Current Psychiatry

Mr. Z, age 38, came to the United States from a predominantly Islamic country to study science and engineering. While in graduate school, he was seen by a primary care physician for complaints of hypersomnia; reduced appetite with an approximate 15-lb weight loss; impaired concentration and memory, which hurt his academic performance; low energy; and occasional thoughts about dying.

Mr. Z’s physical examination and lab results were unremarkable, and he reported no psychiatric history. He was diagnosed with depression and was prescribed sertraline, 50 mg/d, but he refused to take it. He declined referral to a psychiatrist but agreed to weekly psychotherapy with a psychology intern at the student mental health center.

During therapy, Mr. Z said he constantly felt lonely. He feared being ostracized because of his Islamic beliefs and lifestyle, yet reported tremendous guilt over violating Islamic codes forbidding premarital sex. He told his therapist that his longing for a romantic relationship was “contaminating” his soul, and fantasized that death would free him of impure, sexual thoughts.

The severity of Mr. Z’s depression and his preoccupation with death alarmed the therapist. She referred him to a clinic psychiatrist, but Mr. Z refused to see him, saying that his depression was a punishment from God for his sexual sins. He vowed to repent by undergoing psychotherapy.

Continued therapy: A ‘religious awakening’

During the first 4 months of therapy, Mr. Z’s Beck Depression Inventory score fell from 32 to 17, indicating mild depression.

Mr. Z then reported that he experienced a “religious awakening” and began describing his mood and experiences in religious terms. He thanked his therapist for “saving his soul.”

The therapist was stunned by Mr. Z’s sudden transformation in mood and affect. He slept 7 to 8 hours a night, and his academic performance improved dramatically. He exhibited stable (though bright) affect and no thought disorder. His therapist viewed his use of religious terminology, though significant, as a cultural artifact because there were no signs of psychosis. Although no objective signs of mania or hypomania were apparent, the therapist suspected he might have bipolar disorder. She again tried unsuccessfully to refer him to a psychiatrist.

Then came Sept. 11, 2001.

Mr. Z was traumatized by the terrorist attacks on the World Trade Center and the Pentagon. He feared a backlash against Muslims in the United States but showed no signs of paranoia.

A few months later, however, Mr. Z became preoccupied with the attacks and harbored conspiracy theories alleging that the United States government had committed them. His speech was rapid and pressured, and he slept only 2 to 3 hours nightly. We later learned that he had not attended class for months and only sporadically showed up for lab work.

Mr. Z then began to fear he was under surveillance and that his visa would be revoked. His affect became increasingly intense during psychotherapy, and he frequently used religious metaphors and concepts. His therapist realized he was suffering a worsening manic episode, although suicidal or homicidal thoughts were not present.

Down with ‘nonbelievers’

During a subsequent session, Mr. Z reported that he had become engaged to marry a well-known supermodel. He also announced a plan to “rid the world of nonbelievers”—people who were not devout Christians, Jews, or Muslims. His three-stage plan called for:

• gently persuading nonbelievers to change their beliefs and lifestyles
• threatening nonbelievers who did not repent after polite persuasion
• “eliminating all the nonbelievers” who did not respond to intimidation.

Mr. Z viewed his therapist as “commander of the believers” and considered the three-phased plan to be her will. She questioned Mr. Z extensively about how, when, and against whom he intended to carry out this plan. He identified no specific targets, but did say, “I’ll know what do to when the time comes. I am an engineer, and I know a lot about explosives.”

The therapist then recommended an emergency psychiatric evaluation, which Mr. Z declined. She immediately notified the mental health clinic’s attending psychiatrist.

What are the therapist’s options? Can Mr. Z be involuntarily committed based on his threats of violence against “nonbelievers?”

Dr. Kennedy’s and Dr. Klafter’s observations

Two legal principles justify involuntary commitment of a patient who poses a threat to himself or the public:

Police power refers to the government’s role in maintaining public safety. State commitment statutes usually require that a mentally ill person pose a significant and imminent threat to the public. The psychiatrist who files an affidavit alleging danger does not need absolute certainty or perfect information but must act in good faith.¹

Parens patriae, or paternalism, refers to government intervention on behalf of persons incapable of managing their lives.¹

Psychiatric treatment of unwilling patients is possible in some states. Family members and/or mental health professionals can petition the court to compel outpatient psychiatric treatment.

Because an emergency evaluation produces a thorough and controlled psychiatric assessment (and minimal deprivation of personal liberty), a psychiatrist with any doubt about the patient’s condition should move toward commitment.

Box 1

Before resorting to legal coercion, try scheduling more-frequent appointments to monitor symptom progression. This would allow faster response when civil commitment criteria are met.

A psychiatrist or other mental health professional can request an emergency evaluation based on information from a knowledgeable intermediary or family member—even if the clinician did not recently or directly interview the patient.² For example, a psychologist could receive information from a case manager who encountered the patient decompensating. It would be impractical to require a psychiatrist to see a decompensating patient before an evaluation can be ordered.

Hospitalization: A ‘blood-drinking monster’

With no security staff immediately available, the attending psychiatrist and therapist sent Mr. Z home.

The psychiatrist then submitted an application for involuntary hospitalization—in which the doctor summarized the case—and faxed it to the local psychiatric emergency service. The police were notified and—after verifying that the appropriate paperwork had been completed—arrested Mr. Z at his home and brought him to the emergency service for an assessment. Mr. Z was then hospitalized. (Box 1).

Mr. Z was found to be harboring bizarre, grandiose, persecutory, and religious delusions. He claimed that a blood-drinking monster was lurking inside the hospital, and that his hospitalization was part of a conspiracy to persecute Muslims. He considered the Sept. 11 attacks fictitious and claimed that widely broadcast television news footage of the attacks was a computer-animated video. The patient refused all medications while hospitalized.

After 3 days, the court ordered Mr. Z’s discharge, citing lack of evidence that he posed any danger to self or others. At his mental health probate hearing, he managed to conceal his psychotic symptoms while testifying. The court expressed concern over his technical training in explosives but ruled that he was not dangerous because he had never used this knowledge to commit violence.

Upon discharge, Mr. Z declined outpatient psychiatric treatment. The therapist then told Mr. Z that she would terminate psychotherapy after two sessions unless he visited a psychiatrist. Mr. Z again refused, and psychotherapy was terminated.

Box 2

Would you terminate psychotherapy at this point? Could the therapist’s actions be viewed as patient abandonment?

Dr. Kennedy’s and Dr. Klafter’s observations

The formation of a professional relationship establishes a duty of care and requires the clinician to provide reasonable notice of termination and alternative sources of care. Although 30 days’ notice is generally appropriate, several factors may dictate the need for more or less notice (Box 2).

In Mr. Z’s case, we view the psychologist’s behavior as appropriate because:

• Without psychotropics, Mr. Z’s psychosis would likely persist. To continue treating him with psychotherapy alone would fall below the standard of care.
• By threatening to terminate psychotherapy, the therapist tried to use the patient’s transference and desire to maintain the therapeutic relationship as an incentive to accept medication.

Continued observation: A clue from the past

Mr. Z’s brother, who was contacted by the treatment team, reported that the patient had never been violent. He did note, however, that as an adolescent Mr. Z talked about joining a terrorist organization, though he had never followed through. The brother tried to persuade Mr. Z to leave school and live with him on the West Coast, but he instead chose to continue his studies.

Mr. Z’s hospital treatment team realized that his continued work in engineering—where he had access to explosive materials—posed a significant risk given his impaired judgment. Acting on a forensic expert’s advice, the team warned university officials about Mr. Z’s mental state and preoccupation with violence. The FBI was also contacted.

Was the treatment team justified in reporting Mr. Z’s behavior to authorities, even though he never identified any potential victims?

Dr. Kennedy’s and Dr. Klafter’s observations

Various legislative and judicial remedies—some more restrictive than others—address the psychiatrist’s duty to third parties:³

• Some states require psychiatrists to notify or protect third parties when any danger is foreseeable, regardless of threat or victim.
• Other states require specific threats but charge the psychiatrist with foreseeing all potential victims regardless of whether they were named.
• Still other states limit protection to identifiable victims, even if no threat is issued.
• In some states the psychiatrist is responsible only if the patient makes specific threats to identifiable victims.

Again, psychiatrists need to make their best professional judgments in good faith about risk of violence. Hospitalizing a threatening patient provides the most protection to third parties, but this option is intrusive, coercive, and is not always appropriate or feasible. If the threat is directed toward the public rather than specific individuals or groups, law enforcement agencies can reduce the risk somewhat through monitoring and surveillance.

Although it is a judgment call, clinicians should notify:

• all persons or organizations against whom a patient might commit violence
• and those who might be targeted as instruments for violence towards others, such as family members who have guns the patient could obtain.

A terrorist would not likely seek psychiatric help relative to his goals of terrorism because such behavior is not rooted in major mental illness. However, the heightened sense of paranoia and anxiety created by events involving terrorism, religious animosity, and hatred provide patients who struggle with psychosis an outlet for their paranoia. As such, we should take a patient’s terroristic threats seriously.

Conclusion: Going home

The university granted Mr. Z medical leave and placed him on academic probation for 2 months, during which he returned to his native country to stay with his parents.

The faculty later dismissed Mr. Z from the program, citing poor academic and laboratory performance. His visa expired, with renewal contingent upon enrollment in a full-time academic program.

Related resources

• American Academy of Psychiatry and the Law. www.aapl.org.

Drug brand names

• Sertraline • Zoloft

Disclosure

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

Mr. Z, age 38, came to the United States from a predominantly Islamic country to study science and engineering. While in graduate school, he was seen by a primary care physician for complaints of hypersomnia; reduced appetite with an approximate 15-lb weight loss; impaired concentration and memory, which hurt his academic performance; low energy; and occasional thoughts about dying.

Mr. Z’s physical examination and lab results were unremarkable, and he reported no psychiatric history. He was diagnosed with depression and was prescribed sertraline, 50 mg/d, but he refused to take it. He declined referral to a psychiatrist but agreed to weekly psychotherapy with a psychology intern at the student mental health center.

During therapy, Mr. Z said he constantly felt lonely. He feared being ostracized because of his Islamic beliefs and lifestyle, yet reported tremendous guilt over violating Islamic codes forbidding premarital sex. He told his therapist that his longing for a romantic relationship was “contaminating” his soul, and fantasized that death would free him of impure, sexual thoughts.

The severity of Mr. Z’s depression and his preoccupation with death alarmed the therapist. She referred him to a clinic psychiatrist, but Mr. Z refused to see him, saying that his depression was a punishment from God for his sexual sins. He vowed to repent by undergoing psychotherapy.

Continued therapy: A ‘religious awakening’

During the first 4 months of therapy, Mr. Z’s Beck Depression Inventory score fell from 32 to 17, indicating mild depression.

Mr. Z then reported that he experienced a “religious awakening” and began describing his mood and experiences in religious terms. He thanked his therapist for “saving his soul.”

The therapist was stunned by Mr. Z’s sudden transformation in mood and affect. He slept 7 to 8 hours a night, and his academic performance improved dramatically. He exhibited stable (though bright) affect and no thought disorder. His therapist viewed his use of religious terminology, though significant, as a cultural artifact because there were no signs of psychosis. Although no objective signs of mania or hypomania were apparent, the therapist suspected he might have bipolar disorder. She again tried unsuccessfully to refer him to a psychiatrist.

Then came Sept. 11, 2001.

Mr. Z was traumatized by the terrorist attacks on the World Trade Center and the Pentagon. He feared a backlash against Muslims in the United States but showed no signs of paranoia.

A few months later, however, Mr. Z became preoccupied with the attacks and harbored conspiracy theories alleging that the United States government had committed them. His speech was rapid and pressured, and he slept only 2 to 3 hours nightly. We later learned that he had not attended class for months and only sporadically showed up for lab work.

Mr. Z then began to fear he was under surveillance and that his visa would be revoked. His affect became increasingly intense during psychotherapy, and he frequently used religious metaphors and concepts. His therapist realized he was suffering a worsening manic episode, although suicidal or homicidal thoughts were not present.

Down with ‘nonbelievers’

During a subsequent session, Mr. Z reported that he had become engaged to marry a well-known supermodel. He also announced a plan to “rid the world of nonbelievers”—people who were not devout Christians, Jews, or Muslims. His three-stage plan called for:

• gently persuading nonbelievers to change their beliefs and lifestyles
• threatening nonbelievers who did not repent after polite persuasion
• “eliminating all the nonbelievers” who did not respond to intimidation.

Mr. Z viewed his therapist as “commander of the believers” and considered the three-phased plan to be her will. She questioned Mr. Z extensively about how, when, and against whom he intended to carry out this plan. He identified no specific targets, but did say, “I’ll know what do to when the time comes. I am an engineer, and I know a lot about explosives.”

The therapist then recommended an emergency psychiatric evaluation, which Mr. Z declined. She immediately notified the mental health clinic’s attending psychiatrist.

What are the therapist’s options? Can Mr. Z be involuntarily committed based on his threats of violence against “nonbelievers?”

Dr. Kennedy’s and Dr. Klafter’s observations

Two legal principles justify involuntary commitment of a patient who poses a threat to himself or the public:

Police power refers to the government’s role in maintaining public safety. State commitment statutes usually require that a mentally ill person pose a significant and imminent threat to the public. The psychiatrist who files an affidavit alleging danger does not need absolute certainty or perfect information but must act in good faith.¹

Parens patriae, or paternalism, refers to government intervention on behalf of persons incapable of managing their lives.¹

Psychiatric treatment of unwilling patients is possible in some states. Family members and/or mental health professionals can petition the court to compel outpatient psychiatric treatment.

