stavudine | Unknown: confusion, depression, seizures, anxiety, mania, sleep problems |
| Sulfonamides | Unknown: psychosis, delirium, confusion, depression, hallucinations |
| Thiabendazole | Unknown: hallucination, fatigue, irritability, confusion, depression |
| Vinblastine | Unknown: depression |
| Vincristine | Unknown: hallucination |
| Zalcitabine | Unknown: acute psychosis, agitation, amnesia, anxiety, lability, euphoria, hallucination, insomnia, mania, paranoia, suicidal behavior, confusion, impaired concentration, somnolence, depression |
| Zidovudine | Unknown: Insomnia, vivid dreams, agitation, mania, hallucination, confusion |
Table 2
Psychotropic/HIV drug interactions, by cytochrome P-450 isoenzyme
| CYP 3A4 | CYP 2D6 | |
|---|---|---|
| Psychotropics primarily metabolized by isoenzyme | Benzodiazepines Buspirone Carbamazepine Citalopram Clomipramine Imipramine Trazodone | Fluoxetine Fluvoxamine Mirtazapine Antipsychotics (typical and atypical) Paroxetine Sertraline Tricyclics Venlafaxine |
| HIV drugs that inhibit isoenzyme | Protease inhibitors (esp. ritonavir and indinavir) Clarithromycin Erythromycin Itraconazole Ketoconazole Macrolide antibiotics | Protease inhibitors (esp. ritonavir and nelfinavir) |
| Possible clinical effect | Increased plasma levels and increased side effects; for benzodiazepines, sedation and decreased respiratory drive | Increased plasma levels and increased side effects; for tricyclics, increased risk for cardiac conduction delay |
| HIV drugs that induce isoenzyme | Nevirapine Efavirenz Glucocorticoids Rifampin Rifabutin | None |
| Possible clinical effect | Decreased psychotropic plasma levels, decreased effectiveness | None |
| Source: Adapted and reprinted with permission from reference 1, Table 16. Copyright 2000. American Psychiatric Association | ||
The FDA approved enfuvirtide—the first of the new fusion inhibitor class of antiretroviral agents—in March 2003. Enfuvirtide prevents HIV from entering the target CD4 lymphocyte in patients who show continued viral replication despite ongoing antiretroviral therapy. This agent requires twice-daily subcutaneous injections. Because enfuvirtide can be viewed as a medication of last resort, nonresponse may be especially disheartening to an AIDS patient.
Substances of abuse also interact with HIV medications. A lethal overdose of the street drug MDMA (“Ecstasy”) has been reported in a patient treated with ritonavir.10 MDMA is metabolized primarily via CYP 2D6. Other substances of abuse metabolized by CYP 2D6 or 3A4—such as amphetamines, ketamine, heroin, cocaine, and gamma-hydroxybutyrate—may cause toxic reactions in patients being treated with protease inhibitors.
Because substance abuse is a common comorbidity of HIV infection, warn patients that using recreational drugs with antiretroviral medications can cause adverse reactions. Extensive drug interaction lists are available on patient education and physician Web sites (see Related Resources).
Table 3
Diagnostic criteria for HIV-associated minor cognitive motor disorder
Probable diagnosis (must meet all four criteria)
A possible diagnosis of minor cognitive motor disorder can be given if criteria 1-3 are present and either:
|
| Source: Reprinted with permission from reference 14 |
Lipid and hyperglycemic side effects. Antivirals— especially protease inhibitors —appear to be associated with HIV lipodystrophy, which is associated with cosmetic and serum lipid changes as well as hyperglycemia.11 Facial wasting, buffalo humps, and central intra-abdominal obesity may occur, and elevated serum cholesterol and triglycerides often require treatment with cholesterollowering “statin” drugs.
Though it is unclear whether HIV lipodystrophy increases cardiovascular disease risk, carefully consider the potential effects of psychotropics associated with weight gain, hyper-glycemia, and elevated lipids in patients receiving antiretroviral therapy.
Hepatitis. Patients at risk for HIV infection are also at risk for viral hepatitis. One-quarter of persons with HIV are coinfected with hepatitis C, primarily through IV drug use.12 Alpha-interferon treatment of hepatitis B and C has been associated with depression. SSRI treatment—such as paroxetine, 20 mg/d—can ease depressive symptoms.13
HIV-associated cognitive changes
Minor cognitive-motor disorder(Table 3) and HIV-associated dementia (Table 4) 14 are typically seen in late-stage HIV infections and are diagnoses of exclusion. Physical or neurologic examination in a patient with HIV/AIDS and altered mental status may show:
- focal deficits indicating a space-occupying lesion (eg, CNS lymphoma or toxoplasmosis)
- sensory changes that may indicate peripheral neuropathy
- ataxia or gait changes that may indicate myelopathy.
Useful neuropsychological tests include the HIV Dementia Rating Scale,15 Halstead finger-tapping test for motor speed,16 and the Trailmaking Test, which assesses psychomotor speed and sequencing ability.17
Antiretroviral therapy appears to reduce the risk of HIV-associated dementia. In a trial conducted at 42 AIDS Clinical Trials Group sites and 7 National Hemophilia Foundation sites, combination reverse transcriptase inhibitors helped preserve or improve neurologic function.18
Psychostimulants appear to improve HIV-induced brain impairment.19 Immune modulators—such as tumor necrosis factor-alpha blockers (eg, pentoxifylline)20 and interleukin-1 receptor blockers21 —have also been studied for possible beneficial effects on HIV brain disease.
HIV prevention
Because unprotected sex and IV substance use are the primary HIV transmission routes in the United States, assessing psychiatric patients’ sexual and substance use behaviors may help you prevent HIV infection. The CDC offers guidelines for HIV testing, counseling, and referral (see Related Resources).
To identify persons at risk for HIV infection, the CDC recommends asking open-ended questions about risk behaviors, such as: “What are you doing now or what have you done in the past that you think may put you at risk for HIV infection?”22
The shift of new HIV infection disproportionately into African-American and Hispanic populations suggests the need for more-intensive prevention and education in those communities. CDC guidelines emphasize the importance of using culturally sensitive language when asking about risk behavior. Some individuals may engage in same-sex behaviors but do not identify themselves as “homosexual” or “gay.” In some African-American communities, for example, being “on the down low” is used to describe men—oftentimes married—who have sex with men.
To incorporate HIV-prevention messages and brief behavioral interventions into clinical visits:
- speak with patients about sexual and drug use behaviors in simple, everyday language
- learn about interventions shown to be effective
- become familiar with community resources that address HIV risk reduction.23
Training. The CDC and Health Resources and Services Administration of the U.S. Department of Health and Human Services offer free training on risk screening and prevention, as well as opportunities for continuing medical education (see Related Resources).
Table 4
Diagnostic criteria for HIV-associated dementia
|
| Source: Reprinted with permission from reference 14 |
Advances in antibody testing
Psychiatrists play an important supportive role in encouraging HIV screening of at-risk patients of unknown serostatus and in counseling such patients before, during, and after test results are known.
Rapid lab tests. In 2002, the FDA approved a rapid, highly accurate HIV-1 screening test for serum specimens and in March 2004 approved the same test for screening oral fluid specimens. Test results with serum or an oral swab are available from a laboratory in approximately 20 minutes. In clinical studies submitted to the FDA, the OraQuick oral fluid test correctly identified 99.3% of persons infected with HIV-1 (sensitivity) and 99.9% of those not infected (specificity).
CDC guidelines for HIV counseling and testing have been revised to include rapid testing. Screening tests are most accurate at least 3 months after an HIV exposure—the time required for antibodies to develop. When counseling patients after a reactive test result, emphasize that the result is preliminary and further testing is needed to confirm the result. Counsel patients who have a negative result within 3 months of possible infection to be retested to guard against a possible false-negative result.
Home test kits. An FDA-approved consumer-controlled test kit—Home Access HIV-1 Test System24 —is sold at drug stores without a prescription. The customer pricks a finger with a special device, places drops of blood on a specially treated card, and mails the card to a licensed laboratory. Anonymous identification numbers are used when phoning for the results.
Customers may speak to a counselor before taking the test, while awaiting results, and when results are given. All individuals with a reactive test result are referred for a more-specific test and receive information and resources on treatment and support services.
Counseling the HIV patient
The psychological impact of positive HIV antibody test results on psychiatric patients has not been studied. Persons without psychiatric disorders commonly experience anxiety and depression immediately after learning of a positive result. Unless the patient has HIV-related physical symptoms, these psychological sequelae often return to baseline—similar to when the blood sample was drawn—within 2 weeks.25
Patients need to know that a positive HIV test result is no longer associated with death within 2 to 3 years. During a 2-year period, for example, disease progression from HIV infection to AIDS decreased 7-fold among patients who started antiretroviral therapy with a CD4+ T-cell count >350 cells/mm3, compared with others who were monitored without therapy.26 This may be especially important to reinforce with newly-diagnosed patients unfamiliar with advances in HAART.
Medication adherence. To increase patients’ adherence to antiretroviral therapy:
- express interest that they are taking their medications
- use psychotherapy to help them solve problems that interfere with adherence.
Suicide risk. In the 1980s, significantly increased suicide rates were reported among HIV-infected persons. For example, the suicide rate in 1985 for New York City men ages 20 to 59 living with an AIDS diagnosis was 36 times higher than that of similar men without AIDS.27 A later study of HIV infection in New York male suicide victims from 1991 to 1993 suggested that HIV serostatus was associated with a modest increase—at most—in suicide risk. That study considered the interplay of other suicide risk factors, such as substance abuse.28
- Guidelines for HIV counseling, testing, and referral. Centers for Disease Control and Prevention. www.cdc.gov/mmwr/preview/mmwrhtml/rr5019a1.htm
- Training in HIV prevention and counseling. National Network of STD/HIV Prevention Training Centers (http://depts.washington.edu/nnptc) and AIDS Education and Training Centers National Resource Center (http://www.aids-ed.org)
- Rapid HIV testing. Centers for Disease Control and Prevention. http://www.cdc.gov/hiv/rapid_testing/
- Cytochrome P450 drug interaction table. Indiana University School of Medicine. Division of Clinical Pharmacology. www.drug-interactions.com
Drug brand names
- Buspirone • BuSpar
- Carbamazepine • Carbatrol
- Citalopram • Celexa
- Clomipramine • Anafranil
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Imipramine • Tofranil
- Mirtazapine • Remeron
- Paroxetine • Paxil
- Sertraline • Zoloft
- Trazodone • Desyrel
- Venlafaxine • Effexor
Disclosure
Dr. Liang reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products
1. American Psychiatric Association. Practice guideline for the treatment of patients with HIV/AIDS. Am J Psychiatry. 2000 157 11(suppl). Also available at: www.psych.org/psych_pract/treatg/pg/hivaids_revisebook_index.cfm
2. Centers for Disease Control and Prevention National Center for HIV, STD, and TB Prevention. HIV AIDS Surveill Rep December 2001. Available at: http://www.cdc.gov/hiv/stats/hasr1302.htm
3. Centers for Disease Control and Prevention. HIV AIDS Surveill Rep 2002;14:148. Also available at: http://www.cdc.gov/hiv/stats/hasr1402/2002SurveillanceReport.pdf
4. Risk reduction: sex without condoms. HIV Counselor Perspectives [newsletter] 2001;10(2, March).
5. Cournos F, McKinnon K. HIV seroprevalence among people with severe mental illness in the United States: a critical review. Clin Psychol Rev 1997;17:259-69.
6. Steele FR. A moving target: CDC still trying to estimate HIV-1 prevalence. J NIH Res 1994;6:25-6.
7. Paterson DL, Swindells S, Mohr J, et al. Adherence to protease inhibitor therapy and outcomes in patients with HIV infection. Ann Intern Med 2000;133:21-30.
8. Grant I, Atkinson JH, Jr. Neuropsychiatric aspects of HIV infection and AIDS. In: Sadock BJ, Sadock VA (eds). Kaplan and Sadock’s comprehensive textbook of psychiatry. Philadelphia: Lippincott Williams & Wilkins, 1999;308-36.
9. Ayuso JL. Use of psychotropic drugs in patients with HIV infection. Drugs 1994;47:599-610.
10. Mirken B. Danger: possibly fatal interactions between ritonavir and “ecstasy,” some other psychoactive drugs. AIDS Treat News 1997;Feb 21(No 265):5.-
11. Miller KD, Jones E, Yanovski JA, et al. Visceral abdominal-fat accumulation associated with use of indinavir. Lancet 1998;351(9106):871-5.
12. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR 1998;47(No. RR-19):1-39.
13. Kraus MR, Schafer A, Faller H, et al. Paroxetine for the treatment of interferon-alpha-induced depression in chronic hepatitis C. Aliment Pharmacol Ther 2002;16(6):1091-9.
14. Nomenclature and research case definitions for neurologic manifestations of human immunodeficiency virus-type 1 (HIV-1) infection: report of a working group of the American Academy of Neurology AIDS Task Force. Neurology 1991;41:778-85.
15. Power C, Selnes OA, Grim JA, McArthur JC. HIV Dementia Scale: a rapid screening test. J Acquir Immune Defic Syndr Hum Retrovirol 1995 Mar 1;8(3):273-8.
16. Silberstein CH, McKegney FP, O'Dowd MA, et al. A prospective longitudinal study of neuropsychological and psychosocial factors in asymptomatic individuals at risk for HTLV-III/LAV infection in a methadone program: preliminary findings. Int J Neurosci 1987;32(3-4):669-76.
17. Reitan RM. Validity of the trail making test as an indicator of organic brain damage. Percept Mot Skills 1958;8:271-6.
18. Price RW, Yiannoutsos CT, Clifford DB, et al. Neurological outcomes in late HIV infection: adverse impact of neurological impairment on survival and protective effect of antiviral therapy. AIDS Clinical Trial Group and Neurological AIDS Research Consortium study team. AIDS 1999;13(13):1677-85.
19. Perry SW. Organic mental disorders caused by HIV: update on early diagnosis and treatment. Am J Psychiatry 1990;147(6):696-710.
20. Wilt SG, Milward E, Zhou JM, et al. In vitro evidence for a dual role of tumor necrosis factor-alpha in human immunodeficiency virus type 1 encephalopathy. Ann Neurol 1995;37(3):381-94.
21. Boven LA, Gomes L, Hery C, et al. Increased peroxynitrite activity in AIDS dementia complex: implications for the neuropathogenesis of HIV-1 infection. J Immunol 1999;162(7):4319-27.
22. Centers for Disease Control and Prevention. Revised guidelines for HIV counseling, testing, and referral. MMWR Nov. 9, 2001;50(RR19):1-58.
23. Centers for Disease Control and Prevention. Incorporating HIV prevention into the medical care of persons living with HIV. MMWR July 18, 2003;52(RR12):1-24. Also available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5212a1.htm
24. Food and Drug Administration. Home Access HIV-1 Test System: Summary of safety and effectiveness. Available at: http://www.fda.gov/cber/PMAsumm/P950002S.pdf
25. Perry SW, Jacobsberg LB, Fishman B. Psychological responses to serological testing for HIV. AIDS 1990;4(2):145-52.
26. Opravil M, Ledergerber B, Furrer H. et al and the Swiss HIV Cohort Study Clinical benefit of early initiation of HAART in patients with asymptomatic HIV and CD4 counts >350/mm 3 . Abstract LB-6. Chicago, IL: 8th Conference on Retroviruses and Opportunistic Infections, 2001.
27. Marzuk P, Tierney H, Tardiff K, et al. Increased risk of suicide in persons with AIDS. JAMA 1988;259:1333-7.
28. Marzuk PM, Tardiff K, Leon AC, et al. HIV seroprevalence among suicide victims in New York City, 1991-93. Am J Psychiatry 1997;154(6):1720-5.
Psychiatric patients—especially those with substance abuse disorders—are at high risk for HIV infection, which puts psychiatrists on the AIDS pandemic’s front lines.
In the wake of last month’s International AIDS Conference in Thailand, this article supplements American Psychiatric Association guidelines for managing patients with HIV/AIDS.1 Here is updated information on:
- who is at greatest risk for HIV infection today
- neuropsychiatric side effects of HIV medications
- in-office assessment of HIV-associated cognitive changes
- how to avoid psychotropic/antiretroviral interactions.
HIV and psychiatric patients
Psychiatric patients are among those at highest risk for HIV (Box).2-4 Cournos and McKinnon5 found that HIV seroprevalence among persons with severe mental illness was 4% to 23%compared with 0.4% in the general population.6 They defined severe mental illness as schizophrenia, schizoaffective disorder, major depression, or bipolar disorder accompanied by significant functional impairment, disruption of normal life tasks, periods of hospitalization, and need for psychotropics.
Infection rates varied with HIV geographic concentration, presence of comorbid substance use disorders, age, and ethnicity, but not psychiatric diagnosis. Unsafe sex and drug use (including noninjection) were associated with infection, and women were as likely to be infected as men.
Side effects and interactions
‘Triple therapy.’ Combining three antiretroviral agents—highly-active antiretroviral therapy (HAART) or “triple therapy”—is standard treatment for HIV infection in the United States. Initially, HAART was recommended for all patients with early-stage HIV, even if asymptomatic. This changed as antiretrovirals’ side effects—such as peripheral neuropathy with didanosine— and drug resistance from suboptimal adherence became apparent. Viral resistance develops if patients are <95% adherent to antiretroviral regimens.7
Antiretroviral therapy is usually started when:
- CD4 lymphocyte count is <200 cells/mm3 or abruptly decreasing
- plasma viral load is >55,000 copies/mL or abruptly increasing
- symptomatic AIDS emerges.
Psychiatric side effects. Psychiatric symptoms—such as depression, anxiety, confusion, psychosis, hallucinations, insomnia, and mania—are common side effects of antiretrovirals and other drugs used to treat HIV and its opportunistic infections and cancers (Table 1).8 Two antiretrovirals are of particular interest to psychiatrists:
Efavirenz is a non-nucleoside reverse transcriptase inhibitor that causes vivid dreams, especially when initiated.
AIDS death rates have declined in the United States since antiretroviral therapies were introduced in 1996, but the rate of new HIV infection has not changed.2 An estimated 850,000 to 950,000 Americans have HIV, and 25% do not know it.3
Changing demographics. Some 40,000 new HIV infections occur in the United States each year (70% among men), and one-half of the newly-infected are under age 25. African Americans and Hispanics represent 51% of total AIDS cases in men and 77% in women. From 1998 to 2002—the most recent data available from the Centers for Disease Control and Prevention (CDC)—AIDS incidence steadily decreased among whites and Hispanics but increased among blacks, Asian/Pacific Islanders, and American Indian/Alaska Natives.
Transmission routes. Approximately 60% of men with HIV are infected through male-to-male sex, 25% through IV drug use, and 15% through heterosexual sex. Unprotected anal sex appears to be occurring more frequently in some urban centers, particularly among young men who have sex with men.4 Approximately 75% of women with HIV are infected through heterosexual sex and 25% through IV drug use.
Ritonavir is a protease inhibitor that may inhibit psychotropics metabolized by cytochrome P450 3A4 and 2D6 isoenzymes.
Other HIV medications increase or decrease psychotropic blood levels via inhibition or induction of CYP isoenzymes (Table 2).9 When a patient is taking ritonavir or another protease inhibitor, reduced starting dosages of selective serotonin reuptake inhibitors (SSRIs) may be appropriate. Benzodiazepine dosages may need to be increased because of ritonavir induction of the enzyme glucuronosyltransferase.
