Current Psychiatry

I was disappointed to read Dr. Henry Nasrallah’s editorial calling for the use of clinician measurement tools in the management of psychiatric illness (“Long overdue: Measurement-based psychiatric practice,” From the Editor, Current Psychiatry, April 2009). I agree that general and vague comments such as “doing better” are of limited value. I would further argue that such documentation is the psychiatric equivalent of “WNL”—which stands for “we never looked”—in a medical review of systems. But I do not believe the answer is to further dumb down the practice of psychiatry by generating quantifiable, 1-dimensional scores that purport to measure how well our patient is doing.

In the past, when these psychometric tools were developed (approximately from 1960 to 1987), 2 primary concerns were voiced.

First, there was limited data to support their validity and reliability, although that concern is somewhat less now, at least with some of the tests Dr. Nasrallah recommended. These tests still lack criterion-related validity. For example, IQ as measured by an IQ test predicts performance on an IQ test, so it’s reliable. But to use that number to predict fitness for a job or even academic success ends up discriminating against some individuals or groups who are more than just a number.

Second, there was the concern that, similar to schoolteachers who end up teaching to a normative test, we could end up treating a patient’s test score rather than the discomfort with his or her life. I believe this also remains true. Unlike diabetes mellitus, which is defined by increased blood sugars, psychiatric diagnoses are purely syndromal and require “clinically significant distress or impairment” or they are not a disease according to DSM-IV-TR. It’s the distress and the impairment that we treat.

Today, I see 2 positive trends in our field: to find increasingly efficient methods to appropriately tailor and effectively deliver care and to be recovery-focused. It seems to me that routine and indiscriminate use of psychometrics obstructs both of these. Each test takes 30 to 40 minutes to administer and requires skilled and trained clinicians, if not psychiatrists themselves. That at least doubles the length of the visit with no evidence-based benefit. A recovery focus requires that we—as does the DSM—focus on our patients’ perceived impairments, not their test scores.

Lyle B. Forehand, Jr, MD
Modesto, CA

Dr. Nasrallah responds

I thank Dr. Forehand for his comments. I agree that psychiatric diagnoses at this time are purely syndromal and require “clinically significant distress or impairment.” What I am calling for is to quantify the various signs and symptoms of the distress and impairment before and after treatment with a standard scale widely used by all researchers and some clinicians.

The definition of remission, which is the phase that precedes recovery, actually is based on standard rating scales’ severity score for a given psychiatric illness. Therefore, clinicians must rate their patients on the scale corresponding to that illness to recognize when their patients have met the official criteria for remission.

Practitioners do not have to use a scale to rate the patient’s symptoms separate from the standard interviewing process. Rather, once clinicians become familiar with these scales, they could conduct their usual interview and then take a moment when writing their note in the chart to circle the score of each symptom they assessed during their clinical interaction, and cite the total score in the admission or progress note. A copy of the scale can be included as a supplement to the progress note and will ensure that all signs and symptoms related to an illness are assessed, rather than just some of them.

To summarize, until scientific research leads to actual lab tests for psychiatric disorders—and I believe that day will come—psychiatrists should quantify their patients’ clinical distress and impairment with the same objective measures used in evidence-based FDA trials, even if the scales’ reliability and validity are not perfect.

Henry A. Nasrallah, MD
Editor-In-Chief

I was disappointed to read Dr. Henry Nasrallah’s editorial calling for the use of clinician measurement tools in the management of psychiatric illness (“Long overdue: Measurement-based psychiatric practice,” From the Editor, Current Psychiatry, April 2009). I agree that general and vague comments such as “doing better” are of limited value. I would further argue that such documentation is the psychiatric equivalent of “WNL”—which stands for “we never looked”—in a medical review of systems. But I do not believe the answer is to further dumb down the practice of psychiatry by generating quantifiable, 1-dimensional scores that purport to measure how well our patient is doing.

In the past, when these psychometric tools were developed (approximately from 1960 to 1987), 2 primary concerns were voiced.

First, there was limited data to support their validity and reliability, although that concern is somewhat less now, at least with some of the tests Dr. Nasrallah recommended. These tests still lack criterion-related validity. For example, IQ as measured by an IQ test predicts performance on an IQ test, so it’s reliable. But to use that number to predict fitness for a job or even academic success ends up discriminating against some individuals or groups who are more than just a number.

Second, there was the concern that, similar to schoolteachers who end up teaching to a normative test, we could end up treating a patient’s test score rather than the discomfort with his or her life. I believe this also remains true. Unlike diabetes mellitus, which is defined by increased blood sugars, psychiatric diagnoses are purely syndromal and require “clinically significant distress or impairment” or they are not a disease according to DSM-IV-TR. It’s the distress and the impairment that we treat.

Today, I see 2 positive trends in our field: to find increasingly efficient methods to appropriately tailor and effectively deliver care and to be recovery-focused. It seems to me that routine and indiscriminate use of psychometrics obstructs both of these. Each test takes 30 to 40 minutes to administer and requires skilled and trained clinicians, if not psychiatrists themselves. That at least doubles the length of the visit with no evidence-based benefit. A recovery focus requires that we—as does the DSM—focus on our patients’ perceived impairments, not their test scores.

Lyle B. Forehand, Jr, MD
Modesto, CA

Dr. Nasrallah responds

I thank Dr. Forehand for his comments. I agree that psychiatric diagnoses at this time are purely syndromal and require “clinically significant distress or impairment.” What I am calling for is to quantify the various signs and symptoms of the distress and impairment before and after treatment with a standard scale widely used by all researchers and some clinicians.

The definition of remission, which is the phase that precedes recovery, actually is based on standard rating scales’ severity score for a given psychiatric illness. Therefore, clinicians must rate their patients on the scale corresponding to that illness to recognize when their patients have met the official criteria for remission.

Practitioners do not have to use a scale to rate the patient’s symptoms separate from the standard interviewing process. Rather, once clinicians become familiar with these scales, they could conduct their usual interview and then take a moment when writing their note in the chart to circle the score of each symptom they assessed during their clinical interaction, and cite the total score in the admission or progress note. A copy of the scale can be included as a supplement to the progress note and will ensure that all signs and symptoms related to an illness are assessed, rather than just some of them.

To summarize, until scientific research leads to actual lab tests for psychiatric disorders—and I believe that day will come—psychiatrists should quantify their patients’ clinical distress and impairment with the same objective measures used in evidence-based FDA trials, even if the scales’ reliability and validity are not perfect.

Henry A. Nasrallah, MD
Editor-In-Chief

I was disappointed to read Dr. Henry Nasrallah’s editorial calling for the use of clinician measurement tools in the management of psychiatric illness (“Long overdue: Measurement-based psychiatric practice,” From the Editor, Current Psychiatry, April 2009). I agree that general and vague comments such as “doing better” are of limited value. I would further argue that such documentation is the psychiatric equivalent of “WNL”—which stands for “we never looked”—in a medical review of systems. But I do not believe the answer is to further dumb down the practice of psychiatry by generating quantifiable, 1-dimensional scores that purport to measure how well our patient is doing.

In the past, when these psychometric tools were developed (approximately from 1960 to 1987), 2 primary concerns were voiced.

First, there was limited data to support their validity and reliability, although that concern is somewhat less now, at least with some of the tests Dr. Nasrallah recommended. These tests still lack criterion-related validity. For example, IQ as measured by an IQ test predicts performance on an IQ test, so it’s reliable. But to use that number to predict fitness for a job or even academic success ends up discriminating against some individuals or groups who are more than just a number.

Second, there was the concern that, similar to schoolteachers who end up teaching to a normative test, we could end up treating a patient’s test score rather than the discomfort with his or her life. I believe this also remains true. Unlike diabetes mellitus, which is defined by increased blood sugars, psychiatric diagnoses are purely syndromal and require “clinically significant distress or impairment” or they are not a disease according to DSM-IV-TR. It’s the distress and the impairment that we treat.

Today, I see 2 positive trends in our field: to find increasingly efficient methods to appropriately tailor and effectively deliver care and to be recovery-focused. It seems to me that routine and indiscriminate use of psychometrics obstructs both of these. Each test takes 30 to 40 minutes to administer and requires skilled and trained clinicians, if not psychiatrists themselves. That at least doubles the length of the visit with no evidence-based benefit. A recovery focus requires that we—as does the DSM—focus on our patients’ perceived impairments, not their test scores.

Lyle B. Forehand, Jr, MD
Modesto, CA

Dr. Nasrallah responds

I thank Dr. Forehand for his comments. I agree that psychiatric diagnoses at this time are purely syndromal and require “clinically significant distress or impairment.” What I am calling for is to quantify the various signs and symptoms of the distress and impairment before and after treatment with a standard scale widely used by all researchers and some clinicians.

The definition of remission, which is the phase that precedes recovery, actually is based on standard rating scales’ severity score for a given psychiatric illness. Therefore, clinicians must rate their patients on the scale corresponding to that illness to recognize when their patients have met the official criteria for remission.

Practitioners do not have to use a scale to rate the patient’s symptoms separate from the standard interviewing process. Rather, once clinicians become familiar with these scales, they could conduct their usual interview and then take a moment when writing their note in the chart to circle the score of each symptom they assessed during their clinical interaction, and cite the total score in the admission or progress note. A copy of the scale can be included as a supplement to the progress note and will ensure that all signs and symptoms related to an illness are assessed, rather than just some of them.

To summarize, until scientific research leads to actual lab tests for psychiatric disorders—and I believe that day will come—psychiatrists should quantify their patients’ clinical distress and impairment with the same objective measures used in evidence-based FDA trials, even if the scales’ reliability and validity are not perfect.

Henry A. Nasrallah, MD
Editor-In-Chief

I found Dr. James Randolph Hillard’s article on workplace mobbing timely and extremely interesting (“Workplace mobbing: Are they really out to get your patient?” Current Psychiatry, April 2009). As clinical director of a consultation service for corporations, I am asked to assess employees suspected to be at risk for workplace violence and for fitness for duty. Mobbing seems to be more prevalent and the consequences more dire for a victim who is feeling pressured to leave his or her job when there is little hope of getting another one or is taking on responsibilities previously held by others who have been laid off.

This brings to the forefront a very important consideration for individuals who confront such assessment challenges. Gathering collateral information is critical for diagnostic accuracy and well-articulated interventions that may be recommended. Evaluators who do such assessments at the behest of corporate clients should insist that they have access to employee files investigative reports, and—if appropriate—permission to interview supervisors, employee assistance program representatives, and human resources personnel familiar with the case. Mobbing is real and deserves much greater attention by researchers and clinicians in the United States.

Scott Bresler, PhD
Clinical director
Center for Threat Assessment
Institute for Psychiatry and Law
University of Cincinnati
Cincinnati, OH

I found Dr. James Randolph Hillard’s article on workplace mobbing timely and extremely interesting (“Workplace mobbing: Are they really out to get your patient?” Current Psychiatry, April 2009). As clinical director of a consultation service for corporations, I am asked to assess employees suspected to be at risk for workplace violence and for fitness for duty. Mobbing seems to be more prevalent and the consequences more dire for a victim who is feeling pressured to leave his or her job when there is little hope of getting another one or is taking on responsibilities previously held by others who have been laid off.

This brings to the forefront a very important consideration for individuals who confront such assessment challenges. Gathering collateral information is critical for diagnostic accuracy and well-articulated interventions that may be recommended. Evaluators who do such assessments at the behest of corporate clients should insist that they have access to employee files investigative reports, and—if appropriate—permission to interview supervisors, employee assistance program representatives, and human resources personnel familiar with the case. Mobbing is real and deserves much greater attention by researchers and clinicians in the United States.

Scott Bresler, PhD
Clinical director
Center for Threat Assessment
Institute for Psychiatry and Law
University of Cincinnati
Cincinnati, OH

I found Dr. James Randolph Hillard’s article on workplace mobbing timely and extremely interesting (“Workplace mobbing: Are they really out to get your patient?” Current Psychiatry, April 2009). As clinical director of a consultation service for corporations, I am asked to assess employees suspected to be at risk for workplace violence and for fitness for duty. Mobbing seems to be more prevalent and the consequences more dire for a victim who is feeling pressured to leave his or her job when there is little hope of getting another one or is taking on responsibilities previously held by others who have been laid off.

This brings to the forefront a very important consideration for individuals who confront such assessment challenges. Gathering collateral information is critical for diagnostic accuracy and well-articulated interventions that may be recommended. Evaluators who do such assessments at the behest of corporate clients should insist that they have access to employee files investigative reports, and—if appropriate—permission to interview supervisors, employee assistance program representatives, and human resources personnel familiar with the case. Mobbing is real and deserves much greater attention by researchers and clinicians in the United States.

Scott Bresler, PhD
Clinical director
Center for Threat Assessment
Institute for Psychiatry and Law
University of Cincinnati
Cincinnati, OH

I would like to thank Dr. Nasrallah for his wonderful editorial about assessing auditory hallucinations (“The hallucination portrait of psychosis: Probing the voices within,” From the Editor, Current Psychiatry, May 2009). He has eloquently addressed many of the concerns I have had regarding how psychiatrists respond when a patient says “I am hearing voices.” In my experience many psychiatrists simply leave it at that and don’t even attempt the briefest characterization of these hallucinations, let alone the rigorous elucidation that Dr. Nasrallah suggests.

We are doing a disservice to our patients by not performing a thorough evaluation of what a patient means when he says “I am hearing voices.” How can we really understand what our patient is experiencing if we don’t attempt to grasp the specifics of something as remarkable as a hallucination?

Unfortunately, there are patients who use statements such as “I am hearing voices telling me to kill myself and others” in order to be admitted to hospitals or for secondary gain. Getting or attempting to get details about these “voices” and documenting what we are told can be an invaluable part of a patient’s records. Inconsistencies arise that can be taken into consideration during subsequent encounters.