Because an emergency evaluation produces a thorough and controlled psychiatric assessment (and minimal deprivation of personal liberty), a psychiatrist with any doubt about the patient’s condition should move toward commitment.

Box 1

Before resorting to legal coercion, try scheduling more-frequent appointments to monitor symptom progression. This would allow faster response when civil commitment criteria are met.

A psychiatrist or other mental health professional can request an emergency evaluation based on information from a knowledgeable intermediary or family member—even if the clinician did not recently or directly interview the patient.² For example, a psychologist could receive information from a case manager who encountered the patient decompensating. It would be impractical to require a psychiatrist to see a decompensating patient before an evaluation can be ordered.

Hospitalization: A ‘blood-drinking monster’

With no security staff immediately available, the attending psychiatrist and therapist sent Mr. Z home.

The psychiatrist then submitted an application for involuntary hospitalization—in which the doctor summarized the case—and faxed it to the local psychiatric emergency service. The police were notified and—after verifying that the appropriate paperwork had been completed—arrested Mr. Z at his home and brought him to the emergency service for an assessment. Mr. Z was then hospitalized. (Box 1).

Mr. Z was found to be harboring bizarre, grandiose, persecutory, and religious delusions. He claimed that a blood-drinking monster was lurking inside the hospital, and that his hospitalization was part of a conspiracy to persecute Muslims. He considered the Sept. 11 attacks fictitious and claimed that widely broadcast television news footage of the attacks was a computer-animated video. The patient refused all medications while hospitalized.

After 3 days, the court ordered Mr. Z’s discharge, citing lack of evidence that he posed any danger to self or others. At his mental health probate hearing, he managed to conceal his psychotic symptoms while testifying. The court expressed concern over his technical training in explosives but ruled that he was not dangerous because he had never used this knowledge to commit violence.

Upon discharge, Mr. Z declined outpatient psychiatric treatment. The therapist then told Mr. Z that she would terminate psychotherapy after two sessions unless he visited a psychiatrist. Mr. Z again refused, and psychotherapy was terminated.

Box 2

Would you terminate psychotherapy at this point? Could the therapist’s actions be viewed as patient abandonment?

Dr. Kennedy’s and Dr. Klafter’s observations

The formation of a professional relationship establishes a duty of care and requires the clinician to provide reasonable notice of termination and alternative sources of care. Although 30 days’ notice is generally appropriate, several factors may dictate the need for more or less notice (Box 2).

In Mr. Z’s case, we view the psychologist’s behavior as appropriate because:

• Without psychotropics, Mr. Z’s psychosis would likely persist. To continue treating him with psychotherapy alone would fall below the standard of care.
• By threatening to terminate psychotherapy, the therapist tried to use the patient’s transference and desire to maintain the therapeutic relationship as an incentive to accept medication.

Continued observation: A clue from the past

Mr. Z’s brother, who was contacted by the treatment team, reported that the patient had never been violent. He did note, however, that as an adolescent Mr. Z talked about joining a terrorist organization, though he had never followed through. The brother tried to persuade Mr. Z to leave school and live with him on the West Coast, but he instead chose to continue his studies.

Mr. Z’s hospital treatment team realized that his continued work in engineering—where he had access to explosive materials—posed a significant risk given his impaired judgment. Acting on a forensic expert’s advice, the team warned university officials about Mr. Z’s mental state and preoccupation with violence. The FBI was also contacted.

Was the treatment team justified in reporting Mr. Z’s behavior to authorities, even though he never identified any potential victims?

Dr. Kennedy’s and Dr. Klafter’s observations

Various legislative and judicial remedies—some more restrictive than others—address the psychiatrist’s duty to third parties:³

• Some states require psychiatrists to notify or protect third parties when any danger is foreseeable, regardless of threat or victim.
• Other states require specific threats but charge the psychiatrist with foreseeing all potential victims regardless of whether they were named.
• Still other states limit protection to identifiable victims, even if no threat is issued.
• In some states the psychiatrist is responsible only if the patient makes specific threats to identifiable victims.

Again, psychiatrists need to make their best professional judgments in good faith about risk of violence. Hospitalizing a threatening patient provides the most protection to third parties, but this option is intrusive, coercive, and is not always appropriate or feasible. If the threat is directed toward the public rather than specific individuals or groups, law enforcement agencies can reduce the risk somewhat through monitoring and surveillance.

Although it is a judgment call, clinicians should notify:

• all persons or organizations against whom a patient might commit violence
• and those who might be targeted as instruments for violence towards others, such as family members who have guns the patient could obtain.

A terrorist would not likely seek psychiatric help relative to his goals of terrorism because such behavior is not rooted in major mental illness. However, the heightened sense of paranoia and anxiety created by events involving terrorism, religious animosity, and hatred provide patients who struggle with psychosis an outlet for their paranoia. As such, we should take a patient’s terroristic threats seriously.

Conclusion: Going home

The university granted Mr. Z medical leave and placed him on academic probation for 2 months, during which he returned to his native country to stay with his parents.

The faculty later dismissed Mr. Z from the program, citing poor academic and laboratory performance. His visa expired, with renewal contingent upon enrollment in a full-time academic program.

Related resources

• American Academy of Psychiatry and the Law. www.aapl.org.

Drug brand names

• Sertraline • Zoloft

Disclosure

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

Mr. Z, age 38, came to the United States from a predominantly Islamic country to study science and engineering. While in graduate school, he was seen by a primary care physician for complaints of hypersomnia; reduced appetite with an approximate 15-lb weight loss; impaired concentration and memory, which hurt his academic performance; low energy; and occasional thoughts about dying.

Mr. Z’s physical examination and lab results were unremarkable, and he reported no psychiatric history. He was diagnosed with depression and was prescribed sertraline, 50 mg/d, but he refused to take it. He declined referral to a psychiatrist but agreed to weekly psychotherapy with a psychology intern at the student mental health center.

During therapy, Mr. Z said he constantly felt lonely. He feared being ostracized because of his Islamic beliefs and lifestyle, yet reported tremendous guilt over violating Islamic codes forbidding premarital sex. He told his therapist that his longing for a romantic relationship was “contaminating” his soul, and fantasized that death would free him of impure, sexual thoughts.

The severity of Mr. Z’s depression and his preoccupation with death alarmed the therapist. She referred him to a clinic psychiatrist, but Mr. Z refused to see him, saying that his depression was a punishment from God for his sexual sins. He vowed to repent by undergoing psychotherapy.

Continued therapy: A ‘religious awakening’

During the first 4 months of therapy, Mr. Z’s Beck Depression Inventory score fell from 32 to 17, indicating mild depression.

Mr. Z then reported that he experienced a “religious awakening” and began describing his mood and experiences in religious terms. He thanked his therapist for “saving his soul.”

The therapist was stunned by Mr. Z’s sudden transformation in mood and affect. He slept 7 to 8 hours a night, and his academic performance improved dramatically. He exhibited stable (though bright) affect and no thought disorder. His therapist viewed his use of religious terminology, though significant, as a cultural artifact because there were no signs of psychosis. Although no objective signs of mania or hypomania were apparent, the therapist suspected he might have bipolar disorder. She again tried unsuccessfully to refer him to a psychiatrist.

Then came Sept. 11, 2001.

Mr. Z was traumatized by the terrorist attacks on the World Trade Center and the Pentagon. He feared a backlash against Muslims in the United States but showed no signs of paranoia.

A few months later, however, Mr. Z became preoccupied with the attacks and harbored conspiracy theories alleging that the United States government had committed them. His speech was rapid and pressured, and he slept only 2 to 3 hours nightly. We later learned that he had not attended class for months and only sporadically showed up for lab work.

Mr. Z then began to fear he was under surveillance and that his visa would be revoked. His affect became increasingly intense during psychotherapy, and he frequently used religious metaphors and concepts. His therapist realized he was suffering a worsening manic episode, although suicidal or homicidal thoughts were not present.

Down with ‘nonbelievers’

During a subsequent session, Mr. Z reported that he had become engaged to marry a well-known supermodel. He also announced a plan to “rid the world of nonbelievers”—people who were not devout Christians, Jews, or Muslims. His three-stage plan called for:

• gently persuading nonbelievers to change their beliefs and lifestyles
• threatening nonbelievers who did not repent after polite persuasion
• “eliminating all the nonbelievers” who did not respond to intimidation.

Mr. Z viewed his therapist as “commander of the believers” and considered the three-phased plan to be her will. She questioned Mr. Z extensively about how, when, and against whom he intended to carry out this plan. He identified no specific targets, but did say, “I’ll know what do to when the time comes. I am an engineer, and I know a lot about explosives.”

The therapist then recommended an emergency psychiatric evaluation, which Mr. Z declined. She immediately notified the mental health clinic’s attending psychiatrist.

What are the therapist’s options? Can Mr. Z be involuntarily committed based on his threats of violence against “nonbelievers?”

Dr. Kennedy’s and Dr. Klafter’s observations

Two legal principles justify involuntary commitment of a patient who poses a threat to himself or the public:

Police power refers to the government’s role in maintaining public safety. State commitment statutes usually require that a mentally ill person pose a significant and imminent threat to the public. The psychiatrist who files an affidavit alleging danger does not need absolute certainty or perfect information but must act in good faith.¹

Parens patriae, or paternalism, refers to government intervention on behalf of persons incapable of managing their lives.¹

Psychiatric treatment of unwilling patients is possible in some states. Family members and/or mental health professionals can petition the court to compel outpatient psychiatric treatment.

Because an emergency evaluation produces a thorough and controlled psychiatric assessment (and minimal deprivation of personal liberty), a psychiatrist with any doubt about the patient’s condition should move toward commitment.

Box 1

Before resorting to legal coercion, try scheduling more-frequent appointments to monitor symptom progression. This would allow faster response when civil commitment criteria are met.

A psychiatrist or other mental health professional can request an emergency evaluation based on information from a knowledgeable intermediary or family member—even if the clinician did not recently or directly interview the patient.² For example, a psychologist could receive information from a case manager who encountered the patient decompensating. It would be impractical to require a psychiatrist to see a decompensating patient before an evaluation can be ordered.

Hospitalization: A ‘blood-drinking monster’

With no security staff immediately available, the attending psychiatrist and therapist sent Mr. Z home.

The psychiatrist then submitted an application for involuntary hospitalization—in which the doctor summarized the case—and faxed it to the local psychiatric emergency service. The police were notified and—after verifying that the appropriate paperwork had been completed—arrested Mr. Z at his home and brought him to the emergency service for an assessment. Mr. Z was then hospitalized. (Box 1).

Mr. Z was found to be harboring bizarre, grandiose, persecutory, and religious delusions. He claimed that a blood-drinking monster was lurking inside the hospital, and that his hospitalization was part of a conspiracy to persecute Muslims. He considered the Sept. 11 attacks fictitious and claimed that widely broadcast television news footage of the attacks was a computer-animated video. The patient refused all medications while hospitalized.

After 3 days, the court ordered Mr. Z’s discharge, citing lack of evidence that he posed any danger to self or others. At his mental health probate hearing, he managed to conceal his psychotic symptoms while testifying. The court expressed concern over his technical training in explosives but ruled that he was not dangerous because he had never used this knowledge to commit violence.

Upon discharge, Mr. Z declined outpatient psychiatric treatment. The therapist then told Mr. Z that she would terminate psychotherapy after two sessions unless he visited a psychiatrist. Mr. Z again refused, and psychotherapy was terminated.

Box 2

Would you terminate psychotherapy at this point? Could the therapist’s actions be viewed as patient abandonment?

Dr. Kennedy’s and Dr. Klafter’s observations

The formation of a professional relationship establishes a duty of care and requires the clinician to provide reasonable notice of termination and alternative sources of care. Although 30 days’ notice is generally appropriate, several factors may dictate the need for more or less notice (Box 2).

In Mr. Z’s case, we view the psychologist’s behavior as appropriate because:

• Without psychotropics, Mr. Z’s psychosis would likely persist. To continue treating him with psychotherapy alone would fall below the standard of care.
• By threatening to terminate psychotherapy, the therapist tried to use the patient’s transference and desire to maintain the therapeutic relationship as an incentive to accept medication.

Continued observation: A clue from the past

Mr. Z’s brother, who was contacted by the treatment team, reported that the patient had never been violent. He did note, however, that as an adolescent Mr. Z talked about joining a terrorist organization, though he had never followed through. The brother tried to persuade Mr. Z to leave school and live with him on the West Coast, but he instead chose to continue his studies.

Mr. Z’s hospital treatment team realized that his continued work in engineering—where he had access to explosive materials—posed a significant risk given his impaired judgment. Acting on a forensic expert’s advice, the team warned university officials about Mr. Z’s mental state and preoccupation with violence. The FBI was also contacted.

Was the treatment team justified in reporting Mr. Z’s behavior to authorities, even though he never identified any potential victims?

Dr. Kennedy’s and Dr. Klafter’s observations

Various legislative and judicial remedies—some more restrictive than others—address the psychiatrist’s duty to third parties:³

• Some states require psychiatrists to notify or protect third parties when any danger is foreseeable, regardless of threat or victim.
• Other states require specific threats but charge the psychiatrist with foreseeing all potential victims regardless of whether they were named.
• Still other states limit protection to identifiable victims, even if no threat is issued.
• In some states the psychiatrist is responsible only if the patient makes specific threats to identifiable victims.