Table 1
Psychiatric side effects of common HIV medications
| Drug | Side effects, by frequency |
|---|---|
| Acyclovir | Unknown: hallucination, confusion, thought insertion, insomnia |
| Amphotericin B | >5%: confusion, insomnia, somnolence; 1-5%: agitation, anxiety, depression, hallucination, nervousness, psychosis; Unkown: delirium |
| β-Lactam antibiotics | <1%: insomnia, somnolence, anxiety, nervousness, impaired concentration, confusion, nightmares, hallucination; Unkown: paranoia, mania |
| Trimethoprim/sulfamethoxazole | Unknown: hallucinations, depression, apathy, nervousness |
| Cycloserine Unknown: | psychosis, somnolence, depression, confusion, irritability, anxiety |
| Didanosine | Unknown: nervousness, anxiety, confusion, seizures, insomnia |
| Efavirenz | 13-16%: depression; 8-11%: anxiety; 2-6%: nervousness; >5%: headache, seizures, confusion; <2%: suicidal ideation and behavior, aggression |
| Unknown: | agitation, lability, neurosis, psychosis, insomnia, impaired concentration, somnolence, euphoria, amnesia, hallucination |
| Foscarnet | >5%: depression, confusion, anxiety; 1-5%: insomnia, somnolence, amnesia, nervousness, agitation, aggression, hallucination |
| Interferon-a | 6-19%: depression; 12-16%: irritability; 6-12%: insomnia; 3-8%: impaired concentration; >5%: anxiety: <5%: confusion, mania, aggression, delirium, lability, suicidal ideation, psychosis, personality disorder, alcohol intolerance |
| Isoniazid | Unknown: depression, agitation, hallucination, paranoia, anxiety, psychosis |
| Lamivudine | <11%: insomnia; <9%: mania, depressive disorders, dreams |
| Methotrexate | Unknown: cognitive and mood changes |
| Pentamidine | Unknown: confusion, lability, hallucination; Rare: anxiety, fatigue |
| Procarbazine | Unknown: hallucination, depression, nervousness, apprehension, mania, loss of appetite, insomnia, nightmares, confusion, malaise |
| Quinolones | <1%: somnolence, insomnia; Occasional: agitation, anxiety, depression, panic attacks, confusion, hallucination, aggression, psychosis, paranoia; |
| Rare: | suicidal ideation and suicide (no relationship with drug confirmed) |
| Stavudine | Unknown: confusion, depression, seizures, anxiety, mania, sleep problems |
| Sulfonamides | Unknown: psychosis, delirium, confusion, depression, hallucinations |
| Thiabendazole | Unknown: hallucination, fatigue, irritability, confusion, depression |
| Vinblastine | Unknown: depression |
| Vincristine | Unknown: hallucination |
| Zalcitabine | Unknown: acute psychosis, agitation, amnesia, anxiety, lability, euphoria, hallucination, insomnia, mania, paranoia, suicidal behavior, confusion, impaired concentration, somnolence, depression |
| Zidovudine | Unknown: Insomnia, vivid dreams, agitation, mania, hallucination, confusion |
Table 2
Psychotropic/HIV drug interactions, by cytochrome P-450 isoenzyme
| CYP 3A4 | CYP 2D6 | |
|---|---|---|
| Psychotropics primarily metabolized by isoenzyme | Benzodiazepines Buspirone Carbamazepine Citalopram Clomipramine Imipramine Trazodone | Fluoxetine Fluvoxamine Mirtazapine Antipsychotics (typical and atypical) Paroxetine Sertraline Tricyclics Venlafaxine |
| HIV drugs that inhibit isoenzyme | Protease inhibitors (esp. ritonavir and indinavir) Clarithromycin Erythromycin Itraconazole Ketoconazole Macrolide antibiotics | Protease inhibitors (esp. ritonavir and nelfinavir) |
| Possible clinical effect | Increased plasma levels and increased side effects; for benzodiazepines, sedation and decreased respiratory drive | Increased plasma levels and increased side effects; for tricyclics, increased risk for cardiac conduction delay |
| HIV drugs that induce isoenzyme | Nevirapine Efavirenz Glucocorticoids Rifampin Rifabutin | None |
| Possible clinical effect | Decreased psychotropic plasma levels, decreased effectiveness | None |
| Source: Adapted and reprinted with permission from reference 1, Table 16. Copyright 2000. American Psychiatric Association | ||
The FDA approved enfuvirtide—the first of the new fusion inhibitor class of antiretroviral agents—in March 2003. Enfuvirtide prevents HIV from entering the target CD4 lymphocyte in patients who show continued viral replication despite ongoing antiretroviral therapy. This agent requires twice-daily subcutaneous injections. Because enfuvirtide can be viewed as a medication of last resort, nonresponse may be especially disheartening to an AIDS patient.
Substances of abuse also interact with HIV medications. A lethal overdose of the street drug MDMA (“Ecstasy”) has been reported in a patient treated with ritonavir.10 MDMA is metabolized primarily via CYP 2D6. Other substances of abuse metabolized by CYP 2D6 or 3A4—such as amphetamines, ketamine, heroin, cocaine, and gamma-hydroxybutyrate—may cause toxic reactions in patients being treated with protease inhibitors.
Because substance abuse is a common comorbidity of HIV infection, warn patients that using recreational drugs with antiretroviral medications can cause adverse reactions. Extensive drug interaction lists are available on patient education and physician Web sites (see Related Resources).
Table 3
Diagnostic criteria for HIV-associated minor cognitive motor disorder
Probable diagnosis (must meet all four criteria)
A possible diagnosis of minor cognitive motor disorder can be given if criteria 1-3 are present and either:
|
| Source: Reprinted with permission from reference 14 |
Lipid and hyperglycemic side effects. Antivirals— especially protease inhibitors —appear to be associated with HIV lipodystrophy, which is associated with cosmetic and serum lipid changes as well as hyperglycemia.11 Facial wasting, buffalo humps, and central intra-abdominal obesity may occur, and elevated serum cholesterol and triglycerides often require treatment with cholesterollowering “statin” drugs.
Though it is unclear whether HIV lipodystrophy increases cardiovascular disease risk, carefully consider the potential effects of psychotropics associated with weight gain, hyper-glycemia, and elevated lipids in patients receiving antiretroviral therapy.
Hepatitis. Patients at risk for HIV infection are also at risk for viral hepatitis. One-quarter of persons with HIV are coinfected with hepatitis C, primarily through IV drug use.12 Alpha-interferon treatment of hepatitis B and C has been associated with depression. SSRI treatment—such as paroxetine, 20 mg/d—can ease depressive symptoms.13
HIV-associated cognitive changes
Minor cognitive-motor disorder(Table 3) and HIV-associated dementia (Table 4) 14 are typically seen in late-stage HIV infections and are diagnoses of exclusion. Physical or neurologic examination in a patient with HIV/AIDS and altered mental status may show:
- focal deficits indicating a space-occupying lesion (eg, CNS lymphoma or toxoplasmosis)
- sensory changes that may indicate peripheral neuropathy
- ataxia or gait changes that may indicate myelopathy.
Useful neuropsychological tests include the HIV Dementia Rating Scale,15 Halstead finger-tapping test for motor speed,16 and the Trailmaking Test, which assesses psychomotor speed and sequencing ability.17
Antiretroviral therapy appears to reduce the risk of HIV-associated dementia. In a trial conducted at 42 AIDS Clinical Trials Group sites and 7 National Hemophilia Foundation sites, combination reverse transcriptase inhibitors helped preserve or improve neurologic function.18
Psychostimulants appear to improve HIV-induced brain impairment.19 Immune modulators—such as tumor necrosis factor-alpha blockers (eg, pentoxifylline)20 and interleukin-1 receptor blockers21 —have also been studied for possible beneficial effects on HIV brain disease.
HIV prevention
Because unprotected sex and IV substance use are the primary HIV transmission routes in the United States, assessing psychiatric patients’ sexual and substance use behaviors may help you prevent HIV infection. The CDC offers guidelines for HIV testing, counseling, and referral (see Related Resources).
To identify persons at risk for HIV infection, the CDC recommends asking open-ended questions about risk behaviors, such as: “What are you doing now or what have you done in the past that you think may put you at risk for HIV infection?”22
The shift of new HIV infection disproportionately into African-American and Hispanic populations suggests the need for more-intensive prevention and education in those communities. CDC guidelines emphasize the importance of using culturally sensitive language when asking about risk behavior. Some individuals may engage in same-sex behaviors but do not identify themselves as “homosexual” or “gay.” In some African-American communities, for example, being “on the down low” is used to describe men—oftentimes married—who have sex with men.
To incorporate HIV-prevention messages and brief behavioral interventions into clinical visits:
- speak with patients about sexual and drug use behaviors in simple, everyday language
- learn about interventions shown to be effective
- become familiar with community resources that address HIV risk reduction.23
Training. The CDC and Health Resources and Services Administration of the U.S. Department of Health and Human Services offer free training on risk screening and prevention, as well as opportunities for continuing medical education (see Related Resources).
Table 4
Diagnostic criteria for HIV-associated dementia
|
| Source: Reprinted with permission from reference 14 |
Advances in antibody testing
Psychiatrists play an important supportive role in encouraging HIV screening of at-risk patients of unknown serostatus and in counseling such patients before, during, and after test results are known.
Rapid lab tests. In 2002, the FDA approved a rapid, highly accurate HIV-1 screening test for serum specimens and in March 2004 approved the same test for screening oral fluid specimens. Test results with serum or an oral swab are available from a laboratory in approximately 20 minutes. In clinical studies submitted to the FDA, the OraQuick oral fluid test correctly identified 99.3% of persons infected with HIV-1 (sensitivity) and 99.9% of those not infected (specificity).
CDC guidelines for HIV counseling and testing have been revised to include rapid testing. Screening tests are most accurate at least 3 months after an HIV exposure—the time required for antibodies to develop. When counseling patients after a reactive test result, emphasize that the result is preliminary and further testing is needed to confirm the result. Counsel patients who have a negative result within 3 months of possible infection to be retested to guard against a possible false-negative result.
Home test kits. An FDA-approved consumer-controlled test kit—Home Access HIV-1 Test System24 —is sold at drug stores without a prescription. The customer pricks a finger with a special device, places drops of blood on a specially treated card, and mails the card to a licensed laboratory. Anonymous identification numbers are used when phoning for the results.
Customers may speak to a counselor before taking the test, while awaiting results, and when results are given. All individuals with a reactive test result are referred for a more-specific test and receive information and resources on treatment and support services.
Counseling the HIV patient
The psychological impact of positive HIV antibody test results on psychiatric patients has not been studied. Persons without psychiatric disorders commonly experience anxiety and depression immediately after learning of a positive result. Unless the patient has HIV-related physical symptoms, these psychological sequelae often return to baseline—similar to when the blood sample was drawn—within 2 weeks.25
Patients need to know that a positive HIV test result is no longer associated with death within 2 to 3 years. During a 2-year period, for example, disease progression from HIV infection to AIDS decreased 7-fold among patients who started antiretroviral therapy with a CD4+ T-cell count >350 cells/mm3, compared with others who were monitored without therapy.26 This may be especially important to reinforce with newly-diagnosed patients unfamiliar with advances in HAART.
Medication adherence. To increase patients’ adherence to antiretroviral therapy:
- express interest that they are taking their medications
- use psychotherapy to help them solve problems that interfere with adherence.
Suicide risk. In the 1980s, significantly increased suicide rates were reported among HIV-infected persons. For example, the suicide rate in 1985 for New York City men ages 20 to 59 living with an AIDS diagnosis was 36 times higher than that of similar men without AIDS.27 A later study of HIV infection in New York male suicide victims from 1991 to 1993 suggested that HIV serostatus was associated with a modest increase—at most—in suicide risk. That study considered the interplay of other suicide risk factors, such as substance abuse.28
- Guidelines for HIV counseling, testing, and referral. Centers for Disease Control and Prevention. www.cdc.gov/mmwr/preview/mmwrhtml/rr5019a1.htm
- Training in HIV prevention and counseling. National Network of STD/HIV Prevention Training Centers (http://depts.washington.edu/nnptc) and AIDS Education and Training Centers National Resource Center (http://www.aids-ed.org)
- Rapid HIV testing. Centers for Disease Control and Prevention. http://www.cdc.gov/hiv/rapid_testing/
- Cytochrome P450 drug interaction table. Indiana University School of Medicine. Division of Clinical Pharmacology. www.drug-interactions.com
Drug brand names
- Buspirone • BuSpar
- Carbamazepine • Carbatrol
- Citalopram • Celexa
- Clomipramine • Anafranil
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Imipramine • Tofranil
- Mirtazapine • Remeron
- Paroxetine • Paxil
- Sertraline • Zoloft
- Trazodone • Desyrel
- Venlafaxine • Effexor
Disclosure
Dr. Liang reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products
Psychiatric patients—especially those with substance abuse disorders—are at high risk for HIV infection, which puts psychiatrists on the AIDS pandemic’s front lines.
In the wake of last month’s International AIDS Conference in Thailand, this article supplements American Psychiatric Association guidelines for managing patients with HIV/AIDS.1 Here is updated information on:
- who is at greatest risk for HIV infection today
- neuropsychiatric side effects of HIV medications
- in-office assessment of HIV-associated cognitive changes
- how to avoid psychotropic/antiretroviral interactions.
HIV and psychiatric patients
Psychiatric patients are among those at highest risk for HIV (Box).2-4 Cournos and McKinnon5 found that HIV seroprevalence among persons with severe mental illness was 4% to 23%compared with 0.4% in the general population.6 They defined severe mental illness as schizophrenia, schizoaffective disorder, major depression, or bipolar disorder accompanied by significant functional impairment, disruption of normal life tasks, periods of hospitalization, and need for psychotropics.
Infection rates varied with HIV geographic concentration, presence of comorbid substance use disorders, age, and ethnicity, but not psychiatric diagnosis. Unsafe sex and drug use (including noninjection) were associated with infection, and women were as likely to be infected as men.
Side effects and interactions
‘Triple therapy.’ Combining three antiretroviral agents—highly-active antiretroviral therapy (HAART) or “triple therapy”—is standard treatment for HIV infection in the United States. Initially, HAART was recommended for all patients with early-stage HIV, even if asymptomatic. This changed as antiretrovirals’ side effects—such as peripheral neuropathy with didanosine— and drug resistance from suboptimal adherence became apparent. Viral resistance develops if patients are <95% adherent to antiretroviral regimens.7
Antiretroviral therapy is usually started when:
- CD4 lymphocyte count is <200 cells/mm3 or abruptly decreasing
- plasma viral load is >55,000 copies/mL or abruptly increasing
- symptomatic AIDS emerges.
Psychiatric side effects. Psychiatric symptoms—such as depression, anxiety, confusion, psychosis, hallucinations, insomnia, and mania—are common side effects of antiretrovirals and other drugs used to treat HIV and its opportunistic infections and cancers (Table 1).8 Two antiretrovirals are of particular interest to psychiatrists:
Efavirenz is a non-nucleoside reverse transcriptase inhibitor that causes vivid dreams, especially when initiated.
AIDS death rates have declined in the United States since antiretroviral therapies were introduced in 1996, but the rate of new HIV infection has not changed.2 An estimated 850,000 to 950,000 Americans have HIV, and 25% do not know it.3
Changing demographics. Some 40,000 new HIV infections occur in the United States each year (70% among men), and one-half of the newly-infected are under age 25. African Americans and Hispanics represent 51% of total AIDS cases in men and 77% in women. From 1998 to 2002—the most recent data available from the Centers for Disease Control and Prevention (CDC)—AIDS incidence steadily decreased among whites and Hispanics but increased among blacks, Asian/Pacific Islanders, and American Indian/Alaska Natives.
Transmission routes. Approximately 60% of men with HIV are infected through male-to-male sex, 25% through IV drug use, and 15% through heterosexual sex. Unprotected anal sex appears to be occurring more frequently in some urban centers, particularly among young men who have sex with men.4 Approximately 75% of women with HIV are infected through heterosexual sex and 25% through IV drug use.
Ritonavir is a protease inhibitor that may inhibit psychotropics metabolized by cytochrome P450 3A4 and 2D6 isoenzymes.
Other HIV medications increase or decrease psychotropic blood levels via inhibition or induction of CYP isoenzymes (Table 2).9 When a patient is taking ritonavir or another protease inhibitor, reduced starting dosages of selective serotonin reuptake inhibitors (SSRIs) may be appropriate. Benzodiazepine dosages may need to be increased because of ritonavir induction of the enzyme glucuronosyltransferase.
Table 1
Psychiatric side effects of common HIV medications
| Drug | Side effects, by frequency |
|---|---|
| Acyclovir | Unknown: hallucination, confusion, thought insertion, insomnia |
| Amphotericin B | >5%: confusion, insomnia, somnolence; 1-5%: agitation, anxiety, depression, hallucination, nervousness, psychosis; Unkown: delirium |
| β-Lactam antibiotics | <1%: insomnia, somnolence, anxiety, nervousness, impaired concentration, confusion, nightmares, hallucination; Unkown: paranoia, mania |
| Trimethoprim/sulfamethoxazole | Unknown: hallucinations, depression, apathy, nervousness |
| Cycloserine Unknown: | psychosis, somnolence, depression, confusion, irritability, anxiety |
| Didanosine | Unknown: nervousness, anxiety, confusion, seizures, insomnia |
| Efavirenz | 13-16%: depression; 8-11%: anxiety; 2-6%: nervousness; >5%: headache, seizures, confusion; <2%: suicidal ideation and behavior, aggression |
| Unknown: | agitation, lability, neurosis, psychosis, insomnia, impaired concentration, somnolence, euphoria, amnesia, hallucination |
| Foscarnet | >5%: depression, confusion, anxiety; 1-5%: insomnia, somnolence, amnesia, nervousness, agitation, aggression, hallucination |
| Interferon-a | 6-19%: depression; 12-16%: irritability; 6-12%: insomnia; 3-8%: impaired concentration; >5%: anxiety: <5%: confusion, mania, aggression, delirium, lability, suicidal ideation, psychosis, personality disorder, alcohol intolerance |
| Isoniazid | Unknown: depression, agitation, hallucination, paranoia, anxiety, psychosis |
| Lamivudine | <11%: insomnia; <9%: mania, depressive disorders, dreams |
| Methotrexate | Unknown: cognitive and mood changes |
| Pentamidine | Unknown: confusion, lability, hallucination; Rare: anxiety, fatigue |
| Procarbazine | Unknown: hallucination, depression, nervousness, apprehension, mania, loss of appetite, insomnia, nightmares, confusion, malaise |
| Quinolones | <1%: somnolence, insomnia; Occasional: agitation, anxiety, depression, panic attacks, confusion, hallucination, aggression, psychosis, paranoia; |
| Rare: | suicidal ideation and suicide (no relationship with drug confirmed) |
| Stavudine | Unknown: confusion, depression, seizures, anxiety, mania, sleep problems |
| Sulfonamides | Unknown: psychosis, delirium, confusion, depression, hallucinations |
| Thiabendazole | Unknown: hallucination, fatigue, irritability, confusion, depression |
| Vinblastine | Unknown: depression |
| Vincristine | Unknown: hallucination |
| Zalcitabine | Unknown: acute psychosis, agitation, amnesia, anxiety, lability, euphoria, hallucination, insomnia, mania, paranoia, suicidal behavior, confusion, impaired concentration, somnolence, depression |
| Zidovudine | Unknown: Insomnia, vivid dreams, agitation, mania, hallucination, confusion |
Table 2
Psychotropic/HIV drug interactions, by cytochrome P-450 isoenzyme
| CYP 3A4 | CYP 2D6 | |
|---|---|---|
| Psychotropics primarily metabolized by isoenzyme | Benzodiazepines Buspirone Carbamazepine Citalopram Clomipramine Imipramine Trazodone | Fluoxetine Fluvoxamine Mirtazapine Antipsychotics (typical and atypical) Paroxetine Sertraline Tricyclics Venlafaxine |
| HIV drugs that inhibit isoenzyme | Protease inhibitors (esp. ritonavir and indinavir) Clarithromycin Erythromycin Itraconazole Ketoconazole Macrolide antibiotics | Protease inhibitors (esp. ritonavir and nelfinavir) |
| Possible clinical effect | Increased plasma levels and increased side effects; for benzodiazepines, sedation and decreased respiratory drive | Increased plasma levels and increased side effects; for tricyclics, increased risk for cardiac conduction delay |
| HIV drugs that induce isoenzyme | Nevirapine Efavirenz Glucocorticoids Rifampin Rifabutin | None |
| Possible clinical effect | Decreased psychotropic plasma levels, decreased effectiveness | None |
| Source: Adapted and reprinted with permission from reference 1, Table 16. Copyright 2000. American Psychiatric Association | ||
The FDA approved enfuvirtide—the first of the new fusion inhibitor class of antiretroviral agents—in March 2003. Enfuvirtide prevents HIV from entering the target CD4 lymphocyte in patients who show continued viral replication despite ongoing antiretroviral therapy. This agent requires twice-daily subcutaneous injections. Because enfuvirtide can be viewed as a medication of last resort, nonresponse may be especially disheartening to an AIDS patient.