Bennett Cohen, MD
New York, NY

I would like to thank Dr. Nasrallah for his wonderful editorial about assessing auditory hallucinations (“The hallucination portrait of psychosis: Probing the voices within,” From the Editor, Current Psychiatry, May 2009). He has eloquently addressed many of the concerns I have had regarding how psychiatrists respond when a patient says “I am hearing voices.” In my experience many psychiatrists simply leave it at that and don’t even attempt the briefest characterization of these hallucinations, let alone the rigorous elucidation that Dr. Nasrallah suggests.

We are doing a disservice to our patients by not performing a thorough evaluation of what a patient means when he says “I am hearing voices.” How can we really understand what our patient is experiencing if we don’t attempt to grasp the specifics of something as remarkable as a hallucination?

Unfortunately, there are patients who use statements such as “I am hearing voices telling me to kill myself and others” in order to be admitted to hospitals or for secondary gain. Getting or attempting to get details about these “voices” and documenting what we are told can be an invaluable part of a patient’s records. Inconsistencies arise that can be taken into consideration during subsequent encounters.

Bennett Cohen, MD
New York, NY

I would like to thank Dr. Nasrallah for his wonderful editorial about assessing auditory hallucinations (“The hallucination portrait of psychosis: Probing the voices within,” From the Editor, Current Psychiatry, May 2009). He has eloquently addressed many of the concerns I have had regarding how psychiatrists respond when a patient says “I am hearing voices.” In my experience many psychiatrists simply leave it at that and don’t even attempt the briefest characterization of these hallucinations, let alone the rigorous elucidation that Dr. Nasrallah suggests.

We are doing a disservice to our patients by not performing a thorough evaluation of what a patient means when he says “I am hearing voices.” How can we really understand what our patient is experiencing if we don’t attempt to grasp the specifics of something as remarkable as a hallucination?

Unfortunately, there are patients who use statements such as “I am hearing voices telling me to kill myself and others” in order to be admitted to hospitals or for secondary gain. Getting or attempting to get details about these “voices” and documenting what we are told can be an invaluable part of a patient’s records. Inconsistencies arise that can be taken into consideration during subsequent encounters.

Bennett Cohen, MD
New York, NY

The list of interview questions Dr. Henry Nasrallah suggested in “The hallucination portrait of psychosis: Probing the voices within” (From the Editor, Current Psychiatry, May 2009) is a much-needed reminder of the clinical importance of patients’ verbal auditory hallucinations. In 15 years of practice—much of that inpatient psychiatry—I have cared for many patients with hallucinations, and until recently I confess my interview was not as thorough as Dr. Nasrallah advises. Then after attending a workshop in January 2009, I modified my usual clinical interview when a patient reported religious, paranoid, persecutory, and/or command verbal auditory hallucinations. The results have been startling.

Anne M. Stoline, MD
Perryville, MD

The list of interview questions Dr. Henry Nasrallah suggested in “The hallucination portrait of psychosis: Probing the voices within” (From the Editor, Current Psychiatry, May 2009) is a much-needed reminder of the clinical importance of patients’ verbal auditory hallucinations. In 15 years of practice—much of that inpatient psychiatry—I have cared for many patients with hallucinations, and until recently I confess my interview was not as thorough as Dr. Nasrallah advises. Then after attending a workshop in January 2009, I modified my usual clinical interview when a patient reported religious, paranoid, persecutory, and/or command verbal auditory hallucinations. The results have been startling.

Anne M. Stoline, MD
Perryville, MD

The list of interview questions Dr. Henry Nasrallah suggested in “The hallucination portrait of psychosis: Probing the voices within” (From the Editor, Current Psychiatry, May 2009) is a much-needed reminder of the clinical importance of patients’ verbal auditory hallucinations. In 15 years of practice—much of that inpatient psychiatry—I have cared for many patients with hallucinations, and until recently I confess my interview was not as thorough as Dr. Nasrallah advises. Then after attending a workshop in January 2009, I modified my usual clinical interview when a patient reported religious, paranoid, persecutory, and/or command verbal auditory hallucinations. The results have been startling.

Anne M. Stoline, MD
Perryville, MD

Change is coming for continuing medical education (CME). A cloud of conflict of interest has shrouded any person or activity that receives pharmaceutical funding, including the venerable institution of CME. This is a big deal because all health practitioners rely on CME programs to meet requirements for license renewal and to keep up with medical advances.

Attitudes about commercial support of CME have changed, with some organizations calling for elimination of all industry funding (Table). Pressure to strip commercial support from CME is equivalent to draining blood from a living organism; it can have dire consequences if done precipitously.

CME has grown rapidly into a big business. Its commercial support quadrupled from $300 million to $1.2 billion between 1998 and 2006, according to the Accreditation Council for Continuing Medical Education. Another $1.2 billion came from other sources. Here is who received the $2.4 billion in CME funds in 2006: 34% went to publishing and medical education companies, 33% to physician organizations, 18% to medical schools, and 15% to other CME providers (such as hospitals).

The urgent question about sustaining CME has become: where will $1.2 billion come from if not from industry? Eleemosynary is likely to provide only a fraction of support. Shifting the cost to attendees could make CME fees prohibitively high (>$1,000 for a 1-day symposium).

It’s no wonder that CME providers feel anxious about the perception of undue influence on their programs, while at the same time pharmaceutical companies are pulling back from sponsoring CME. But how do psychiatric practitioners feel about this issue?

Table

Industry support of CME: Evolution of standards

Practitioners’ attitudes about CME funding

To find out, I polled 200 mental health professionals at a CME symposium in October 2008. The results are interesting and contrary to what one might assume to be prevailing perceptions. Most respondents (69%) said industry support biases CME content at least sometimes. Most agreed CME programs with multiple sponsors are less likely to be biased than single-sponsored programs (29% “strongly agree,” 53% “agree”). Nearly all (90%) said CME programs generally meet their educational needs.

If CME funding must come from nonindustry sources, only 17% of respondents favored higher registration fees. Other sources they endorsed were private foundations (39%), online CME (30%), and grand rounds (5%). View complete survey results.

Based on these responses, here are my predictions:

• CME will survive, but its funding sources will change.
• Industry sponsorship of CME will not disappear, but it will decline substantially (a trend that has already begun). Funds from multiple pharmaceutical companies might be pooled and allocated to applicants by a third party.
• Eleemosynary will probably increase, but charity will remain a small fraction of CME support.
• The number of CME programs will decline (the American Psychiatric Association has cut sponsored CME symposia at their annual meeting by about 70%).
• Online CME will grow.
• Health professionals will increasingly participate in online learning through educational Web sites, including those of medical journals.

Change is coming for continuing medical education (CME). A cloud of conflict of interest has shrouded any person or activity that receives pharmaceutical funding, including the venerable institution of CME. This is a big deal because all health practitioners rely on CME programs to meet requirements for license renewal and to keep up with medical advances.

Attitudes about commercial support of CME have changed, with some organizations calling for elimination of all industry funding (Table). Pressure to strip commercial support from CME is equivalent to draining blood from a living organism; it can have dire consequences if done precipitously.

CME has grown rapidly into a big business. Its commercial support quadrupled from $300 million to $1.2 billion between 1998 and 2006, according to the Accreditation Council for Continuing Medical Education. Another $1.2 billion came from other sources. Here is who received the $2.4 billion in CME funds in 2006: 34% went to publishing and medical education companies, 33% to physician organizations, 18% to medical schools, and 15% to other CME providers (such as hospitals).

The urgent question about sustaining CME has become: where will $1.2 billion come from if not from industry? Eleemosynary is likely to provide only a fraction of support. Shifting the cost to attendees could make CME fees prohibitively high (>$1,000 for a 1-day symposium).

It’s no wonder that CME providers feel anxious about the perception of undue influence on their programs, while at the same time pharmaceutical companies are pulling back from sponsoring CME. But how do psychiatric practitioners feel about this issue?

Table

Industry support of CME: Evolution of standards

Practitioners’ attitudes about CME funding

To find out, I polled 200 mental health professionals at a CME symposium in October 2008. The results are interesting and contrary to what one might assume to be prevailing perceptions. Most respondents (69%) said industry support biases CME content at least sometimes. Most agreed CME programs with multiple sponsors are less likely to be biased than single-sponsored programs (29% “strongly agree,” 53% “agree”). Nearly all (90%) said CME programs generally meet their educational needs.

If CME funding must come from nonindustry sources, only 17% of respondents favored higher registration fees. Other sources they endorsed were private foundations (39%), online CME (30%), and grand rounds (5%). View complete survey results.

Based on these responses, here are my predictions:

• CME will survive, but its funding sources will change.
• Industry sponsorship of CME will not disappear, but it will decline substantially (a trend that has already begun). Funds from multiple pharmaceutical companies might be pooled and allocated to applicants by a third party.
• Eleemosynary will probably increase, but charity will remain a small fraction of CME support.
• The number of CME programs will decline (the American Psychiatric Association has cut sponsored CME symposia at their annual meeting by about 70%).
• Online CME will grow.
• Health professionals will increasingly participate in online learning through educational Web sites, including those of medical journals.

Change is coming for continuing medical education (CME). A cloud of conflict of interest has shrouded any person or activity that receives pharmaceutical funding, including the venerable institution of CME. This is a big deal because all health practitioners rely on CME programs to meet requirements for license renewal and to keep up with medical advances.

Attitudes about commercial support of CME have changed, with some organizations calling for elimination of all industry funding (Table). Pressure to strip commercial support from CME is equivalent to draining blood from a living organism; it can have dire consequences if done precipitously.

CME has grown rapidly into a big business. Its commercial support quadrupled from $300 million to $1.2 billion between 1998 and 2006, according to the Accreditation Council for Continuing Medical Education. Another $1.2 billion came from other sources. Here is who received the $2.4 billion in CME funds in 2006: 34% went to publishing and medical education companies, 33% to physician organizations, 18% to medical schools, and 15% to other CME providers (such as hospitals).

The urgent question about sustaining CME has become: where will $1.2 billion come from if not from industry? Eleemosynary is likely to provide only a fraction of support. Shifting the cost to attendees could make CME fees prohibitively high (>$1,000 for a 1-day symposium).

It’s no wonder that CME providers feel anxious about the perception of undue influence on their programs, while at the same time pharmaceutical companies are pulling back from sponsoring CME. But how do psychiatric practitioners feel about this issue?

Table

Industry support of CME: Evolution of standards

Practitioners’ attitudes about CME funding

To find out, I polled 200 mental health professionals at a CME symposium in October 2008. The results are interesting and contrary to what one might assume to be prevailing perceptions. Most respondents (69%) said industry support biases CME content at least sometimes. Most agreed CME programs with multiple sponsors are less likely to be biased than single-sponsored programs (29% “strongly agree,” 53% “agree”). Nearly all (90%) said CME programs generally meet their educational needs.

If CME funding must come from nonindustry sources, only 17% of respondents favored higher registration fees. Other sources they endorsed were private foundations (39%), online CME (30%), and grand rounds (5%). View complete survey results.

Based on these responses, here are my predictions:

• CME will survive, but its funding sources will change.
• Industry sponsorship of CME will not disappear, but it will decline substantially (a trend that has already begun). Funds from multiple pharmaceutical companies might be pooled and allocated to applicants by a third party.
• Eleemosynary will probably increase, but charity will remain a small fraction of CME support.
• The number of CME programs will decline (the American Psychiatric Association has cut sponsored CME symposia at their annual meeting by about 70%).
• Online CME will grow.
• Health professionals will increasingly participate in online learning through educational Web sites, including those of medical journals.

CASE: A ‘high utilizer’

Ms. Y, a 49-year-old intensive care registered nurse, is admitted to the psychiatric hospital for suicidal ideation for the eighth time in 1 year. Ms. Y has chronic suicidal ideation with multiple attempts and has been on disability for 3 years for treatment of severe depression. She has been hospitalized for depression with suicide ideation 49 times since her divorce 6 years ago. She is prescribed fluoxetine, 60 mg/d, quetiapine, 400 mg/d, and clonazepam, 2 mg/d.

The authors’ observations

Ms. Y possesses 7 of the 11 characteristics of a high utilizer of psychiatric services (Table 1),^1,2 defined as a patient who is:

• 2 standard deviations above the mean number of visits to an urban psychiatric emergency service in 6 months or
  
• has 4 inpatient admissions in a quarter or 6 inpatient admissions in 1 year.
  

Table 1

Common characteristics of high utilizers* of psychiatric services

The author’s observations

Because previous hospitalizations and courses of ECT have provided Ms. Y with only minimal, short-lived improvement, the treatment team decides to reconsider her diagnosis and treatment plan. Ms. Y’s first psychiatrist diagnosed her with major depressive disorder. After thoroughly interviewing Ms. Y and reviewing her history, the hospital psychiatrist determines that she meets criteria for borderline personality disorder (BPD) in addition to major depression. The psychiatrist explains this diagnosis to Ms. Y, provides her with education and support, and recommends dialectical behavioral therapy (DBT) and case management. She rejects the new diagnosis and treatment plan and pleads for help establishing treatment with a new psychiatrist.

The team at the psychiatric hospital feels Ms. Y needs to receive ongoing treatment from a psychiatrist. In the hope that she will be able to establish a therapeutic alliance with a new psychiatrist and therapist, they decide to continue working with Ms. Y if she accepts the BPD diagnosis and agrees to undergo DBT.

EVALUATION: A troubling pattern

Before Ms. Y’s husband divorced her, she had not received psychiatric care and had no psychiatric diagnosis. During the contentious divorce, she experienced depressive symptoms that later intensified, and she was unable to return to her previous high level of functioning.

Ms. Y became suicidal and was hospitalized for the first time shortly after the divorce was finalized and her ex-husband remarried. She began treatment with a psychiatrist, whom she idealized and saw for 5 years.