Again, psychiatrists need to make their best professional judgments in good faith about risk of violence. Hospitalizing a threatening patient provides the most protection to third parties, but this option is intrusive, coercive, and is not always appropriate or feasible. If the threat is directed toward the public rather than specific individuals or groups, law enforcement agencies can reduce the risk somewhat through monitoring and surveillance.

Although it is a judgment call, clinicians should notify:

• all persons or organizations against whom a patient might commit violence
• and those who might be targeted as instruments for violence towards others, such as family members who have guns the patient could obtain.

A terrorist would not likely seek psychiatric help relative to his goals of terrorism because such behavior is not rooted in major mental illness. However, the heightened sense of paranoia and anxiety created by events involving terrorism, religious animosity, and hatred provide patients who struggle with psychosis an outlet for their paranoia. As such, we should take a patient’s terroristic threats seriously.

Conclusion: Going home

The university granted Mr. Z medical leave and placed him on academic probation for 2 months, during which he returned to his native country to stay with his parents.

The faculty later dismissed Mr. Z from the program, citing poor academic and laboratory performance. His visa expired, with renewal contingent upon enrollment in a full-time academic program.

Related resources

• American Academy of Psychiatry and the Law. www.aapl.org.

Drug brand names

• Sertraline • Zoloft

Disclosure

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

Patients with chronic schizophrenia are notoriously inconsistent in adhering to medications.¹ Partial compliance is a serious problem because the resulting psychotic relapses often lead to progressive neurologic and clinical deterioration as well as social and vocational impairment.

Long-acting, “depot” formulations of first-generation antipsychotics (haloperidol decanoate and fluphenazine decanoate) have been used over the past 25 years to ensure adherence in the least-compliant patients. These formulations, however, are not widely used because of the risks of tardive dyskinesia (TD) and other movement disorders.

Atypical antipsychotics—with their reduced risk of TD—have become the standard of care in managing schizophrenia and related psychosis over the long term.² All are administered orally, however, and—until now—none has been available in a long-acting formulation.

The FDA recently approved a long-acting, injectable form of risperidone (Table 1), based on results of a 12-week, placebo-controlled trial and a 1-year open-label trial. The clinical and functional improvements seen in chronic schizophrenia patients who received long-acting risperidone for 1 to 3 years may change prevailing notions of the potential to stabilize and restore function in this severe brain disorder.

Table 1

Injectable, long-acting risperidone: Fast facts

HOW LONG-ACTING RISPERIDONE WORKS

Long-acting injectable risperidone has the same mechanism of action as oral risperidone. The injectable form is delivered into muscle tissue by microspheres that encapsulate the drug into a biodegradable polymer. The microspheres undergo gradual hydrolysis, resulting in a gradual release of risperidone into the blood stream. The drug then crosses the blood-brain barrier to block dopamine D2 and serotonin 5HT2A receptors in brain tissue, which is accepted as the pharmacodynamic basis for the efficacy of atypical antipsychotics. Risperidone’s receptor-binding profile is shown in Table 2.

CLINICAL PHARMACOKINETICS

Full release of long-acting risperidone from the gradually hydrolyzing microspheres starts about 3 weeks after an intramuscular (IM) injection. Thus, supplemental oral risperidone is recommended during the first 3 weeks of IM injections. Release is then maintained for 4 to 6 weeks. Steady-state plasma levels are reached after four biweekly injections. Risperidone is absorbed completely from the microspheres, which are biodegradable to carbon dioxide and water.

In plasma, risperidone is oxidized by the cytochrome P-450 isoenzyme CYP 2D6 to 9-hydroxy risperidone, an active metabolite similar to risperidone in its pharmacologic characteristics and efficacy. Risperidone is also metabolized via N-dealkylation. The plasma protein binding of risperidone is 90% and that of 9-hydroxy risperidone is 77%. After several biweekly IM injections of 25 or 50 mg during clinical trials, median trough and peak plasma concentrations of active moiety fluctuated between 9.9 and 19.2 ng/ml and 17.9 and 45.5 ng/ml, respectively.

Table 2

Receptor-binding profile of risperidone long-acting formulation

Risperidone plasma concentrations may be affected by interactions with other psychotropics that inhibit or induce the oxidative enzyme CYP 2D6 (Table 3).

Clearance of risperidone and 9-hydroxy risperidone is decreased by 60% in patients with severe kidney disease, as compared with healthy subjects. Plasma levels and maximum drug concentrations are 25 to 32% lower with long-acting risperidone than with oral risperidone. This difference may account for the injectable formulation’s more favorable side-effect profile because lower peaks means a lower likelihood of side effects.

Table 3

Potential drug-drug interactions with risperidone long-acting microspheres

RESULTS FROM CLINICAL TRIALS

Long-acting risperidone was tested at doses of 25, 50, and 75 mg in a 12-week, double-blind trial of 400 patients with acute relapse of schizophrenia.⁴ During the 3-week initial titration, patients also received the usual dosage of oral risperidone (3 to 5 mg/d) for schizophrenia. Oral risperidone can be discontinued 3 weeks after the first injection (ie, 1 week after the second injection). Measurement of serum concentrations is not needed because the microspheres encapsulating risperidone have been shown in bioavailability studies to begin disintegrating and releasing risperidone 3 weeks after being deposited into muscle tissue.

All three doses were more effective than placebo in reducing total, positive, and negative symptom scores, as measured by the Positive and Negative Syndrome Scale (PANSS). The 75-mg dose showed no greater efficacy than the 50-mg dose.

In a second, open-label study, 775 stable outpatients with schizophrenia or schizoaffective disorder received biweekly injections of 25, 50, or 75 mg of long-acting risperidone for 1 year. All three doses improved the baseline PANSS scores significantly, above and beyond the patients’ stable clinical status. These results indicate that injectable long-acting risperidone can further stabilize schizophrenia beyond the usual response to oral antipsychotics.⁵

Notably, patients’ quality-of-life scores—as measured by the 36-item Short-Form Health Survey (SF-36)—were significantly lower than U.S. norms at baseline. At the end of the study, patients’ scores had increased to within the norm range.⁶ The completion rate in this 1-year study was 65%; patients dropped out because of insufficient response (7%) or adverse events (5%), or they withdrew consent (15%) or were lost to follow-up (3%).

SAFETY AND TOLERABILITY

Few side effects were seen in the 12-week and 1-year trials. Extrapyramidal symptoms as measured by the Extrapyramidal Symptom Rating Scale declined from baseline by 67% with the 25-mg dose, by 50% with the 50-mg dose, and by 33% with the 75-mg dose in the 12-week study. Patients who had TD at baseline also improved by the end of the 1-year study, suggesting that long-acting risperidone has a low risk of TD.⁷ Also:

• Although prolactin levels were elevated compared with baseline, they were 18% lower with long-acting risperidone than with oral risperidone, possibly because of lower plasma peaks of the drug in the long-acting formulation.
• Injection site pain or redness was minimal, as measured by patient ratings.
• Mean weight gain after 12 weeks was 0.5 kg with the 25-mg dose, 1.2 kg with the 50-mg dose, and 1.9 kg with the 75-mg dose. After 52 weeks, weight gain was 1.8 kg, 2.1 kg, and 2.7 kg, respectively.
• QTc prolongation—as measured with random ECGs—was negligible with all doses.

REPARATIVE EFFECTS?

Based on clinical trial results, long-acting risperidone appears to be highly effective in treating and preventing relapse of acute psychotic episodes in schizophrenia. Its injectable formulation ensures that compliance is far more consistent than with oral atypical antipsychotics.

Patients who had been disabled with chronic schizophrenia improved dramatically after about 1 year of biweekly injections of long-acting risperidone. Many were able to return to school to finish a degree, go back to holding full-time jobs, or develop close personal relationships such as dating. Total PANSS scores after 1 year of treatment approached the low 40s in some patients, which is similar to what a healthy person might score on the PANSS on certain days. This pattern, which justifies the term “recovery,” suggests that uninterrupted, long-term atypical antipsychotic treatment may have reparative and/or neuroprotective effects on the brain in schizophrenia.⁸

Candidates for long-acting injectable risperidone include:

• first-episode patients
• patients with a history of partial or complete noncompliance
• patients who become violent or assaultive when they relapse
• and those receiving depot injections of haloperidol decanoate or fluphenazine decanoate.

Long-acting injectable atypical antipsychotics may become the standard of care for treating newonset schizophrenia.⁹ The goal would be to return patients to baseline functioning as soon as possible, rather than resorting to a long-acting antipsychotic only after repetitive relapses, adverse neuroplastic changes, and psychosocial decline.

Related resources

• Lasser R, Bossie C, Zhu Y, Gharahawi G. Does constant therapy infer optimal efficacy in schizophrenia? Moving to an advanced pharmacotherapeutic option. Schizophr Res 2003;60:291.
• Risperdal Consta Web site. www.risperdalconsta.com

Drug brand names

• Carbamazepine • Tegretol
• Fluphenazine • Prolixin
• Haloperidol • Haldol
• Paroxetine • Paxil

Disclosure

The author participated in the 12-week controlled clinical trial of long-acting, injectable risperidone and in an open-label extension for more than 3 additional years.

Dr. Nasrallah reports that he also receives research/grant support from and is a consultant to and speaker for AstraZeneca Pharmaceuticals, Janssen Pharmaceutica, and Pfizer Inc., and is a consultant to and speaker for Bristol-Myers Squibb Co. and Abbott Laboratories.

Acknowledgment

The author thanks Peggy Grause for her assistance in preparing this manuscript for publication.

Patients with chronic schizophrenia are notoriously inconsistent in adhering to medications.¹ Partial compliance is a serious problem because the resulting psychotic relapses often lead to progressive neurologic and clinical deterioration as well as social and vocational impairment.

Long-acting, “depot” formulations of first-generation antipsychotics (haloperidol decanoate and fluphenazine decanoate) have been used over the past 25 years to ensure adherence in the least-compliant patients. These formulations, however, are not widely used because of the risks of tardive dyskinesia (TD) and other movement disorders.

Atypical antipsychotics—with their reduced risk of TD—have become the standard of care in managing schizophrenia and related psychosis over the long term.² All are administered orally, however, and—until now—none has been available in a long-acting formulation.

The FDA recently approved a long-acting, injectable form of risperidone (Table 1), based on results of a 12-week, placebo-controlled trial and a 1-year open-label trial. The clinical and functional improvements seen in chronic schizophrenia patients who received long-acting risperidone for 1 to 3 years may change prevailing notions of the potential to stabilize and restore function in this severe brain disorder.

Table 1

Injectable, long-acting risperidone: Fast facts

HOW LONG-ACTING RISPERIDONE WORKS

Long-acting injectable risperidone has the same mechanism of action as oral risperidone. The injectable form is delivered into muscle tissue by microspheres that encapsulate the drug into a biodegradable polymer. The microspheres undergo gradual hydrolysis, resulting in a gradual release of risperidone into the blood stream. The drug then crosses the blood-brain barrier to block dopamine D2 and serotonin 5HT2A receptors in brain tissue, which is accepted as the pharmacodynamic basis for the efficacy of atypical antipsychotics. Risperidone’s receptor-binding profile is shown in Table 2.

CLINICAL PHARMACOKINETICS

Full release of long-acting risperidone from the gradually hydrolyzing microspheres starts about 3 weeks after an intramuscular (IM) injection. Thus, supplemental oral risperidone is recommended during the first 3 weeks of IM injections. Release is then maintained for 4 to 6 weeks. Steady-state plasma levels are reached after four biweekly injections. Risperidone is absorbed completely from the microspheres, which are biodegradable to carbon dioxide and water.

In plasma, risperidone is oxidized by the cytochrome P-450 isoenzyme CYP 2D6 to 9-hydroxy risperidone, an active metabolite similar to risperidone in its pharmacologic characteristics and efficacy. Risperidone is also metabolized via N-dealkylation. The plasma protein binding of risperidone is 90% and that of 9-hydroxy risperidone is 77%. After several biweekly IM injections of 25 or 50 mg during clinical trials, median trough and peak plasma concentrations of active moiety fluctuated between 9.9 and 19.2 ng/ml and 17.9 and 45.5 ng/ml, respectively.

Table 2

Receptor-binding profile of risperidone long-acting formulation

Risperidone plasma concentrations may be affected by interactions with other psychotropics that inhibit or induce the oxidative enzyme CYP 2D6 (Table 3).

Clearance of risperidone and 9-hydroxy risperidone is decreased by 60% in patients with severe kidney disease, as compared with healthy subjects. Plasma levels and maximum drug concentrations are 25 to 32% lower with long-acting risperidone than with oral risperidone. This difference may account for the injectable formulation’s more favorable side-effect profile because lower peaks means a lower likelihood of side effects.

Table 3

Potential drug-drug interactions with risperidone long-acting microspheres

RESULTS FROM CLINICAL TRIALS

Long-acting risperidone was tested at doses of 25, 50, and 75 mg in a 12-week, double-blind trial of 400 patients with acute relapse of schizophrenia.⁴ During the 3-week initial titration, patients also received the usual dosage of oral risperidone (3 to 5 mg/d) for schizophrenia. Oral risperidone can be discontinued 3 weeks after the first injection (ie, 1 week after the second injection). Measurement of serum concentrations is not needed because the microspheres encapsulating risperidone have been shown in bioavailability studies to begin disintegrating and releasing risperidone 3 weeks after being deposited into muscle tissue.

All three doses were more effective than placebo in reducing total, positive, and negative symptom scores, as measured by the Positive and Negative Syndrome Scale (PANSS). The 75-mg dose showed no greater efficacy than the 50-mg dose.