Substances of abuse also interact with HIV medications. A lethal overdose of the street drug MDMA (“Ecstasy”) has been reported in a patient treated with ritonavir.10 MDMA is metabolized primarily via CYP 2D6. Other substances of abuse metabolized by CYP 2D6 or 3A4—such as amphetamines, ketamine, heroin, cocaine, and gamma-hydroxybutyrate—may cause toxic reactions in patients being treated with protease inhibitors.
Because substance abuse is a common comorbidity of HIV infection, warn patients that using recreational drugs with antiretroviral medications can cause adverse reactions. Extensive drug interaction lists are available on patient education and physician Web sites (see Related Resources).
Table 3
Diagnostic criteria for HIV-associated minor cognitive motor disorder
Probable diagnosis (must meet all four criteria)
A possible diagnosis of minor cognitive motor disorder can be given if criteria 1-3 are present and either:
|
| Source: Reprinted with permission from reference 14 |
Lipid and hyperglycemic side effects. Antivirals— especially protease inhibitors —appear to be associated with HIV lipodystrophy, which is associated with cosmetic and serum lipid changes as well as hyperglycemia.11 Facial wasting, buffalo humps, and central intra-abdominal obesity may occur, and elevated serum cholesterol and triglycerides often require treatment with cholesterollowering “statin” drugs.
Though it is unclear whether HIV lipodystrophy increases cardiovascular disease risk, carefully consider the potential effects of psychotropics associated with weight gain, hyper-glycemia, and elevated lipids in patients receiving antiretroviral therapy.
Hepatitis. Patients at risk for HIV infection are also at risk for viral hepatitis. One-quarter of persons with HIV are coinfected with hepatitis C, primarily through IV drug use.12 Alpha-interferon treatment of hepatitis B and C has been associated with depression. SSRI treatment—such as paroxetine, 20 mg/d—can ease depressive symptoms.13
HIV-associated cognitive changes
Minor cognitive-motor disorder(Table 3) and HIV-associated dementia (Table 4) 14 are typically seen in late-stage HIV infections and are diagnoses of exclusion. Physical or neurologic examination in a patient with HIV/AIDS and altered mental status may show:
- focal deficits indicating a space-occupying lesion (eg, CNS lymphoma or toxoplasmosis)
- sensory changes that may indicate peripheral neuropathy
- ataxia or gait changes that may indicate myelopathy.
Useful neuropsychological tests include the HIV Dementia Rating Scale,15 Halstead finger-tapping test for motor speed,16 and the Trailmaking Test, which assesses psychomotor speed and sequencing ability.17
Antiretroviral therapy appears to reduce the risk of HIV-associated dementia. In a trial conducted at 42 AIDS Clinical Trials Group sites and 7 National Hemophilia Foundation sites, combination reverse transcriptase inhibitors helped preserve or improve neurologic function.18
Psychostimulants appear to improve HIV-induced brain impairment.19 Immune modulators—such as tumor necrosis factor-alpha blockers (eg, pentoxifylline)20 and interleukin-1 receptor blockers21 —have also been studied for possible beneficial effects on HIV brain disease.
HIV prevention
Because unprotected sex and IV substance use are the primary HIV transmission routes in the United States, assessing psychiatric patients’ sexual and substance use behaviors may help you prevent HIV infection. The CDC offers guidelines for HIV testing, counseling, and referral (see Related Resources).
To identify persons at risk for HIV infection, the CDC recommends asking open-ended questions about risk behaviors, such as: “What are you doing now or what have you done in the past that you think may put you at risk for HIV infection?”22
The shift of new HIV infection disproportionately into African-American and Hispanic populations suggests the need for more-intensive prevention and education in those communities. CDC guidelines emphasize the importance of using culturally sensitive language when asking about risk behavior. Some individuals may engage in same-sex behaviors but do not identify themselves as “homosexual” or “gay.” In some African-American communities, for example, being “on the down low” is used to describe men—oftentimes married—who have sex with men.
To incorporate HIV-prevention messages and brief behavioral interventions into clinical visits:
- speak with patients about sexual and drug use behaviors in simple, everyday language
- learn about interventions shown to be effective
- become familiar with community resources that address HIV risk reduction.23
Training. The CDC and Health Resources and Services Administration of the U.S. Department of Health and Human Services offer free training on risk screening and prevention, as well as opportunities for continuing medical education (see Related Resources).
Table 4
Diagnostic criteria for HIV-associated dementia
|
| Source: Reprinted with permission from reference 14 |
Advances in antibody testing
Psychiatrists play an important supportive role in encouraging HIV screening of at-risk patients of unknown serostatus and in counseling such patients before, during, and after test results are known.
Rapid lab tests. In 2002, the FDA approved a rapid, highly accurate HIV-1 screening test for serum specimens and in March 2004 approved the same test for screening oral fluid specimens. Test results with serum or an oral swab are available from a laboratory in approximately 20 minutes. In clinical studies submitted to the FDA, the OraQuick oral fluid test correctly identified 99.3% of persons infected with HIV-1 (sensitivity) and 99.9% of those not infected (specificity).
CDC guidelines for HIV counseling and testing have been revised to include rapid testing. Screening tests are most accurate at least 3 months after an HIV exposure—the time required for antibodies to develop. When counseling patients after a reactive test result, emphasize that the result is preliminary and further testing is needed to confirm the result. Counsel patients who have a negative result within 3 months of possible infection to be retested to guard against a possible false-negative result.
Home test kits. An FDA-approved consumer-controlled test kit—Home Access HIV-1 Test System24 —is sold at drug stores without a prescription. The customer pricks a finger with a special device, places drops of blood on a specially treated card, and mails the card to a licensed laboratory. Anonymous identification numbers are used when phoning for the results.
Customers may speak to a counselor before taking the test, while awaiting results, and when results are given. All individuals with a reactive test result are referred for a more-specific test and receive information and resources on treatment and support services.
Counseling the HIV patient
The psychological impact of positive HIV antibody test results on psychiatric patients has not been studied. Persons without psychiatric disorders commonly experience anxiety and depression immediately after learning of a positive result. Unless the patient has HIV-related physical symptoms, these psychological sequelae often return to baseline—similar to when the blood sample was drawn—within 2 weeks.25
Patients need to know that a positive HIV test result is no longer associated with death within 2 to 3 years. During a 2-year period, for example, disease progression from HIV infection to AIDS decreased 7-fold among patients who started antiretroviral therapy with a CD4+ T-cell count >350 cells/mm3, compared with others who were monitored without therapy.26 This may be especially important to reinforce with newly-diagnosed patients unfamiliar with advances in HAART.
Medication adherence. To increase patients’ adherence to antiretroviral therapy:
- express interest that they are taking their medications
- use psychotherapy to help them solve problems that interfere with adherence.
Suicide risk. In the 1980s, significantly increased suicide rates were reported among HIV-infected persons. For example, the suicide rate in 1985 for New York City men ages 20 to 59 living with an AIDS diagnosis was 36 times higher than that of similar men without AIDS.27 A later study of HIV infection in New York male suicide victims from 1991 to 1993 suggested that HIV serostatus was associated with a modest increase—at most—in suicide risk. That study considered the interplay of other suicide risk factors, such as substance abuse.28
- Guidelines for HIV counseling, testing, and referral. Centers for Disease Control and Prevention. www.cdc.gov/mmwr/preview/mmwrhtml/rr5019a1.htm
- Training in HIV prevention and counseling. National Network of STD/HIV Prevention Training Centers (http://depts.washington.edu/nnptc) and AIDS Education and Training Centers National Resource Center (http://www.aids-ed.org)
- Rapid HIV testing. Centers for Disease Control and Prevention. http://www.cdc.gov/hiv/rapid_testing/
- Cytochrome P450 drug interaction table. Indiana University School of Medicine. Division of Clinical Pharmacology. www.drug-interactions.com
Drug brand names
- Buspirone • BuSpar
- Carbamazepine • Carbatrol
- Citalopram • Celexa
- Clomipramine • Anafranil
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Imipramine • Tofranil
- Mirtazapine • Remeron
- Paroxetine • Paxil
- Sertraline • Zoloft
- Trazodone • Desyrel
- Venlafaxine • Effexor
Disclosure
Dr. Liang reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products
1. American Psychiatric Association. Practice guideline for the treatment of patients with HIV/AIDS. Am J Psychiatry. 2000 157 11(suppl). Also available at: www.psych.org/psych_pract/treatg/pg/hivaids_revisebook_index.cfm
2. Centers for Disease Control and Prevention National Center for HIV, STD, and TB Prevention. HIV AIDS Surveill Rep December 2001. Available at: http://www.cdc.gov/hiv/stats/hasr1302.htm
3. Centers for Disease Control and Prevention. HIV AIDS Surveill Rep 2002;14:148. Also available at: http://www.cdc.gov/hiv/stats/hasr1402/2002SurveillanceReport.pdf
4. Risk reduction: sex without condoms. HIV Counselor Perspectives [newsletter] 2001;10(2, March).
5. Cournos F, McKinnon K. HIV seroprevalence among people with severe mental illness in the United States: a critical review. Clin Psychol Rev 1997;17:259-69.
6. Steele FR. A moving target: CDC still trying to estimate HIV-1 prevalence. J NIH Res 1994;6:25-6.
7. Paterson DL, Swindells S, Mohr J, et al. Adherence to protease inhibitor therapy and outcomes in patients with HIV infection. Ann Intern Med 2000;133:21-30.
8. Grant I, Atkinson JH, Jr. Neuropsychiatric aspects of HIV infection and AIDS. In: Sadock BJ, Sadock VA (eds). Kaplan and Sadock’s comprehensive textbook of psychiatry. Philadelphia: Lippincott Williams & Wilkins, 1999;308-36.
9. Ayuso JL. Use of psychotropic drugs in patients with HIV infection. Drugs 1994;47:599-610.
10. Mirken B. Danger: possibly fatal interactions between ritonavir and “ecstasy,” some other psychoactive drugs. AIDS Treat News 1997;Feb 21(No 265):5.-
11. Miller KD, Jones E, Yanovski JA, et al. Visceral abdominal-fat accumulation associated with use of indinavir. Lancet 1998;351(9106):871-5.
12. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR 1998;47(No. RR-19):1-39.
13. Kraus MR, Schafer A, Faller H, et al. Paroxetine for the treatment of interferon-alpha-induced depression in chronic hepatitis C. Aliment Pharmacol Ther 2002;16(6):1091-9.
14. Nomenclature and research case definitions for neurologic manifestations of human immunodeficiency virus-type 1 (HIV-1) infection: report of a working group of the American Academy of Neurology AIDS Task Force. Neurology 1991;41:778-85.
15. Power C, Selnes OA, Grim JA, McArthur JC. HIV Dementia Scale: a rapid screening test. J Acquir Immune Defic Syndr Hum Retrovirol 1995 Mar 1;8(3):273-8.
16. Silberstein CH, McKegney FP, O'Dowd MA, et al. A prospective longitudinal study of neuropsychological and psychosocial factors in asymptomatic individuals at risk for HTLV-III/LAV infection in a methadone program: preliminary findings. Int J Neurosci 1987;32(3-4):669-76.
17. Reitan RM. Validity of the trail making test as an indicator of organic brain damage. Percept Mot Skills 1958;8:271-6.
18. Price RW, Yiannoutsos CT, Clifford DB, et al. Neurological outcomes in late HIV infection: adverse impact of neurological impairment on survival and protective effect of antiviral therapy. AIDS Clinical Trial Group and Neurological AIDS Research Consortium study team. AIDS 1999;13(13):1677-85.
19. Perry SW. Organic mental disorders caused by HIV: update on early diagnosis and treatment. Am J Psychiatry 1990;147(6):696-710.
20. Wilt SG, Milward E, Zhou JM, et al. In vitro evidence for a dual role of tumor necrosis factor-alpha in human immunodeficiency virus type 1 encephalopathy. Ann Neurol 1995;37(3):381-94.
21. Boven LA, Gomes L, Hery C, et al. Increased peroxynitrite activity in AIDS dementia complex: implications for the neuropathogenesis of HIV-1 infection. J Immunol 1999;162(7):4319-27.
22. Centers for Disease Control and Prevention. Revised guidelines for HIV counseling, testing, and referral. MMWR Nov. 9, 2001;50(RR19):1-58.
23. Centers for Disease Control and Prevention. Incorporating HIV prevention into the medical care of persons living with HIV. MMWR July 18, 2003;52(RR12):1-24. Also available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5212a1.htm
24. Food and Drug Administration. Home Access HIV-1 Test System: Summary of safety and effectiveness. Available at: http://www.fda.gov/cber/PMAsumm/P950002S.pdf
25. Perry SW, Jacobsberg LB, Fishman B. Psychological responses to serological testing for HIV. AIDS 1990;4(2):145-52.
26. Opravil M, Ledergerber B, Furrer H. et al and the Swiss HIV Cohort Study Clinical benefit of early initiation of HAART in patients with asymptomatic HIV and CD4 counts >350/mm 3 . Abstract LB-6. Chicago, IL: 8th Conference on Retroviruses and Opportunistic Infections, 2001.
27. Marzuk P, Tierney H, Tardiff K, et al. Increased risk of suicide in persons with AIDS. JAMA 1988;259:1333-7.
28. Marzuk PM, Tardiff K, Leon AC, et al. HIV seroprevalence among suicide victims in New York City, 1991-93. Am J Psychiatry 1997;154(6):1720-5.
1. American Psychiatric Association. Practice guideline for the treatment of patients with HIV/AIDS. Am J Psychiatry. 2000 157 11(suppl). Also available at: www.psych.org/psych_pract/treatg/pg/hivaids_revisebook_index.cfm
2. Centers for Disease Control and Prevention National Center for HIV, STD, and TB Prevention. HIV AIDS Surveill Rep December 2001. Available at: http://www.cdc.gov/hiv/stats/hasr1302.htm
3. Centers for Disease Control and Prevention. HIV AIDS Surveill Rep 2002;14:148. Also available at: http://www.cdc.gov/hiv/stats/hasr1402/2002SurveillanceReport.pdf
4. Risk reduction: sex without condoms. HIV Counselor Perspectives [newsletter] 2001;10(2, March).
5. Cournos F, McKinnon K. HIV seroprevalence among people with severe mental illness in the United States: a critical review. Clin Psychol Rev 1997;17:259-69.
6. Steele FR. A moving target: CDC still trying to estimate HIV-1 prevalence. J NIH Res 1994;6:25-6.
7. Paterson DL, Swindells S, Mohr J, et al. Adherence to protease inhibitor therapy and outcomes in patients with HIV infection. Ann Intern Med 2000;133:21-30.
8. Grant I, Atkinson JH, Jr. Neuropsychiatric aspects of HIV infection and AIDS. In: Sadock BJ, Sadock VA (eds). Kaplan and Sadock’s comprehensive textbook of psychiatry. Philadelphia: Lippincott Williams & Wilkins, 1999;308-36.
9. Ayuso JL. Use of psychotropic drugs in patients with HIV infection. Drugs 1994;47:599-610.
10. Mirken B. Danger: possibly fatal interactions between ritonavir and “ecstasy,” some other psychoactive drugs. AIDS Treat News 1997;Feb 21(No 265):5.-
11. Miller KD, Jones E, Yanovski JA, et al. Visceral abdominal-fat accumulation associated with use of indinavir. Lancet 1998;351(9106):871-5.
12. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR 1998;47(No. RR-19):1-39.
13. Kraus MR, Schafer A, Faller H, et al. Paroxetine for the treatment of interferon-alpha-induced depression in chronic hepatitis C. Aliment Pharmacol Ther 2002;16(6):1091-9.
14. Nomenclature and research case definitions for neurologic manifestations of human immunodeficiency virus-type 1 (HIV-1) infection: report of a working group of the American Academy of Neurology AIDS Task Force. Neurology 1991;41:778-85.
15. Power C, Selnes OA, Grim JA, McArthur JC. HIV Dementia Scale: a rapid screening test. J Acquir Immune Defic Syndr Hum Retrovirol 1995 Mar 1;8(3):273-8.
16. Silberstein CH, McKegney FP, O'Dowd MA, et al. A prospective longitudinal study of neuropsychological and psychosocial factors in asymptomatic individuals at risk for HTLV-III/LAV infection in a methadone program: preliminary findings. Int J Neurosci 1987;32(3-4):669-76.
17. Reitan RM. Validity of the trail making test as an indicator of organic brain damage. Percept Mot Skills 1958;8:271-6.
18. Price RW, Yiannoutsos CT, Clifford DB, et al. Neurological outcomes in late HIV infection: adverse impact of neurological impairment on survival and protective effect of antiviral therapy. AIDS Clinical Trial Group and Neurological AIDS Research Consortium study team. AIDS 1999;13(13):1677-85.
19. Perry SW. Organic mental disorders caused by HIV: update on early diagnosis and treatment. Am J Psychiatry 1990;147(6):696-710.
20. Wilt SG, Milward E, Zhou JM, et al. In vitro evidence for a dual role of tumor necrosis factor-alpha in human immunodeficiency virus type 1 encephalopathy. Ann Neurol 1995;37(3):381-94.
21. Boven LA, Gomes L, Hery C, et al. Increased peroxynitrite activity in AIDS dementia complex: implications for the neuropathogenesis of HIV-1 infection. J Immunol 1999;162(7):4319-27.
22. Centers for Disease Control and Prevention. Revised guidelines for HIV counseling, testing, and referral. MMWR Nov. 9, 2001;50(RR19):1-58.
23. Centers for Disease Control and Prevention. Incorporating HIV prevention into the medical care of persons living with HIV. MMWR July 18, 2003;52(RR12):1-24. Also available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5212a1.htm
24. Food and Drug Administration. Home Access HIV-1 Test System: Summary of safety and effectiveness. Available at: http://www.fda.gov/cber/PMAsumm/P950002S.pdf
25. Perry SW, Jacobsberg LB, Fishman B. Psychological responses to serological testing for HIV. AIDS 1990;4(2):145-52.
26. Opravil M, Ledergerber B, Furrer H. et al and the Swiss HIV Cohort Study Clinical benefit of early initiation of HAART in patients with asymptomatic HIV and CD4 counts >350/mm 3 . Abstract LB-6. Chicago, IL: 8th Conference on Retroviruses and Opportunistic Infections, 2001.
27. Marzuk P, Tierney H, Tardiff K, et al. Increased risk of suicide in persons with AIDS. JAMA 1988;259:1333-7.
28. Marzuk PM, Tardiff K, Leon AC, et al. HIV seroprevalence among suicide victims in New York City, 1991-93. Am J Psychiatry 1997;154(6):1720-5.
A troubled patient’s secret life
History: Threatened by an ‘angel’
Mr. M, age 32, began hearing voices at age 16. He had been diagnosed as having bipolar disorder with psychotic features before presenting to our hospital in 1995. He often experienced hypomania (euphoria, decreased sleep, free spending) followed by depressive periods (lack of energy, tearfulness, decreased concentration), and heard commands to kill himself or saw menacing shadows or “angels.”