When this psychiatrist—who had been one of the few stable relationships in Ms. Y’s life—moved to another state, Ms. Y experienced a rapid recurrence of depression. She began treatment with 3 other psychiatrists but fired them because they “never understand me” like her first psychiatrist did, and she never felt she received the consistent, supportive care she deserved. She become suicidal and again required psychiatric hospitalization. This pattern continued up to her current admission.

The authors’ observations

Ms. Y briefly returns to work between hospitalizations but is not able to tolerate the stress. At one point she was admitted to an out-of-state facility; after this 2-month stay, she remained out of the local psychiatric hospital for 6 months but then became unable to function and was readmitted to the local psychiatric hospital.

When interviewed, Ms. Y describes feeling hopeless, empty, and alone each time 2 of her 3 children return to college after summer break. Her youngest child lives at home but is involved in extracurricular high school activities, and doesn’t seem to need her. Ms. Y is estranged from both parents. Her social support is unreliable because she tends to push others away and isolate herself.

The authors’ observations

Because she has no history of mania, Ms. Y does not meet criteria for bipolar affective disorder. Her multidisciplinary treatment team feels she is too fragile to transfer care to new providers or to foster care, so we schedule a care conference and carefully compose a 6-month contract to formally articulate limits and boundaries within which we will continue to treat her.

The contract specifies that Ms. Y will participate in DBT, take her medications exactly as prescribed, and not receive any early refills of her prescriptions. We arrange with Ms. Y’s health plan to have a home healthcare agency provide her medications weekly. This benefit was not available to other health plan members. Ms. Y signs the contract.

TREATMENT: Contract violation

Ms. Y complies with the contract for 2 months, then abruptly fires her long-term therapist, whom she claims violated confidentiality by giving false information to another provider. At her next session, Ms. Y will not provide details about the alleged incident, and the issue never is resolved. She admits she did not start DBT and is not taking her medications as prescribed.

Ms. Y expresses her disagreement with the terms of the contract. She becomes very upset and asks for her care to be transferred to another psychiatrist. She demands to be followed at the current clinic because “I was born here.” She denies being actively suicidal and terminates the session early. That afternoon, she calls 1 of the inpatient psychiatrists and asks if he would treat her. She also calls the first psychiatrist she had seen to enlist help in obtaining care.

The authors’ observations

In Groves’ description of 4 types of “hateful patients,” Ms. Y represents a combination of an entitled demander and a manipulative help-rejecter. The behaviors and personality disorders associated with these types of patients—and effective management strategies—are listed in (Table 2).³ (Table 3) offers tips for successfully dealing with high utilizers of psychiatric services. High utilizers of medical services other than psychiatry are more likely than patients who are not high utilizers to have a psychiatric disorder (Box).^4-9

Box

Some members of our treatment team began to experience countertransference, which also interfered with Ms. Y’s treatment. They viewed her behavior as entitled, demanding, and manipulative and dreaded caring for her. Failing to recognize such defenses can lead to consequences such as malignant alienation—a progressive deterioration in the patient’s relationship with others that includes loss of sympathy and support from staff members—which can put a patient at high risk for suicide.¹⁰

• fear of Ms. Y committing suicide
  
• fear of setting limits
  
• fear of being reported to the Medical Board
  
• fear of a lawsuit.
  

Table 2

Strategies for helping 4 types of ‘hateful patients’

Table 3

Tips for managing high utilizers

OUTCOME: The pattern continues

Ms. Y continues to receive treatment with a different outpatient psychiatrist and therapist in the area. She has not been hospitalized for almost 2 years but her financial state has deteriorated and she has had a recurrence of depression. Ms. Y’s psychiatrist recently called the hospital to ask for direct admission on the patient’s behalf, stating that Ms. Y did not want to wait hours to be seen in the ER. Hospital staff explained that she needs to first come to the ER for evaluation. Ms. Y refused to come to the ER and was not admitted. About 1 month later, Ms. Y’s psychiatrist called again, and she was directly admitted to the psychiatric hospital.

Related resource

• National Suicide Prevention Lifeline. 1-800-273-TALK (8255). www.suicidepreventionlifeline.org.
  

• Clonazepam • Klonopin
  
• Fluoxetine • Prozac
  
• Quetiapine • Seroquel
  

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

CASE: A ‘high utilizer’

Ms. Y, a 49-year-old intensive care registered nurse, is admitted to the psychiatric hospital for suicidal ideation for the eighth time in 1 year. Ms. Y has chronic suicidal ideation with multiple attempts and has been on disability for 3 years for treatment of severe depression. She has been hospitalized for depression with suicide ideation 49 times since her divorce 6 years ago. She is prescribed fluoxetine, 60 mg/d, quetiapine, 400 mg/d, and clonazepam, 2 mg/d.

The authors’ observations

Ms. Y possesses 7 of the 11 characteristics of a high utilizer of psychiatric services (Table 1),^1,2 defined as a patient who is:

• 2 standard deviations above the mean number of visits to an urban psychiatric emergency service in 6 months or
  
• has 4 inpatient admissions in a quarter or 6 inpatient admissions in 1 year.
  

Table 1

Common characteristics of high utilizers* of psychiatric services

The author’s observations

Because previous hospitalizations and courses of ECT have provided Ms. Y with only minimal, short-lived improvement, the treatment team decides to reconsider her diagnosis and treatment plan. Ms. Y’s first psychiatrist diagnosed her with major depressive disorder. After thoroughly interviewing Ms. Y and reviewing her history, the hospital psychiatrist determines that she meets criteria for borderline personality disorder (BPD) in addition to major depression. The psychiatrist explains this diagnosis to Ms. Y, provides her with education and support, and recommends dialectical behavioral therapy (DBT) and case management. She rejects the new diagnosis and treatment plan and pleads for help establishing treatment with a new psychiatrist.

The team at the psychiatric hospital feels Ms. Y needs to receive ongoing treatment from a psychiatrist. In the hope that she will be able to establish a therapeutic alliance with a new psychiatrist and therapist, they decide to continue working with Ms. Y if she accepts the BPD diagnosis and agrees to undergo DBT.

EVALUATION: A troubling pattern

Before Ms. Y’s husband divorced her, she had not received psychiatric care and had no psychiatric diagnosis. During the contentious divorce, she experienced depressive symptoms that later intensified, and she was unable to return to her previous high level of functioning.

Ms. Y became suicidal and was hospitalized for the first time shortly after the divorce was finalized and her ex-husband remarried. She began treatment with a psychiatrist, whom she idealized and saw for 5 years.

When this psychiatrist—who had been one of the few stable relationships in Ms. Y’s life—moved to another state, Ms. Y experienced a rapid recurrence of depression. She began treatment with 3 other psychiatrists but fired them because they “never understand me” like her first psychiatrist did, and she never felt she received the consistent, supportive care she deserved. She become suicidal and again required psychiatric hospitalization. This pattern continued up to her current admission.

The authors’ observations

Ms. Y briefly returns to work between hospitalizations but is not able to tolerate the stress. At one point she was admitted to an out-of-state facility; after this 2-month stay, she remained out of the local psychiatric hospital for 6 months but then became unable to function and was readmitted to the local psychiatric hospital.

When interviewed, Ms. Y describes feeling hopeless, empty, and alone each time 2 of her 3 children return to college after summer break. Her youngest child lives at home but is involved in extracurricular high school activities, and doesn’t seem to need her. Ms. Y is estranged from both parents. Her social support is unreliable because she tends to push others away and isolate herself.

The authors’ observations

Because she has no history of mania, Ms. Y does not meet criteria for bipolar affective disorder. Her multidisciplinary treatment team feels she is too fragile to transfer care to new providers or to foster care, so we schedule a care conference and carefully compose a 6-month contract to formally articulate limits and boundaries within which we will continue to treat her.

The contract specifies that Ms. Y will participate in DBT, take her medications exactly as prescribed, and not receive any early refills of her prescriptions. We arrange with Ms. Y’s health plan to have a home healthcare agency provide her medications weekly. This benefit was not available to other health plan members. Ms. Y signs the contract.

TREATMENT: Contract violation

Ms. Y complies with the contract for 2 months, then abruptly fires her long-term therapist, whom she claims violated confidentiality by giving false information to another provider. At her next session, Ms. Y will not provide details about the alleged incident, and the issue never is resolved. She admits she did not start DBT and is not taking her medications as prescribed.

Ms. Y expresses her disagreement with the terms of the contract. She becomes very upset and asks for her care to be transferred to another psychiatrist. She demands to be followed at the current clinic because “I was born here.” She denies being actively suicidal and terminates the session early. That afternoon, she calls 1 of the inpatient psychiatrists and asks if he would treat her. She also calls the first psychiatrist she had seen to enlist help in obtaining care.

The authors’ observations

In Groves’ description of 4 types of “hateful patients,” Ms. Y represents a combination of an entitled demander and a manipulative help-rejecter. The behaviors and personality disorders associated with these types of patients—and effective management strategies—are listed in (Table 2).³ (Table 3) offers tips for successfully dealing with high utilizers of psychiatric services. High utilizers of medical services other than psychiatry are more likely than patients who are not high utilizers to have a psychiatric disorder (Box).^4-9

Box

Some members of our treatment team began to experience countertransference, which also interfered with Ms. Y’s treatment. They viewed her behavior as entitled, demanding, and manipulative and dreaded caring for her. Failing to recognize such defenses can lead to consequences such as malignant alienation—a progressive deterioration in the patient’s relationship with others that includes loss of sympathy and support from staff members—which can put a patient at high risk for suicide.¹⁰

• fear of Ms. Y committing suicide
  
• fear of setting limits
  
• fear of being reported to the Medical Board
  
• fear of a lawsuit.
  

Table 2

Strategies for helping 4 types of ‘hateful patients’

Table 3

Tips for managing high utilizers

OUTCOME: The pattern continues

Ms. Y continues to receive treatment with a different outpatient psychiatrist and therapist in the area. She has not been hospitalized for almost 2 years but her financial state has deteriorated and she has had a recurrence of depression. Ms. Y’s psychiatrist recently called the hospital to ask for direct admission on the patient’s behalf, stating that Ms. Y did not want to wait hours to be seen in the ER. Hospital staff explained that she needs to first come to the ER for evaluation. Ms. Y refused to come to the ER and was not admitted. About 1 month later, Ms. Y’s psychiatrist called again, and she was directly admitted to the psychiatric hospital.

Related resource

• National Suicide Prevention Lifeline. 1-800-273-TALK (8255). www.suicidepreventionlifeline.org.
  

• Clonazepam • Klonopin
  
• Fluoxetine • Prozac
  
• Quetiapine • Seroquel
  

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

CASE: A ‘high utilizer’

Ms. Y, a 49-year-old intensive care registered nurse, is admitted to the psychiatric hospital for suicidal ideation for the eighth time in 1 year. Ms. Y has chronic suicidal ideation with multiple attempts and has been on disability for 3 years for treatment of severe depression. She has been hospitalized for depression with suicide ideation 49 times since her divorce 6 years ago. She is prescribed fluoxetine, 60 mg/d, quetiapine, 400 mg/d, and clonazepam, 2 mg/d.

The authors’ observations

Ms. Y possesses 7 of the 11 characteristics of a high utilizer of psychiatric services (Table 1),^1,2 defined as a patient who is:

• 2 standard deviations above the mean number of visits to an urban psychiatric emergency service in 6 months or
  
• has 4 inpatient admissions in a quarter or 6 inpatient admissions in 1 year.
  

Table 1

Common characteristics of high utilizers* of psychiatric services

The author’s observations

Because previous hospitalizations and courses of ECT have provided Ms. Y with only minimal, short-lived improvement, the treatment team decides to reconsider her diagnosis and treatment plan. Ms. Y’s first psychiatrist diagnosed her with major depressive disorder. After thoroughly interviewing Ms. Y and reviewing her history, the hospital psychiatrist determines that she meets criteria for borderline personality disorder (BPD) in addition to major depression. The psychiatrist explains this diagnosis to Ms. Y, provides her with education and support, and recommends dialectical behavioral therapy (DBT) and case management. She rejects the new diagnosis and treatment plan and pleads for help establishing treatment with a new psychiatrist.

The team at the psychiatric hospital feels Ms. Y needs to receive ongoing treatment from a psychiatrist. In the hope that she will be able to establish a therapeutic alliance with a new psychiatrist and therapist, they decide to continue working with Ms. Y if she accepts the BPD diagnosis and agrees to undergo DBT.

EVALUATION: A troubling pattern

Before Ms. Y’s husband divorced her, she had not received psychiatric care and had no psychiatric diagnosis. During the contentious divorce, she experienced depressive symptoms that later intensified, and she was unable to return to her previous high level of functioning.

Ms. Y became suicidal and was hospitalized for the first time shortly after the divorce was finalized and her ex-husband remarried. She began treatment with a psychiatrist, whom she idealized and saw for 5 years.

When this psychiatrist—who had been one of the few stable relationships in Ms. Y’s life—moved to another state, Ms. Y experienced a rapid recurrence of depression. She began treatment with 3 other psychiatrists but fired them because they “never understand me” like her first psychiatrist did, and she never felt she received the consistent, supportive care she deserved. She become suicidal and again required psychiatric hospitalization. This pattern continued up to her current admission.

The authors’ observations

Ms. Y briefly returns to work between hospitalizations but is not able to tolerate the stress. At one point she was admitted to an out-of-state facility; after this 2-month stay, she remained out of the local psychiatric hospital for 6 months but then became unable to function and was readmitted to the local psychiatric hospital.

When interviewed, Ms. Y describes feeling hopeless, empty, and alone each time 2 of her 3 children return to college after summer break. Her youngest child lives at home but is involved in extracurricular high school activities, and doesn’t seem to need her. Ms. Y is estranged from both parents. Her social support is unreliable because she tends to push others away and isolate herself.

The authors’ observations

Because she has no history of mania, Ms. Y does not meet criteria for bipolar affective disorder. Her multidisciplinary treatment team feels she is too fragile to transfer care to new providers or to foster care, so we schedule a care conference and carefully compose a 6-month contract to formally articulate limits and boundaries within which we will continue to treat her.