In a second, open-label study, 775 stable outpatients with schizophrenia or schizoaffective disorder received biweekly injections of 25, 50, or 75 mg of long-acting risperidone for 1 year. All three doses improved the baseline PANSS scores significantly, above and beyond the patients’ stable clinical status. These results indicate that injectable long-acting risperidone can further stabilize schizophrenia beyond the usual response to oral antipsychotics.⁵

Notably, patients’ quality-of-life scores—as measured by the 36-item Short-Form Health Survey (SF-36)—were significantly lower than U.S. norms at baseline. At the end of the study, patients’ scores had increased to within the norm range.⁶ The completion rate in this 1-year study was 65%; patients dropped out because of insufficient response (7%) or adverse events (5%), or they withdrew consent (15%) or were lost to follow-up (3%).

SAFETY AND TOLERABILITY

Few side effects were seen in the 12-week and 1-year trials. Extrapyramidal symptoms as measured by the Extrapyramidal Symptom Rating Scale declined from baseline by 67% with the 25-mg dose, by 50% with the 50-mg dose, and by 33% with the 75-mg dose in the 12-week study. Patients who had TD at baseline also improved by the end of the 1-year study, suggesting that long-acting risperidone has a low risk of TD.⁷ Also:

• Although prolactin levels were elevated compared with baseline, they were 18% lower with long-acting risperidone than with oral risperidone, possibly because of lower plasma peaks of the drug in the long-acting formulation.
• Injection site pain or redness was minimal, as measured by patient ratings.
• Mean weight gain after 12 weeks was 0.5 kg with the 25-mg dose, 1.2 kg with the 50-mg dose, and 1.9 kg with the 75-mg dose. After 52 weeks, weight gain was 1.8 kg, 2.1 kg, and 2.7 kg, respectively.
• QTc prolongation—as measured with random ECGs—was negligible with all doses.

REPARATIVE EFFECTS?

Based on clinical trial results, long-acting risperidone appears to be highly effective in treating and preventing relapse of acute psychotic episodes in schizophrenia. Its injectable formulation ensures that compliance is far more consistent than with oral atypical antipsychotics.

Patients who had been disabled with chronic schizophrenia improved dramatically after about 1 year of biweekly injections of long-acting risperidone. Many were able to return to school to finish a degree, go back to holding full-time jobs, or develop close personal relationships such as dating. Total PANSS scores after 1 year of treatment approached the low 40s in some patients, which is similar to what a healthy person might score on the PANSS on certain days. This pattern, which justifies the term “recovery,” suggests that uninterrupted, long-term atypical antipsychotic treatment may have reparative and/or neuroprotective effects on the brain in schizophrenia.⁸

Candidates for long-acting injectable risperidone include:

• first-episode patients
• patients with a history of partial or complete noncompliance
• patients who become violent or assaultive when they relapse
• and those receiving depot injections of haloperidol decanoate or fluphenazine decanoate.

Long-acting injectable atypical antipsychotics may become the standard of care for treating newonset schizophrenia.⁹ The goal would be to return patients to baseline functioning as soon as possible, rather than resorting to a long-acting antipsychotic only after repetitive relapses, adverse neuroplastic changes, and psychosocial decline.

Related resources

• Lasser R, Bossie C, Zhu Y, Gharahawi G. Does constant therapy infer optimal efficacy in schizophrenia? Moving to an advanced pharmacotherapeutic option. Schizophr Res 2003;60:291.
• Risperdal Consta Web site. www.risperdalconsta.com

Drug brand names

• Carbamazepine • Tegretol
• Fluphenazine • Prolixin
• Haloperidol • Haldol
• Paroxetine • Paxil

Disclosure

The author participated in the 12-week controlled clinical trial of long-acting, injectable risperidone and in an open-label extension for more than 3 additional years.

Dr. Nasrallah reports that he also receives research/grant support from and is a consultant to and speaker for AstraZeneca Pharmaceuticals, Janssen Pharmaceutica, and Pfizer Inc., and is a consultant to and speaker for Bristol-Myers Squibb Co. and Abbott Laboratories.

Acknowledgment

The author thanks Peggy Grause for her assistance in preparing this manuscript for publication.

Patients with chronic schizophrenia are notoriously inconsistent in adhering to medications.¹ Partial compliance is a serious problem because the resulting psychotic relapses often lead to progressive neurologic and clinical deterioration as well as social and vocational impairment.

Long-acting, “depot” formulations of first-generation antipsychotics (haloperidol decanoate and fluphenazine decanoate) have been used over the past 25 years to ensure adherence in the least-compliant patients. These formulations, however, are not widely used because of the risks of tardive dyskinesia (TD) and other movement disorders.

Atypical antipsychotics—with their reduced risk of TD—have become the standard of care in managing schizophrenia and related psychosis over the long term.² All are administered orally, however, and—until now—none has been available in a long-acting formulation.

The FDA recently approved a long-acting, injectable form of risperidone (Table 1), based on results of a 12-week, placebo-controlled trial and a 1-year open-label trial. The clinical and functional improvements seen in chronic schizophrenia patients who received long-acting risperidone for 1 to 3 years may change prevailing notions of the potential to stabilize and restore function in this severe brain disorder.

Table 1

Injectable, long-acting risperidone: Fast facts

HOW LONG-ACTING RISPERIDONE WORKS

Long-acting injectable risperidone has the same mechanism of action as oral risperidone. The injectable form is delivered into muscle tissue by microspheres that encapsulate the drug into a biodegradable polymer. The microspheres undergo gradual hydrolysis, resulting in a gradual release of risperidone into the blood stream. The drug then crosses the blood-brain barrier to block dopamine D2 and serotonin 5HT2A receptors in brain tissue, which is accepted as the pharmacodynamic basis for the efficacy of atypical antipsychotics. Risperidone’s receptor-binding profile is shown in Table 2.

CLINICAL PHARMACOKINETICS

Full release of long-acting risperidone from the gradually hydrolyzing microspheres starts about 3 weeks after an intramuscular (IM) injection. Thus, supplemental oral risperidone is recommended during the first 3 weeks of IM injections. Release is then maintained for 4 to 6 weeks. Steady-state plasma levels are reached after four biweekly injections. Risperidone is absorbed completely from the microspheres, which are biodegradable to carbon dioxide and water.

In plasma, risperidone is oxidized by the cytochrome P-450 isoenzyme CYP 2D6 to 9-hydroxy risperidone, an active metabolite similar to risperidone in its pharmacologic characteristics and efficacy. Risperidone is also metabolized via N-dealkylation. The plasma protein binding of risperidone is 90% and that of 9-hydroxy risperidone is 77%. After several biweekly IM injections of 25 or 50 mg during clinical trials, median trough and peak plasma concentrations of active moiety fluctuated between 9.9 and 19.2 ng/ml and 17.9 and 45.5 ng/ml, respectively.

Table 2

Receptor-binding profile of risperidone long-acting formulation

Risperidone plasma concentrations may be affected by interactions with other psychotropics that inhibit or induce the oxidative enzyme CYP 2D6 (Table 3).

Clearance of risperidone and 9-hydroxy risperidone is decreased by 60% in patients with severe kidney disease, as compared with healthy subjects. Plasma levels and maximum drug concentrations are 25 to 32% lower with long-acting risperidone than with oral risperidone. This difference may account for the injectable formulation’s more favorable side-effect profile because lower peaks means a lower likelihood of side effects.

Table 3

Potential drug-drug interactions with risperidone long-acting microspheres

RESULTS FROM CLINICAL TRIALS

Long-acting risperidone was tested at doses of 25, 50, and 75 mg in a 12-week, double-blind trial of 400 patients with acute relapse of schizophrenia.⁴ During the 3-week initial titration, patients also received the usual dosage of oral risperidone (3 to 5 mg/d) for schizophrenia. Oral risperidone can be discontinued 3 weeks after the first injection (ie, 1 week after the second injection). Measurement of serum concentrations is not needed because the microspheres encapsulating risperidone have been shown in bioavailability studies to begin disintegrating and releasing risperidone 3 weeks after being deposited into muscle tissue.

All three doses were more effective than placebo in reducing total, positive, and negative symptom scores, as measured by the Positive and Negative Syndrome Scale (PANSS). The 75-mg dose showed no greater efficacy than the 50-mg dose.

In a second, open-label study, 775 stable outpatients with schizophrenia or schizoaffective disorder received biweekly injections of 25, 50, or 75 mg of long-acting risperidone for 1 year. All three doses improved the baseline PANSS scores significantly, above and beyond the patients’ stable clinical status. These results indicate that injectable long-acting risperidone can further stabilize schizophrenia beyond the usual response to oral antipsychotics.⁵

Notably, patients’ quality-of-life scores—as measured by the 36-item Short-Form Health Survey (SF-36)—were significantly lower than U.S. norms at baseline. At the end of the study, patients’ scores had increased to within the norm range.⁶ The completion rate in this 1-year study was 65%; patients dropped out because of insufficient response (7%) or adverse events (5%), or they withdrew consent (15%) or were lost to follow-up (3%).

SAFETY AND TOLERABILITY

Few side effects were seen in the 12-week and 1-year trials. Extrapyramidal symptoms as measured by the Extrapyramidal Symptom Rating Scale declined from baseline by 67% with the 25-mg dose, by 50% with the 50-mg dose, and by 33% with the 75-mg dose in the 12-week study. Patients who had TD at baseline also improved by the end of the 1-year study, suggesting that long-acting risperidone has a low risk of TD.⁷ Also:

• Although prolactin levels were elevated compared with baseline, they were 18% lower with long-acting risperidone than with oral risperidone, possibly because of lower plasma peaks of the drug in the long-acting formulation.
• Injection site pain or redness was minimal, as measured by patient ratings.
• Mean weight gain after 12 weeks was 0.5 kg with the 25-mg dose, 1.2 kg with the 50-mg dose, and 1.9 kg with the 75-mg dose. After 52 weeks, weight gain was 1.8 kg, 2.1 kg, and 2.7 kg, respectively.
• QTc prolongation—as measured with random ECGs—was negligible with all doses.

REPARATIVE EFFECTS?

Based on clinical trial results, long-acting risperidone appears to be highly effective in treating and preventing relapse of acute psychotic episodes in schizophrenia. Its injectable formulation ensures that compliance is far more consistent than with oral atypical antipsychotics.

Patients who had been disabled with chronic schizophrenia improved dramatically after about 1 year of biweekly injections of long-acting risperidone. Many were able to return to school to finish a degree, go back to holding full-time jobs, or develop close personal relationships such as dating. Total PANSS scores after 1 year of treatment approached the low 40s in some patients, which is similar to what a healthy person might score on the PANSS on certain days. This pattern, which justifies the term “recovery,” suggests that uninterrupted, long-term atypical antipsychotic treatment may have reparative and/or neuroprotective effects on the brain in schizophrenia.⁸

Candidates for long-acting injectable risperidone include:

• first-episode patients
• patients with a history of partial or complete noncompliance
• patients who become violent or assaultive when they relapse
• and those receiving depot injections of haloperidol decanoate or fluphenazine decanoate.

Long-acting injectable atypical antipsychotics may become the standard of care for treating newonset schizophrenia.⁹ The goal would be to return patients to baseline functioning as soon as possible, rather than resorting to a long-acting antipsychotic only after repetitive relapses, adverse neuroplastic changes, and psychosocial decline.

Related resources

• Lasser R, Bossie C, Zhu Y, Gharahawi G. Does constant therapy infer optimal efficacy in schizophrenia? Moving to an advanced pharmacotherapeutic option. Schizophr Res 2003;60:291.
• Risperdal Consta Web site. www.risperdalconsta.com

Drug brand names

• Carbamazepine • Tegretol
• Fluphenazine • Prolixin
• Haloperidol • Haldol
• Paroxetine • Paxil

Disclosure

The author participated in the 12-week controlled clinical trial of long-acting, injectable risperidone and in an open-label extension for more than 3 additional years.

Dr. Nasrallah reports that he also receives research/grant support from and is a consultant to and speaker for AstraZeneca Pharmaceuticals, Janssen Pharmaceutica, and Pfizer Inc., and is a consultant to and speaker for Bristol-Myers Squibb Co. and Abbott Laboratories.

Acknowledgment

The author thanks Peggy Grause for her assistance in preparing this manuscript for publication.

Potentially fatal neuroleptic malignant syndrome (NMS)—though less common than in the past—can happen with either conventional or atypical antipsychotics.^1,2 To help you protect patients when prescribing antipsychotics or consulting with other clinicians about these drugs, this article discusses:

• risk factors and clinical features that warn of NMS onset
• differential diagnosis of disease states most often confused with NMS
• management recommendations, including supportive measures and specific interventions such as benzodiazepines, dopamine agonists, dantrolene, and electroconvulsive therapy (ECT).

WHY NMS REMAINS RELEVANT

NMS remains a risk in susceptible patients receiving atypical antipsychotics, according to clinical reports and drug adverse event surveys (Figure).²

Moreover, NMS continues to be reported with conventional antipsychotics, which remain in widespread use. Patients who receive long-acting depot conventional antipsychotics are at risk for prolonged NMS episodes.

Figure 55 NMS cases reported with use of antipsychotics, 1998-2002

Probable or definite neuroleptic malignant syndrome cases associated with antipsychotic monotherapy reported to the Neuroleptic Malignant Syndrome Information Service.NMS in medical settings. Psychiatrists may be consulted when patients develop NMS while receiving conventional antipsychotics or other dopaminereceptor antagonists used in medical settings.^3,4 Haloperidol remains the recommended drug of choice for treating agitation and delirium and continues to be the single most common trigger of NMS. Although often overlooked, antiemetics and sedatives with neuroleptic properties—such as prochlorperazine, metoclopramide, and promethazine—also have triggered NMS.