Several psychiatrists tried various psychotropics across 6 years, but Mr. M’s odd behaviors persisted. One night he physically threatened his father, who tried to stop Mr. M from eating a sandwich wrapped in a plastic bag. Mr. M was hospitalized that night, and his diagnosis was changed to schizoaffective disorder based on recurrent auditory and visual hallucinations when mood symptoms were absent.
Mr. M was hospitalized nine times within 6 years for psychotic or depressive symptoms— including twice in 1 month for depression and suicidal ideation. Two months later, he attempted suicide by taking 1,200 mg of ziprasidone (about 10 times the normal daily dosage) and an unknown amount of lorazepam, after which he was treated in the ER and released. He presented to me shortly afterward, frightened by his suicide attempt.
At intake, Mr. M was taking lorazepam, 1 mg tid for anxiety, and ziprasidone, 20 mg bid.
Single and unemployed, Mr. M lived with his parents and a brother, and was collecting disability benefits because of his psychiatric problems. He told me that he had been off cocaine for 3 years but had used marijuana 2 weeks earlier. He also reported ongoing family problems but did not elaborate. He said he did not feel suicidal but described continued depressive episodes.
Dr. Fraser’s observations
Mr. M’s last six psychiatric hospitalizations and at least 5 years of outpatient notes by other psychiatrists indicated a history of schizoaffective disorder. Mr. M’s psychotic symptoms persisted for substantial periods while mood symptoms were absent, thus supporting the diagnosis. By contrast, mood and psychotic symptoms in major depression with psychotic features are almost always simultaneous.
Mr. M’s substance use should be considered. Fifty percent of persons with schizophrenia or an affective disorder have a lifetime prevalence of substance abuse disorder.1 The rate climbs to 60% to 90% for patients with schizophrenia seen in emergency rooms, inpatient psychiatric units, and community settings.2
Mr. M’s last documented cocaine use was in 1998; subsequent urine drug screens showed only marijuana.
Cocaine abuse could have contributed to Mr. M’s psychotic symptoms, and marijuana use could have caused his inertia, lack of motivation, and difficulty concentrating. It is unclear why previous doctors attributed most of his psychotic symptoms to a major mental illness rather than cocaine use.
Ask patients about substance use along with a chronology of psychiatric symptoms. Encourage patients who are regularly using substances to stop for a trial period to see if symptoms abate during abstinence. Refer patients for substance use treatment if necessary.
Treatment: A waighty issue
I feared that Mr. M’s psychotic symptoms would recur, but he was more concerned about his depression and obesity. He said he gained 50 pounds over 3 1/2 years while taking olanzapine, 10 to 15 mg/d, and divalproex at various dosages. He stopped both agents on his own and lost 35 pounds across 6 months but was still obese (197 lbs., body mass index [BMI] 32.9).
I prescribed bupropion SR—100 mg/d titrated over several weeks to 200 mg each morning and 100 mg at night—because of its association with weight loss. I also:
- continued ziprasidone, 20 mg bid, to prevent psychosis
- continued lorazepam, 1 mg tid, to reduce anxiety stemming from his family problems. I asked Mr. M to slowly taper off the agent—which he had been taking for 8 years—across 6 to 12 months because a protracted benzodiazepine regimen can contribute to depression.
- referred him to a psychotherapist for cognitive-behavioral therapy to help reduce his depressive thinking and suicide risk
- recommended that he stop using marijuana.
At his second visit, Mr. M reported more auditory hallucinations. I increased ziprasidone to 40 mg bid.
By this time, Mr. M was becoming more comfortable in therapy. He began discussing his family problems in more detail, telling me that his brother is addicted to heroin.
I asked Mr. M if he was again threatening family members or other people. He replied that he had not been violent, but that his mother often slaps him and others in his family. I commended him for not retaliating, but warned him that his mother’s aggression was perpetuating his depression.
I encouraged Mr. M to find an apartment, but he said he could not yet afford to live on his own. I referred him to case management services to help him find affordable housing and urged him to avoid his mother’s assaults. He seemed to appreciate my concern for him.
- Respect the patient’s goals. You fear psychotic symptoms will resurface, but the patient is more concerned about weight gain or other side effects. When possible, choose an agent that targets symptoms without causing the feared side effects.
- Enhance motivation for change. Remind the patient of past successes. Break the broad goal into smaller, achievable goals. Find out the patient’s unique motivations for change.
- Become the patient’s advocate. Accept responsibility for patient care problems. Refer the patient to needed social services.
- Keep an open mind about diagnosis and prognosis. Despite being the definitive diagnostic reference, DSM-IV-TR does not neatly fit all patients, nor account for all human suffering.
Twelve days later, Mr. M made an unplanned visit. He was angry because our pharmacy had not refilled his prescriptions and no one had returned his call asking about the refills. He was irritable but nonthreatening, although he planned to complain to the psychiatric center’s medical director.
I had received no phone messages, and my notes indicated the prescriptions were refilled. Nonetheless, my assuming responsibility for this problem was key to preserving our therapeutic alliance (Box). I resolved the matter and apologized for the miscommunication. Mr. M accepted my apology and scheduled a return visit.
About 1 month later, Mr. M’s self-esteem had increased. He stopped using marijuana, went on a low-calorie diet, and exercised at least 1 hour daily at a local gym. He lost 27 lbs. over 2 months, dropping his weight to 170 lbs. (BMI 28.3). He finished group (15 sessions) and individual (four sessions) psychotherapy, and avoided his mother when she became aggressive.
Before his next monthly visit, Mr. M had called the state vocational rehabilitation department to begin employment. I tapered lorazepam to 0.5 mg nightly while continuing ziprasidone and bupropion. His weight was near normal (150 lbs., BMI 25).
Six months into treatment, Mr. M. applied for a job and moved out of his parents’ home to live with another brother, who does not take drugs. He said that he “felt at peace” for the first time in years. His weight stayed in the 140s. I stopped lorazepam and he requested to see me 3 months later.
Dr. Fraser’s observations
Many patients with schizophrenia or schizoaffective disorder struggle with weight gain, substance use, employment problems, and family conflict, and some make slow progress with one or more of these issues. Mr. M’s rapid improvement on all fronts was striking, however.
Recovery from schizophrenia has been documented,3 and the prognosis for schizoaffective disorder is often more positive than for schizophrenia or severe bipolar disorder.4 Still, Mr. M’s apparent recovery seemed incredible.
To prevent symptom recurrence, I left the bupropion/ziprasidone regimen unchanged. Even after a chronically ill patient responds to medication, I feel dosages should be maintained unless side effects occur or a medication loses effectiveness.
Table
PTSD symptoms that suggest other diagnoses
| PTSD symptoms | Similar to | Diagnosis suggested |
|---|---|---|
| Depersonalization, derealization, dissociation | Psychosis | Schizophrenia, schizoaffective disorder |
| Anxiety, hypervigilance, insomnia | Anxiety | Exacerbations of schizophrenia, schizoaffective disorder, bipolar disorder (mania) |
| Flashbacks, fear of trauma recurrence | Paranoia | Schizophrenia, schizoaffective disorder |
Follow-up: Mr. M’s story
Since the mix-up with Mr. M’s medications, our therapeutic alliance grew stronger. He told me more about himself with each visit. Four months into treatment, he revealed that he is gay and feels “liberated” after years of keeping it secret.
Five months later, Mr. M confided that an older male partner had physically, sexually, and emotionally abused him for about 10 years, starting when Mr. M was 16—about the time his auditory hallucinations began. The abusive relationship ended when the partner died of an unspecified overdose.
Mr. M’s gay friends advised him to seek closure. He visited his ex-partner’s grave, placed a rose, said goodbye, and left vowing he’d never again become an abuse victim. He said he had never told any health professional this story.
Mr. M then asked to be tapered off medications. I was afraid his psychotic symptoms could resurface, although I now wondered whether his schizoaffective disorder diagnosis had been correct. We tapered bupropion and ziprasidone over the next month.
Twenty-four months later, his schizoaffective symptoms had not resurfaced. He worked as a security guard, maintained an apartment, and continued exercising and eating right. His weight stayed normal (140 lbs., BMI 23.3). No signs of hypomania were present, and he was finding fulfillment in nonabusive relationships.
Dr. Fraser’s observations
Some patients progress to schizophrenia’s residual “burnout” phase and become asymptomatic. Mr. M, however, was much younger than other patients with residual schizophrenia, and his mental and physical health were more robust.
Instead, Mr. M may have had complex PTSD secondary to 10 years of abuse by a partner and lifelong abuse by his mother, with drug-induced psychotic symptoms. PTSD can mimic schizoaffective disorder and schizophrenia (Table), and DSM-IV trains us to manage the differential diagnosis first. Mr. M’s revelation about his abusive mother could have raised suspicion of PTSD, but I was targeting apparent psychotic symptoms.
Mr. M’s shame over being gay and his inability to discuss his guilt with family and friends likely contributed to his isolation and perpetuated both the abuse and psychiatric symptoms. Although his ex-partner’s death ended an abusive relationship, his mother’s ongoing abuse prolonged its emotional effects.
If Mr. M. had not revealed his mother’s aggression—in response to a question about his abusive behavior—his psychiatric symptoms may have continued unabated. For years, despite many psychiatric consultations and hospitalizations, Mr. M kept his abusive relationships a secret.
Ask patients about ongoing physical, sexual, and emotional abuse as part of the initial evaluation. Even if the patient denies abuse at first, he or she may reveal this information as the therapeutic alliance develops. As treatment continues—particularly when the patient seems more stressed—ask again about abuse by or toward the patient. If necessary, be direct: “Is anyone hitting or hurting you in any way? Are you hurting someone else in any way?”
Building an alliance
Although clinicians often harbor low expectations for chronically ill patients, I believe that recovery from major psychiatric illness is possible.
Whatever his diagnosis, a strong therapeutic alliance hastened Mr. M’s recovery. Respecting his treatment goals, enhancing motivation to change, being his advocate, and considering alternate diagnoses helped me gain his trust (Box). Because I accepted responsibility for Mr. M’s prescription problems, for example, he sensed that I was on his side. This trust may have ultimately encouraged him to share secrets with me that he had not told other psychiatrists.
Related resources
- National Center for Post-Traumatic Stress Disorder. www.ncptsd.org
- Heim C, Meinlschmidt G, Nemeroff CB. Neurobiology of early-life stress. Psychiatric Annals 2003;33(1):18-26.
- Yehuda R. Post-traumatic stress disorder. N Engl J Med 2002;346:108-14.
Drug brand names
- Bupropion • Wellbutrin
- Divalproex • Depakote
- Lorazepam •Ativan
- Olanzapine • Zyprexa
- Ziprasidone • Geodon
Disclosure
The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
The author thanks Mr. M for permission to publish this case report.
1. Regier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse. Results from the Epidemiologic Catchment Area (ECA) Study. JAMA 1990;264:2511-8.
2. Ziedonis DM, Trudeau K. Motivation to quit using substances among individuals with schizophrenia: implications for a motivation-based treatment model. Schizophr Bull. 1997;23:229-38.
3. Moran M. Skepticism greets report of schizophrenia recovery. Psychiatry News. 2003;38:32-7.
4. Tsuang MT, Levitt JJ, Simpson JC. Schizoaffective disorder. In: Hirsch SR, Weinberger DR (eds). Schizophrenia. Oxford, UK: Blackwell Sciences, 1995;46-57.
History: Threatened by an ‘angel’
Mr. M, age 32, began hearing voices at age 16. He had been diagnosed as having bipolar disorder with psychotic features before presenting to our hospital in 1995. He often experienced hypomania (euphoria, decreased sleep, free spending) followed by depressive periods (lack of energy, tearfulness, decreased concentration), and heard commands to kill himself or saw menacing shadows or “angels.”
Several psychiatrists tried various psychotropics across 6 years, but Mr. M’s odd behaviors persisted. One night he physically threatened his father, who tried to stop Mr. M from eating a sandwich wrapped in a plastic bag. Mr. M was hospitalized that night, and his diagnosis was changed to schizoaffective disorder based on recurrent auditory and visual hallucinations when mood symptoms were absent.
Mr. M was hospitalized nine times within 6 years for psychotic or depressive symptoms— including twice in 1 month for depression and suicidal ideation. Two months later, he attempted suicide by taking 1,200 mg of ziprasidone (about 10 times the normal daily dosage) and an unknown amount of lorazepam, after which he was treated in the ER and released. He presented to me shortly afterward, frightened by his suicide attempt.
At intake, Mr. M was taking lorazepam, 1 mg tid for anxiety, and ziprasidone, 20 mg bid.
Single and unemployed, Mr. M lived with his parents and a brother, and was collecting disability benefits because of his psychiatric problems. He told me that he had been off cocaine for 3 years but had used marijuana 2 weeks earlier. He also reported ongoing family problems but did not elaborate. He said he did not feel suicidal but described continued depressive episodes.
Dr. Fraser’s observations
Mr. M’s last six psychiatric hospitalizations and at least 5 years of outpatient notes by other psychiatrists indicated a history of schizoaffective disorder. Mr. M’s psychotic symptoms persisted for substantial periods while mood symptoms were absent, thus supporting the diagnosis. By contrast, mood and psychotic symptoms in major depression with psychotic features are almost always simultaneous.
Mr. M’s substance use should be considered. Fifty percent of persons with schizophrenia or an affective disorder have a lifetime prevalence of substance abuse disorder.1 The rate climbs to 60% to 90% for patients with schizophrenia seen in emergency rooms, inpatient psychiatric units, and community settings.2
Mr. M’s last documented cocaine use was in 1998; subsequent urine drug screens showed only marijuana.
Cocaine abuse could have contributed to Mr. M’s psychotic symptoms, and marijuana use could have caused his inertia, lack of motivation, and difficulty concentrating. It is unclear why previous doctors attributed most of his psychotic symptoms to a major mental illness rather than cocaine use.
Ask patients about substance use along with a chronology of psychiatric symptoms. Encourage patients who are regularly using substances to stop for a trial period to see if symptoms abate during abstinence. Refer patients for substance use treatment if necessary.
Treatment: A waighty issue
I feared that Mr. M’s psychotic symptoms would recur, but he was more concerned about his depression and obesity. He said he gained 50 pounds over 3 1/2 years while taking olanzapine, 10 to 15 mg/d, and divalproex at various dosages. He stopped both agents on his own and lost 35 pounds across 6 months but was still obese (197 lbs., body mass index [BMI] 32.9).
I prescribed bupropion SR—100 mg/d titrated over several weeks to 200 mg each morning and 100 mg at night—because of its association with weight loss. I also:
- continued ziprasidone, 20 mg bid, to prevent psychosis
- continued lorazepam, 1 mg tid, to reduce anxiety stemming from his family problems. I asked Mr. M to slowly taper off the agent—which he had been taking for 8 years—across 6 to 12 months because a protracted benzodiazepine regimen can contribute to depression.
- referred him to a psychotherapist for cognitive-behavioral therapy to help reduce his depressive thinking and suicide risk
- recommended that he stop using marijuana.
At his second visit, Mr. M reported more auditory hallucinations. I increased ziprasidone to 40 mg bid.
By this time, Mr. M was becoming more comfortable in therapy. He began discussing his family problems in more detail, telling me that his brother is addicted to heroin.
I asked Mr. M if he was again threatening family members or other people. He replied that he had not been violent, but that his mother often slaps him and others in his family. I commended him for not retaliating, but warned him that his mother’s aggression was perpetuating his depression.
I encouraged Mr. M to find an apartment, but he said he could not yet afford to live on his own. I referred him to case management services to help him find affordable housing and urged him to avoid his mother’s assaults. He seemed to appreciate my concern for him.
- Respect the patient’s goals. You fear psychotic symptoms will resurface, but the patient is more concerned about weight gain or other side effects. When possible, choose an agent that targets symptoms without causing the feared side effects.
- Enhance motivation for change. Remind the patient of past successes. Break the broad goal into smaller, achievable goals. Find out the patient’s unique motivations for change.
- Become the patient’s advocate. Accept responsibility for patient care problems. Refer the patient to needed social services.
- Keep an open mind about diagnosis and prognosis. Despite being the definitive diagnostic reference, DSM-IV-TR does not neatly fit all patients, nor account for all human suffering.
Twelve days later, Mr. M made an unplanned visit. He was angry because our pharmacy had not refilled his prescriptions and no one had returned his call asking about the refills. He was irritable but nonthreatening, although he planned to complain to the psychiatric center’s medical director.
I had received no phone messages, and my notes indicated the prescriptions were refilled. Nonetheless, my assuming responsibility for this problem was key to preserving our therapeutic alliance (Box). I resolved the matter and apologized for the miscommunication. Mr. M accepted my apology and scheduled a return visit.
About 1 month later, Mr. M’s self-esteem had increased. He stopped using marijuana, went on a low-calorie diet, and exercised at least 1 hour daily at a local gym. He lost 27 lbs. over 2 months, dropping his weight to 170 lbs. (BMI 28.3). He finished group (15 sessions) and individual (four sessions) psychotherapy, and avoided his mother when she became aggressive.
Before his next monthly visit, Mr. M had called the state vocational rehabilitation department to begin employment. I tapered lorazepam to 0.5 mg nightly while continuing ziprasidone and bupropion. His weight was near normal (150 lbs., BMI 25).
Six months into treatment, Mr. M. applied for a job and moved out of his parents’ home to live with another brother, who does not take drugs. He said that he “felt at peace” for the first time in years. His weight stayed in the 140s. I stopped lorazepam and he requested to see me 3 months later.
Dr. Fraser’s observations
Many patients with schizophrenia or schizoaffective disorder struggle with weight gain, substance use, employment problems, and family conflict, and some make slow progress with one or more of these issues. Mr. M’s rapid improvement on all fronts was striking, however.
Recovery from schizophrenia has been documented,3 and the prognosis for schizoaffective disorder is often more positive than for schizophrenia or severe bipolar disorder.4 Still, Mr. M’s apparent recovery seemed incredible.
To prevent symptom recurrence, I left the bupropion/ziprasidone regimen unchanged. Even after a chronically ill patient responds to medication, I feel dosages should be maintained unless side effects occur or a medication loses effectiveness.
Table
PTSD symptoms that suggest other diagnoses
| PTSD symptoms | Similar to | Diagnosis suggested |
|---|---|---|
| Depersonalization, derealization, dissociation | Psychosis | Schizophrenia, schizoaffective disorder |
| Anxiety, hypervigilance, insomnia | Anxiety | Exacerbations of schizophrenia, schizoaffective disorder, bipolar disorder (mania) |
| Flashbacks, fear of trauma recurrence | Paranoia | Schizophrenia, schizoaffective disorder |
Follow-up: Mr. M’s story
Since the mix-up with Mr. M’s medications, our therapeutic alliance grew stronger. He told me more about himself with each visit. Four months into treatment, he revealed that he is gay and feels “liberated” after years of keeping it secret.
Five months later, Mr. M confided that an older male partner had physically, sexually, and emotionally abused him for about 10 years, starting when Mr. M was 16—about the time his auditory hallucinations began. The abusive relationship ended when the partner died of an unspecified overdose.
Mr. M’s gay friends advised him to seek closure. He visited his ex-partner’s grave, placed a rose, said goodbye, and left vowing he’d never again become an abuse victim. He said he had never told any health professional this story.
Mr. M then asked to be tapered off medications. I was afraid his psychotic symptoms could resurface, although I now wondered whether his schizoaffective disorder diagnosis had been correct. We tapered bupropion and ziprasidone over the next month.
Twenty-four months later, his schizoaffective symptoms had not resurfaced. He worked as a security guard, maintained an apartment, and continued exercising and eating right. His weight stayed normal (140 lbs., BMI 23.3). No signs of hypomania were present, and he was finding fulfillment in nonabusive relationships.
Dr. Fraser’s observations
Some patients progress to schizophrenia’s residual “burnout” phase and become asymptomatic. Mr. M, however, was much younger than other patients with residual schizophrenia, and his mental and physical health were more robust.