The contract specifies that Ms. Y will participate in DBT, take her medications exactly as prescribed, and not receive any early refills of her prescriptions. We arrange with Ms. Y’s health plan to have a home healthcare agency provide her medications weekly. This benefit was not available to other health plan members. Ms. Y signs the contract.

TREATMENT: Contract violation

Ms. Y complies with the contract for 2 months, then abruptly fires her long-term therapist, whom she claims violated confidentiality by giving false information to another provider. At her next session, Ms. Y will not provide details about the alleged incident, and the issue never is resolved. She admits she did not start DBT and is not taking her medications as prescribed.

Ms. Y expresses her disagreement with the terms of the contract. She becomes very upset and asks for her care to be transferred to another psychiatrist. She demands to be followed at the current clinic because “I was born here.” She denies being actively suicidal and terminates the session early. That afternoon, she calls 1 of the inpatient psychiatrists and asks if he would treat her. She also calls the first psychiatrist she had seen to enlist help in obtaining care.

The authors’ observations

In Groves’ description of 4 types of “hateful patients,” Ms. Y represents a combination of an entitled demander and a manipulative help-rejecter. The behaviors and personality disorders associated with these types of patients—and effective management strategies—are listed in (Table 2).³ (Table 3) offers tips for successfully dealing with high utilizers of psychiatric services. High utilizers of medical services other than psychiatry are more likely than patients who are not high utilizers to have a psychiatric disorder (Box).^4-9

Box

Some members of our treatment team began to experience countertransference, which also interfered with Ms. Y’s treatment. They viewed her behavior as entitled, demanding, and manipulative and dreaded caring for her. Failing to recognize such defenses can lead to consequences such as malignant alienation—a progressive deterioration in the patient’s relationship with others that includes loss of sympathy and support from staff members—which can put a patient at high risk for suicide.¹⁰

• fear of Ms. Y committing suicide
  
• fear of setting limits
  
• fear of being reported to the Medical Board
  
• fear of a lawsuit.
  

Table 2

Strategies for helping 4 types of ‘hateful patients’

Table 3

Tips for managing high utilizers

OUTCOME: The pattern continues

Ms. Y continues to receive treatment with a different outpatient psychiatrist and therapist in the area. She has not been hospitalized for almost 2 years but her financial state has deteriorated and she has had a recurrence of depression. Ms. Y’s psychiatrist recently called the hospital to ask for direct admission on the patient’s behalf, stating that Ms. Y did not want to wait hours to be seen in the ER. Hospital staff explained that she needs to first come to the ER for evaluation. Ms. Y refused to come to the ER and was not admitted. About 1 month later, Ms. Y’s psychiatrist called again, and she was directly admitted to the psychiatric hospital.

Related resource

• National Suicide Prevention Lifeline. 1-800-273-TALK (8255). www.suicidepreventionlifeline.org.
  

• Clonazepam • Klonopin
  
• Fluoxetine • Prozac
  
• Quetiapine • Seroquel
  

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

Comment on this article

“A patient I’ve seen for a number of years had been diagnosed in the pervasive developmental disorder spectrum, but she was quite atypical. Her perseverative thinking focused on a fantasy world, and she was so preoccupied that it was very difficult to pull her out of it. Now at age 12, she has a full-blown psychotic disorder, and the fantasy world is enveloping her. She hears people talking to her all day long.”

Jean A. Frazier, MD, who treats this patient and other children with psychotic disorders, was 1 of 4 principal investigators in the Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS) study, a randomized, double-blind, multisite trial funded by the National Institute of Mental Health. The study, published in November 2008,¹ compared the efficacy and tolerability of 3 antipsychotics—olanzapine, risperidone, and molindone—in pediatric patients with schizophrenia or schizoaffective disorder (Box 1).

Dr. Frazier discusses the unexpected findings of the TEOSS trial with Current Psychiatry Section Editor Robert A. Kowatch, MD, PhD. Based on the trial findings and her experience, she tells how she makes decisions when prescribing antipsychotics for children and adolescents with schizophrenia and related disorders.

DR. KOWATCH: The TEOSS trial found no significant differences in efficacy between molindone and the atypical antipsychotics (olanzapine and risperidone) included in the study. You’ve prescribed both typical and atypical antipsychotics in research and in your clinical practice. Do you believe there’s any difference between the 2 classes?

DR. FRAZIER: There are some differences. For example, treatment-refractory patients, especially young children, sometimes need more D2 blockade than some atypical antipsychotics provide. I’ve seen more extra pyramidal side effects with the typical antipsychotics than the atypicals, although it’s not uncommon to see some akathisia with aripiprazole or some dystonia and dyskinesia with risperidone.

DR. KOWATCH: What are the benefits and risks of using antipsychotics in young children?

DR. FRAZIER: The benefit is that antipsychotics can decrease children’s suffering and get them more centered in reality so they can enjoy their friends and progress in school. And when that happens, it’s wonderful. What are the risks? With the atypicals my greatest concern is weight gain, and with the typical agents it’s tardive dyskinesia.

DR. KOWATCH: Have you changed the way you prescribe antipsychotics as a result of the TEOSS study?

DR. FRAZIER: Actually, I have. Clinicians have to be very careful about selecting psychotropic agents that can worsen pediatric-onset obesity. Olanzapine is an effective agent for targeting psychosis and mood symptoms, but the weight gain associated with it is a concern. I do not prescribe olanzapine as much as I have in the past, although I keep it in my armamentarium and tend to reserve it for third- or fourth-line therapy.

I have found molindone to be quite effective in children with schizophrenia or schizoaffective disorder, especially in those who have gained a lot of weight on atypical antipsychotics. They usually lose weight on molindone.

DR. KOWATCH: Do you think the TEOSS study had adequate power to demonstrate differences among molindone, olanzapine, and risperidone?

DR. FRAZIER: We enrolled 119 patients—which is large for a study such as this—but we did not reach our target of 168 patients, which might have increased our power to detect differences. Among the children we did enroll, the 3 antipsychotics showed no difference in efficacy, but the meaningful finding of this study to me was the side effect profile of these agents.

DR. KOWATCH: You mean weight gain with olanzapine and extrapyramidal symptoms with molindone?

DR. FRAZIER: Yes.

Managing side effects

DR. KOWATCH: How do you manage antipsychotic side effects?

DR. FRAZIER: For any of the antipsychotics’ side effects, you have to decide whether to continue the agent or switch to another anti psychotic. For example, I’ve had a number of children—many with significant weight problems—whose psychotic symptoms have responded only to risperidone. So we put them back on risperidone, and the decision then becomes what can we do to help with the weight gain while continuing that agent.

For weight gain, I think the best intervention is diet, exercise, and drinking a lot of water, but that can be effective only if you engage the patient’s entire family in the intervention as well. Short of that, a number of pharmacologic interventions have been studied, although not specifically in children.

In an open-label trial our group conducted with 11 children age 10 to 18 years who had gained weight while taking atypical antipsychotics, metformin decreased lipid levels and body mass index but not significantly. I’ve followed these children in my practice, however, and all those who continued taking metformin over a period of months lost weight.

Box 1

Antipsychotics in children with schizophrenia:
TEOSS study adds to debate about efficacy and tolerability

The 5-year National Institute of Mental Health-funded Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS) trial began with an ambitious goal: to compare the efficacy and safety of 1 typical and 2 atypical antipsychotics in children age 8 to 19 with schizophrenia. The primary hypothesis was that atypical agents would show greater efficacy and tolerability when given for 8 weeks. Instead, the atypical agents showed no greater efficacy, and adverse effects occurred with all 3 antipsychotics. Because the trial was designed for 168 subjects but enrolled 119, it may not have been adequately powered to detect differences among the 3 agents.

Medications: Most of the 116 children who received medications were severely ill with psychotic symptoms when randomly assigned to 1 of the 3 antipsychotics for 8 weeks of double-blind treatment. Administration began at the lowest dose in a set range and usually was increased to midrange within 10 to 14 days. Dosing remained flexible within these ranges:

• molindone, 10 to 140 mg/d (mean endpoint dose 59.9 mg/d)
• olanzapine, 2.5 to 20 mg/d (mean endpoint dose 11.4 mg/d)
• risperidone, 0.5 to 6 mg/d (mean endpoint dose 2.8 mg/d).

Benztropine, ≥1 mg/d, was given to all patients treated with molindone, 14% of those treated with olanzapine, and 34% of those treated with risperidone to prevent or manage akathisia.

Efficacy: Two criteria defined treatment response: a Clinical Global Impression improvement score of 1 or 2 and a ≥20% reduction in baseline Positive and Negative Syndrome Scale (PANSS) score. Tolerability outcomes included neurologic side effects, weight changes, laboratory analyses, vital signs, ECG, serious adverse events, and treatment discontinuation. Extrapyramidal symptoms were monitored with involuntary movement and akathisia scales.

Observed PANSS total score by week of treatment

Mean Positive and Negative Symptom Scale (PANSS) total scores of observed cases during each week of the TEOSS trial. Minimum possible PANSS score is 30; scores >60 typically are viewed as problematic.

Among the 70 patients who completed treatment (25 of 40 with molindone, 17 of 35 olanzapine, and 28 of 41 with risperidone), more than one-half failed to achieve an adequate response. Response rates were 50% with molindone, 34% with olanzapine, and 46% with risperidone. The atypical antipsychotics did not show greater efficacy than molindone, and mean reductions in psychotic symptoms were modest (20% to 34% on the PANSS). Mean medication doses were midrange and considered moderate.

Tolerability: Sedation, irritability, and anxiety were frequent adverse events. Patients receiving molindone reported significantly higher rates of akathisia (P < .0008). Those receiving olanzapine reported significantly higher rates of weight gain (P < .0001) and were the only group with increased lipid and insulin serum levels and liver function tests. Patients in the risperidone group reported significantly higher rates of constipation (P < .021) and were the only group that experienced elevated serum prolactin.

Source: Sikich L, Frazier JA, McClellan J, et al. Double-blind comparison of first- and second-generation antipsychotics in early-onset schizophrenia and schizoaffective disorder: findings from the Treatment of Early-Onset Schizophrenia Spectrum disorders (TEOSS) study. Am J Psychiatry. 2008;165:1420-1431

Choosing antipsychotics

DR. KOWATCH: Let’s say you’re seeing psychosis in a 12-year-old whom you think is schizophrenic, and he or she has not yet received an antipsychotic. What are your top 3 treatment choices?

DR. FRAZIER: The first agent I usually select is risperidone. We have the most data on the use of this atypical antipsychotic in children and adolescents, and most psychotic children I see do better with a bit more D2 blockade than some of the other atypicals provide. That said, I remain concerned about risperidone’s side effects—such as weight gain and increased serum prolactin—so my usual second-line agent is aripiprazole.

Box 2

DR. KOWATCH: Why do you like aripiprazole for this patient population?

DR. FRAZIER: Aripiprazole doesn’t tend to be associated with as much weight gain as olanzapine or risperidone, although I’ve had children—especially in the autism spectrum—who have gained quite a bit of weight on aripiprazole. Clinically, I’ve noticed that aripiprazole seems to brighten up children’s affect. It also seems to help many children in my practice with attentional symptoms, although that’s anecdotal.

Although we don’t have a lot of data to inform this discussion about aripiprazole, a placebo-controlled study of 302 adolescents diagnosed with schizophrenia showed that aripiprazole, 10 mg/d, targeted negative symptoms fairly well, based on changes from baseline in PANSS (Positive and Negative Syndrome Scale) total scores. This was a 6-week multicenter, double-blind, randomized, trial.²

Ultimately, cognition in patients with schizophrenia is the strongest predictor of success in the workplace and in school. We need data on what happens to neurocognitive functioning with aripiprazole—and all the other atypical agents.

DR. KOWATCH: What would be your third-line agent?

DR. FRAZIER: Well, that varies for me. I’m trying to match the medication I use with the individual patient, and at this point I prescribe based on the side-effect profile more than anything else. I also consider if the child has a family member who has suffered from a similar condition and what agents the family member responded to.

Let’s say I have a child who has tried 1 or 2 atypical antipsychotics and has not had a good response. Many times I decide to try yet another atypical, and often I will try quetiapine. But after a patient has not responded to 2 atypicals, I might start thinking about a typical agent or clozapine. I use clozapine quite a bit. I find it is the most efficacious agent available, and the data speak to this as well.^3,4 It has been truly remarkable for some children in my practice.

Less than 50% chance of efficacy?

DR. KOWATCH: The TEOSS study found 50% or lower response rates across 8 weeks of antipsychotic treatment. Clinically, what kind of response rates do you see with antipsychotics in children and adolescents?

DR. FRAZIER: I probably see about a 50% response rate in my practice as well. It’s variable, and the earlier the onset of the illness, the harder it is to treat.

DR. KOWATCH: Do you ever combine a typical antipsychotic with an atypical?

DR. FRAZIER: I try not to, but a number of children in the schizophrenia spectrum have enduring positive symptoms after 2 or 3 trials of atypical antipsychotics. Sometimes adding a touch of a typical agent can improve the situation. The typicals I usually try are perphenazine (around 8 to 16 mg/d) or molin done (around 20 to 60 mg/d). Sometimes I use a very low dose of haloperidol (such as 0.5 to 2 mg/d) with an atypical agent, and it can be quite effective.

DR. KOWATCH: That has been our experience as well; sometimes combining typical and atypical agents improves response. Besides medications, what do you consider an optimal treatment plan for a child or adolescent with psychosis?

DR. FRAZIER: These children need a multi-modal approach. Pharmacotherapy is the cornerstone because you want to decrease positive symptoms of psychosis, but often these children require therapeutic school placements or residential programs. If they’re old enough, cognitive-behavioral therapy can help by teaching them skills to manage ongoing psychotic symptoms. Older teens often have comorbid substance abuse and may require substance abuse intervention.