Other hyperthermic conditions. NMS is often considered in the differential diagnosis of patients who develop fever or encephalopathy while being treated with psychotropics. In these acute, complex, and often grave situations, psychiatrists may be consulted to recommend treatment for behavioral control or to distinguish NMS from other conditions.

NEWER VS. OLDER ANTIPSYCHOTICS

Has NMS incidence declined with the atypical agents? Probably, but providing proof is difficult:

• NMS is uncommon; its incidence in psychiatric patients treated with conventional antipsychotics is approximately 0.2%.⁵ To demonstrate reduced NMS incidence with atypicals, a very large sample of patients would be required to reach statistical significance.
• As doctors have used lower doses of conventional agents—which reduces the risk of NMS—any beneficial impact from atypicals has become more difficult to detect.^5,6
• Reports of NMS frequency with atypicals may be inflated by bias in publishing adverse events with newer versus older agents.
• Patients switched to atypicals may represent a high-risk group that is intolerant or resistant to conventional antipsychotics.

So far, few unequivocal cases of NMS have been attributed to the use of quetiapine, ziprasidone, or aripiprazole, the most recently introduced atypicals. Moreover, case reports of NMS associated with clozapine, risperidone, or olanzapine² are often difficult to interpret because of incomplete clinical details, varying diagnostic criteria, and concomitant use of more than one antipsychotic.

Milder NMS? Do the newer antipsychotics produce an “atypical” or milder form of NMS? Case reports indicate that extreme temperature elevations and extrapyramidal dysfunction are less frequent in NMS associated with atypical compared with conventional antipsychotics.² However, case descriptions of NMS were heterogeneous even with conventional agents, and clinicians’ growing awareness of NMS even before atypicals were introduced allowed for earlier diagnosis of mild and partial NMS cases.⁷

CLINICAL FEATURES OF NMS

Regardless of drug selection, it is important to recognize early and mild signs of NMS. Any case can progress to a fulminant form that is more difficult to treat.

Patients at risk. NMS may be more likely to develop in patients with:^5,6,8

• dehydration
• agitation
• low serum iron
• underlying brain damage
• catatonia.

Some patients may have genetic abnormalities in central dopamine systems that increase their susceptibility to NMS.^6,9

Fifteen to 20% of patients who develop NMS have experienced a previous episode while taking antipsychotics, which is why taking a careful drug history is important.^5,6 Although most often reported with therapeutic antipsychotic doses, NMS has been associated with rapid dose titration, especially when given parenterally.⁸

On the other hand, the practical value of these risk factors is often limited in individual cases and may lead one to overestimate NMS risk. NMS is rare and idiosyncratic. Risk factors may not outweigh antipsychotics’ benefits when these drugs are indicated for a patient with psychosis.

Incipient NMS. Identifying early signs of NMS may be impossible in fulminant cases, but patients with incipient NMS may show:

• unexpected mental status changes
• new-onset catatonia
• refractory extrapyramidal and bulbar signs such as rigidity, dysphagia, or dysarthria.^5,7,10

Other clues to NMS onset include tachycardia, tachypnea, and elevated temperature or serum creatine phosphokinase (CPK). These signs, however, do not precede or progress to NMS in all cases. A high index of suspicion for NMS, tempered by sound clinical judgment, is called for when assessing all patients receiving antipsychotics.

Diagnostic criteria. Clinical signs of NMS as a fullblown hypermetabolic syndrome are distinctive and well described (Table 1).^5,6,11,12 Elevated temperature is accompanied by profuse sweating. Extreme temperatures (>104° F), especially if prolonged or associated with hypoxia or hypotension, pose a high risk for brain damage, rhabdomyolysis, disseminated intravascular coagulation, multisystem organ failure, and death.

Muscle rigidity is a characteristic finding and may be accompanied by tremors, cogwheeling, myoclonus, or rhabdomyolysis. Changes in vital signs—such as tachycardia and tachypnea—are typical.

Mental status examination usually reveals catatonic signs of mutism and stupor, but delirium and coma also have been described. No laboratory findings are specific for NMS, but elevated white blood cell counts, low serum iron, metabolic acidosis, hypoxia, and elevated serum CPK and catecholamines have been reported.

Table 1

Common clinical features of NMS

Resolution. If recognized promptly, NMS resolves within 1 to 2 weeks in two-thirds of patients after antipsychotics are discontinued. The average recovery time of 7 to 10 days may be prolonged in patients who were taking long-acting depot antipsychotics or in those with persistent residual catatonic symptoms.¹³

Risk of death. NMS remains potentially fatal, especially if high temperatures develop or episodes are prolonged. Causes of death include cardiorespiratory arrest, renal failure, pulmonary emboli, pneumonia, sepsis, disseminated intravascular coagulation, and multisystem organ failure.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis of NMS encompasses disorders that present with fever and encephalopathy.^5,6,12 Primary brain disorders that resemble NMS include:^9,14-16

• infections
• acute psychotic disorders that progress to malignant catatonia or delirious mania
• midbrain structural lesions
• seizures.

Also exclude hormonal and autoimmune disorders and environmental heatstroke (Table 2).^17,18 Similar hyperthermic syndromes have been reported with other toxins and drugs, including malignant hyperthermia of anesthesia, serotonin syndrome, and dopamine agonist withdrawal in patients with Parkinson’s disease (Table 3).^5,6,19

Table 2

7 disease states most often confused with NMS

Table 3

Drugs that can cause NMS-like hyperthermic syndromes

MANAGING NMS

The standard approach to managing patients with NMS includes four steps:

• recognize the diagnosis early
• exclude alternate causes of symptoms
• discontinue suspected triggering drugs
• provide supportive care to reduce temperatures, ensure fluid balance, and detect complications.^5,6,20

Beyond supportive care, several specific therapies have been proposed based on theoretical mechanisms of NMS and meta-analyses of offlabel use in anecdotal clinical reports (Table 4). If benzodiazepines, dopamine agonists, or dantrolene are effective, taper slowly after recovery to prevent rebound symptoms.

Benzodiazepines. Given the concept of NMS as a form of catatonia, benzodiazepines have been used effectively in some cases.^20,21 A trial of lorazepam, 1 to 2 mg parenterally, is a reasonable first step. Higher doses may be required, with adequate monitoring of respiratory status. Oral lorazepam can maintain the therapeutic effect.

Dopamine agonists. To reverse the parkinsonism and dopamine antagonist properties of antipsychotics, dopamine agonists such as bromocriptine or amantadine have been tried and have reduced NMS duration and mortality.^20,22,23 Newer drugs such as ropinorole and pramipexole may also be useful. Dopaminergic drugs, however, can worsen psychosis and cause hypotension and emesis.

Dantrolene may reduce hyperthermia related to skeletal muscle hypermetabolism of any cause and has been effective in rapidly reducing extreme temperatures in some NMS cases.^20,22-26 Dantrolene is given IV, 1 to 2.5 mg/kg every 6 hours. An oral form can be substituted if a response is obtained. Dantrolene can impair respiratory and hepatic function and should not be combined with calcium channel blockers.

ECT is increasingly recognized as an effective NMS treatment and should not be overlooked for patients:

• who fail to respond to drug therapy or supportive care
• with residual catatonic symptoms.^13,20,27,28

Standard ECT is given, although nondepolarizing muscle relaxants instead of succinylcholine are used in patients with serious rhabdomyolysis to avoid the risk of hyperkalemia.²⁰

Recommendation. Although these modalities offer a spectrum of therapeutic options, it is premature to recommend any single remedy over others or over supportive care alone because:

• randomized, controlled trials have not been conducted
• NMS episodes are heterogeneous in presentation and outcome
• the syndrome is often self-limited after antipsychotics are discontinued.

I recommend that you choose therapies empirically, based on the character, severity, and duration of symptoms in a given case.^5,6,20

Table 4

How to treat neuroleptic malignant syndrome

REDUCING RISK OF RECURRENCE

Patients vary in susceptibility to recurrence after they recover from NMS, but the risk approaches 30% with future exposure to antipsychotics.^5,6 You may be able to minimize recurrence risk by:

• reducing risk factors, such as dehydration
• considering alternatives to antipsychotics, such as treating bipolar disorder with lithium or ECT
• using atypical instead of conventional antipsychotics, starting with low dosages and titrating slowly.

Before you reintroduce antipsychotics, carefully document informed consent and your rationale for treatment decisions in the patient’s chart.

Related resources

• Neuroleptic Malignant Syndrome Information Service. Hotline for health professionals. (888) 667-8367. www.nmsis.org
• Mann SC, Caroff SN, Keck PE Jr, Lazarus A. Neuroleptic malignant syndrome and related conditions (2nd ed). Washington, DC: American Psychiatric Publishing, 2003.
• Caroff SN, Mann SC, Francis A, Fricchione GL. Catatonia: from psychopathology to neurobiology. Washington, DC: American Psychiatric Publishing (in press).

Drug brand names

• Amantadine • Symmetrel
• Aripiprazole • Abilify
• Bromocriptine • Parlodel
• Clozapine • Clozaril
• Dantrolene • Dantrium
• Haloperidol • Haldol
• Lorazepam • Ativan
• Metoclopramide • Reglan
• Olanzapine • Zyprexa
• Pramipexole • Mirapex
• Prochlorperazine • Compazine
• Promethazine • Phenergan
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Ropinirole • Requip
• Ziprasidone • Geodon

Disclosure

Dr. Caroff receives research support from Janssen Pharmaceutica and Pfizer Inc., and is a consultant to Eli Lilly and Co. and Bristol-Myers Squibb Co.

Potentially fatal neuroleptic malignant syndrome (NMS)—though less common than in the past—can happen with either conventional or atypical antipsychotics.^1,2 To help you protect patients when prescribing antipsychotics or consulting with other clinicians about these drugs, this article discusses:

• risk factors and clinical features that warn of NMS onset
• differential diagnosis of disease states most often confused with NMS
• management recommendations, including supportive measures and specific interventions such as benzodiazepines, dopamine agonists, dantrolene, and electroconvulsive therapy (ECT).

WHY NMS REMAINS RELEVANT

NMS remains a risk in susceptible patients receiving atypical antipsychotics, according to clinical reports and drug adverse event surveys (Figure).²

Moreover, NMS continues to be reported with conventional antipsychotics, which remain in widespread use. Patients who receive long-acting depot conventional antipsychotics are at risk for prolonged NMS episodes.

Figure 55 NMS cases reported with use of antipsychotics, 1998-2002

Probable or definite neuroleptic malignant syndrome cases associated with antipsychotic monotherapy reported to the Neuroleptic Malignant Syndrome Information Service.NMS in medical settings. Psychiatrists may be consulted when patients develop NMS while receiving conventional antipsychotics or other dopaminereceptor antagonists used in medical settings.^3,4 Haloperidol remains the recommended drug of choice for treating agitation and delirium and continues to be the single most common trigger of NMS. Although often overlooked, antiemetics and sedatives with neuroleptic properties—such as prochlorperazine, metoclopramide, and promethazine—also have triggered NMS.

Other hyperthermic conditions. NMS is often considered in the differential diagnosis of patients who develop fever or encephalopathy while being treated with psychotropics. In these acute, complex, and often grave situations, psychiatrists may be consulted to recommend treatment for behavioral control or to distinguish NMS from other conditions.

NEWER VS. OLDER ANTIPSYCHOTICS

Has NMS incidence declined with the atypical agents? Probably, but providing proof is difficult:

• NMS is uncommon; its incidence in psychiatric patients treated with conventional antipsychotics is approximately 0.2%.⁵ To demonstrate reduced NMS incidence with atypicals, a very large sample of patients would be required to reach statistical significance.
• As doctors have used lower doses of conventional agents—which reduces the risk of NMS—any beneficial impact from atypicals has become more difficult to detect.^5,6
• Reports of NMS frequency with atypicals may be inflated by bias in publishing adverse events with newer versus older agents.
• Patients switched to atypicals may represent a high-risk group that is intolerant or resistant to conventional antipsychotics.

So far, few unequivocal cases of NMS have been attributed to the use of quetiapine, ziprasidone, or aripiprazole, the most recently introduced atypicals. Moreover, case reports of NMS associated with clozapine, risperidone, or olanzapine² are often difficult to interpret because of incomplete clinical details, varying diagnostic criteria, and concomitant use of more than one antipsychotic.

Milder NMS? Do the newer antipsychotics produce an “atypical” or milder form of NMS? Case reports indicate that extreme temperature elevations and extrapyramidal dysfunction are less frequent in NMS associated with atypical compared with conventional antipsychotics.² However, case descriptions of NMS were heterogeneous even with conventional agents, and clinicians’ growing awareness of NMS even before atypicals were introduced allowed for earlier diagnosis of mild and partial NMS cases.⁷

CLINICAL FEATURES OF NMS

Regardless of drug selection, it is important to recognize early and mild signs of NMS. Any case can progress to a fulminant form that is more difficult to treat.

Patients at risk. NMS may be more likely to develop in patients with:^5,6,8

• dehydration
• agitation
• low serum iron
• underlying brain damage
• catatonia.