Instead, Mr. M may have had complex PTSD secondary to 10 years of abuse by a partner and lifelong abuse by his mother, with drug-induced psychotic symptoms. PTSD can mimic schizoaffective disorder and schizophrenia (Table), and DSM-IV trains us to manage the differential diagnosis first. Mr. M’s revelation about his abusive mother could have raised suspicion of PTSD, but I was targeting apparent psychotic symptoms.
Mr. M’s shame over being gay and his inability to discuss his guilt with family and friends likely contributed to his isolation and perpetuated both the abuse and psychiatric symptoms. Although his ex-partner’s death ended an abusive relationship, his mother’s ongoing abuse prolonged its emotional effects.
If Mr. M. had not revealed his mother’s aggression—in response to a question about his abusive behavior—his psychiatric symptoms may have continued unabated. For years, despite many psychiatric consultations and hospitalizations, Mr. M kept his abusive relationships a secret.
Ask patients about ongoing physical, sexual, and emotional abuse as part of the initial evaluation. Even if the patient denies abuse at first, he or she may reveal this information as the therapeutic alliance develops. As treatment continues—particularly when the patient seems more stressed—ask again about abuse by or toward the patient. If necessary, be direct: “Is anyone hitting or hurting you in any way? Are you hurting someone else in any way?”
Building an alliance
Although clinicians often harbor low expectations for chronically ill patients, I believe that recovery from major psychiatric illness is possible.
Whatever his diagnosis, a strong therapeutic alliance hastened Mr. M’s recovery. Respecting his treatment goals, enhancing motivation to change, being his advocate, and considering alternate diagnoses helped me gain his trust (Box). Because I accepted responsibility for Mr. M’s prescription problems, for example, he sensed that I was on his side. This trust may have ultimately encouraged him to share secrets with me that he had not told other psychiatrists.
Related resources
- National Center for Post-Traumatic Stress Disorder. www.ncptsd.org
- Heim C, Meinlschmidt G, Nemeroff CB. Neurobiology of early-life stress. Psychiatric Annals 2003;33(1):18-26.
- Yehuda R. Post-traumatic stress disorder. N Engl J Med 2002;346:108-14.
Drug brand names
- Bupropion • Wellbutrin
- Divalproex • Depakote
- Lorazepam •Ativan
- Olanzapine • Zyprexa
- Ziprasidone • Geodon
Disclosure
The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
The author thanks Mr. M for permission to publish this case report.
History: Threatened by an ‘angel’
Mr. M, age 32, began hearing voices at age 16. He had been diagnosed as having bipolar disorder with psychotic features before presenting to our hospital in 1995. He often experienced hypomania (euphoria, decreased sleep, free spending) followed by depressive periods (lack of energy, tearfulness, decreased concentration), and heard commands to kill himself or saw menacing shadows or “angels.”
Several psychiatrists tried various psychotropics across 6 years, but Mr. M’s odd behaviors persisted. One night he physically threatened his father, who tried to stop Mr. M from eating a sandwich wrapped in a plastic bag. Mr. M was hospitalized that night, and his diagnosis was changed to schizoaffective disorder based on recurrent auditory and visual hallucinations when mood symptoms were absent.
Mr. M was hospitalized nine times within 6 years for psychotic or depressive symptoms— including twice in 1 month for depression and suicidal ideation. Two months later, he attempted suicide by taking 1,200 mg of ziprasidone (about 10 times the normal daily dosage) and an unknown amount of lorazepam, after which he was treated in the ER and released. He presented to me shortly afterward, frightened by his suicide attempt.
At intake, Mr. M was taking lorazepam, 1 mg tid for anxiety, and ziprasidone, 20 mg bid.
Single and unemployed, Mr. M lived with his parents and a brother, and was collecting disability benefits because of his psychiatric problems. He told me that he had been off cocaine for 3 years but had used marijuana 2 weeks earlier. He also reported ongoing family problems but did not elaborate. He said he did not feel suicidal but described continued depressive episodes.
Dr. Fraser’s observations
Mr. M’s last six psychiatric hospitalizations and at least 5 years of outpatient notes by other psychiatrists indicated a history of schizoaffective disorder. Mr. M’s psychotic symptoms persisted for substantial periods while mood symptoms were absent, thus supporting the diagnosis. By contrast, mood and psychotic symptoms in major depression with psychotic features are almost always simultaneous.
Mr. M’s substance use should be considered. Fifty percent of persons with schizophrenia or an affective disorder have a lifetime prevalence of substance abuse disorder.1 The rate climbs to 60% to 90% for patients with schizophrenia seen in emergency rooms, inpatient psychiatric units, and community settings.2
Mr. M’s last documented cocaine use was in 1998; subsequent urine drug screens showed only marijuana.
Cocaine abuse could have contributed to Mr. M’s psychotic symptoms, and marijuana use could have caused his inertia, lack of motivation, and difficulty concentrating. It is unclear why previous doctors attributed most of his psychotic symptoms to a major mental illness rather than cocaine use.
Ask patients about substance use along with a chronology of psychiatric symptoms. Encourage patients who are regularly using substances to stop for a trial period to see if symptoms abate during abstinence. Refer patients for substance use treatment if necessary.
Treatment: A waighty issue
I feared that Mr. M’s psychotic symptoms would recur, but he was more concerned about his depression and obesity. He said he gained 50 pounds over 3 1/2 years while taking olanzapine, 10 to 15 mg/d, and divalproex at various dosages. He stopped both agents on his own and lost 35 pounds across 6 months but was still obese (197 lbs., body mass index [BMI] 32.9).
I prescribed bupropion SR—100 mg/d titrated over several weeks to 200 mg each morning and 100 mg at night—because of its association with weight loss. I also:
- continued ziprasidone, 20 mg bid, to prevent psychosis
- continued lorazepam, 1 mg tid, to reduce anxiety stemming from his family problems. I asked Mr. M to slowly taper off the agent—which he had been taking for 8 years—across 6 to 12 months because a protracted benzodiazepine regimen can contribute to depression.
- referred him to a psychotherapist for cognitive-behavioral therapy to help reduce his depressive thinking and suicide risk
- recommended that he stop using marijuana.
At his second visit, Mr. M reported more auditory hallucinations. I increased ziprasidone to 40 mg bid.
By this time, Mr. M was becoming more comfortable in therapy. He began discussing his family problems in more detail, telling me that his brother is addicted to heroin.
I asked Mr. M if he was again threatening family members or other people. He replied that he had not been violent, but that his mother often slaps him and others in his family. I commended him for not retaliating, but warned him that his mother’s aggression was perpetuating his depression.
I encouraged Mr. M to find an apartment, but he said he could not yet afford to live on his own. I referred him to case management services to help him find affordable housing and urged him to avoid his mother’s assaults. He seemed to appreciate my concern for him.
- Respect the patient’s goals. You fear psychotic symptoms will resurface, but the patient is more concerned about weight gain or other side effects. When possible, choose an agent that targets symptoms without causing the feared side effects.
- Enhance motivation for change. Remind the patient of past successes. Break the broad goal into smaller, achievable goals. Find out the patient’s unique motivations for change.
- Become the patient’s advocate. Accept responsibility for patient care problems. Refer the patient to needed social services.
- Keep an open mind about diagnosis and prognosis. Despite being the definitive diagnostic reference, DSM-IV-TR does not neatly fit all patients, nor account for all human suffering.
Twelve days later, Mr. M made an unplanned visit. He was angry because our pharmacy had not refilled his prescriptions and no one had returned his call asking about the refills. He was irritable but nonthreatening, although he planned to complain to the psychiatric center’s medical director.
I had received no phone messages, and my notes indicated the prescriptions were refilled. Nonetheless, my assuming responsibility for this problem was key to preserving our therapeutic alliance (Box). I resolved the matter and apologized for the miscommunication. Mr. M accepted my apology and scheduled a return visit.
About 1 month later, Mr. M’s self-esteem had increased. He stopped using marijuana, went on a low-calorie diet, and exercised at least 1 hour daily at a local gym. He lost 27 lbs. over 2 months, dropping his weight to 170 lbs. (BMI 28.3). He finished group (15 sessions) and individual (four sessions) psychotherapy, and avoided his mother when she became aggressive.
Before his next monthly visit, Mr. M had called the state vocational rehabilitation department to begin employment. I tapered lorazepam to 0.5 mg nightly while continuing ziprasidone and bupropion. His weight was near normal (150 lbs., BMI 25).
Six months into treatment, Mr. M. applied for a job and moved out of his parents’ home to live with another brother, who does not take drugs. He said that he “felt at peace” for the first time in years. His weight stayed in the 140s. I stopped lorazepam and he requested to see me 3 months later.
Dr. Fraser’s observations
Many patients with schizophrenia or schizoaffective disorder struggle with weight gain, substance use, employment problems, and family conflict, and some make slow progress with one or more of these issues. Mr. M’s rapid improvement on all fronts was striking, however.
Recovery from schizophrenia has been documented,3 and the prognosis for schizoaffective disorder is often more positive than for schizophrenia or severe bipolar disorder.4 Still, Mr. M’s apparent recovery seemed incredible.
To prevent symptom recurrence, I left the bupropion/ziprasidone regimen unchanged. Even after a chronically ill patient responds to medication, I feel dosages should be maintained unless side effects occur or a medication loses effectiveness.
Table
PTSD symptoms that suggest other diagnoses
| PTSD symptoms | Similar to | Diagnosis suggested |
|---|---|---|
| Depersonalization, derealization, dissociation | Psychosis | Schizophrenia, schizoaffective disorder |
| Anxiety, hypervigilance, insomnia | Anxiety | Exacerbations of schizophrenia, schizoaffective disorder, bipolar disorder (mania) |
| Flashbacks, fear of trauma recurrence | Paranoia | Schizophrenia, schizoaffective disorder |
Follow-up: Mr. M’s story
Since the mix-up with Mr. M’s medications, our therapeutic alliance grew stronger. He told me more about himself with each visit. Four months into treatment, he revealed that he is gay and feels “liberated” after years of keeping it secret.
Five months later, Mr. M confided that an older male partner had physically, sexually, and emotionally abused him for about 10 years, starting when Mr. M was 16—about the time his auditory hallucinations began. The abusive relationship ended when the partner died of an unspecified overdose.
Mr. M’s gay friends advised him to seek closure. He visited his ex-partner’s grave, placed a rose, said goodbye, and left vowing he’d never again become an abuse victim. He said he had never told any health professional this story.
Mr. M then asked to be tapered off medications. I was afraid his psychotic symptoms could resurface, although I now wondered whether his schizoaffective disorder diagnosis had been correct. We tapered bupropion and ziprasidone over the next month.
Twenty-four months later, his schizoaffective symptoms had not resurfaced. He worked as a security guard, maintained an apartment, and continued exercising and eating right. His weight stayed normal (140 lbs., BMI 23.3). No signs of hypomania were present, and he was finding fulfillment in nonabusive relationships.
Dr. Fraser’s observations
Some patients progress to schizophrenia’s residual “burnout” phase and become asymptomatic. Mr. M, however, was much younger than other patients with residual schizophrenia, and his mental and physical health were more robust.
Instead, Mr. M may have had complex PTSD secondary to 10 years of abuse by a partner and lifelong abuse by his mother, with drug-induced psychotic symptoms. PTSD can mimic schizoaffective disorder and schizophrenia (Table), and DSM-IV trains us to manage the differential diagnosis first. Mr. M’s revelation about his abusive mother could have raised suspicion of PTSD, but I was targeting apparent psychotic symptoms.
Mr. M’s shame over being gay and his inability to discuss his guilt with family and friends likely contributed to his isolation and perpetuated both the abuse and psychiatric symptoms. Although his ex-partner’s death ended an abusive relationship, his mother’s ongoing abuse prolonged its emotional effects.
If Mr. M. had not revealed his mother’s aggression—in response to a question about his abusive behavior—his psychiatric symptoms may have continued unabated. For years, despite many psychiatric consultations and hospitalizations, Mr. M kept his abusive relationships a secret.
Ask patients about ongoing physical, sexual, and emotional abuse as part of the initial evaluation. Even if the patient denies abuse at first, he or she may reveal this information as the therapeutic alliance develops. As treatment continues—particularly when the patient seems more stressed—ask again about abuse by or toward the patient. If necessary, be direct: “Is anyone hitting or hurting you in any way? Are you hurting someone else in any way?”
Building an alliance
Although clinicians often harbor low expectations for chronically ill patients, I believe that recovery from major psychiatric illness is possible.
Whatever his diagnosis, a strong therapeutic alliance hastened Mr. M’s recovery. Respecting his treatment goals, enhancing motivation to change, being his advocate, and considering alternate diagnoses helped me gain his trust (Box). Because I accepted responsibility for Mr. M’s prescription problems, for example, he sensed that I was on his side. This trust may have ultimately encouraged him to share secrets with me that he had not told other psychiatrists.
Related resources
- National Center for Post-Traumatic Stress Disorder. www.ncptsd.org
- Heim C, Meinlschmidt G, Nemeroff CB. Neurobiology of early-life stress. Psychiatric Annals 2003;33(1):18-26.
- Yehuda R. Post-traumatic stress disorder. N Engl J Med 2002;346:108-14.
Drug brand names
- Bupropion • Wellbutrin
- Divalproex • Depakote
- Lorazepam •Ativan
- Olanzapine • Zyprexa
- Ziprasidone • Geodon
Disclosure
The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
The author thanks Mr. M for permission to publish this case report.
1. Regier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse. Results from the Epidemiologic Catchment Area (ECA) Study. JAMA 1990;264:2511-8.
2. Ziedonis DM, Trudeau K. Motivation to quit using substances among individuals with schizophrenia: implications for a motivation-based treatment model. Schizophr Bull. 1997;23:229-38.
3. Moran M. Skepticism greets report of schizophrenia recovery. Psychiatry News. 2003;38:32-7.
4. Tsuang MT, Levitt JJ, Simpson JC. Schizoaffective disorder. In: Hirsch SR, Weinberger DR (eds). Schizophrenia. Oxford, UK: Blackwell Sciences, 1995;46-57.
1. Regier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse. Results from the Epidemiologic Catchment Area (ECA) Study. JAMA 1990;264:2511-8.
2. Ziedonis DM, Trudeau K. Motivation to quit using substances among individuals with schizophrenia: implications for a motivation-based treatment model. Schizophr Bull. 1997;23:229-38.
3. Moran M. Skepticism greets report of schizophrenia recovery. Psychiatry News. 2003;38:32-7.
4. Tsuang MT, Levitt JJ, Simpson JC. Schizoaffective disorder. In: Hirsch SR, Weinberger DR (eds). Schizophrenia. Oxford, UK: Blackwell Sciences, 1995;46-57.
Bedside psychotherapy: Brief and surprisingly effective
Bedside psychotherapy is not only possible but invaluable for some medical-surgical patients, despite hospitals’ distractions, lack of privacy, and short stays. If you are asked to evaluate a hospitalized patient, a 5-step strategy can help you:
- identify acute psychiatric problems that psychotherapy can help
- watch for common psychodynamic themes
- choose a beneficial psychotherapy
- integrate drug/psychotherapy, as needed
- quickly establish rapport by using an effective bedside manner.
Case report: A deeply wounded patient
Ms. T, age 45, was admitted to the trauma unit with gunshot wounds. Her estranged husband shot her during an argument and killed her 14-year-old son, who tried to help her.
She underwent multiple surgeries to repair internal organs and endured intense pain. She was medically stable after 10 days, and the surgical team called on the psychiatric consultation-liaison (C-L) service to evaluate her “depression.”
Table 1
5 steps to bedside psychotherapy
|
Ms. T told the psychiatrist she was having nightmares and re-experiencing the shootings. She felt overwhelming guilt and blamed herself for her son’s death. She reported hyperarousal, muscle tension, and palpitations. She also worried about facing her son’s killer in court.
The C-L psychiatrist felt Ms. T would benefit from medication and psychotherapy for anxiety while hospitalized.
Obstacles to bedside psychotherapy
Hospitalized patients do not usually seek psychiatric consultation but are referred by their physicians. Pain and injuries, medications, and illness can limit patients’ energy and motivation to participate in therapy, as well as their concentration and cognition. Moreover, bedside psychotherapy sessions are likely to be interrupted for blood draws, medical rounds, investigations, and procedures.
Despite these obstacles, medical patients are often receptive to psychiatric care.1 An alliance often develops within minutes, and the psychiatrist can achieve effective psychotherapy during a single bedside visit.2
The Academy of Psychosomatic Medicine considers psychotherapy a required skill for anyone who evaluates and treats psychiatric disorders in general medical settings.3
How to overcome obstacles
STEP 1. Identify when psychotherapy may help. Not every problem or patient benefits from bedside psychotherapy. The C-L psychiatrist’s first task is to identify:
- Problems that warrant psychotherapy. These may include depression, bereavement, adjustment disorder, maladaptive coping, anxiety related to medical procedures, acute stress disorder, posttraumatic stress disorder (PTSD), and demoralization.
- Patients likely to benefit. Look for evidence of ego strength, ability to interact in the first session, psychological-mindedness, ability to experience feeling, and absence of severe cognitive deficit.2
These patient traits are not prerequisites, however, and clinical judgment applies on a case-by-case basis.
Demoralization is the most common reason for psychiatric evaluation of medically-ill patients, though their physicians typically request a “depression” evaluation.4 Demoralization is an understandable response to serious illness or disabling, agonizing, or deforming treatment.5 Symptoms include anxiety, guilt, shame, depression, diminished self-worth, and possibly somatic complaints or preoccupation.6
Ms. T was experiencing survivor guilt—she blamed herself for her son’s death—and she described herself as feeling “lost.” Four strategies can treat demoralization (Table 2).
STEP 2. Watch for common psychodynamic themes, such as denial of illness, loss of control, dependency and regression, fear of abandonment, loss of identity, and fear of death.7 Other issues include survivor guilt, anger at the treatment team or family, and knowing someone who had a negative experience with the same illness or treatment.
Identifying these themes and integrating them into the treatment plan can improve outcomes. For example:
- Giving an empathic validation can help overcome fear of abandonment.
- Letting the patient choose the time when blood is drawn increases feelings of control.
Table 2
4 bedside strategies to treat demoralization
| Strategy | Examples |
|---|---|
| Validate the patient’s feeling and experience | Say, “I can see this is frustrating to you to be in the hospital so long,” or “You must feel as if everything is out of your control” |
| Reassure the patient that demoralization is a natural response to a difficult situation | Say, “I can imagine that anyone in your place would feel the same way,” or “It’s only natural to feel this way after what you’ve been through; this does not mean you have a mental illness or are ‘going crazy’” |
| Make simple gestures that promote an improved outlook | Use an effective bedside manner (Box 1) |
| Alleviate feelings of isolation, and foster a sense of hope | Use resilience-building questions (Box 2) |
STEP 3. Select appropriate psychotherapy. The psychiatrist’s challenge is to know:
- when to use which approach
- when to combine approaches
- what problems each approach targets.
A hospitalized medical patient often has a fluctuating course and may require more than one approach—or even a different approach at each visit. Thus, flexibility and creativity are keys to successful bedside psychotherapy.
STEP 4. Integrate psychotherapy with medication, as needed. Consider target symptoms for using psychotropics and how medication may help the patient attain treatment goals. Does the patient require medication to allow psychotherapy to occur?
STEP 5. Combine steps 1 to 4 with a good bedside manner. An empathetic approach will help most patients, no matter which psychotherapy model you use (Box 1).4,8,9
Case continued: First aid for the ego
The C-L psychiatrist diagnosed Ms. T as having acute stress disorder and identified four target symptoms: bereavement, demoralization, anxiety, and hyperarousal. During the initial interview, Ms. T appeared to be psychologically-minded and open to psychiatric intervention.
The psychiatrist considered her at high risk for PTSD and prescribed citalopram, 20 mg/d, because selective serotonin reuptake inhibitors may prevent PTSD. Ms. T was also given clonazepam, 0.25 mg as needed, for severe anxiety.