Are antipsychotics overused?

DR. KOWATCH: Do you think antipsychotics are overused in pediatric patients with psychosis?

DR. FRAZIER: In pediatric patients with psychosis? No.

DR. KOWATCH: What about in pediatric patients with behavioral disorders?

DR. FRAZIER: We need more studies to inform our practice and to be mindful of the evidence. Most children with schizophrenia have substantial developmental challenges (Box 2).⁵ In the autism spectrum, often an atypical antipsychotic is the only agent that can help a patient who is aggressive, self-injurious, or agitated.

In terms of bipolar disorder in children and adolescents, it would be ideal if we had more head-to-head comparator studies to inform our prescriptive practice. For example, we need more studies comparing traditional mood stabilizers such as lithium with the atypical agents.

Of course it would be ideal if we could use monotherapy in children who suffer from bipolar disorder and schizophrenia. But early-onset bipolar disorder—like early-onset schizophrenia—can be very difficult to treat and often requires more than 1 agent.

In a recent study of a pharmacotherapy algorithm for treating pediatric bipolar disorder,³ the children who did the best were on a combination of a mood stabilizer and an atypical antipsychotic. That has been my experience, too. I do my best to manage children on a mood stabilizer alone, but I rarely have been able to do that.

In terms of attention-deficit/hyperactivity disorder (ADHD), it depends on what’s going on with the child. Certain children with an ADHD diagnosis have complicated behavioral issues. First I would wonder if they have a different diagnosis, particularly if it gets to the point that an atypical agent is being considered. But sometimes it becomes a question of treating pronounced aggression. We need more studies to inform what we do. Some studies indicate that stimulants can be quite helpful for the aggressive child with ADHD.⁷

DR. KOWATCH: I don’t see any child and adolescent psychiatrist in the United States using antipsychotics to treat uncomplicated ADHD. The kids we see [at specialty clinics] have comorbid problems such as conduct disorder, oppositional-defiant disorder, mood instability—whatever you want to call it. And we’re seeing these patients because they haven’t done well on other medications, such as stimulants. Usually the parents are desperate because these children are moody and aggressive. I don’t think anybody wants to treat children with antipsychotics or mood stabilizers, but it’s what keeps these children well.

DR. FRAZIER: Yes, I agree.

Related resources

• Longitudinal assessment and monitoring of clinical status and brain function in adolescents and adults. Boston Center for Intervention Development and Applied Research (CIDAR) study. www.bostoncidar.org.
• Frazier JA, Hodge S, Breeze JL, et al. Diagnostic and sex effects on limbic volumes in early-onset bipolar disorder and schizophrenia. Schizophr Bull. 2008;34(1):37-46.
• Frazier JA, McClellan J, Findling RL, et al. Treatment of Early-Onset Schizophrenia Spectrum disorders (TEOSS): demographic and clinical characteristics. J Am Acad Child Adolesc Psychiatry. 2007;46:979-988.

Drug brand names

• Aripiprazole • Abilify
• Benztropine • Cogentin
• Clozapine • Clozaril
• Haloperidol • Haldol
• Metformin • Glucophage
• Molindone • Moban
• Olanzapine • Zyprexa
• Perphenazine • Trilafon
• Quetiapine • Seroquel
• Risperidone • Risperdal

Disclosures

Dr. Kowatch receives grant/research support from the Stanley Foundation, National Institute of Mental Health, National Institute of Child Health and Human Development, and the National Alliance for Research on Schizophrenia and Depression. He is a consultant to AstraZeneca and Forest Pharmaceuticals and a speaker for AstraZeneca.

Dr. Frazier receives grant/research support from Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, Johnson & Johnson, Neuropharm, Otsuka America Pharmaceuticals, and Pfizer Inc.

Comment on this article

“A patient I’ve seen for a number of years had been diagnosed in the pervasive developmental disorder spectrum, but she was quite atypical. Her perseverative thinking focused on a fantasy world, and she was so preoccupied that it was very difficult to pull her out of it. Now at age 12, she has a full-blown psychotic disorder, and the fantasy world is enveloping her. She hears people talking to her all day long.”

Jean A. Frazier, MD, who treats this patient and other children with psychotic disorders, was 1 of 4 principal investigators in the Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS) study, a randomized, double-blind, multisite trial funded by the National Institute of Mental Health. The study, published in November 2008,¹ compared the efficacy and tolerability of 3 antipsychotics—olanzapine, risperidone, and molindone—in pediatric patients with schizophrenia or schizoaffective disorder (Box 1).

Dr. Frazier discusses the unexpected findings of the TEOSS trial with Current Psychiatry Section Editor Robert A. Kowatch, MD, PhD. Based on the trial findings and her experience, she tells how she makes decisions when prescribing antipsychotics for children and adolescents with schizophrenia and related disorders.

DR. KOWATCH: The TEOSS trial found no significant differences in efficacy between molindone and the atypical antipsychotics (olanzapine and risperidone) included in the study. You’ve prescribed both typical and atypical antipsychotics in research and in your clinical practice. Do you believe there’s any difference between the 2 classes?

DR. FRAZIER: There are some differences. For example, treatment-refractory patients, especially young children, sometimes need more D2 blockade than some atypical antipsychotics provide. I’ve seen more extra pyramidal side effects with the typical antipsychotics than the atypicals, although it’s not uncommon to see some akathisia with aripiprazole or some dystonia and dyskinesia with risperidone.

DR. KOWATCH: What are the benefits and risks of using antipsychotics in young children?

DR. FRAZIER: The benefit is that antipsychotics can decrease children’s suffering and get them more centered in reality so they can enjoy their friends and progress in school. And when that happens, it’s wonderful. What are the risks? With the atypicals my greatest concern is weight gain, and with the typical agents it’s tardive dyskinesia.

DR. KOWATCH: Have you changed the way you prescribe antipsychotics as a result of the TEOSS study?

DR. FRAZIER: Actually, I have. Clinicians have to be very careful about selecting psychotropic agents that can worsen pediatric-onset obesity. Olanzapine is an effective agent for targeting psychosis and mood symptoms, but the weight gain associated with it is a concern. I do not prescribe olanzapine as much as I have in the past, although I keep it in my armamentarium and tend to reserve it for third- or fourth-line therapy.

I have found molindone to be quite effective in children with schizophrenia or schizoaffective disorder, especially in those who have gained a lot of weight on atypical antipsychotics. They usually lose weight on molindone.

DR. KOWATCH: Do you think the TEOSS study had adequate power to demonstrate differences among molindone, olanzapine, and risperidone?

DR. FRAZIER: We enrolled 119 patients—which is large for a study such as this—but we did not reach our target of 168 patients, which might have increased our power to detect differences. Among the children we did enroll, the 3 antipsychotics showed no difference in efficacy, but the meaningful finding of this study to me was the side effect profile of these agents.

DR. KOWATCH: You mean weight gain with olanzapine and extrapyramidal symptoms with molindone?

DR. FRAZIER: Yes.

Managing side effects

DR. KOWATCH: How do you manage antipsychotic side effects?

DR. FRAZIER: For any of the antipsychotics’ side effects, you have to decide whether to continue the agent or switch to another anti psychotic. For example, I’ve had a number of children—many with significant weight problems—whose psychotic symptoms have responded only to risperidone. So we put them back on risperidone, and the decision then becomes what can we do to help with the weight gain while continuing that agent.

For weight gain, I think the best intervention is diet, exercise, and drinking a lot of water, but that can be effective only if you engage the patient’s entire family in the intervention as well. Short of that, a number of pharmacologic interventions have been studied, although not specifically in children.

In an open-label trial our group conducted with 11 children age 10 to 18 years who had gained weight while taking atypical antipsychotics, metformin decreased lipid levels and body mass index but not significantly. I’ve followed these children in my practice, however, and all those who continued taking metformin over a period of months lost weight.

Box 1

Antipsychotics in children with schizophrenia:
TEOSS study adds to debate about efficacy and tolerability

The 5-year National Institute of Mental Health-funded Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS) trial began with an ambitious goal: to compare the efficacy and safety of 1 typical and 2 atypical antipsychotics in children age 8 to 19 with schizophrenia. The primary hypothesis was that atypical agents would show greater efficacy and tolerability when given for 8 weeks. Instead, the atypical agents showed no greater efficacy, and adverse effects occurred with all 3 antipsychotics. Because the trial was designed for 168 subjects but enrolled 119, it may not have been adequately powered to detect differences among the 3 agents.

Medications: Most of the 116 children who received medications were severely ill with psychotic symptoms when randomly assigned to 1 of the 3 antipsychotics for 8 weeks of double-blind treatment. Administration began at the lowest dose in a set range and usually was increased to midrange within 10 to 14 days. Dosing remained flexible within these ranges:

• molindone, 10 to 140 mg/d (mean endpoint dose 59.9 mg/d)
• olanzapine, 2.5 to 20 mg/d (mean endpoint dose 11.4 mg/d)
• risperidone, 0.5 to 6 mg/d (mean endpoint dose 2.8 mg/d).

Benztropine, ≥1 mg/d, was given to all patients treated with molindone, 14% of those treated with olanzapine, and 34% of those treated with risperidone to prevent or manage akathisia.

Efficacy: Two criteria defined treatment response: a Clinical Global Impression improvement score of 1 or 2 and a ≥20% reduction in baseline Positive and Negative Syndrome Scale (PANSS) score. Tolerability outcomes included neurologic side effects, weight changes, laboratory analyses, vital signs, ECG, serious adverse events, and treatment discontinuation. Extrapyramidal symptoms were monitored with involuntary movement and akathisia scales.

Observed PANSS total score by week of treatment

Mean Positive and Negative Symptom Scale (PANSS) total scores of observed cases during each week of the TEOSS trial. Minimum possible PANSS score is 30; scores >60 typically are viewed as problematic.

Among the 70 patients who completed treatment (25 of 40 with molindone, 17 of 35 olanzapine, and 28 of 41 with risperidone), more than one-half failed to achieve an adequate response. Response rates were 50% with molindone, 34% with olanzapine, and 46% with risperidone. The atypical antipsychotics did not show greater efficacy than molindone, and mean reductions in psychotic symptoms were modest (20% to 34% on the PANSS). Mean medication doses were midrange and considered moderate.

Tolerability: Sedation, irritability, and anxiety were frequent adverse events. Patients receiving molindone reported significantly higher rates of akathisia (P < .0008). Those receiving olanzapine reported significantly higher rates of weight gain (P < .0001) and were the only group with increased lipid and insulin serum levels and liver function tests. Patients in the risperidone group reported significantly higher rates of constipation (P < .021) and were the only group that experienced elevated serum prolactin.

Source: Sikich L, Frazier JA, McClellan J, et al. Double-blind comparison of first- and second-generation antipsychotics in early-onset schizophrenia and schizoaffective disorder: findings from the Treatment of Early-Onset Schizophrenia Spectrum disorders (TEOSS) study. Am J Psychiatry. 2008;165:1420-1431

Choosing antipsychotics

DR. KOWATCH: Let’s say you’re seeing psychosis in a 12-year-old whom you think is schizophrenic, and he or she has not yet received an antipsychotic. What are your top 3 treatment choices?

DR. FRAZIER: The first agent I usually select is risperidone. We have the most data on the use of this atypical antipsychotic in children and adolescents, and most psychotic children I see do better with a bit more D2 blockade than some of the other atypicals provide. That said, I remain concerned about risperidone’s side effects—such as weight gain and increased serum prolactin—so my usual second-line agent is aripiprazole.

Box 2

DR. KOWATCH: Why do you like aripiprazole for this patient population?

DR. FRAZIER: Aripiprazole doesn’t tend to be associated with as much weight gain as olanzapine or risperidone, although I’ve had children—especially in the autism spectrum—who have gained quite a bit of weight on aripiprazole. Clinically, I’ve noticed that aripiprazole seems to brighten up children’s affect. It also seems to help many children in my practice with attentional symptoms, although that’s anecdotal.

Although we don’t have a lot of data to inform this discussion about aripiprazole, a placebo-controlled study of 302 adolescents diagnosed with schizophrenia showed that aripiprazole, 10 mg/d, targeted negative symptoms fairly well, based on changes from baseline in PANSS (Positive and Negative Syndrome Scale) total scores. This was a 6-week multicenter, double-blind, randomized, trial.²

Ultimately, cognition in patients with schizophrenia is the strongest predictor of success in the workplace and in school. We need data on what happens to neurocognitive functioning with aripiprazole—and all the other atypical agents.

DR. KOWATCH: What would be your third-line agent?

DR. FRAZIER: Well, that varies for me. I’m trying to match the medication I use with the individual patient, and at this point I prescribe based on the side-effect profile more than anything else. I also consider if the child has a family member who has suffered from a similar condition and what agents the family member responded to.

Let’s say I have a child who has tried 1 or 2 atypical antipsychotics and has not had a good response. Many times I decide to try yet another atypical, and often I will try quetiapine. But after a patient has not responded to 2 atypicals, I might start thinking about a typical agent or clozapine. I use clozapine quite a bit. I find it is the most efficacious agent available, and the data speak to this as well.^3,4 It has been truly remarkable for some children in my practice.

Less than 50% chance of efficacy?

DR. KOWATCH: The TEOSS study found 50% or lower response rates across 8 weeks of antipsychotic treatment. Clinically, what kind of response rates do you see with antipsychotics in children and adolescents?

DR. FRAZIER: I probably see about a 50% response rate in my practice as well. It’s variable, and the earlier the onset of the illness, the harder it is to treat.

DR. KOWATCH: Do you ever combine a typical antipsychotic with an atypical?

DR. FRAZIER: I try not to, but a number of children in the schizophrenia spectrum have enduring positive symptoms after 2 or 3 trials of atypical antipsychotics. Sometimes adding a touch of a typical agent can improve the situation. The typicals I usually try are perphenazine (around 8 to 16 mg/d) or molin done (around 20 to 60 mg/d). Sometimes I use a very low dose of haloperidol (such as 0.5 to 2 mg/d) with an atypical agent, and it can be quite effective.