Some patients may have genetic abnormalities in central dopamine systems that increase their susceptibility to NMS.^6,9

Fifteen to 20% of patients who develop NMS have experienced a previous episode while taking antipsychotics, which is why taking a careful drug history is important.^5,6 Although most often reported with therapeutic antipsychotic doses, NMS has been associated with rapid dose titration, especially when given parenterally.⁸

On the other hand, the practical value of these risk factors is often limited in individual cases and may lead one to overestimate NMS risk. NMS is rare and idiosyncratic. Risk factors may not outweigh antipsychotics’ benefits when these drugs are indicated for a patient with psychosis.

Incipient NMS. Identifying early signs of NMS may be impossible in fulminant cases, but patients with incipient NMS may show:

• unexpected mental status changes
• new-onset catatonia
• refractory extrapyramidal and bulbar signs such as rigidity, dysphagia, or dysarthria.^5,7,10

Other clues to NMS onset include tachycardia, tachypnea, and elevated temperature or serum creatine phosphokinase (CPK). These signs, however, do not precede or progress to NMS in all cases. A high index of suspicion for NMS, tempered by sound clinical judgment, is called for when assessing all patients receiving antipsychotics.

Diagnostic criteria. Clinical signs of NMS as a fullblown hypermetabolic syndrome are distinctive and well described (Table 1).^5,6,11,12 Elevated temperature is accompanied by profuse sweating. Extreme temperatures (>104° F), especially if prolonged or associated with hypoxia or hypotension, pose a high risk for brain damage, rhabdomyolysis, disseminated intravascular coagulation, multisystem organ failure, and death.

Muscle rigidity is a characteristic finding and may be accompanied by tremors, cogwheeling, myoclonus, or rhabdomyolysis. Changes in vital signs—such as tachycardia and tachypnea—are typical.

Mental status examination usually reveals catatonic signs of mutism and stupor, but delirium and coma also have been described. No laboratory findings are specific for NMS, but elevated white blood cell counts, low serum iron, metabolic acidosis, hypoxia, and elevated serum CPK and catecholamines have been reported.

Table 1

Common clinical features of NMS

Resolution. If recognized promptly, NMS resolves within 1 to 2 weeks in two-thirds of patients after antipsychotics are discontinued. The average recovery time of 7 to 10 days may be prolonged in patients who were taking long-acting depot antipsychotics or in those with persistent residual catatonic symptoms.¹³

Risk of death. NMS remains potentially fatal, especially if high temperatures develop or episodes are prolonged. Causes of death include cardiorespiratory arrest, renal failure, pulmonary emboli, pneumonia, sepsis, disseminated intravascular coagulation, and multisystem organ failure.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis of NMS encompasses disorders that present with fever and encephalopathy.^5,6,12 Primary brain disorders that resemble NMS include:^9,14-16

• infections
• acute psychotic disorders that progress to malignant catatonia or delirious mania
• midbrain structural lesions
• seizures.

Also exclude hormonal and autoimmune disorders and environmental heatstroke (Table 2).^17,18 Similar hyperthermic syndromes have been reported with other toxins and drugs, including malignant hyperthermia of anesthesia, serotonin syndrome, and dopamine agonist withdrawal in patients with Parkinson’s disease (Table 3).^5,6,19

Table 2

7 disease states most often confused with NMS

Table 3

Drugs that can cause NMS-like hyperthermic syndromes

MANAGING NMS

The standard approach to managing patients with NMS includes four steps:

• recognize the diagnosis early
• exclude alternate causes of symptoms
• discontinue suspected triggering drugs
• provide supportive care to reduce temperatures, ensure fluid balance, and detect complications.^5,6,20

Beyond supportive care, several specific therapies have been proposed based on theoretical mechanisms of NMS and meta-analyses of offlabel use in anecdotal clinical reports (Table 4). If benzodiazepines, dopamine agonists, or dantrolene are effective, taper slowly after recovery to prevent rebound symptoms.

Benzodiazepines. Given the concept of NMS as a form of catatonia, benzodiazepines have been used effectively in some cases.^20,21 A trial of lorazepam, 1 to 2 mg parenterally, is a reasonable first step. Higher doses may be required, with adequate monitoring of respiratory status. Oral lorazepam can maintain the therapeutic effect.

Dopamine agonists. To reverse the parkinsonism and dopamine antagonist properties of antipsychotics, dopamine agonists such as bromocriptine or amantadine have been tried and have reduced NMS duration and mortality.^20,22,23 Newer drugs such as ropinorole and pramipexole may also be useful. Dopaminergic drugs, however, can worsen psychosis and cause hypotension and emesis.

Dantrolene may reduce hyperthermia related to skeletal muscle hypermetabolism of any cause and has been effective in rapidly reducing extreme temperatures in some NMS cases.^20,22-26 Dantrolene is given IV, 1 to 2.5 mg/kg every 6 hours. An oral form can be substituted if a response is obtained. Dantrolene can impair respiratory and hepatic function and should not be combined with calcium channel blockers.

ECT is increasingly recognized as an effective NMS treatment and should not be overlooked for patients:

• who fail to respond to drug therapy or supportive care
• with residual catatonic symptoms.^13,20,27,28

Standard ECT is given, although nondepolarizing muscle relaxants instead of succinylcholine are used in patients with serious rhabdomyolysis to avoid the risk of hyperkalemia.²⁰

Recommendation. Although these modalities offer a spectrum of therapeutic options, it is premature to recommend any single remedy over others or over supportive care alone because:

• randomized, controlled trials have not been conducted
• NMS episodes are heterogeneous in presentation and outcome
• the syndrome is often self-limited after antipsychotics are discontinued.

I recommend that you choose therapies empirically, based on the character, severity, and duration of symptoms in a given case.^5,6,20

Table 4

How to treat neuroleptic malignant syndrome

REDUCING RISK OF RECURRENCE

Patients vary in susceptibility to recurrence after they recover from NMS, but the risk approaches 30% with future exposure to antipsychotics.^5,6 You may be able to minimize recurrence risk by:

• reducing risk factors, such as dehydration
• considering alternatives to antipsychotics, such as treating bipolar disorder with lithium or ECT
• using atypical instead of conventional antipsychotics, starting with low dosages and titrating slowly.

Before you reintroduce antipsychotics, carefully document informed consent and your rationale for treatment decisions in the patient’s chart.

Related resources

• Neuroleptic Malignant Syndrome Information Service. Hotline for health professionals. (888) 667-8367. www.nmsis.org
• Mann SC, Caroff SN, Keck PE Jr, Lazarus A. Neuroleptic malignant syndrome and related conditions (2nd ed). Washington, DC: American Psychiatric Publishing, 2003.
• Caroff SN, Mann SC, Francis A, Fricchione GL. Catatonia: from psychopathology to neurobiology. Washington, DC: American Psychiatric Publishing (in press).

Drug brand names

• Amantadine • Symmetrel
• Aripiprazole • Abilify
• Bromocriptine • Parlodel
• Clozapine • Clozaril
• Dantrolene • Dantrium
• Haloperidol • Haldol
• Lorazepam • Ativan
• Metoclopramide • Reglan
• Olanzapine • Zyprexa
• Pramipexole • Mirapex
• Prochlorperazine • Compazine
• Promethazine • Phenergan
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Ropinirole • Requip
• Ziprasidone • Geodon

Disclosure

Dr. Caroff receives research support from Janssen Pharmaceutica and Pfizer Inc., and is a consultant to Eli Lilly and Co. and Bristol-Myers Squibb Co.

Potentially fatal neuroleptic malignant syndrome (NMS)—though less common than in the past—can happen with either conventional or atypical antipsychotics.^1,2 To help you protect patients when prescribing antipsychotics or consulting with other clinicians about these drugs, this article discusses:

• risk factors and clinical features that warn of NMS onset
• differential diagnosis of disease states most often confused with NMS
• management recommendations, including supportive measures and specific interventions such as benzodiazepines, dopamine agonists, dantrolene, and electroconvulsive therapy (ECT).

WHY NMS REMAINS RELEVANT

NMS remains a risk in susceptible patients receiving atypical antipsychotics, according to clinical reports and drug adverse event surveys (Figure).²

Moreover, NMS continues to be reported with conventional antipsychotics, which remain in widespread use. Patients who receive long-acting depot conventional antipsychotics are at risk for prolonged NMS episodes.

Figure 55 NMS cases reported with use of antipsychotics, 1998-2002

Probable or definite neuroleptic malignant syndrome cases associated with antipsychotic monotherapy reported to the Neuroleptic Malignant Syndrome Information Service.NMS in medical settings. Psychiatrists may be consulted when patients develop NMS while receiving conventional antipsychotics or other dopaminereceptor antagonists used in medical settings.^3,4 Haloperidol remains the recommended drug of choice for treating agitation and delirium and continues to be the single most common trigger of NMS. Although often overlooked, antiemetics and sedatives with neuroleptic properties—such as prochlorperazine, metoclopramide, and promethazine—also have triggered NMS.

Other hyperthermic conditions. NMS is often considered in the differential diagnosis of patients who develop fever or encephalopathy while being treated with psychotropics. In these acute, complex, and often grave situations, psychiatrists may be consulted to recommend treatment for behavioral control or to distinguish NMS from other conditions.

NEWER VS. OLDER ANTIPSYCHOTICS

Has NMS incidence declined with the atypical agents? Probably, but providing proof is difficult:

• NMS is uncommon; its incidence in psychiatric patients treated with conventional antipsychotics is approximately 0.2%.⁵ To demonstrate reduced NMS incidence with atypicals, a very large sample of patients would be required to reach statistical significance.
• As doctors have used lower doses of conventional agents—which reduces the risk of NMS—any beneficial impact from atypicals has become more difficult to detect.^5,6
• Reports of NMS frequency with atypicals may be inflated by bias in publishing adverse events with newer versus older agents.
• Patients switched to atypicals may represent a high-risk group that is intolerant or resistant to conventional antipsychotics.

So far, few unequivocal cases of NMS have been attributed to the use of quetiapine, ziprasidone, or aripiprazole, the most recently introduced atypicals. Moreover, case reports of NMS associated with clozapine, risperidone, or olanzapine² are often difficult to interpret because of incomplete clinical details, varying diagnostic criteria, and concomitant use of more than one antipsychotic.

Milder NMS? Do the newer antipsychotics produce an “atypical” or milder form of NMS? Case reports indicate that extreme temperature elevations and extrapyramidal dysfunction are less frequent in NMS associated with atypical compared with conventional antipsychotics.² However, case descriptions of NMS were heterogeneous even with conventional agents, and clinicians’ growing awareness of NMS even before atypicals were introduced allowed for earlier diagnosis of mild and partial NMS cases.⁷

CLINICAL FEATURES OF NMS

Regardless of drug selection, it is important to recognize early and mild signs of NMS. Any case can progress to a fulminant form that is more difficult to treat.

Patients at risk. NMS may be more likely to develop in patients with:^5,6,8

• dehydration
• agitation
• low serum iron
• underlying brain damage
• catatonia.

Some patients may have genetic abnormalities in central dopamine systems that increase their susceptibility to NMS.^6,9

Fifteen to 20% of patients who develop NMS have experienced a previous episode while taking antipsychotics, which is why taking a careful drug history is important.^5,6 Although most often reported with therapeutic antipsychotic doses, NMS has been associated with rapid dose titration, especially when given parenterally.⁸

On the other hand, the practical value of these risk factors is often limited in individual cases and may lead one to overestimate NMS risk. NMS is rare and idiosyncratic. Risk factors may not outweigh antipsychotics’ benefits when these drugs are indicated for a patient with psychosis.

Incipient NMS. Identifying early signs of NMS may be impossible in fulminant cases, but patients with incipient NMS may show:

• unexpected mental status changes
• new-onset catatonia
• refractory extrapyramidal and bulbar signs such as rigidity, dysphagia, or dysarthria.^5,7,10

Other clues to NMS onset include tachycardia, tachypnea, and elevated temperature or serum creatine phosphokinase (CPK). These signs, however, do not precede or progress to NMS in all cases. A high index of suspicion for NMS, tempered by sound clinical judgment, is called for when assessing all patients receiving antipsychotics.

Diagnostic criteria. Clinical signs of NMS as a fullblown hypermetabolic syndrome are distinctive and well described (Table 1).^5,6,11,12 Elevated temperature is accompanied by profuse sweating. Extreme temperatures (>104° F), especially if prolonged or associated with hypoxia or hypotension, pose a high risk for brain damage, rhabdomyolysis, disseminated intravascular coagulation, multisystem organ failure, and death.

Muscle rigidity is a characteristic finding and may be accompanied by tremors, cogwheeling, myoclonus, or rhabdomyolysis. Changes in vital signs—such as tachycardia and tachypnea—are typical.

Mental status examination usually reveals catatonic signs of mutism and stupor, but delirium and coma also have been described. No laboratory findings are specific for NMS, but elevated white blood cell counts, low serum iron, metabolic acidosis, hypoxia, and elevated serum CPK and catecholamines have been reported.

Table 1

Common clinical features of NMS

Resolution. If recognized promptly, NMS resolves within 1 to 2 weeks in two-thirds of patients after antipsychotics are discontinued. The average recovery time of 7 to 10 days may be prolonged in patients who were taking long-acting depot antipsychotics or in those with persistent residual catatonic symptoms.¹³

Risk of death. NMS remains potentially fatal, especially if high temperatures develop or episodes are prolonged. Causes of death include cardiorespiratory arrest, renal failure, pulmonary emboli, pneumonia, sepsis, disseminated intravascular coagulation, and multisystem organ failure.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis of NMS encompasses disorders that present with fever and encephalopathy.^5,6,12 Primary brain disorders that resemble NMS include:^9,14-16

• infections
• acute psychotic disorders that progress to malignant catatonia or delirious mania
• midbrain structural lesions
• seizures.