The psychiatrist visited her 20 to 30 minutes daily. Initial psychotherapy focused on supporting Ms. T’s ego. Resilience-building interviews—using questions to counter feelings of despair, meaninglessness, and sorrow—addressed her demoralization and grief. She regained some sense of meaning and hope by focusing on caring for her other son and on her family’s love. She also found a sense of peace through prayer and by visualizing her lost son safe in God’s hands.
The psychiatrist also taught her relaxation skills to manage her anxiety symptoms. These included abdominal breathing and guided imagery (picturing herself in a safe, comforting place).
- Start by attending to basic physical needs (help the patient get some water or move into a more comfortable position)
- Sit down, even for a brief session
- Smile and touch the patient when appropriate
- Ask “What troubles you most?”
- Inquire about the patient’s experience (ask what the medical illness or treatment was like, not just what happened)
- Look for opportunities to comment on the patient’s strength and accomplishments
- Avoid using confusing medical terms or psychiatric jargon
- Be sensitive to cross-cultural, spiritual, and religious issues, as well as culture-specific health beliefs
Psychotherapeutic options
Three psychotherapeutic approaches are particularly useful at bedside—supportive therapy and resilience-building, cognitive-behavioral therapy (CBT), and psychodynamic therapy.
Supportive therapy and resilience-building is the most common bedside model. Supportive therapy’s goal is to strengthen coping skills, thereby reducing anxiety and enhancing well-being, self-esteem, and function.
Fostering a good working relationship is the first priority.10 The therapist works to contain the patient’s anxiety and provide an “auxiliary ego” to supplement his or her reality testing, planning and judgment, and sense of self.2,10 Supportive techniques include suggestion, clarification, limit-setting, reinforcement, reassurance, and empathic listening.
Much of the work relies on positive transference to build the supportive relationship.8,10 Transference is interpreted only when negative transference disrupts treatment; the therapeutic goal is to decrease the patient’s anxiety. Resilience-building questions (Box 2)4,11 help identify the patient’s skills and competencies and mobilize his or her internal resources.
CBT attempts to identify, challenge, and correct a patient’s inaccurate or dysfunctional beliefs about illness, treatment, or self-image. For example:
- a patient with second-degree burns may be convinced she is the world’s ugliest person
- a patient facing an operation may believe he will be permanently disabled, as was his father after a similar procedure.
CBT can also help dispel beliefs that psychiatric treatment is for “crazy” people.
Behavioral therapy can help patients manage distress related to their medical care, such as shortness of breath while being weaned from a ventilator or arousal and anxiety related to procedures. Techniques that work in office settings—systematic desensitization, in vivo exposure, breathing exercises, progressive muscle relaxation, guided imagery, meditation, and hypnosis—also can be effective at bedside.12
Psychodynamic therapy. Patients can develop insight through psychodynamic therapy, even in brief therapeutic relationships. Useful bedside techniques include clarification, confrontation, and interpretation of behavior, conflict, and transference.
For example, a patient who survived heart surgery later developed depression and suicidal ideation. Psychiatric interview revealed she was experiencing survivor guilt because her mother had died from a heart attack. Emphatic clarification and validation of feelings often can help lift such a patient’s mood and allow a dialogue to begin.
A “psychodynamic life-narrative” approach1 can help treat depression in medically ill patients. The therapist first asks the patient to describe the illness’ meaning in his or her lifespan, then formulates a statement (the “narrative”) of its meaning at the moment. The narrative is intended to:
- create a new perspective
- increase self-esteem by emphasizing the patient’s strengths
- support coping mechanisms that worked in the past.
This approach also can help the patient understand that a psychiatric symptom is an understandable response when a previously successful adaptive method cannot be used.
Choosing a psychotherapy
Three factors—patient characteristics, therapist characteristics, and evidence—determine the psychotherapeutic approach.
Patient characteristics include ego functioning level and maturity, object relationship stability,13 history and experience of psychotherapeutic treatment, personality and coping style, and physical condition. For example:
- CBT and education may be effective for patients who cope through analytical thinking, controlling emotional expression, and managing situations.
- Psychodynamic methods may help those who cope through expressing feelings, self-reflection, and a wish to be understood.
Therapist characteristics include experience, preference, and degree of comfort in conducting each therapeutic approach, as well as time and schedule.
The goal of a resilience-building interview is to enable patients under stress to focus their attention and mobilize their emotions while answering each question.10,14 Here are sample questions, grouped by issues the psychiatrist wishes to address.
Countering isolation
- Who understands your situation?
- In whose presence do you feel peaceful?
Countering meaninglessness
- For whom or what does it matter that you continue to live?
Countering despair
- What keeps you from giving up on difficult days?
- From what sources do you draw hope?
Countering sorrow
- What sustains your capacity for joy in the midst of pain?
- What has this experience added to your life?
- Are there things that take your mind off your illness and comfort you?
Promoting resilience
- What part of you is strongest right now?
- What is still possible?
Promoting continuity of self/role preservation
- What should I know about you as a person that lies beyond this illness?
- How have you prevented this illness from taking charge of your life and identity?
- What did you do before you were sick that was important to you?
- What about yourself or your life are you most proud of?
- What have you learned about your life during your illness that you would want to pass along to others?
Evidence of efficacy. Psychiatric literature supports using CBT for depressive cognition in major depression,14 resilience-building interviews for demoralization,4 and behavioral therapy and relaxation for anxiety related to medical procedures.12
Case continued: Coming home
As Ms. T’s medical condition improved over several days and her discharge was planned, the psychiatrist began to emphasize practical issues, such as:
- limiting visitation to allow her time to grieve
- addressing her anxieties about outpatient treatment and moving in with her parents.
At discharge, Ms. T was taking citalopram, 40 mg/d, and clonazepam, 0.25 mg as needed. With this regimen, her nightmares and re-experiencing had decreased. The psychiatrist had treated Ms. T in the hospital for 21 days. She continued psychiatric care for acute stress disorder at a local outpatient center.
Related resources
- Academy of Psychosomatic Medicine. www.apm.org
- American Psychosomatic Society. www.psychosomatic.org
- Griffith JL, Griffith ME. Encountering the sacred in psychotherapy: how to talk with people about their spiritual lives. New York: Guilford Press, 2002.
- Dewan MJ, Steenbarger BN, Greenberg RP (eds). The art and science of brief psychotherapies: a practitioner’s guide. Washington, DC: American Psychiatric Publishing, 2004
Drug brand names
- Citalopram • Celexa
- Clonazepam • Klonopin
Disclosure
Dr. Lolak reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgments
The author thanks James Griffith, MD, and Thomas Wise, MD, for their valuable contributions to this article.
1. Viederman M, Perry SW, 3rd. Use of a psychodynamic life narrative in the treatment of depression in the physically ill. Gen Hosp Psychiatry 1980;2(3):177-85.
2. Lipsitt D. Psychotherapy. In: Wise MG, Rundell JR (eds). Textbook of consultation-liaison psychiatry: psychiatry in the medically ill (2nd ed). Washington, DC: American Psychiatric Publishing, 2002;1027-51.
3. Bronheim HE, Fulop G, Kunkel EJ, et al. The Academy of Psychosomatic Medicine practice guidelines for psychiatric consultation in the general medical setting. Psychosomatics 1998;39(4):S8-S30.
4. Griffith JL, Gaby L. Brief psychotherapy at the bedside: countering demoralization from medical Illness. In press.
5. Slavney PR. Diagnosing demoralization in consultation psychiatry. Psychosomatics 1999;40(4):325-9.
6. Goldberg RL, Green S. Medical psychotherapy. Am Fam Physician 1985;31(1):173-8.
7. Postone N. Psychotherapy with cancer patients. Am J Psychother 1998;52(4):412-24.
8. Muskin PR. The combined use of psychotherapy and pharmacotherapy in the medical setting. Psychiatr Clin North Am 1990;13(2):341-53.
9. Yager J. Specific components of bedside manner in the general hospital psychiatric consultation: 12 concrete suggestions. Psychosomatics 1989;30(2):209-12.
10. Ursano RJ, Silberman EK. Psychoanalysis, psychoanalytic psychotherapy, and supportive psychotherapy. In: Hales RE, Yudofsky SC (eds). Textbook of clinical psychiatry (4th ed). Washington, DC: American Psychiatric Publishing, 2003;1177-1203.
11. Chochinov HM. Dignity-conserving care—a new model for palliative care: helping the patient feel valued. JAMA 2002;287(17):2253-60.
12. Barrows KA, Jacobs BP. Mind-body medicine. An introduction and review of the literature. Med Clin North Am 2002;86(1):11-31.
13. O’Dowd MA, Gomez MF. Psychotherapy in consultation-liaison psychiatry. Am J Psychother 2001;55(1):122-32.
14. Wright JH, Beck AT, Thase ME. Cognitive therapy. In: Hales RE, Yudofsky SC (eds). Textbook of clinical psychiatry (4th ed). Washington, DC: American Psychiatric Publishing, 2003;1245-84.
Bedside psychotherapy is not only possible but invaluable for some medical-surgical patients, despite hospitals’ distractions, lack of privacy, and short stays. If you are asked to evaluate a hospitalized patient, a 5-step strategy can help you:
- identify acute psychiatric problems that psychotherapy can help
- watch for common psychodynamic themes
- choose a beneficial psychotherapy
- integrate drug/psychotherapy, as needed
- quickly establish rapport by using an effective bedside manner.
Case report: A deeply wounded patient
Ms. T, age 45, was admitted to the trauma unit with gunshot wounds. Her estranged husband shot her during an argument and killed her 14-year-old son, who tried to help her.
She underwent multiple surgeries to repair internal organs and endured intense pain. She was medically stable after 10 days, and the surgical team called on the psychiatric consultation-liaison (C-L) service to evaluate her “depression.”
Table 1
5 steps to bedside psychotherapy
|
Ms. T told the psychiatrist she was having nightmares and re-experiencing the shootings. She felt overwhelming guilt and blamed herself for her son’s death. She reported hyperarousal, muscle tension, and palpitations. She also worried about facing her son’s killer in court.
The C-L psychiatrist felt Ms. T would benefit from medication and psychotherapy for anxiety while hospitalized.
Obstacles to bedside psychotherapy
Hospitalized patients do not usually seek psychiatric consultation but are referred by their physicians. Pain and injuries, medications, and illness can limit patients’ energy and motivation to participate in therapy, as well as their concentration and cognition. Moreover, bedside psychotherapy sessions are likely to be interrupted for blood draws, medical rounds, investigations, and procedures.
Despite these obstacles, medical patients are often receptive to psychiatric care.1 An alliance often develops within minutes, and the psychiatrist can achieve effective psychotherapy during a single bedside visit.2
The Academy of Psychosomatic Medicine considers psychotherapy a required skill for anyone who evaluates and treats psychiatric disorders in general medical settings.3
How to overcome obstacles
STEP 1. Identify when psychotherapy may help. Not every problem or patient benefits from bedside psychotherapy. The C-L psychiatrist’s first task is to identify:
- Problems that warrant psychotherapy. These may include depression, bereavement, adjustment disorder, maladaptive coping, anxiety related to medical procedures, acute stress disorder, posttraumatic stress disorder (PTSD), and demoralization.
- Patients likely to benefit. Look for evidence of ego strength, ability to interact in the first session, psychological-mindedness, ability to experience feeling, and absence of severe cognitive deficit.2
These patient traits are not prerequisites, however, and clinical judgment applies on a case-by-case basis.
Demoralization is the most common reason for psychiatric evaluation of medically-ill patients, though their physicians typically request a “depression” evaluation.4 Demoralization is an understandable response to serious illness or disabling, agonizing, or deforming treatment.5 Symptoms include anxiety, guilt, shame, depression, diminished self-worth, and possibly somatic complaints or preoccupation.6
Ms. T was experiencing survivor guilt—she blamed herself for her son’s death—and she described herself as feeling “lost.” Four strategies can treat demoralization (Table 2).
STEP 2. Watch for common psychodynamic themes, such as denial of illness, loss of control, dependency and regression, fear of abandonment, loss of identity, and fear of death.7 Other issues include survivor guilt, anger at the treatment team or family, and knowing someone who had a negative experience with the same illness or treatment.
Identifying these themes and integrating them into the treatment plan can improve outcomes. For example:
- Giving an empathic validation can help overcome fear of abandonment.
- Letting the patient choose the time when blood is drawn increases feelings of control.
Table 2
4 bedside strategies to treat demoralization
| Strategy | Examples |
|---|---|
| Validate the patient’s feeling and experience | Say, “I can see this is frustrating to you to be in the hospital so long,” or “You must feel as if everything is out of your control” |
| Reassure the patient that demoralization is a natural response to a difficult situation | Say, “I can imagine that anyone in your place would feel the same way,” or “It’s only natural to feel this way after what you’ve been through; this does not mean you have a mental illness or are ‘going crazy’” |
| Make simple gestures that promote an improved outlook | Use an effective bedside manner (Box 1) |
| Alleviate feelings of isolation, and foster a sense of hope | Use resilience-building questions (Box 2) |
STEP 3. Select appropriate psychotherapy. The psychiatrist’s challenge is to know:
- when to use which approach
- when to combine approaches
- what problems each approach targets.
A hospitalized medical patient often has a fluctuating course and may require more than one approach—or even a different approach at each visit. Thus, flexibility and creativity are keys to successful bedside psychotherapy.
STEP 4. Integrate psychotherapy with medication, as needed. Consider target symptoms for using psychotropics and how medication may help the patient attain treatment goals. Does the patient require medication to allow psychotherapy to occur?
STEP 5. Combine steps 1 to 4 with a good bedside manner. An empathetic approach will help most patients, no matter which psychotherapy model you use (Box 1).4,8,9
Case continued: First aid for the ego
The C-L psychiatrist diagnosed Ms. T as having acute stress disorder and identified four target symptoms: bereavement, demoralization, anxiety, and hyperarousal. During the initial interview, Ms. T appeared to be psychologically-minded and open to psychiatric intervention.
The psychiatrist considered her at high risk for PTSD and prescribed citalopram, 20 mg/d, because selective serotonin reuptake inhibitors may prevent PTSD. Ms. T was also given clonazepam, 0.25 mg as needed, for severe anxiety.
The psychiatrist visited her 20 to 30 minutes daily. Initial psychotherapy focused on supporting Ms. T’s ego. Resilience-building interviews—using questions to counter feelings of despair, meaninglessness, and sorrow—addressed her demoralization and grief. She regained some sense of meaning and hope by focusing on caring for her other son and on her family’s love. She also found a sense of peace through prayer and by visualizing her lost son safe in God’s hands.
The psychiatrist also taught her relaxation skills to manage her anxiety symptoms. These included abdominal breathing and guided imagery (picturing herself in a safe, comforting place).
- Start by attending to basic physical needs (help the patient get some water or move into a more comfortable position)
- Sit down, even for a brief session
- Smile and touch the patient when appropriate
- Ask “What troubles you most?”
- Inquire about the patient’s experience (ask what the medical illness or treatment was like, not just what happened)
- Look for opportunities to comment on the patient’s strength and accomplishments
- Avoid using confusing medical terms or psychiatric jargon
- Be sensitive to cross-cultural, spiritual, and religious issues, as well as culture-specific health beliefs
Psychotherapeutic options
Three psychotherapeutic approaches are particularly useful at bedside—supportive therapy and resilience-building, cognitive-behavioral therapy (CBT), and psychodynamic therapy.
Supportive therapy and resilience-building is the most common bedside model. Supportive therapy’s goal is to strengthen coping skills, thereby reducing anxiety and enhancing well-being, self-esteem, and function.
Fostering a good working relationship is the first priority.10 The therapist works to contain the patient’s anxiety and provide an “auxiliary ego” to supplement his or her reality testing, planning and judgment, and sense of self.2,10 Supportive techniques include suggestion, clarification, limit-setting, reinforcement, reassurance, and empathic listening.
Much of the work relies on positive transference to build the supportive relationship.8,10 Transference is interpreted only when negative transference disrupts treatment; the therapeutic goal is to decrease the patient’s anxiety. Resilience-building questions (Box 2)4,11 help identify the patient’s skills and competencies and mobilize his or her internal resources.
CBT attempts to identify, challenge, and correct a patient’s inaccurate or dysfunctional beliefs about illness, treatment, or self-image. For example:
- a patient with second-degree burns may be convinced she is the world’s ugliest person
- a patient facing an operation may believe he will be permanently disabled, as was his father after a similar procedure.
CBT can also help dispel beliefs that psychiatric treatment is for “crazy” people.
Behavioral therapy can help patients manage distress related to their medical care, such as shortness of breath while being weaned from a ventilator or arousal and anxiety related to procedures. Techniques that work in office settings—systematic desensitization, in vivo exposure, breathing exercises, progressive muscle relaxation, guided imagery, meditation, and hypnosis—also can be effective at bedside.12
Psychodynamic therapy. Patients can develop insight through psychodynamic therapy, even in brief therapeutic relationships. Useful bedside techniques include clarification, confrontation, and interpretation of behavior, conflict, and transference.
For example, a patient who survived heart surgery later developed depression and suicidal ideation. Psychiatric interview revealed she was experiencing survivor guilt because her mother had died from a heart attack. Emphatic clarification and validation of feelings often can help lift such a patient’s mood and allow a dialogue to begin.
A “psychodynamic life-narrative” approach1 can help treat depression in medically ill patients. The therapist first asks the patient to describe the illness’ meaning in his or her lifespan, then formulates a statement (the “narrative”) of its meaning at the moment. The narrative is intended to:
- create a new perspective
- increase self-esteem by emphasizing the patient’s strengths
- support coping mechanisms that worked in the past.
This approach also can help the patient understand that a psychiatric symptom is an understandable response when a previously successful adaptive method cannot be used.
Choosing a psychotherapy
Three factors—patient characteristics, therapist characteristics, and evidence—determine the psychotherapeutic approach.
Patient characteristics include ego functioning level and maturity, object relationship stability,13 history and experience of psychotherapeutic treatment, personality and coping style, and physical condition. For example:
- CBT and education may be effective for patients who cope through analytical thinking, controlling emotional expression, and managing situations.
- Psychodynamic methods may help those who cope through expressing feelings, self-reflection, and a wish to be understood.
Therapist characteristics include experience, preference, and degree of comfort in conducting each therapeutic approach, as well as time and schedule.
The goal of a resilience-building interview is to enable patients under stress to focus their attention and mobilize their emotions while answering each question.10,14 Here are sample questions, grouped by issues the psychiatrist wishes to address.
Countering isolation
- Who understands your situation?
- In whose presence do you feel peaceful?
Countering meaninglessness
- For whom or what does it matter that you continue to live?
Countering despair
- What keeps you from giving up on difficult days?
- From what sources do you draw hope?
Countering sorrow
- What sustains your capacity for joy in the midst of pain?
- What has this experience added to your life?
- Are there things that take your mind off your illness and comfort you?
Promoting resilience
- What part of you is strongest right now?
- What is still possible?
Promoting continuity of self/role preservation
- What should I know about you as a person that lies beyond this illness?
- How have you prevented this illness from taking charge of your life and identity?
- What did you do before you were sick that was important to you?
- What about yourself or your life are you most proud of?
- What have you learned about your life during your illness that you would want to pass along to others?
Evidence of efficacy. Psychiatric literature supports using CBT for depressive cognition in major depression,14 resilience-building interviews for demoralization,4 and behavioral therapy and relaxation for anxiety related to medical procedures.12
Case continued: Coming home
As Ms. T’s medical condition improved over several days and her discharge was planned, the psychiatrist began to emphasize practical issues, such as:
- limiting visitation to allow her time to grieve
- addressing her anxieties about outpatient treatment and moving in with her parents.
At discharge, Ms. T was taking citalopram, 40 mg/d, and clonazepam, 0.25 mg as needed. With this regimen, her nightmares and re-experiencing had decreased. The psychiatrist had treated Ms. T in the hospital for 21 days. She continued psychiatric care for acute stress disorder at a local outpatient center.