DR. KOWATCH: That has been our experience as well; sometimes combining typical and atypical agents improves response. Besides medications, what do you consider an optimal treatment plan for a child or adolescent with psychosis?

DR. FRAZIER: These children need a multi-modal approach. Pharmacotherapy is the cornerstone because you want to decrease positive symptoms of psychosis, but often these children require therapeutic school placements or residential programs. If they’re old enough, cognitive-behavioral therapy can help by teaching them skills to manage ongoing psychotic symptoms. Older teens often have comorbid substance abuse and may require substance abuse intervention.

Are antipsychotics overused?

DR. KOWATCH: Do you think antipsychotics are overused in pediatric patients with psychosis?

DR. FRAZIER: In pediatric patients with psychosis? No.

DR. KOWATCH: What about in pediatric patients with behavioral disorders?

DR. FRAZIER: We need more studies to inform our practice and to be mindful of the evidence. Most children with schizophrenia have substantial developmental challenges (Box 2).⁵ In the autism spectrum, often an atypical antipsychotic is the only agent that can help a patient who is aggressive, self-injurious, or agitated.

In terms of bipolar disorder in children and adolescents, it would be ideal if we had more head-to-head comparator studies to inform our prescriptive practice. For example, we need more studies comparing traditional mood stabilizers such as lithium with the atypical agents.

Of course it would be ideal if we could use monotherapy in children who suffer from bipolar disorder and schizophrenia. But early-onset bipolar disorder—like early-onset schizophrenia—can be very difficult to treat and often requires more than 1 agent.

In a recent study of a pharmacotherapy algorithm for treating pediatric bipolar disorder,³ the children who did the best were on a combination of a mood stabilizer and an atypical antipsychotic. That has been my experience, too. I do my best to manage children on a mood stabilizer alone, but I rarely have been able to do that.

In terms of attention-deficit/hyperactivity disorder (ADHD), it depends on what’s going on with the child. Certain children with an ADHD diagnosis have complicated behavioral issues. First I would wonder if they have a different diagnosis, particularly if it gets to the point that an atypical agent is being considered. But sometimes it becomes a question of treating pronounced aggression. We need more studies to inform what we do. Some studies indicate that stimulants can be quite helpful for the aggressive child with ADHD.⁷

DR. KOWATCH: I don’t see any child and adolescent psychiatrist in the United States using antipsychotics to treat uncomplicated ADHD. The kids we see [at specialty clinics] have comorbid problems such as conduct disorder, oppositional-defiant disorder, mood instability—whatever you want to call it. And we’re seeing these patients because they haven’t done well on other medications, such as stimulants. Usually the parents are desperate because these children are moody and aggressive. I don’t think anybody wants to treat children with antipsychotics or mood stabilizers, but it’s what keeps these children well.

DR. FRAZIER: Yes, I agree.

Related resources

• Longitudinal assessment and monitoring of clinical status and brain function in adolescents and adults. Boston Center for Intervention Development and Applied Research (CIDAR) study. www.bostoncidar.org.
• Frazier JA, Hodge S, Breeze JL, et al. Diagnostic and sex effects on limbic volumes in early-onset bipolar disorder and schizophrenia. Schizophr Bull. 2008;34(1):37-46.
• Frazier JA, McClellan J, Findling RL, et al. Treatment of Early-Onset Schizophrenia Spectrum disorders (TEOSS): demographic and clinical characteristics. J Am Acad Child Adolesc Psychiatry. 2007;46:979-988.

Drug brand names

• Aripiprazole • Abilify
• Benztropine • Cogentin
• Clozapine • Clozaril
• Haloperidol • Haldol
• Metformin • Glucophage
• Molindone • Moban
• Olanzapine • Zyprexa
• Perphenazine • Trilafon
• Quetiapine • Seroquel
• Risperidone • Risperdal

Disclosures

Dr. Kowatch receives grant/research support from the Stanley Foundation, National Institute of Mental Health, National Institute of Child Health and Human Development, and the National Alliance for Research on Schizophrenia and Depression. He is a consultant to AstraZeneca and Forest Pharmaceuticals and a speaker for AstraZeneca.

Dr. Frazier receives grant/research support from Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, Johnson & Johnson, Neuropharm, Otsuka America Pharmaceuticals, and Pfizer Inc.

Comment on this article

“A patient I’ve seen for a number of years had been diagnosed in the pervasive developmental disorder spectrum, but she was quite atypical. Her perseverative thinking focused on a fantasy world, and she was so preoccupied that it was very difficult to pull her out of it. Now at age 12, she has a full-blown psychotic disorder, and the fantasy world is enveloping her. She hears people talking to her all day long.”

Jean A. Frazier, MD, who treats this patient and other children with psychotic disorders, was 1 of 4 principal investigators in the Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS) study, a randomized, double-blind, multisite trial funded by the National Institute of Mental Health. The study, published in November 2008,¹ compared the efficacy and tolerability of 3 antipsychotics—olanzapine, risperidone, and molindone—in pediatric patients with schizophrenia or schizoaffective disorder (Box 1).

Dr. Frazier discusses the unexpected findings of the TEOSS trial with Current Psychiatry Section Editor Robert A. Kowatch, MD, PhD. Based on the trial findings and her experience, she tells how she makes decisions when prescribing antipsychotics for children and adolescents with schizophrenia and related disorders.

DR. KOWATCH: The TEOSS trial found no significant differences in efficacy between molindone and the atypical antipsychotics (olanzapine and risperidone) included in the study. You’ve prescribed both typical and atypical antipsychotics in research and in your clinical practice. Do you believe there’s any difference between the 2 classes?

DR. FRAZIER: There are some differences. For example, treatment-refractory patients, especially young children, sometimes need more D2 blockade than some atypical antipsychotics provide. I’ve seen more extra pyramidal side effects with the typical antipsychotics than the atypicals, although it’s not uncommon to see some akathisia with aripiprazole or some dystonia and dyskinesia with risperidone.

DR. KOWATCH: What are the benefits and risks of using antipsychotics in young children?

DR. FRAZIER: The benefit is that antipsychotics can decrease children’s suffering and get them more centered in reality so they can enjoy their friends and progress in school. And when that happens, it’s wonderful. What are the risks? With the atypicals my greatest concern is weight gain, and with the typical agents it’s tardive dyskinesia.

DR. KOWATCH: Have you changed the way you prescribe antipsychotics as a result of the TEOSS study?

DR. FRAZIER: Actually, I have. Clinicians have to be very careful about selecting psychotropic agents that can worsen pediatric-onset obesity. Olanzapine is an effective agent for targeting psychosis and mood symptoms, but the weight gain associated with it is a concern. I do not prescribe olanzapine as much as I have in the past, although I keep it in my armamentarium and tend to reserve it for third- or fourth-line therapy.

I have found molindone to be quite effective in children with schizophrenia or schizoaffective disorder, especially in those who have gained a lot of weight on atypical antipsychotics. They usually lose weight on molindone.

DR. KOWATCH: Do you think the TEOSS study had adequate power to demonstrate differences among molindone, olanzapine, and risperidone?

DR. FRAZIER: We enrolled 119 patients—which is large for a study such as this—but we did not reach our target of 168 patients, which might have increased our power to detect differences. Among the children we did enroll, the 3 antipsychotics showed no difference in efficacy, but the meaningful finding of this study to me was the side effect profile of these agents.

DR. KOWATCH: You mean weight gain with olanzapine and extrapyramidal symptoms with molindone?

DR. FRAZIER: Yes.

Managing side effects

DR. KOWATCH: How do you manage antipsychotic side effects?

DR. FRAZIER: For any of the antipsychotics’ side effects, you have to decide whether to continue the agent or switch to another anti psychotic. For example, I’ve had a number of children—many with significant weight problems—whose psychotic symptoms have responded only to risperidone. So we put them back on risperidone, and the decision then becomes what can we do to help with the weight gain while continuing that agent.

For weight gain, I think the best intervention is diet, exercise, and drinking a lot of water, but that can be effective only if you engage the patient’s entire family in the intervention as well. Short of that, a number of pharmacologic interventions have been studied, although not specifically in children.

In an open-label trial our group conducted with 11 children age 10 to 18 years who had gained weight while taking atypical antipsychotics, metformin decreased lipid levels and body mass index but not significantly. I’ve followed these children in my practice, however, and all those who continued taking metformin over a period of months lost weight.

Box 1

Antipsychotics in children with schizophrenia:
TEOSS study adds to debate about efficacy and tolerability

The 5-year National Institute of Mental Health-funded Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS) trial began with an ambitious goal: to compare the efficacy and safety of 1 typical and 2 atypical antipsychotics in children age 8 to 19 with schizophrenia. The primary hypothesis was that atypical agents would show greater efficacy and tolerability when given for 8 weeks. Instead, the atypical agents showed no greater efficacy, and adverse effects occurred with all 3 antipsychotics. Because the trial was designed for 168 subjects but enrolled 119, it may not have been adequately powered to detect differences among the 3 agents.

Medications: Most of the 116 children who received medications were severely ill with psychotic symptoms when randomly assigned to 1 of the 3 antipsychotics for 8 weeks of double-blind treatment. Administration began at the lowest dose in a set range and usually was increased to midrange within 10 to 14 days. Dosing remained flexible within these ranges:

• molindone, 10 to 140 mg/d (mean endpoint dose 59.9 mg/d)
• olanzapine, 2.5 to 20 mg/d (mean endpoint dose 11.4 mg/d)
• risperidone, 0.5 to 6 mg/d (mean endpoint dose 2.8 mg/d).

Benztropine, ≥1 mg/d, was given to all patients treated with molindone, 14% of those treated with olanzapine, and 34% of those treated with risperidone to prevent or manage akathisia.

Efficacy: Two criteria defined treatment response: a Clinical Global Impression improvement score of 1 or 2 and a ≥20% reduction in baseline Positive and Negative Syndrome Scale (PANSS) score. Tolerability outcomes included neurologic side effects, weight changes, laboratory analyses, vital signs, ECG, serious adverse events, and treatment discontinuation. Extrapyramidal symptoms were monitored with involuntary movement and akathisia scales.

Observed PANSS total score by week of treatment

Mean Positive and Negative Symptom Scale (PANSS) total scores of observed cases during each week of the TEOSS trial. Minimum possible PANSS score is 30; scores >60 typically are viewed as problematic.

Among the 70 patients who completed treatment (25 of 40 with molindone, 17 of 35 olanzapine, and 28 of 41 with risperidone), more than one-half failed to achieve an adequate response. Response rates were 50% with molindone, 34% with olanzapine, and 46% with risperidone. The atypical antipsychotics did not show greater efficacy than molindone, and mean reductions in psychotic symptoms were modest (20% to 34% on the PANSS). Mean medication doses were midrange and considered moderate.

Tolerability: Sedation, irritability, and anxiety were frequent adverse events. Patients receiving molindone reported significantly higher rates of akathisia (P < .0008). Those receiving olanzapine reported significantly higher rates of weight gain (P < .0001) and were the only group with increased lipid and insulin serum levels and liver function tests. Patients in the risperidone group reported significantly higher rates of constipation (P < .021) and were the only group that experienced elevated serum prolactin.

Source: Sikich L, Frazier JA, McClellan J, et al. Double-blind comparison of first- and second-generation antipsychotics in early-onset schizophrenia and schizoaffective disorder: findings from the Treatment of Early-Onset Schizophrenia Spectrum disorders (TEOSS) study. Am J Psychiatry. 2008;165:1420-1431

Choosing antipsychotics

DR. KOWATCH: Let’s say you’re seeing psychosis in a 12-year-old whom you think is schizophrenic, and he or she has not yet received an antipsychotic. What are your top 3 treatment choices?

DR. FRAZIER: The first agent I usually select is risperidone. We have the most data on the use of this atypical antipsychotic in children and adolescents, and most psychotic children I see do better with a bit more D2 blockade than some of the other atypicals provide. That said, I remain concerned about risperidone’s side effects—such as weight gain and increased serum prolactin—so my usual second-line agent is aripiprazole.

Box 2

DR. KOWATCH: Why do you like aripiprazole for this patient population?

DR. FRAZIER: Aripiprazole doesn’t tend to be associated with as much weight gain as olanzapine or risperidone, although I’ve had children—especially in the autism spectrum—who have gained quite a bit of weight on aripiprazole. Clinically, I’ve noticed that aripiprazole seems to brighten up children’s affect. It also seems to help many children in my practice with attentional symptoms, although that’s anecdotal.

Although we don’t have a lot of data to inform this discussion about aripiprazole, a placebo-controlled study of 302 adolescents diagnosed with schizophrenia showed that aripiprazole, 10 mg/d, targeted negative symptoms fairly well, based on changes from baseline in PANSS (Positive and Negative Syndrome Scale) total scores. This was a 6-week multicenter, double-blind, randomized, trial.²

Ultimately, cognition in patients with schizophrenia is the strongest predictor of success in the workplace and in school. We need data on what happens to neurocognitive functioning with aripiprazole—and all the other atypical agents.

DR. KOWATCH: What would be your third-line agent?

DR. FRAZIER: Well, that varies for me. I’m trying to match the medication I use with the individual patient, and at this point I prescribe based on the side-effect profile more than anything else. I also consider if the child has a family member who has suffered from a similar condition and what agents the family member responded to.

Let’s say I have a child who has tried 1 or 2 atypical antipsychotics and has not had a good response. Many times I decide to try yet another atypical, and often I will try quetiapine. But after a patient has not responded to 2 atypicals, I might start thinking about a typical agent or clozapine. I use clozapine quite a bit. I find it is the most efficacious agent available, and the data speak to this as well.^3,4 It has been truly remarkable for some children in my practice.

Less than 50% chance of efficacy?