Also exclude hormonal and autoimmune disorders and environmental heatstroke (Table 2).^17,18 Similar hyperthermic syndromes have been reported with other toxins and drugs, including malignant hyperthermia of anesthesia, serotonin syndrome, and dopamine agonist withdrawal in patients with Parkinson’s disease (Table 3).^5,6,19

Table 2

7 disease states most often confused with NMS

Table 3

Drugs that can cause NMS-like hyperthermic syndromes

MANAGING NMS

The standard approach to managing patients with NMS includes four steps:

• recognize the diagnosis early
• exclude alternate causes of symptoms
• discontinue suspected triggering drugs
• provide supportive care to reduce temperatures, ensure fluid balance, and detect complications.^5,6,20

Beyond supportive care, several specific therapies have been proposed based on theoretical mechanisms of NMS and meta-analyses of offlabel use in anecdotal clinical reports (Table 4). If benzodiazepines, dopamine agonists, or dantrolene are effective, taper slowly after recovery to prevent rebound symptoms.

Benzodiazepines. Given the concept of NMS as a form of catatonia, benzodiazepines have been used effectively in some cases.^20,21 A trial of lorazepam, 1 to 2 mg parenterally, is a reasonable first step. Higher doses may be required, with adequate monitoring of respiratory status. Oral lorazepam can maintain the therapeutic effect.

Dopamine agonists. To reverse the parkinsonism and dopamine antagonist properties of antipsychotics, dopamine agonists such as bromocriptine or amantadine have been tried and have reduced NMS duration and mortality.^20,22,23 Newer drugs such as ropinorole and pramipexole may also be useful. Dopaminergic drugs, however, can worsen psychosis and cause hypotension and emesis.

Dantrolene may reduce hyperthermia related to skeletal muscle hypermetabolism of any cause and has been effective in rapidly reducing extreme temperatures in some NMS cases.^20,22-26 Dantrolene is given IV, 1 to 2.5 mg/kg every 6 hours. An oral form can be substituted if a response is obtained. Dantrolene can impair respiratory and hepatic function and should not be combined with calcium channel blockers.

ECT is increasingly recognized as an effective NMS treatment and should not be overlooked for patients:

• who fail to respond to drug therapy or supportive care
• with residual catatonic symptoms.^13,20,27,28

Standard ECT is given, although nondepolarizing muscle relaxants instead of succinylcholine are used in patients with serious rhabdomyolysis to avoid the risk of hyperkalemia.²⁰

Recommendation. Although these modalities offer a spectrum of therapeutic options, it is premature to recommend any single remedy over others or over supportive care alone because:

• randomized, controlled trials have not been conducted
• NMS episodes are heterogeneous in presentation and outcome
• the syndrome is often self-limited after antipsychotics are discontinued.

I recommend that you choose therapies empirically, based on the character, severity, and duration of symptoms in a given case.^5,6,20

Table 4

How to treat neuroleptic malignant syndrome

REDUCING RISK OF RECURRENCE

Patients vary in susceptibility to recurrence after they recover from NMS, but the risk approaches 30% with future exposure to antipsychotics.^5,6 You may be able to minimize recurrence risk by:

• reducing risk factors, such as dehydration
• considering alternatives to antipsychotics, such as treating bipolar disorder with lithium or ECT
• using atypical instead of conventional antipsychotics, starting with low dosages and titrating slowly.

Before you reintroduce antipsychotics, carefully document informed consent and your rationale for treatment decisions in the patient’s chart.

Related resources

• Neuroleptic Malignant Syndrome Information Service. Hotline for health professionals. (888) 667-8367. www.nmsis.org
• Mann SC, Caroff SN, Keck PE Jr, Lazarus A. Neuroleptic malignant syndrome and related conditions (2nd ed). Washington, DC: American Psychiatric Publishing, 2003.
• Caroff SN, Mann SC, Francis A, Fricchione GL. Catatonia: from psychopathology to neurobiology. Washington, DC: American Psychiatric Publishing (in press).

Drug brand names

• Amantadine • Symmetrel
• Aripiprazole • Abilify
• Bromocriptine • Parlodel
• Clozapine • Clozaril
• Dantrolene • Dantrium
• Haloperidol • Haldol
• Lorazepam • Ativan
• Metoclopramide • Reglan
• Olanzapine • Zyprexa
• Pramipexole • Mirapex
• Prochlorperazine • Compazine
• Promethazine • Phenergan
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Ropinirole • Requip
• Ziprasidone • Geodon

Disclosure

Dr. Caroff receives research support from Janssen Pharmaceutica and Pfizer Inc., and is a consultant to Eli Lilly and Co. and Bristol-Myers Squibb Co.

Psychiatrists’ risk of malpractice liability¹ is broadening as courts consider the uncertainties of off-label prescribing, telemedicine, and confidentiality. Juries are holding mental health practitioners responsible for harm done both to and by psychiatric patients.

How you keep medical records, communicate with patients and colleagues, and arrange consultations can reduce your malpractice risk (Box 1).^4-9 We offer recommendations based on court decisions and other evidence for managing:

• traditional risks—such as patient violence and suicide, adverse drug reactions, sex with patients, faulty termination of treatment, and supervisory and consultative relationships⁴
• newer risks—such as recovered memory, off-label prescribing, practice guidelines, and e-mail and confidentiality.

Box 1

This article describes general guidelines and is not intended to constitute legal advice. All practitioners have a responsibility to know the laws of the jurisdictions in which they practice.

PREVENTING PATIENT VIOLENCE

The case that opened Pandora’s box. Prosenjit Poddar, a student at the University of California at Berkeley, was infatuated with coed Tanya Tarasoff and told his psychologist he intended to kill her. The psychologist notified his psychiatric supervisor and called campus police.

The psychologist told police Poddar was dangerous to himself and others. He stated that he would sign an emergency hold if they would bring Poddar to the hospital.

The police apprehended Poddar but released him. Poddar dropped out of therapy and 2 months later fatally stabbed Ms. Tarasoff.

Ms. Tarasoff’s parents sued those who treated Poddar and the University of California.² After a complicated legal course, the California Supreme Court ruled that once a therapist determines—or should have determined—that a patient poses a serious danger of violence to others, “he bears a duty to exercise reasonable care to protect the foreseeable victim of that danger.”³

The 1976 Tarasoff ruling has become a national standard of practice, leading to numerous other patient violence lawsuits. In these cases, psychiatrists are most likely to be found liable when recently released inpatients commit violent acts, particularly if the physician had reason to know the patient was dangerous and failed to take adequate precautions or appropriately assess the patient.⁴

Wider interpretations. Cases in several states have extended the Tarasoff ruling. In at least two cases, this standard has been applied when the patient threatened no specific victim before committing violence:

• A New Jersey court (McIntosh v. Milano, 1979) found a psychiatrist liable for malpractice on grounds that a therapist has a duty to protect society, just as a doctor must protect society by reporting carriers of dangerous diseases.
• A Nebraska court (Lipari v. Sears, Roebuck, and Co., 1980) held that physicians have a duty to protect—even if the specific identity of victims is unknown—so long as the physician should know that the patient presents an unreasonable risk of harm to others.²

Auto accidents. Tarasoff liability also has been extended to auto accidents. In Washington state (Petersen v. Washington, 1983), a psychiatrist was held liable for injuries to victims of an accident caused by a psychiatric patient. The court ruled that the psychiatrist had a duty to take reasonable precautions to protect any foreseeable persons from being endangered by the patient.

In a similar case in Wisconsin (Schuster and Schuster v. Altenberg, et al., 1988), the court ruled that damages could be awarded to anyone whose harm could have been prevented had the physician practiced according to professional standards.²

Other extensions include cases such as Naidu v. Laird, 1988, in which patient violence occurred more than 5 months after hospitalization.² Vermont has extended the Tarasoff precedent to property destruction by psychiatric patients.¹⁰

Recommendation. Most states require a psychiatrist to protect against only specific threats to identifiable victims.¹⁰ To defend yourself against a Tarasoff-type suit, you must show that you:

• carefully assessed the patient’s risk for violence
• provided appropriate care
• and took appropriate precautions.

The most protective evidence is a medical record documenting that you thoroughly assessed a patient for risk of violence (Table).^4,11

If you are unsure about how to manage a patient you believe may be dangerous to himself or others, consult with supervisors, peers, and legal advisors. Many states have Tarasoff-like statutes that specify the conditions that require action and the appropriate actions.

In states without specific statutes, options that generally satisfy Tarasoff requirements include hospitalizing the patient, notifying authorities, and/or warning the potential victim.¹⁰ As the Tarasoff case demonstrated, notifying authorities may not substitute for warning or hospitalizing.²

SUICIDE RISK? DOCUMENT CAREFULLY

Patient suicide accounts for one-fifth of claims covered by the American Psychiatric Association (APA) insurance plan.

In court, key points of challenge to a physician’s judgment in a suicide case include the admission evaluation and any status changes. Thorough risk assessment includes carefully reviewing existing records, evaluating risk factors for suicide, and seeking advice from colleagues or supervisors when appropriate.⁴

Recommendation. Document for every inpatient admission, discharge, or status change that the patient’s risk for suicide was assessed. List risk factors, protective factors, and risk for self-harm.

Explicitly address in the patient’s chart any comments about suicidality (such as heard by nursing staff).⁹ Document your rationale for medical decisions and orders, consistently follow unit policies, and explain risks and benefits of hospitalization to patients and their families.

Before discharge, schedule appropriate follow-up and make reasonable efforts to ensure medication adherence.⁴

SEX WITH PATIENTS IS UNPROTECTED

Sexual involvement with patients is indefensible and uncontestable in malpractice cases. Even so, up to 9% of male therapists and 3% of female therapists report in surveys that they have had sexual interaction with their patients.⁴

In 1985 the APA excluded sex with patients from its malpractice insurance coverage. Courts generally consider a treatment to be within the standard of care if a respectable minority of physicians consider it to be appropriate. Sex with patients is considered an absolute deviation from the standard of care, and no respectable minority of practitioners supports this practice. Because patients are substantially harmed, sex with patients is considered prima facie malpractice.¹²

Table

Is this patient dangerous? Risk factors for violence

WHEN MEDICATIONS CAUSE HARM

Adverse drug reactions—particularly tardive dyskinesia (TD)—are a source of significant losses in malpractice cases. Multimillion-dollar awards have been granted, especially when neuroleptic antipsychotics have been given in excessive dosages without proper monitoring.¹³

Informed consent has been a particularly difficult issue with the use of neuroleptic medications. Many doctors worry that patients who fear developing TD will not take prescribed neuroleptics. A study of North Carolina psychiatrists in the 1980s revealed that only 30% mentioned TD when telling their patients about neuroleptics’ possible side effects.¹³

The fact that a patient develops TD while taking an antipsychotic does not establish grounds for malpractice; a valid malpractice suit must also establish negligence. Negligence could include failing to obtain appropriate informed consent or continuing to prescribe an antipsychotic without adequately examining the patient.⁴

Informed consent does not require a patient to fully understand everything about a medication. The patient must understand the information a reasonable patient would want to know. Obvious misunderstandings must be corrected.

Recommendation. Consider informed consent a process, rather than one event—especially when you give neuroleptics for acute psychotic episodes. You can establish, review, and refresh consent in follow-up visits as medications help patients become more coherent and organized.

If you doubt a patient’s capacity to provide informed consent, a court determination may be necessary. In emergencies, however, treatment becomes a priority, even if the patient’s capacity to make rational decisions has not been established.¹³

TERMINATE TREATMENT WITH CAUTION

Terminating treatment can lead to malpractice, particularly if a patient becomes suicidal or violent. Psychiatrists have the right to choose their patients but cannot terminate care if a patient is acutely ill or requires emergency care.

Ensuring appropriate follow-up for patients at risk for decompensation often requires more than providing a referral or phone number. With the patient’s permission, for example, you could contact his subsequent psychiatrist or work with his support network to ensure that he receives follow-up care.¹⁴

Recommendation. With stable patients, send a written notice of termination and specify a reasonable period, usually 30 days. Send the letter by certified mail, and request a return receipt. Offer to help the patient find a new doctor, and say that you will forward the patient’s records to the new doctor when you receive appropriate release-of-information paperwork.¹⁵

LET THE SUPERVISOR BEWARE

Under the legal concept of respondeat superior (“let the master reply”), liability for the actions of subordinates may be transferred upward to the supervisor.⁴ For psychiatrists, supervisory liability obviously applies to teaching residents but may also apply in joint care, as with psychologists or social workers.

Recommendation. As a co-treating psychiatrist, you may be liable for other therapists’ actions unless you formally distinguish your role as a prescriber and not as a supervisor.⁹

When you prescribe medications for patients of nonphysician therapists, be sure you, the therapist, and patient understand the nature of your collaboration. Document the type of relationship and your discussion with the patient in the patient’s chart.

WATCH OUT FOR ‘CURBSIDE’ CONSULTS

Consult-liaison psychiatrists typically face a lower malpractice risk than do those who provide primary treatment. Duty to care for the patient is usually established by a formal consult request, after which the psychiatrist examines the patient and recommends treatment to the primary team.