Related resources
- Academy of Psychosomatic Medicine. www.apm.org
- American Psychosomatic Society. www.psychosomatic.org
- Griffith JL, Griffith ME. Encountering the sacred in psychotherapy: how to talk with people about their spiritual lives. New York: Guilford Press, 2002.
- Dewan MJ, Steenbarger BN, Greenberg RP (eds). The art and science of brief psychotherapies: a practitioner’s guide. Washington, DC: American Psychiatric Publishing, 2004
Drug brand names
- Citalopram • Celexa
- Clonazepam • Klonopin
Disclosure
Dr. Lolak reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgments
The author thanks James Griffith, MD, and Thomas Wise, MD, for their valuable contributions to this article.
Bedside psychotherapy is not only possible but invaluable for some medical-surgical patients, despite hospitals’ distractions, lack of privacy, and short stays. If you are asked to evaluate a hospitalized patient, a 5-step strategy can help you:
- identify acute psychiatric problems that psychotherapy can help
- watch for common psychodynamic themes
- choose a beneficial psychotherapy
- integrate drug/psychotherapy, as needed
- quickly establish rapport by using an effective bedside manner.
Case report: A deeply wounded patient
Ms. T, age 45, was admitted to the trauma unit with gunshot wounds. Her estranged husband shot her during an argument and killed her 14-year-old son, who tried to help her.
She underwent multiple surgeries to repair internal organs and endured intense pain. She was medically stable after 10 days, and the surgical team called on the psychiatric consultation-liaison (C-L) service to evaluate her “depression.”
Table 1
5 steps to bedside psychotherapy
|
Ms. T told the psychiatrist she was having nightmares and re-experiencing the shootings. She felt overwhelming guilt and blamed herself for her son’s death. She reported hyperarousal, muscle tension, and palpitations. She also worried about facing her son’s killer in court.
The C-L psychiatrist felt Ms. T would benefit from medication and psychotherapy for anxiety while hospitalized.
Obstacles to bedside psychotherapy
Hospitalized patients do not usually seek psychiatric consultation but are referred by their physicians. Pain and injuries, medications, and illness can limit patients’ energy and motivation to participate in therapy, as well as their concentration and cognition. Moreover, bedside psychotherapy sessions are likely to be interrupted for blood draws, medical rounds, investigations, and procedures.
Despite these obstacles, medical patients are often receptive to psychiatric care.1 An alliance often develops within minutes, and the psychiatrist can achieve effective psychotherapy during a single bedside visit.2
The Academy of Psychosomatic Medicine considers psychotherapy a required skill for anyone who evaluates and treats psychiatric disorders in general medical settings.3
How to overcome obstacles
STEP 1. Identify when psychotherapy may help. Not every problem or patient benefits from bedside psychotherapy. The C-L psychiatrist’s first task is to identify:
- Problems that warrant psychotherapy. These may include depression, bereavement, adjustment disorder, maladaptive coping, anxiety related to medical procedures, acute stress disorder, posttraumatic stress disorder (PTSD), and demoralization.
- Patients likely to benefit. Look for evidence of ego strength, ability to interact in the first session, psychological-mindedness, ability to experience feeling, and absence of severe cognitive deficit.2
These patient traits are not prerequisites, however, and clinical judgment applies on a case-by-case basis.
Demoralization is the most common reason for psychiatric evaluation of medically-ill patients, though their physicians typically request a “depression” evaluation.4 Demoralization is an understandable response to serious illness or disabling, agonizing, or deforming treatment.5 Symptoms include anxiety, guilt, shame, depression, diminished self-worth, and possibly somatic complaints or preoccupation.6
Ms. T was experiencing survivor guilt—she blamed herself for her son’s death—and she described herself as feeling “lost.” Four strategies can treat demoralization (Table 2).
STEP 2. Watch for common psychodynamic themes, such as denial of illness, loss of control, dependency and regression, fear of abandonment, loss of identity, and fear of death.7 Other issues include survivor guilt, anger at the treatment team or family, and knowing someone who had a negative experience with the same illness or treatment.
Identifying these themes and integrating them into the treatment plan can improve outcomes. For example:
- Giving an empathic validation can help overcome fear of abandonment.
- Letting the patient choose the time when blood is drawn increases feelings of control.
Table 2
4 bedside strategies to treat demoralization
| Strategy | Examples |
|---|---|
| Validate the patient’s feeling and experience | Say, “I can see this is frustrating to you to be in the hospital so long,” or “You must feel as if everything is out of your control” |
| Reassure the patient that demoralization is a natural response to a difficult situation | Say, “I can imagine that anyone in your place would feel the same way,” or “It’s only natural to feel this way after what you’ve been through; this does not mean you have a mental illness or are ‘going crazy’” |
| Make simple gestures that promote an improved outlook | Use an effective bedside manner (Box 1) |
| Alleviate feelings of isolation, and foster a sense of hope | Use resilience-building questions (Box 2) |
STEP 3. Select appropriate psychotherapy. The psychiatrist’s challenge is to know:
- when to use which approach
- when to combine approaches
- what problems each approach targets.
A hospitalized medical patient often has a fluctuating course and may require more than one approach—or even a different approach at each visit. Thus, flexibility and creativity are keys to successful bedside psychotherapy.
STEP 4. Integrate psychotherapy with medication, as needed. Consider target symptoms for using psychotropics and how medication may help the patient attain treatment goals. Does the patient require medication to allow psychotherapy to occur?
STEP 5. Combine steps 1 to 4 with a good bedside manner. An empathetic approach will help most patients, no matter which psychotherapy model you use (Box 1).4,8,9
Case continued: First aid for the ego
The C-L psychiatrist diagnosed Ms. T as having acute stress disorder and identified four target symptoms: bereavement, demoralization, anxiety, and hyperarousal. During the initial interview, Ms. T appeared to be psychologically-minded and open to psychiatric intervention.
The psychiatrist considered her at high risk for PTSD and prescribed citalopram, 20 mg/d, because selective serotonin reuptake inhibitors may prevent PTSD. Ms. T was also given clonazepam, 0.25 mg as needed, for severe anxiety.
The psychiatrist visited her 20 to 30 minutes daily. Initial psychotherapy focused on supporting Ms. T’s ego. Resilience-building interviews—using questions to counter feelings of despair, meaninglessness, and sorrow—addressed her demoralization and grief. She regained some sense of meaning and hope by focusing on caring for her other son and on her family’s love. She also found a sense of peace through prayer and by visualizing her lost son safe in God’s hands.
The psychiatrist also taught her relaxation skills to manage her anxiety symptoms. These included abdominal breathing and guided imagery (picturing herself in a safe, comforting place).
- Start by attending to basic physical needs (help the patient get some water or move into a more comfortable position)
- Sit down, even for a brief session
- Smile and touch the patient when appropriate
- Ask “What troubles you most?”
- Inquire about the patient’s experience (ask what the medical illness or treatment was like, not just what happened)
- Look for opportunities to comment on the patient’s strength and accomplishments
- Avoid using confusing medical terms or psychiatric jargon
- Be sensitive to cross-cultural, spiritual, and religious issues, as well as culture-specific health beliefs
Psychotherapeutic options
Three psychotherapeutic approaches are particularly useful at bedside—supportive therapy and resilience-building, cognitive-behavioral therapy (CBT), and psychodynamic therapy.
Supportive therapy and resilience-building is the most common bedside model. Supportive therapy’s goal is to strengthen coping skills, thereby reducing anxiety and enhancing well-being, self-esteem, and function.
Fostering a good working relationship is the first priority.10 The therapist works to contain the patient’s anxiety and provide an “auxiliary ego” to supplement his or her reality testing, planning and judgment, and sense of self.2,10 Supportive techniques include suggestion, clarification, limit-setting, reinforcement, reassurance, and empathic listening.
Much of the work relies on positive transference to build the supportive relationship.8,10 Transference is interpreted only when negative transference disrupts treatment; the therapeutic goal is to decrease the patient’s anxiety. Resilience-building questions (Box 2)4,11 help identify the patient’s skills and competencies and mobilize his or her internal resources.
CBT attempts to identify, challenge, and correct a patient’s inaccurate or dysfunctional beliefs about illness, treatment, or self-image. For example:
- a patient with second-degree burns may be convinced she is the world’s ugliest person
- a patient facing an operation may believe he will be permanently disabled, as was his father after a similar procedure.
CBT can also help dispel beliefs that psychiatric treatment is for “crazy” people.
Behavioral therapy can help patients manage distress related to their medical care, such as shortness of breath while being weaned from a ventilator or arousal and anxiety related to procedures. Techniques that work in office settings—systematic desensitization, in vivo exposure, breathing exercises, progressive muscle relaxation, guided imagery, meditation, and hypnosis—also can be effective at bedside.12
Psychodynamic therapy. Patients can develop insight through psychodynamic therapy, even in brief therapeutic relationships. Useful bedside techniques include clarification, confrontation, and interpretation of behavior, conflict, and transference.
For example, a patient who survived heart surgery later developed depression and suicidal ideation. Psychiatric interview revealed she was experiencing survivor guilt because her mother had died from a heart attack. Emphatic clarification and validation of feelings often can help lift such a patient’s mood and allow a dialogue to begin.
A “psychodynamic life-narrative” approach1 can help treat depression in medically ill patients. The therapist first asks the patient to describe the illness’ meaning in his or her lifespan, then formulates a statement (the “narrative”) of its meaning at the moment. The narrative is intended to:
- create a new perspective
- increase self-esteem by emphasizing the patient’s strengths
- support coping mechanisms that worked in the past.
This approach also can help the patient understand that a psychiatric symptom is an understandable response when a previously successful adaptive method cannot be used.
Choosing a psychotherapy
Three factors—patient characteristics, therapist characteristics, and evidence—determine the psychotherapeutic approach.
Patient characteristics include ego functioning level and maturity, object relationship stability,13 history and experience of psychotherapeutic treatment, personality and coping style, and physical condition. For example:
- CBT and education may be effective for patients who cope through analytical thinking, controlling emotional expression, and managing situations.
- Psychodynamic methods may help those who cope through expressing feelings, self-reflection, and a wish to be understood.
Therapist characteristics include experience, preference, and degree of comfort in conducting each therapeutic approach, as well as time and schedule.
The goal of a resilience-building interview is to enable patients under stress to focus their attention and mobilize their emotions while answering each question.10,14 Here are sample questions, grouped by issues the psychiatrist wishes to address.
Countering isolation
- Who understands your situation?
- In whose presence do you feel peaceful?
Countering meaninglessness
- For whom or what does it matter that you continue to live?
Countering despair
- What keeps you from giving up on difficult days?
- From what sources do you draw hope?
Countering sorrow
- What sustains your capacity for joy in the midst of pain?
- What has this experience added to your life?
- Are there things that take your mind off your illness and comfort you?
Promoting resilience
- What part of you is strongest right now?
- What is still possible?
Promoting continuity of self/role preservation
- What should I know about you as a person that lies beyond this illness?
- How have you prevented this illness from taking charge of your life and identity?
- What did you do before you were sick that was important to you?
- What about yourself or your life are you most proud of?
- What have you learned about your life during your illness that you would want to pass along to others?
Evidence of efficacy. Psychiatric literature supports using CBT for depressive cognition in major depression,14 resilience-building interviews for demoralization,4 and behavioral therapy and relaxation for anxiety related to medical procedures.12
Case continued: Coming home
As Ms. T’s medical condition improved over several days and her discharge was planned, the psychiatrist began to emphasize practical issues, such as:
- limiting visitation to allow her time to grieve
- addressing her anxieties about outpatient treatment and moving in with her parents.
At discharge, Ms. T was taking citalopram, 40 mg/d, and clonazepam, 0.25 mg as needed. With this regimen, her nightmares and re-experiencing had decreased. The psychiatrist had treated Ms. T in the hospital for 21 days. She continued psychiatric care for acute stress disorder at a local outpatient center.
Related resources
- Academy of Psychosomatic Medicine. www.apm.org
- American Psychosomatic Society. www.psychosomatic.org
- Griffith JL, Griffith ME. Encountering the sacred in psychotherapy: how to talk with people about their spiritual lives. New York: Guilford Press, 2002.
- Dewan MJ, Steenbarger BN, Greenberg RP (eds). The art and science of brief psychotherapies: a practitioner’s guide. Washington, DC: American Psychiatric Publishing, 2004
Drug brand names
- Citalopram • Celexa
- Clonazepam • Klonopin
Disclosure
Dr. Lolak reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgments
The author thanks James Griffith, MD, and Thomas Wise, MD, for their valuable contributions to this article.
1. Viederman M, Perry SW, 3rd. Use of a psychodynamic life narrative in the treatment of depression in the physically ill. Gen Hosp Psychiatry 1980;2(3):177-85.
2. Lipsitt D. Psychotherapy. In: Wise MG, Rundell JR (eds). Textbook of consultation-liaison psychiatry: psychiatry in the medically ill (2nd ed). Washington, DC: American Psychiatric Publishing, 2002;1027-51.
3. Bronheim HE, Fulop G, Kunkel EJ, et al. The Academy of Psychosomatic Medicine practice guidelines for psychiatric consultation in the general medical setting. Psychosomatics 1998;39(4):S8-S30.
4. Griffith JL, Gaby L. Brief psychotherapy at the bedside: countering demoralization from medical Illness. In press.
5. Slavney PR. Diagnosing demoralization in consultation psychiatry. Psychosomatics 1999;40(4):325-9.
6. Goldberg RL, Green S. Medical psychotherapy. Am Fam Physician 1985;31(1):173-8.
7. Postone N. Psychotherapy with cancer patients. Am J Psychother 1998;52(4):412-24.
8. Muskin PR. The combined use of psychotherapy and pharmacotherapy in the medical setting. Psychiatr Clin North Am 1990;13(2):341-53.
9. Yager J. Specific components of bedside manner in the general hospital psychiatric consultation: 12 concrete suggestions. Psychosomatics 1989;30(2):209-12.
10. Ursano RJ, Silberman EK. Psychoanalysis, psychoanalytic psychotherapy, and supportive psychotherapy. In: Hales RE, Yudofsky SC (eds). Textbook of clinical psychiatry (4th ed). Washington, DC: American Psychiatric Publishing, 2003;1177-1203.
11. Chochinov HM. Dignity-conserving care—a new model for palliative care: helping the patient feel valued. JAMA 2002;287(17):2253-60.
12. Barrows KA, Jacobs BP. Mind-body medicine. An introduction and review of the literature. Med Clin North Am 2002;86(1):11-31.
13. O’Dowd MA, Gomez MF. Psychotherapy in consultation-liaison psychiatry. Am J Psychother 2001;55(1):122-32.
14. Wright JH, Beck AT, Thase ME. Cognitive therapy. In: Hales RE, Yudofsky SC (eds). Textbook of clinical psychiatry (4th ed). Washington, DC: American Psychiatric Publishing, 2003;1245-84.
1. Viederman M, Perry SW, 3rd. Use of a psychodynamic life narrative in the treatment of depression in the physically ill. Gen Hosp Psychiatry 1980;2(3):177-85.
2. Lipsitt D. Psychotherapy. In: Wise MG, Rundell JR (eds). Textbook of consultation-liaison psychiatry: psychiatry in the medically ill (2nd ed). Washington, DC: American Psychiatric Publishing, 2002;1027-51.
3. Bronheim HE, Fulop G, Kunkel EJ, et al. The Academy of Psychosomatic Medicine practice guidelines for psychiatric consultation in the general medical setting. Psychosomatics 1998;39(4):S8-S30.
4. Griffith JL, Gaby L. Brief psychotherapy at the bedside: countering demoralization from medical Illness. In press.
5. Slavney PR. Diagnosing demoralization in consultation psychiatry. Psychosomatics 1999;40(4):325-9.
6. Goldberg RL, Green S. Medical psychotherapy. Am Fam Physician 1985;31(1):173-8.
7. Postone N. Psychotherapy with cancer patients. Am J Psychother 1998;52(4):412-24.
8. Muskin PR. The combined use of psychotherapy and pharmacotherapy in the medical setting. Psychiatr Clin North Am 1990;13(2):341-53.
9. Yager J. Specific components of bedside manner in the general hospital psychiatric consultation: 12 concrete suggestions. Psychosomatics 1989;30(2):209-12.
10. Ursano RJ, Silberman EK. Psychoanalysis, psychoanalytic psychotherapy, and supportive psychotherapy. In: Hales RE, Yudofsky SC (eds). Textbook of clinical psychiatry (4th ed). Washington, DC: American Psychiatric Publishing, 2003;1177-1203.
11. Chochinov HM. Dignity-conserving care—a new model for palliative care: helping the patient feel valued. JAMA 2002;287(17):2253-60.
12. Barrows KA, Jacobs BP. Mind-body medicine. An introduction and review of the literature. Med Clin North Am 2002;86(1):11-31.
13. O’Dowd MA, Gomez MF. Psychotherapy in consultation-liaison psychiatry. Am J Psychother 2001;55(1):122-32.
14. Wright JH, Beck AT, Thase ME. Cognitive therapy. In: Hales RE, Yudofsky SC (eds). Textbook of clinical psychiatry (4th ed). Washington, DC: American Psychiatric Publishing, 2003;1245-84.
Exercise and depression
Exercise is an important component of depression treatment (Current Psychiatry, June 2004). Exercise:
- helps metabolize cortisol, which is directly toxic to CNS neurons. Lowering cortisol levels improves neuronal connections.
- raises endorphin levels, which increases global feelings of well-being and activates reward centers in the brain.
- raises core body temperature, which promotes deeper and more restful sleep, during which serotonin is replenished.
Common reasons patients resist exercise include:
Lack of energy associated with a depressive episode. When I explain the benefits of exercise, however, patients are more likely to consider it.
Self-consciousness. Physically inactive patients are often reluctant to exercise in public, so help them choose an acceptable regimen and location.
Time management. I tell patients that exercise will increase their energy, making them more efficient. I also mention that exercise is a lifelong necessity for maintaining health.
I work primarily with young adults in a university health center. The key to getting students to exercise is to start very slowly—5 to 10 minutes of brisk walking three to five times weekly—then add 5 minutes per week until they are exercising about 30 minutes at a time.
I also preach persistence and patience, since the patient must exercise for 6 to 8 weeks to see a benefit. In the interim, I may help them choose a regular time to exercise, then encourage them to reward themselves by purchasing new walking shoes or exercise clothes if they are still exercising after 2 weeks. If a patient cannot follow a self-imposed schedule, participation in a fitness class may be more effective.
Linda L. Keeler MD
Counseling and Psychological Services
University of Kansas, Lawrence
The article, “Exercise for depression: Here’s how to get patients moving” shows the value of exercise in relieving depressive symptoms.
The authors summarize the evidence clinicians need for recommending that an exercise program may be just as effective as psychotherapy or pharmacotherapy for treating depression.
I plan to use the article to educate trainees in medicine, psychiatry, psychology, and social work. Thanks for publishing such a balanced, health-oriented discussion.
Stanley E. Harrris, MD, DFAPA
University psychiatrist
Clinical professor of psychiatry and the behavioral sciences
Keck School of Medicine
University of Southern California
Los Angeles
Exercise is an important component of depression treatment (Current Psychiatry, June 2004). Exercise:
- helps metabolize cortisol, which is directly toxic to CNS neurons. Lowering cortisol levels improves neuronal connections.
- raises endorphin levels, which increases global feelings of well-being and activates reward centers in the brain.
- raises core body temperature, which promotes deeper and more restful sleep, during which serotonin is replenished.
Common reasons patients resist exercise include:
Lack of energy associated with a depressive episode. When I explain the benefits of exercise, however, patients are more likely to consider it.
Self-consciousness. Physically inactive patients are often reluctant to exercise in public, so help them choose an acceptable regimen and location.
Time management. I tell patients that exercise will increase their energy, making them more efficient. I also mention that exercise is a lifelong necessity for maintaining health.