DR. KOWATCH: The TEOSS study found 50% or lower response rates across 8 weeks of antipsychotic treatment. Clinically, what kind of response rates do you see with antipsychotics in children and adolescents?

DR. FRAZIER: I probably see about a 50% response rate in my practice as well. It’s variable, and the earlier the onset of the illness, the harder it is to treat.

DR. KOWATCH: Do you ever combine a typical antipsychotic with an atypical?

DR. FRAZIER: I try not to, but a number of children in the schizophrenia spectrum have enduring positive symptoms after 2 or 3 trials of atypical antipsychotics. Sometimes adding a touch of a typical agent can improve the situation. The typicals I usually try are perphenazine (around 8 to 16 mg/d) or molin done (around 20 to 60 mg/d). Sometimes I use a very low dose of haloperidol (such as 0.5 to 2 mg/d) with an atypical agent, and it can be quite effective.

DR. KOWATCH: That has been our experience as well; sometimes combining typical and atypical agents improves response. Besides medications, what do you consider an optimal treatment plan for a child or adolescent with psychosis?

DR. FRAZIER: These children need a multi-modal approach. Pharmacotherapy is the cornerstone because you want to decrease positive symptoms of psychosis, but often these children require therapeutic school placements or residential programs. If they’re old enough, cognitive-behavioral therapy can help by teaching them skills to manage ongoing psychotic symptoms. Older teens often have comorbid substance abuse and may require substance abuse intervention.

Are antipsychotics overused?

DR. KOWATCH: Do you think antipsychotics are overused in pediatric patients with psychosis?

DR. FRAZIER: In pediatric patients with psychosis? No.

DR. KOWATCH: What about in pediatric patients with behavioral disorders?

DR. FRAZIER: We need more studies to inform our practice and to be mindful of the evidence. Most children with schizophrenia have substantial developmental challenges (Box 2).⁵ In the autism spectrum, often an atypical antipsychotic is the only agent that can help a patient who is aggressive, self-injurious, or agitated.

In terms of bipolar disorder in children and adolescents, it would be ideal if we had more head-to-head comparator studies to inform our prescriptive practice. For example, we need more studies comparing traditional mood stabilizers such as lithium with the atypical agents.

Of course it would be ideal if we could use monotherapy in children who suffer from bipolar disorder and schizophrenia. But early-onset bipolar disorder—like early-onset schizophrenia—can be very difficult to treat and often requires more than 1 agent.

In a recent study of a pharmacotherapy algorithm for treating pediatric bipolar disorder,³ the children who did the best were on a combination of a mood stabilizer and an atypical antipsychotic. That has been my experience, too. I do my best to manage children on a mood stabilizer alone, but I rarely have been able to do that.

In terms of attention-deficit/hyperactivity disorder (ADHD), it depends on what’s going on with the child. Certain children with an ADHD diagnosis have complicated behavioral issues. First I would wonder if they have a different diagnosis, particularly if it gets to the point that an atypical agent is being considered. But sometimes it becomes a question of treating pronounced aggression. We need more studies to inform what we do. Some studies indicate that stimulants can be quite helpful for the aggressive child with ADHD.⁷

DR. KOWATCH: I don’t see any child and adolescent psychiatrist in the United States using antipsychotics to treat uncomplicated ADHD. The kids we see [at specialty clinics] have comorbid problems such as conduct disorder, oppositional-defiant disorder, mood instability—whatever you want to call it. And we’re seeing these patients because they haven’t done well on other medications, such as stimulants. Usually the parents are desperate because these children are moody and aggressive. I don’t think anybody wants to treat children with antipsychotics or mood stabilizers, but it’s what keeps these children well.

DR. FRAZIER: Yes, I agree.

Related resources

• Longitudinal assessment and monitoring of clinical status and brain function in adolescents and adults. Boston Center for Intervention Development and Applied Research (CIDAR) study. www.bostoncidar.org.
• Frazier JA, Hodge S, Breeze JL, et al. Diagnostic and sex effects on limbic volumes in early-onset bipolar disorder and schizophrenia. Schizophr Bull. 2008;34(1):37-46.
• Frazier JA, McClellan J, Findling RL, et al. Treatment of Early-Onset Schizophrenia Spectrum disorders (TEOSS): demographic and clinical characteristics. J Am Acad Child Adolesc Psychiatry. 2007;46:979-988.

Drug brand names

• Aripiprazole • Abilify
• Benztropine • Cogentin
• Clozapine • Clozaril
• Haloperidol • Haldol
• Metformin • Glucophage
• Molindone • Moban
• Olanzapine • Zyprexa
• Perphenazine • Trilafon
• Quetiapine • Seroquel
• Risperidone • Risperdal

Disclosures

Dr. Kowatch receives grant/research support from the Stanley Foundation, National Institute of Mental Health, National Institute of Child Health and Human Development, and the National Alliance for Research on Schizophrenia and Depression. He is a consultant to AstraZeneca and Forest Pharmaceuticals and a speaker for AstraZeneca.

Dr. Frazier receives grant/research support from Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, Johnson & Johnson, Neuropharm, Otsuka America Pharmaceuticals, and Pfizer Inc.

WEB AUDIO

Comment on this article

At least 25% and possibly up to 50% of patients with recurrent major depressive disorder (MDD) have features of mild hypomania (the “soft end” of the bipolar spectrum¹) and might be better conceptualized as suffering from a broadly defined bipolar (BP) II disorder.² The challenge is to differentiate MDD from BP II so that we make treatment decisions—such as antidepressants vs mood stabilizers—shown to improve the long-term course of patients’ depressive symptoms.

Diagnosis of BP II often is not straightforward and unfortunately may be delayed several years after patients first present for evaluation. To help clinicians make correct diagnostic decisions, this article:

• describes diagnostic criteria outside of DSM-IV-TR that can assist in identifying BP II disorder
  
• identifies subgroups of recurrently depressed patients whose primary disorder is more likely to be bipolar than unipolar
  
• provides a screening tool validated for identifying “soft” bipolarity
  
• offers a pragmatic clinical perspective on the treatment of BP II disorder.
  

How common is BP II disorder?

As with all psychiatric diagnoses, the prevalence of BP II disorder is a function of the diagnostic criteria used to define it.³ BP II—1 or more depressive episodes with at least 1 hypomanic episode—affects 1% to 2% of the population, based on DSM-IV-TR criteria for hypomania (Box 1). However, the DSM definition of BP II might be too restrictive. Regarding the diagnosis of hypomania, in particular:

• the symptom of “overactivity” should be given as much weight as the stem criteria of “euphoria” and “irritability”
  
• the 4-day threshold for a hypomanic episode probably is too long.
  

These deficiencies in DSM-IV-TR exclude many patients who experience brief but clinically significant periods of hypomania. A more realistic definition of hypomania within BP II disorder would:

• include overactivity as an additional stem criterion
  
• specify a threshold duration for hypomanic symptoms of at least 1 day rather than 4 days
  
• stipulate the experience of negative consequences of the episode as necessary for the diagnosis (Table 1).
  

Box 1

Proposed hypomania criteria in broadly defined BP II

Depression’s subgroups

Recurrent MDD is an extremely heterogeneous diagnosis. It includes many clinical presentations of depressive illness that may share little in terms of etiology, pathophysiology, and response to treatment. When carefully assessed, 2 subgroups of recurrently depressed patients in particular appear to be more likely to have a primary bipolar disorder:

• young patients with early-onset severe depression
  
• older adults with difficult-to-treat or treatment-resistant depression.
  

Higher rates of unrecognized bipolar disorder have been identified in patients with treatment-resistant depression. In a prospective study of 61 consecutive MDD patients referred to a mood disorders clinic, 59% satisfied DSM-IV-TR criteria for bipolar disorder.⁸

Consequences. Undiagnosed BP II disorder is an important clinical issue because bipolar features in patients presumed to have recurrent MDD can adversely affect long-term outcomes. Many of these patients will be treated exclusively with antidepressants despite evidence that antidepressant monotherapy for bipolar depression—at least for some patients—can cause more frequent mood episodes, mood destabilization, and possibly an increase in suicidal behaviors.^9,10

This point is highlighted in the United Kingdom’s National Institute of Health and Clinical Excellence (NICE) guidelines for bipolar disorder, which recommended that antidepressants be prescribed for bipolar depression only in combination with mood stabilizer treatment and withdrawn within 2 to 3 months of recovery.¹¹

The American Psychiatric Association’s (APA) practice guideline for treating bipolar disorder, published in 2002, advises against antidepressants as monotherapy for bipolar depression, recommending instead that lithium or lamotrigine be used first-line. A revised APA guideline is scheduled for publication this year.¹²

Why is BP II underdiagnosed?

Notwithstanding the limitations of DSMIV-TR criteria for hypomania, additional factors contribute to under-recognition of BP II in clinical practice.

Dominant depressive symptoms. The clinical course of bipolar disorders is dominated by low-grade depressive symptoms and recurrent depressive episodes rather than mania or hypomania. This is especially true for BP II disorder, where the ratio of time spent with depressive symptoms relative to time with hypomanic symptoms is approximately 30:1.¹³ The fact that BP II patients in general seek help only during depressive periods means that consultations inevitably focus on the diagnosis and treatment of depression, rather than long-term prophylaxis of both depressive and hypomanic episodes.

Indistinguishable symptoms? Bipolar depressions are generally thought to be clinically indistinguishable from unipolar depressions, but this might not be clear-cut. Although differentiating symptoms of unipolar and bipolar depression can be difficult in clinical practice, evidence suggests that certain symptoms may be more common in bipolar than unipolar depression:

• atypical depressive features such as mood reactivity, overeating, oversleeping, and excessive fatigue¹⁴
  
• depressive psychotic symptoms, especially in younger patients¹⁵
  
• “mixed” depressive episodes (depressive episodes with concurrent manic symptoms).¹⁶
  

How to recognize BP II disorder

To detect and diagnose BP II disorder, systematically assess hypomanic features in all patients who present with recurrent MDD, especially those who have an early age of onset or don’t seem to be responding well to antidepressant monotherapy. As noted, a corroborative history from a close relative is essential. Within a full clinical assessment, use the features listed in Table 2 to help differentiate bipolar depression from unipolar depression.

Screening instruments for hypomania are no substitute for a careful psychiatric history but can be very helpful in everyday clinical practice. The most well-known is the Mood Disorder Questionnaire (MDQ);¹⁷ other options include the Hypomania Checklist (HCL-32)¹⁸ and the Bipolar Spectrum Diagnostic Scale (BSDS).¹⁹ In general, the MDQ performs better at detecting BP I in psychiatric practice settings, whereas the HCL-32 and BSDS may be more useful in primary care and general population settings.²⁰

The BSDS has a particular focus on the softer end of the bipolar spectrum,¹⁹ and in my experience patients like its narrative structure. It can help prompt discussions about previous hypomania symptoms and mood instability. In this sense, the BSDS is a useful adjunct to the routine clinical assessment of patients with recurrent depressive disorders. Click here to view the BSDS.

Table 2

Possible indicators of bipolarity in apparently unipolar depression

Treatment strategies for BP II

As with all psychiatric disorders, treatment needs to multimodal and tailored to the individual. For a detailed assessment of pharmacologic and psychological options, see Goodwin and Jamison’s authoritative text, chapters 17 to 20.²¹

Pharmacologic options. Because few clinical trials have focused exclusively on BP II patients, much psychiatric practice has been extrapolated from trials involving BP I patients. Obviously, trials with BP II samples are needed, but these may be limited by the restrictive DSM-IV-TR definition of hypomania.

Lithium has the most supporting evidence, showing efficacy for all 3 phases of BP II—treatment of hypomania, treatment of bipolar depression, and prophylaxis against hypomanic and depressive relapses.²² Different medications used in bipolar disorder appear to have different efficacy profiles, however. For example, a systematic review of 14 randomized controlled trials with 2,526 patients found that although lithium, lamotrigine, olanzapine, and valproate were more effective than placebo at preventing relapse due to any mood episode:

• only lithium and olanzapine significantly reduced manic relapses
  
• only lamotrigine and valproate significantly reduced depressive relapses.²³
  

The Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) trial did not find any therapeutic benefit or increased risk of switching to mania for anti depressants plus mood stabilizer vs mood stabilizer alone.²⁶ Many trials of bipolar depression have recruited such heterogeneous groups of patients (including BP I, BP II, and BP NOS; schizoaffective disorder, bipolar type; and even recurrent MDD) that it is difficult to make firm recommendations about pharmacologic options for the depressive phase of BP II disorder.

In my experience, approximately one-third of BP II patients have a history of poor response to antidepressants or adverse effects from antidepressants (extreme irritability, activation, and antidepressant-induced hypomania). In the long term, these patients often do much better on mood stabilizer monotherapy or a combination of mood stabilizers such as lithium plus lamotrigine. The key is to be flexible with treatment options within recommended guidelines and to tailor treatment choices to the individual’s pattern of illness and treatment preferences.

Psychological interventions. Some evidence supports cognitive-behavioral therapy (CBT) and interpersonal and social rhythm therapy (IPSRT) in long-term treatment of bipolar disorders, although—as with medication trials—we need to be careful about extrapolating these findings to BP II disorder.²⁹ For example, a recent large-scale randomized controlled trial of CBT for bipolar disorder was largely negative.³⁰ Psychoeducation given in families and groups can be effective long-term options when used as adjuncts to medications.³¹

Table 3

Recommendations for treating patients with BP II disorder

• Goodwin GM and the Consensus Group of the British Association for Psychopharmacology. Evidence-based guidelines for treating bipolar disorder: revised second edition—recommendations from the British Association for Psychopharmacology. J Psychopharmacol. 2009;23(4):346-388. www.bap.org.uk/pdfs/Bipolar_guidelines.pdf.
  
• Goodwin FK, Jamison KR. Manic-depressive illness: bipolar disorders and recurrent depression. 2nd ed. New York, NY: Oxford University Press; 2007.
  