You can, however, establish duty without meeting a patient. If sufficiently detailed, an informal “curbside” consult may establish a duty and corresponding liability¹⁶ (Box 2).^4,5,9,17.18

Liability is usually shared with the primary team but may be related to how much responsibility you assume in the patient’s care. Any direct treatment—electroconvulsive therapy, psychotherapy, prescribing, writing orders in the chart—can elevate your risk to the primary level. Similarly, if the patient is harmed because the primary treater followed a consulting psychiatrist’s negligent advice, the psychiatrist can be found solely liable.

When you recommend a treatment, you share a portion of liability for informed consent. If neither you nor the provider obtains appropriate informed consent, you may both share liability for adverse outcomes. Both teams also share the duty to report child and elder abuse.¹⁶

Recommendation. Establish an explicit division of responsibilities with the primary team, including who writes orders and manages medications and who provides follow-up and discharge planning.

For curbside consults, inform the primary physician that you are providing general information and not a specific treatment recommendation. If the case is too complicated for general information to be useful, a formal consultation would serve the patient better. In written consultations, specify:

• the reason for the consult
• the issues addressed
• and the parties responsible for follow-up.¹⁶

RECOVERED MEMORY? FORGET PROSECUTION

In 1994, a father successfully sued his daughter’s therapists for implanting false memories of incest. A California court awarded him $500,000 on grounds that the therapists owed a duty of care to the patient’s parents as well as to the patient. Since then, multimillion-dollar cases have been litigated on grounds of false recovered memories, and some insurers exclude coverage for “revival of memory.”¹²

Most therapists who have been found liable have strongly supported the accuracy of their patients’ memories. These memories have usually contained bizarre features, including satanic abuse, baby breeding, human sacrifice, and cannibalism. Therapists in these cases have often recommended that their patients press charges or file lawsuits against their alleged abusers.

Lawsuits against therapists have been won on grounds that they used unorthodox procedures without informed consent, negligently or recklessly implanted memories of abuse, negligently reinforced such memories, and failed to sufficiently investigate the memories’ accuracy.¹⁹

Box 2

Recommendation. Patients in therapy sometimes report newly found memories. To reduce your risk:

• obtain informed consent from patients before you begin any psychotherapy
• carefully document therapy session details when patients divulge new memories—particularly of abuse
• avoid encouraging patients to act on recovered memories.¹⁹

OFF-LABEL DRUG USE: KNOW THE LITERATURE

Off-label prescribing is both common and legal but may increase a physician’s liability risk if adverse events occur. Cases in Minnesota, Texas, and Louisiana have established precedents for using the Physician’s Desk Reference or package inserts to establish a standard of care.

In 1970 the Minnesota Supreme Court held that deviating from the package insert constituted prima facie evidence of negligence. This interpretation shifts the burden of proof from the plaintiff to the physician, who must then prove that he or she was not negligent when prescribing the drug.²⁰

Recommendation. Off-label prescribing is an important component of modern psychiatric care. Research supports most accepted off-label prescribing, at least to the point of establishing a respectable minority for a standard of care (Box 2).

When prescribing, know which indications are FDA-approved and which are off-label. For off-label prescribing, know the literature supporting that use and notify patients of off-label status as you document informed consent.²⁰

PROS AND CONS OF PRACTICE GUIDELINES

Clinical practice guidelines developed by professional organizations to assist physicians have also acquired legal ramifications. Difficult questions about guidelines include:

• Do they set the standard of care, or are they merely suggestions?
• Do they provide a defense against liability?
• How does a practitioner select between conflicting guidelines?

On the other hand, following clinical guidelines can protect you in cases with adverse outcomes. In a study of insurance company claims, approximately one-fourth of plaintiff’s attorneys who were surveyed said they had refused cases because the physician had followed practice guidelines. Conversely, one-fourth of defense attorneys said they had been influenced to settle cases because the physicians they represented had not followed practice guidelines.²¹

Liability cases involving practice guidelines have produced varying decisions. As a rule of thumb, courts tend to find that more-specific guidelines constitute a standard of care, whereas more-general guidelines are flexible suggestions.

Recommendation. If the court finds that existing guidelines establish the standard of care and your care has deviated from the guidelines with adverse consequences, the burden of proof shifts to you to prove that you were not negligent.¹⁸ When guidelines exist, know them and be prepared to defend decisions that deviate from them.

TELEMEDICINE: DANGERS IN CYBERSPACE

Unauthorized use or disclosure of patients’ electronic information can leave physicians liable for invasion of privacy and breach of confidentiality.²²

E-mail communication with a patient may also be sufficient to establish a duty of care, especially if the patient presents diagnostic information and the physician provides medical advice. Once duty to care is established, the physician is responsible for ongoing care or may face charges of abandonment.

Establishing duty to patients through e-mail is particularly troublesome, as patients may be writing from another state where you are not licensed to practice. Several states have explicitly forbidden unlicensed telemedicine; others have offered limited licenses for telemedicine practice.²²

Using e-mail to communicate with established patients introduces other liabilities. E-mail is legally considered part of the medical record and is subject to discovery in legal proceedings. Failure to preserve important patient e-mail may be evidence of negligence, especially in cases involving the medical record.

On the other hand, e-mail can be surprisingly permanent; it is virtually impossible to definitively delete e-mail that contains sensitive or embarrassing information. Deleted e-mail frequently can be recovered, and every e-mail exists in multiple copies, including the sender’s, the receiver’s, and at least one in a centralized server.²³

Recommendation. Reduce liability risks with informed consent if you use e-mail to communicate with existing patients. Minimize e-mail contact with nonestablished patients, and make sure the confidentiality of patients’ communications is secure.²²

Related resources

• Gutheil TG, Appelbaum PS. Clinical handbook of psychiatry and the law (3rd ed). Philadelphia: Lippincott Williams & Wilkins, 2000.
• American Psychiatric Association. Practice guidelines. http://www.psych.org/clin_res/prac_guide.cfm

Psychiatrists’ risk of malpractice liability¹ is broadening as courts consider the uncertainties of off-label prescribing, telemedicine, and confidentiality. Juries are holding mental health practitioners responsible for harm done both to and by psychiatric patients.

How you keep medical records, communicate with patients and colleagues, and arrange consultations can reduce your malpractice risk (Box 1).^4-9 We offer recommendations based on court decisions and other evidence for managing:

• traditional risks—such as patient violence and suicide, adverse drug reactions, sex with patients, faulty termination of treatment, and supervisory and consultative relationships⁴
• newer risks—such as recovered memory, off-label prescribing, practice guidelines, and e-mail and confidentiality.

Box 1

This article describes general guidelines and is not intended to constitute legal advice. All practitioners have a responsibility to know the laws of the jurisdictions in which they practice.

PREVENTING PATIENT VIOLENCE

The case that opened Pandora’s box. Prosenjit Poddar, a student at the University of California at Berkeley, was infatuated with coed Tanya Tarasoff and told his psychologist he intended to kill her. The psychologist notified his psychiatric supervisor and called campus police.

The psychologist told police Poddar was dangerous to himself and others. He stated that he would sign an emergency hold if they would bring Poddar to the hospital.

The police apprehended Poddar but released him. Poddar dropped out of therapy and 2 months later fatally stabbed Ms. Tarasoff.

Ms. Tarasoff’s parents sued those who treated Poddar and the University of California.² After a complicated legal course, the California Supreme Court ruled that once a therapist determines—or should have determined—that a patient poses a serious danger of violence to others, “he bears a duty to exercise reasonable care to protect the foreseeable victim of that danger.”³

The 1976 Tarasoff ruling has become a national standard of practice, leading to numerous other patient violence lawsuits. In these cases, psychiatrists are most likely to be found liable when recently released inpatients commit violent acts, particularly if the physician had reason to know the patient was dangerous and failed to take adequate precautions or appropriately assess the patient.⁴

Wider interpretations. Cases in several states have extended the Tarasoff ruling. In at least two cases, this standard has been applied when the patient threatened no specific victim before committing violence:

• A New Jersey court (McIntosh v. Milano, 1979) found a psychiatrist liable for malpractice on grounds that a therapist has a duty to protect society, just as a doctor must protect society by reporting carriers of dangerous diseases.
• A Nebraska court (Lipari v. Sears, Roebuck, and Co., 1980) held that physicians have a duty to protect—even if the specific identity of victims is unknown—so long as the physician should know that the patient presents an unreasonable risk of harm to others.²

Auto accidents. Tarasoff liability also has been extended to auto accidents. In Washington state (Petersen v. Washington, 1983), a psychiatrist was held liable for injuries to victims of an accident caused by a psychiatric patient. The court ruled that the psychiatrist had a duty to take reasonable precautions to protect any foreseeable persons from being endangered by the patient.

In a similar case in Wisconsin (Schuster and Schuster v. Altenberg, et al., 1988), the court ruled that damages could be awarded to anyone whose harm could have been prevented had the physician practiced according to professional standards.²

Other extensions include cases such as Naidu v. Laird, 1988, in which patient violence occurred more than 5 months after hospitalization.² Vermont has extended the Tarasoff precedent to property destruction by psychiatric patients.¹⁰

Recommendation. Most states require a psychiatrist to protect against only specific threats to identifiable victims.¹⁰ To defend yourself against a Tarasoff-type suit, you must show that you:

• carefully assessed the patient’s risk for violence
• provided appropriate care
• and took appropriate precautions.

The most protective evidence is a medical record documenting that you thoroughly assessed a patient for risk of violence (Table).^4,11

If you are unsure about how to manage a patient you believe may be dangerous to himself or others, consult with supervisors, peers, and legal advisors. Many states have Tarasoff-like statutes that specify the conditions that require action and the appropriate actions.

In states without specific statutes, options that generally satisfy Tarasoff requirements include hospitalizing the patient, notifying authorities, and/or warning the potential victim.¹⁰ As the Tarasoff case demonstrated, notifying authorities may not substitute for warning or hospitalizing.²

SUICIDE RISK? DOCUMENT CAREFULLY

Patient suicide accounts for one-fifth of claims covered by the American Psychiatric Association (APA) insurance plan.

In court, key points of challenge to a physician’s judgment in a suicide case include the admission evaluation and any status changes. Thorough risk assessment includes carefully reviewing existing records, evaluating risk factors for suicide, and seeking advice from colleagues or supervisors when appropriate.⁴

Recommendation. Document for every inpatient admission, discharge, or status change that the patient’s risk for suicide was assessed. List risk factors, protective factors, and risk for self-harm.

Explicitly address in the patient’s chart any comments about suicidality (such as heard by nursing staff).⁹ Document your rationale for medical decisions and orders, consistently follow unit policies, and explain risks and benefits of hospitalization to patients and their families.

Before discharge, schedule appropriate follow-up and make reasonable efforts to ensure medication adherence.⁴

SEX WITH PATIENTS IS UNPROTECTED

Sexual involvement with patients is indefensible and uncontestable in malpractice cases. Even so, up to 9% of male therapists and 3% of female therapists report in surveys that they have had sexual interaction with their patients.⁴

In 1985 the APA excluded sex with patients from its malpractice insurance coverage. Courts generally consider a treatment to be within the standard of care if a respectable minority of physicians consider it to be appropriate. Sex with patients is considered an absolute deviation from the standard of care, and no respectable minority of practitioners supports this practice. Because patients are substantially harmed, sex with patients is considered prima facie malpractice.¹²

Table

Is this patient dangerous? Risk factors for violence

WHEN MEDICATIONS CAUSE HARM

Adverse drug reactions—particularly tardive dyskinesia (TD)—are a source of significant losses in malpractice cases. Multimillion-dollar awards have been granted, especially when neuroleptic antipsychotics have been given in excessive dosages without proper monitoring.¹³

Informed consent has been a particularly difficult issue with the use of neuroleptic medications. Many doctors worry that patients who fear developing TD will not take prescribed neuroleptics. A study of North Carolina psychiatrists in the 1980s revealed that only 30% mentioned TD when telling their patients about neuroleptics’ possible side effects.¹³

The fact that a patient develops TD while taking an antipsychotic does not establish grounds for malpractice; a valid malpractice suit must also establish negligence. Negligence could include failing to obtain appropriate informed consent or continuing to prescribe an antipsychotic without adequately examining the patient.⁴

Informed consent does not require a patient to fully understand everything about a medication. The patient must understand the information a reasonable patient would want to know. Obvious misunderstandings must be corrected.

Recommendation. Consider informed consent a process, rather than one event—especially when you give neuroleptics for acute psychotic episodes. You can establish, review, and refresh consent in follow-up visits as medications help patients become more coherent and organized.

If you doubt a patient’s capacity to provide informed consent, a court determination may be necessary. In emergencies, however, treatment becomes a priority, even if the patient’s capacity to make rational decisions has not been established.¹³

TERMINATE TREATMENT WITH CAUTION

Terminating treatment can lead to malpractice, particularly if a patient becomes suicidal or violent. Psychiatrists have the right to choose their patients but cannot terminate care if a patient is acutely ill or requires emergency care.

Ensuring appropriate follow-up for patients at risk for decompensation often requires more than providing a referral or phone number. With the patient’s permission, for example, you could contact his subsequent psychiatrist or work with his support network to ensure that he receives follow-up care.¹⁴

Recommendation. With stable patients, send a written notice of termination and specify a reasonable period, usually 30 days. Send the letter by certified mail, and request a return receipt. Offer to help the patient find a new doctor, and say that you will forward the patient’s records to the new doctor when you receive appropriate release-of-information paperwork.¹⁵

LET THE SUPERVISOR BEWARE

Under the legal concept of respondeat superior (“let the master reply”), liability for the actions of subordinates may be transferred upward to the supervisor.⁴ For psychiatrists, supervisory liability obviously applies to teaching residents but may also apply in joint care, as with psychologists or social workers.