I work primarily with young adults in a university health center. The key to getting students to exercise is to start very slowly—5 to 10 minutes of brisk walking three to five times weekly—then add 5 minutes per week until they are exercising about 30 minutes at a time.
I also preach persistence and patience, since the patient must exercise for 6 to 8 weeks to see a benefit. In the interim, I may help them choose a regular time to exercise, then encourage them to reward themselves by purchasing new walking shoes or exercise clothes if they are still exercising after 2 weeks. If a patient cannot follow a self-imposed schedule, participation in a fitness class may be more effective.
Linda L. Keeler MD
Counseling and Psychological Services
University of Kansas, Lawrence
The article, “Exercise for depression: Here’s how to get patients moving” shows the value of exercise in relieving depressive symptoms.
The authors summarize the evidence clinicians need for recommending that an exercise program may be just as effective as psychotherapy or pharmacotherapy for treating depression.
I plan to use the article to educate trainees in medicine, psychiatry, psychology, and social work. Thanks for publishing such a balanced, health-oriented discussion.
Stanley E. Harrris, MD, DFAPA
University psychiatrist
Clinical professor of psychiatry and the behavioral sciences
Keck School of Medicine
University of Southern California
Los Angeles
Exercise is an important component of depression treatment (Current Psychiatry, June 2004). Exercise:
- helps metabolize cortisol, which is directly toxic to CNS neurons. Lowering cortisol levels improves neuronal connections.
- raises endorphin levels, which increases global feelings of well-being and activates reward centers in the brain.
- raises core body temperature, which promotes deeper and more restful sleep, during which serotonin is replenished.
Common reasons patients resist exercise include:
Lack of energy associated with a depressive episode. When I explain the benefits of exercise, however, patients are more likely to consider it.
Self-consciousness. Physically inactive patients are often reluctant to exercise in public, so help them choose an acceptable regimen and location.
Time management. I tell patients that exercise will increase their energy, making them more efficient. I also mention that exercise is a lifelong necessity for maintaining health.
I work primarily with young adults in a university health center. The key to getting students to exercise is to start very slowly—5 to 10 minutes of brisk walking three to five times weekly—then add 5 minutes per week until they are exercising about 30 minutes at a time.
I also preach persistence and patience, since the patient must exercise for 6 to 8 weeks to see a benefit. In the interim, I may help them choose a regular time to exercise, then encourage them to reward themselves by purchasing new walking shoes or exercise clothes if they are still exercising after 2 weeks. If a patient cannot follow a self-imposed schedule, participation in a fitness class may be more effective.
Linda L. Keeler MD
Counseling and Psychological Services
University of Kansas, Lawrence
The article, “Exercise for depression: Here’s how to get patients moving” shows the value of exercise in relieving depressive symptoms.
The authors summarize the evidence clinicians need for recommending that an exercise program may be just as effective as psychotherapy or pharmacotherapy for treating depression.
I plan to use the article to educate trainees in medicine, psychiatry, psychology, and social work. Thanks for publishing such a balanced, health-oriented discussion.
Stanley E. Harrris, MD, DFAPA
University psychiatrist
Clinical professor of psychiatry and the behavioral sciences
Keck School of Medicine
University of Southern California
Los Angeles
Is conduct disorder real?
I am rebutting “How to reduce aggression in patients with conduct disorder” (Current Psychiatry, April 2004).
A 15-year-old ended his first two visits with me under police custody and was committed both times. After the first commitment, his grandmother filed a petition alleging unruly/delinquent behavior, and a judge ordered the boy to take his prescribed mood stabilizers. That was necessary because the hospital psychiatrist had determined that the boy was not mentally ill and that his grandmother needed parenting classes. The youth’s original diagnosis—conduct disorder and oppositional-defiant disorder (ODD)—contradicted my diagnosis: bipolar disorder, mixed.
During the second hospitalization, a psychiatrist diagnosed the youth as having attentiondeficit/hyperactivity disorder (ADHD). The doctor prescribed methylphenidate and oxcarbazepine, but the patient’s guardian did not consent to the medications.
Facing a sentence at the county juvenile detention center, the youth started taking olanzapine, 10 mg at bedtime, and lamotrigine, 25 mg bid titrated to 50 mg bid, as I had prescribed. His grandmother says that he no longer exhibits defiant behavior. At his third visit, he shook my hand and said, “Thank you for finding the right medications for me.”
I have seen hundreds of similar cases over 10 years. To paraphrase a colleague, diagnosing somebody with conduct disorder or ODD is like diagnosing a patient with a runny nose after a thorough emergency room examination.
I applaud the American Association of Community Psychiatry’s efforts to urge the American Psychiatric Association (APA) to abolish the conduct disorder diagnosis. I also support the many researchers who are requesting elimination of conduct disorder and ODD. These are not real and specific diagnoses but are alleged syndromes that express several conditions.
Manuel Mota-Castillo MD
Orlando, FL
Dr. Malone responds
It is hard to assess Dr. Mota-Castillo’s case based on the information he provided. Still, one would not refute any psychiatric syndrome by citing a single case.
Most psychiatric disorders are syndromes and affect heterogeneous groups. This is true for disorders that are more prevalent in adults—such as schizophrenia and mania—and for those that present in childhood and adolescence—such as conduct disorder, ODD, and ADHD. Heterogeneity within disorders is no doubt related to underlying individual differences in genetics and environment and contributes to differences in symptom expression and treatment response.
Dr. Mota-Castillo did not present symptoms listed under DSM-IV-TR, so it is unclear how the patient was diagnosed. Diagnoses:
- are one clinician’s impression or the consensus of several clinicians
- are based on one patient encounter or ongoing treatment
- occur with or without input from other sources, such as parents and school
- are made with or without validated structured interviews.
Conduct disorder and ODDare part of DSM diagnostic nomenclature,1 and the APA and American Academy of Child and Adolescent Psychiatry recognize both disorders. Reducing aggression associated with either disorder has long been the most common reason for psychiatric consultation in children.2
Also, Dr. Mota-Castillo prescribed olanzapine and lamotrigine, apparently for simultaneous use. The main point of our case was to discourage polypharmacy—something most experts agree should be avoided3 —by carefully starting one drug before adding a second. When a child receives two drugs at once, we cannot know the effect of either.
In the 15-year-old’s case, as often happens, the prescribed treatment might not have changed the symptoms; some symptoms remit spontaneously.
Nor does drug response clarify diagnosis. For example, both bipolar disorder and aggression in conduct disorder (and in many other conditions) may respond to an antipsychotic.4 Lithium and other treatments for mania have been shown to reduce severe aggression in nonmanic children and adolescents with conduct disorder.5,6
Richard P. Malone, MD
Associate professor
Eastern Pennsylvania Psychiatric Institute
Drexel University College of Medicine
Philadelphia, PA
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (4th ed-rev). Washington, DC: American Psychiatric Association, 2000.
- Kazdin AE. Conduct disorders in childhood and adolescence, vol. 9: developmental clinical psychology and psychiatry series. Newbury Park, CA: Sage Publications, 1987.
- Pappadopulos E, Macintyre JC II, Crismon ML, et al. Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY): Part II. J Am Acad Child Adolesc Psychiatry 2003;42(2):145–61.
- Malone RP, Delaney MA. Psychopharmacologic interventions in children with aggression: neuroleptics, lithium, and anticonvulsants. In: Coccaro EF (ed). Aggression: assessment and treatment.New York: Marcel Dekker, 2003:331–49.
- Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry 2000;57(7):649–54.
- Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry 1995;34(4):445–53.
I am rebutting “How to reduce aggression in patients with conduct disorder” (Current Psychiatry, April 2004).
A 15-year-old ended his first two visits with me under police custody and was committed both times. After the first commitment, his grandmother filed a petition alleging unruly/delinquent behavior, and a judge ordered the boy to take his prescribed mood stabilizers. That was necessary because the hospital psychiatrist had determined that the boy was not mentally ill and that his grandmother needed parenting classes. The youth’s original diagnosis—conduct disorder and oppositional-defiant disorder (ODD)—contradicted my diagnosis: bipolar disorder, mixed.
During the second hospitalization, a psychiatrist diagnosed the youth as having attentiondeficit/hyperactivity disorder (ADHD). The doctor prescribed methylphenidate and oxcarbazepine, but the patient’s guardian did not consent to the medications.
Facing a sentence at the county juvenile detention center, the youth started taking olanzapine, 10 mg at bedtime, and lamotrigine, 25 mg bid titrated to 50 mg bid, as I had prescribed. His grandmother says that he no longer exhibits defiant behavior. At his third visit, he shook my hand and said, “Thank you for finding the right medications for me.”
I have seen hundreds of similar cases over 10 years. To paraphrase a colleague, diagnosing somebody with conduct disorder or ODD is like diagnosing a patient with a runny nose after a thorough emergency room examination.
I applaud the American Association of Community Psychiatry’s efforts to urge the American Psychiatric Association (APA) to abolish the conduct disorder diagnosis. I also support the many researchers who are requesting elimination of conduct disorder and ODD. These are not real and specific diagnoses but are alleged syndromes that express several conditions.
Manuel Mota-Castillo MD
Orlando, FL
Dr. Malone responds
It is hard to assess Dr. Mota-Castillo’s case based on the information he provided. Still, one would not refute any psychiatric syndrome by citing a single case.
Most psychiatric disorders are syndromes and affect heterogeneous groups. This is true for disorders that are more prevalent in adults—such as schizophrenia and mania—and for those that present in childhood and adolescence—such as conduct disorder, ODD, and ADHD. Heterogeneity within disorders is no doubt related to underlying individual differences in genetics and environment and contributes to differences in symptom expression and treatment response.
Dr. Mota-Castillo did not present symptoms listed under DSM-IV-TR, so it is unclear how the patient was diagnosed. Diagnoses:
- are one clinician’s impression or the consensus of several clinicians
- are based on one patient encounter or ongoing treatment
- occur with or without input from other sources, such as parents and school
- are made with or without validated structured interviews.
Conduct disorder and ODDare part of DSM diagnostic nomenclature,1 and the APA and American Academy of Child and Adolescent Psychiatry recognize both disorders. Reducing aggression associated with either disorder has long been the most common reason for psychiatric consultation in children.2
Also, Dr. Mota-Castillo prescribed olanzapine and lamotrigine, apparently for simultaneous use. The main point of our case was to discourage polypharmacy—something most experts agree should be avoided3 —by carefully starting one drug before adding a second. When a child receives two drugs at once, we cannot know the effect of either.
In the 15-year-old’s case, as often happens, the prescribed treatment might not have changed the symptoms; some symptoms remit spontaneously.
Nor does drug response clarify diagnosis. For example, both bipolar disorder and aggression in conduct disorder (and in many other conditions) may respond to an antipsychotic.4 Lithium and other treatments for mania have been shown to reduce severe aggression in nonmanic children and adolescents with conduct disorder.5,6
Richard P. Malone, MD
Associate professor
Eastern Pennsylvania Psychiatric Institute
Drexel University College of Medicine
Philadelphia, PA
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (4th ed-rev). Washington, DC: American Psychiatric Association, 2000.
- Kazdin AE. Conduct disorders in childhood and adolescence, vol. 9: developmental clinical psychology and psychiatry series. Newbury Park, CA: Sage Publications, 1987.
- Pappadopulos E, Macintyre JC II, Crismon ML, et al. Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY): Part II. J Am Acad Child Adolesc Psychiatry 2003;42(2):145–61.
- Malone RP, Delaney MA. Psychopharmacologic interventions in children with aggression: neuroleptics, lithium, and anticonvulsants. In: Coccaro EF (ed). Aggression: assessment and treatment.New York: Marcel Dekker, 2003:331–49.
- Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry 2000;57(7):649–54.
- Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry 1995;34(4):445–53.
I am rebutting “How to reduce aggression in patients with conduct disorder” (Current Psychiatry, April 2004).
A 15-year-old ended his first two visits with me under police custody and was committed both times. After the first commitment, his grandmother filed a petition alleging unruly/delinquent behavior, and a judge ordered the boy to take his prescribed mood stabilizers. That was necessary because the hospital psychiatrist had determined that the boy was not mentally ill and that his grandmother needed parenting classes. The youth’s original diagnosis—conduct disorder and oppositional-defiant disorder (ODD)—contradicted my diagnosis: bipolar disorder, mixed.
During the second hospitalization, a psychiatrist diagnosed the youth as having attentiondeficit/hyperactivity disorder (ADHD). The doctor prescribed methylphenidate and oxcarbazepine, but the patient’s guardian did not consent to the medications.
Facing a sentence at the county juvenile detention center, the youth started taking olanzapine, 10 mg at bedtime, and lamotrigine, 25 mg bid titrated to 50 mg bid, as I had prescribed. His grandmother says that he no longer exhibits defiant behavior. At his third visit, he shook my hand and said, “Thank you for finding the right medications for me.”
I have seen hundreds of similar cases over 10 years. To paraphrase a colleague, diagnosing somebody with conduct disorder or ODD is like diagnosing a patient with a runny nose after a thorough emergency room examination.
I applaud the American Association of Community Psychiatry’s efforts to urge the American Psychiatric Association (APA) to abolish the conduct disorder diagnosis. I also support the many researchers who are requesting elimination of conduct disorder and ODD. These are not real and specific diagnoses but are alleged syndromes that express several conditions.
Manuel Mota-Castillo MD
Orlando, FL
Dr. Malone responds
It is hard to assess Dr. Mota-Castillo’s case based on the information he provided. Still, one would not refute any psychiatric syndrome by citing a single case.
Most psychiatric disorders are syndromes and affect heterogeneous groups. This is true for disorders that are more prevalent in adults—such as schizophrenia and mania—and for those that present in childhood and adolescence—such as conduct disorder, ODD, and ADHD. Heterogeneity within disorders is no doubt related to underlying individual differences in genetics and environment and contributes to differences in symptom expression and treatment response.
Dr. Mota-Castillo did not present symptoms listed under DSM-IV-TR, so it is unclear how the patient was diagnosed. Diagnoses:
- are one clinician’s impression or the consensus of several clinicians
- are based on one patient encounter or ongoing treatment
- occur with or without input from other sources, such as parents and school
- are made with or without validated structured interviews.
Conduct disorder and ODDare part of DSM diagnostic nomenclature,1 and the APA and American Academy of Child and Adolescent Psychiatry recognize both disorders. Reducing aggression associated with either disorder has long been the most common reason for psychiatric consultation in children.2
Also, Dr. Mota-Castillo prescribed olanzapine and lamotrigine, apparently for simultaneous use. The main point of our case was to discourage polypharmacy—something most experts agree should be avoided3 —by carefully starting one drug before adding a second. When a child receives two drugs at once, we cannot know the effect of either.
In the 15-year-old’s case, as often happens, the prescribed treatment might not have changed the symptoms; some symptoms remit spontaneously.
Nor does drug response clarify diagnosis. For example, both bipolar disorder and aggression in conduct disorder (and in many other conditions) may respond to an antipsychotic.4 Lithium and other treatments for mania have been shown to reduce severe aggression in nonmanic children and adolescents with conduct disorder.5,6
Richard P. Malone, MD
Associate professor
Eastern Pennsylvania Psychiatric Institute
Drexel University College of Medicine
Philadelphia, PA
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (4th ed-rev). Washington, DC: American Psychiatric Association, 2000.
- Kazdin AE. Conduct disorders in childhood and adolescence, vol. 9: developmental clinical psychology and psychiatry series. Newbury Park, CA: Sage Publications, 1987.
- Pappadopulos E, Macintyre JC II, Crismon ML, et al. Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY): Part II. J Am Acad Child Adolesc Psychiatry 2003;42(2):145–61.
- Malone RP, Delaney MA. Psychopharmacologic interventions in children with aggression: neuroleptics, lithium, and anticonvulsants. In: Coccaro EF (ed). Aggression: assessment and treatment.New York: Marcel Dekker, 2003:331–49.
- Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry 2000;57(7):649–54.
- Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry 1995;34(4):445–53.
Antipsychotic dosage correction
In Dr. Willem Martens’ article, “Recovery from schizophrenia: Fact or fiction” (Current Psychiatry, July 2004), dosages listed for several antipsychotics in Table 3 were inaccurate—specifically risperidone (25-50 mg/d) and ziprasidone (10 mg/d). Some clozapine side effects, such as increased blood glucose and weight gain, were omitted.
Also omitted was the fact that haloperidol reduces positive symptoms, while the atypical antipsychotics reduce negative symptoms.
James Patras MD
Assistant professor of clinical psychiatry
University of Illinois at Chicago School of Medicine
Dr. Martens responds
The recommended risperidone dosage was incorrect because the decimals were omitted. The correct dosage is 2.5 to 5 mg/d.
Concerning haloperidol, severely disturbed patients often receive 30 to 40 mg/d, and particularly resistant patients have received up to 100 mg/d. Haloperidol is useful for managing acute and chronic psychosis as well as aggression and agitated behavior.
The normal ziprasidone dosage is between 80 and 160 mg/d but can range from 10 mg/d for less-severe cases to 200 mg/d for exceptionally severe and treatment-resistant patients.
Finally, I did not list all possible side effects; there are too many to mention in such a short space.
Willem HJ Martens, MD, PhD
Director, W. Kahn Institute of Theoretical Psychiatry and Neuroscience
Elst (Utrecht), The Netherlands
In Dr. Willem Martens’ article, “Recovery from schizophrenia: Fact or fiction” (Current Psychiatry, July 2004), dosages listed for several antipsychotics in Table 3 were inaccurate—specifically risperidone (25-50 mg/d) and ziprasidone (10 mg/d). Some clozapine side effects, such as increased blood glucose and weight gain, were omitted.
Also omitted was the fact that haloperidol reduces positive symptoms, while the atypical antipsychotics reduce negative symptoms.
James Patras MD
Assistant professor of clinical psychiatry
University of Illinois at Chicago School of Medicine
Dr. Martens responds
The recommended risperidone dosage was incorrect because the decimals were omitted. The correct dosage is 2.5 to 5 mg/d.
Concerning haloperidol, severely disturbed patients often receive 30 to 40 mg/d, and particularly resistant patients have received up to 100 mg/d. Haloperidol is useful for managing acute and chronic psychosis as well as aggression and agitated behavior.
The normal ziprasidone dosage is between 80 and 160 mg/d but can range from 10 mg/d for less-severe cases to 200 mg/d for exceptionally severe and treatment-resistant patients.
Finally, I did not list all possible side effects; there are too many to mention in such a short space.
Willem HJ Martens, MD, PhD
Director, W. Kahn Institute of Theoretical Psychiatry and Neuroscience
Elst (Utrecht), The Netherlands
In Dr. Willem Martens’ article, “Recovery from schizophrenia: Fact or fiction” (Current Psychiatry, July 2004), dosages listed for several antipsychotics in Table 3 were inaccurate—specifically risperidone (25-50 mg/d) and ziprasidone (10 mg/d). Some clozapine side effects, such as increased blood glucose and weight gain, were omitted.
Also omitted was the fact that haloperidol reduces positive symptoms, while the atypical antipsychotics reduce negative symptoms.
James Patras MD
Assistant professor of clinical psychiatry
University of Illinois at Chicago School of Medicine
Dr. Martens responds
The recommended risperidone dosage was incorrect because the decimals were omitted. The correct dosage is 2.5 to 5 mg/d.
Concerning haloperidol, severely disturbed patients often receive 30 to 40 mg/d, and particularly resistant patients have received up to 100 mg/d. Haloperidol is useful for managing acute and chronic psychosis as well as aggression and agitated behavior.
The normal ziprasidone dosage is between 80 and 160 mg/d but can range from 10 mg/d for less-severe cases to 200 mg/d for exceptionally severe and treatment-resistant patients.
Finally, I did not list all possible side effects; there are too many to mention in such a short space.
Willem HJ Martens, MD, PhD
Director, W. Kahn Institute of Theoretical Psychiatry and Neuroscience
Elst (Utrecht), The Netherlands