• Phelps J. Bipolar psychoeducation. www.psycheducation.org.
  
• Mood Disorders Treatment Team, Cardiff University. Interactive online psychoeducational treatment for bipolar disorder. www.BeatingBipolar.org.
  
• Goodwin GM, Geddes JR. What is the heartland of psychiatry? Br J Psychiatry. 2007;191(3):189-191.
  

• Lamotrigine • Lamictal
  
• Lithium • Various
  
• Olanzapine • Zyprexa
  
• Quetiapine • Seroquel
  
• Valproate • Depakon
  

Dr. Smith receives research funding from the National Institute of Health Research UK, the MRC/Welsh Assembly Government, NARSAD, and the American Psychiatric Institute for Research and Education. He is a speaker for Eli Lilly and Company, AstraZeneca, and Bristol-Myers Squibb and is a consultant to Shire Pharmaceuticals.

WEB AUDIO

Comment on this article

At least 25% and possibly up to 50% of patients with recurrent major depressive disorder (MDD) have features of mild hypomania (the “soft end” of the bipolar spectrum¹) and might be better conceptualized as suffering from a broadly defined bipolar (BP) II disorder.² The challenge is to differentiate MDD from BP II so that we make treatment decisions—such as antidepressants vs mood stabilizers—shown to improve the long-term course of patients’ depressive symptoms.

Diagnosis of BP II often is not straightforward and unfortunately may be delayed several years after patients first present for evaluation. To help clinicians make correct diagnostic decisions, this article:

• describes diagnostic criteria outside of DSM-IV-TR that can assist in identifying BP II disorder
  
• identifies subgroups of recurrently depressed patients whose primary disorder is more likely to be bipolar than unipolar
  
• provides a screening tool validated for identifying “soft” bipolarity
  
• offers a pragmatic clinical perspective on the treatment of BP II disorder.
  

How common is BP II disorder?

As with all psychiatric diagnoses, the prevalence of BP II disorder is a function of the diagnostic criteria used to define it.³ BP II—1 or more depressive episodes with at least 1 hypomanic episode—affects 1% to 2% of the population, based on DSM-IV-TR criteria for hypomania (Box 1). However, the DSM definition of BP II might be too restrictive. Regarding the diagnosis of hypomania, in particular:

• the symptom of “overactivity” should be given as much weight as the stem criteria of “euphoria” and “irritability”
  
• the 4-day threshold for a hypomanic episode probably is too long.
  

These deficiencies in DSM-IV-TR exclude many patients who experience brief but clinically significant periods of hypomania. A more realistic definition of hypomania within BP II disorder would:

• include overactivity as an additional stem criterion
  
• specify a threshold duration for hypomanic symptoms of at least 1 day rather than 4 days
  
• stipulate the experience of negative consequences of the episode as necessary for the diagnosis (Table 1).
  

Box 1

Proposed hypomania criteria in broadly defined BP II

Depression’s subgroups

Recurrent MDD is an extremely heterogeneous diagnosis. It includes many clinical presentations of depressive illness that may share little in terms of etiology, pathophysiology, and response to treatment. When carefully assessed, 2 subgroups of recurrently depressed patients in particular appear to be more likely to have a primary bipolar disorder:

• young patients with early-onset severe depression
  
• older adults with difficult-to-treat or treatment-resistant depression.
  

Higher rates of unrecognized bipolar disorder have been identified in patients with treatment-resistant depression. In a prospective study of 61 consecutive MDD patients referred to a mood disorders clinic, 59% satisfied DSM-IV-TR criteria for bipolar disorder.⁸

Consequences. Undiagnosed BP II disorder is an important clinical issue because bipolar features in patients presumed to have recurrent MDD can adversely affect long-term outcomes. Many of these patients will be treated exclusively with antidepressants despite evidence that antidepressant monotherapy for bipolar depression—at least for some patients—can cause more frequent mood episodes, mood destabilization, and possibly an increase in suicidal behaviors.^9,10

This point is highlighted in the United Kingdom’s National Institute of Health and Clinical Excellence (NICE) guidelines for bipolar disorder, which recommended that antidepressants be prescribed for bipolar depression only in combination with mood stabilizer treatment and withdrawn within 2 to 3 months of recovery.¹¹

The American Psychiatric Association’s (APA) practice guideline for treating bipolar disorder, published in 2002, advises against antidepressants as monotherapy for bipolar depression, recommending instead that lithium or lamotrigine be used first-line. A revised APA guideline is scheduled for publication this year.¹²

Why is BP II underdiagnosed?

Notwithstanding the limitations of DSMIV-TR criteria for hypomania, additional factors contribute to under-recognition of BP II in clinical practice.

Dominant depressive symptoms. The clinical course of bipolar disorders is dominated by low-grade depressive symptoms and recurrent depressive episodes rather than mania or hypomania. This is especially true for BP II disorder, where the ratio of time spent with depressive symptoms relative to time with hypomanic symptoms is approximately 30:1.¹³ The fact that BP II patients in general seek help only during depressive periods means that consultations inevitably focus on the diagnosis and treatment of depression, rather than long-term prophylaxis of both depressive and hypomanic episodes.

Indistinguishable symptoms? Bipolar depressions are generally thought to be clinically indistinguishable from unipolar depressions, but this might not be clear-cut. Although differentiating symptoms of unipolar and bipolar depression can be difficult in clinical practice, evidence suggests that certain symptoms may be more common in bipolar than unipolar depression:

• atypical depressive features such as mood reactivity, overeating, oversleeping, and excessive fatigue¹⁴
  
• depressive psychotic symptoms, especially in younger patients¹⁵
  
• “mixed” depressive episodes (depressive episodes with concurrent manic symptoms).¹⁶
  

How to recognize BP II disorder

To detect and diagnose BP II disorder, systematically assess hypomanic features in all patients who present with recurrent MDD, especially those who have an early age of onset or don’t seem to be responding well to antidepressant monotherapy. As noted, a corroborative history from a close relative is essential. Within a full clinical assessment, use the features listed in Table 2 to help differentiate bipolar depression from unipolar depression.

Screening instruments for hypomania are no substitute for a careful psychiatric history but can be very helpful in everyday clinical practice. The most well-known is the Mood Disorder Questionnaire (MDQ);¹⁷ other options include the Hypomania Checklist (HCL-32)¹⁸ and the Bipolar Spectrum Diagnostic Scale (BSDS).¹⁹ In general, the MDQ performs better at detecting BP I in psychiatric practice settings, whereas the HCL-32 and BSDS may be more useful in primary care and general population settings.²⁰

The BSDS has a particular focus on the softer end of the bipolar spectrum,¹⁹ and in my experience patients like its narrative structure. It can help prompt discussions about previous hypomania symptoms and mood instability. In this sense, the BSDS is a useful adjunct to the routine clinical assessment of patients with recurrent depressive disorders. Click here to view the BSDS.

Table 2

Possible indicators of bipolarity in apparently unipolar depression

Treatment strategies for BP II

As with all psychiatric disorders, treatment needs to multimodal and tailored to the individual. For a detailed assessment of pharmacologic and psychological options, see Goodwin and Jamison’s authoritative text, chapters 17 to 20.²¹

Pharmacologic options. Because few clinical trials have focused exclusively on BP II patients, much psychiatric practice has been extrapolated from trials involving BP I patients. Obviously, trials with BP II samples are needed, but these may be limited by the restrictive DSM-IV-TR definition of hypomania.

Lithium has the most supporting evidence, showing efficacy for all 3 phases of BP II—treatment of hypomania, treatment of bipolar depression, and prophylaxis against hypomanic and depressive relapses.²² Different medications used in bipolar disorder appear to have different efficacy profiles, however. For example, a systematic review of 14 randomized controlled trials with 2,526 patients found that although lithium, lamotrigine, olanzapine, and valproate were more effective than placebo at preventing relapse due to any mood episode:

• only lithium and olanzapine significantly reduced manic relapses
  
• only lamotrigine and valproate significantly reduced depressive relapses.²³
  

The Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) trial did not find any therapeutic benefit or increased risk of switching to mania for anti depressants plus mood stabilizer vs mood stabilizer alone.²⁶ Many trials of bipolar depression have recruited such heterogeneous groups of patients (including BP I, BP II, and BP NOS; schizoaffective disorder, bipolar type; and even recurrent MDD) that it is difficult to make firm recommendations about pharmacologic options for the depressive phase of BP II disorder.

In my experience, approximately one-third of BP II patients have a history of poor response to antidepressants or adverse effects from antidepressants (extreme irritability, activation, and antidepressant-induced hypomania). In the long term, these patients often do much better on mood stabilizer monotherapy or a combination of mood stabilizers such as lithium plus lamotrigine. The key is to be flexible with treatment options within recommended guidelines and to tailor treatment choices to the individual’s pattern of illness and treatment preferences.

Psychological interventions. Some evidence supports cognitive-behavioral therapy (CBT) and interpersonal and social rhythm therapy (IPSRT) in long-term treatment of bipolar disorders, although—as with medication trials—we need to be careful about extrapolating these findings to BP II disorder.²⁹ For example, a recent large-scale randomized controlled trial of CBT for bipolar disorder was largely negative.³⁰ Psychoeducation given in families and groups can be effective long-term options when used as adjuncts to medications.³¹

Table 3

Recommendations for treating patients with BP II disorder

• Goodwin GM and the Consensus Group of the British Association for Psychopharmacology. Evidence-based guidelines for treating bipolar disorder: revised second edition—recommendations from the British Association for Psychopharmacology. J Psychopharmacol. 2009;23(4):346-388. www.bap.org.uk/pdfs/Bipolar_guidelines.pdf.
  
• Goodwin FK, Jamison KR. Manic-depressive illness: bipolar disorders and recurrent depression. 2nd ed. New York, NY: Oxford University Press; 2007.
  
• Phelps J. Bipolar psychoeducation. www.psycheducation.org.
  
• Mood Disorders Treatment Team, Cardiff University. Interactive online psychoeducational treatment for bipolar disorder. www.BeatingBipolar.org.
  
• Goodwin GM, Geddes JR. What is the heartland of psychiatry? Br J Psychiatry. 2007;191(3):189-191.
  

• Lamotrigine • Lamictal
  
• Lithium • Various
  
• Olanzapine • Zyprexa
  
• Quetiapine • Seroquel
  
• Valproate • Depakon
  

Dr. Smith receives research funding from the National Institute of Health Research UK, the MRC/Welsh Assembly Government, NARSAD, and the American Psychiatric Institute for Research and Education. He is a speaker for Eli Lilly and Company, AstraZeneca, and Bristol-Myers Squibb and is a consultant to Shire Pharmaceuticals.

WEB AUDIO

Comment on this article

At least 25% and possibly up to 50% of patients with recurrent major depressive disorder (MDD) have features of mild hypomania (the “soft end” of the bipolar spectrum¹) and might be better conceptualized as suffering from a broadly defined bipolar (BP) II disorder.² The challenge is to differentiate MDD from BP II so that we make treatment decisions—such as antidepressants vs mood stabilizers—shown to improve the long-term course of patients’ depressive symptoms.

Diagnosis of BP II often is not straightforward and unfortunately may be delayed several years after patients first present for evaluation. To help clinicians make correct diagnostic decisions, this article:

• describes diagnostic criteria outside of DSM-IV-TR that can assist in identifying BP II disorder
  
• identifies subgroups of recurrently depressed patients whose primary disorder is more likely to be bipolar than unipolar
  
• provides a screening tool validated for identifying “soft” bipolarity
  
• offers a pragmatic clinical perspective on the treatment of BP II disorder.
  

How common is BP II disorder?

As with all psychiatric diagnoses, the prevalence of BP II disorder is a function of the diagnostic criteria used to define it.³ BP II—1 or more depressive episodes with at least 1 hypomanic episode—affects 1% to 2% of the population, based on DSM-IV-TR criteria for hypomania (Box 1). However, the DSM definition of BP II might be too restrictive. Regarding the diagnosis of hypomania, in particular:

• the symptom of “overactivity” should be given as much weight as the stem criteria of “euphoria” and “irritability”
  
• the 4-day threshold for a hypomanic episode probably is too long.
  

These deficiencies in DSM-IV-TR exclude many patients who experience brief but clinically significant periods of hypomania. A more realistic definition of hypomania within BP II disorder would:

• include overactivity as an additional stem criterion
  
• specify a threshold duration for hypomanic symptoms of at least 1 day rather than 4 days
  
• stipulate the experience of negative consequences of the episode as necessary for the diagnosis (Table 1).
  

Box 1

Proposed hypomania criteria in broadly defined BP II

Depression’s subgroups

Recurrent MDD is an extremely heterogeneous diagnosis. It includes many clinical presentations of depressive illness that may share little in terms of etiology, pathophysiology, and response to treatment. When carefully assessed, 2 subgroups of recurrently depressed patients in particular appear to be more likely to have a primary bipolar disorder:

• young patients with early-onset severe depression
  
• older adults with difficult-to-treat or treatment-resistant depression.
  

Higher rates of unrecognized bipolar disorder have been identified in patients with treatment-resistant depression. In a prospective study of 61 consecutive MDD patients referred to a mood disorders clinic, 59% satisfied DSM-IV-TR criteria for bipolar disorder.⁸

Consequences. Undiagnosed BP II disorder is an important clinical issue because bipolar features in patients presumed to have recurrent MDD can adversely affect long-term outcomes. Many of these patients will be treated exclusively with antidepressants despite evidence that antidepressant monotherapy for bipolar depression—at least for some patients—can cause more frequent mood episodes, mood destabilization, and possibly an increase in suicidal behaviors.^9,10

This point is highlighted in the United Kingdom’s National Institute of Health and Clinical Excellence (NICE) guidelines for bipolar disorder, which recommended that antidepressants be prescribed for bipolar depression only in combination with mood stabilizer treatment and withdrawn within 2 to 3 months of recovery.¹¹

The American Psychiatric Association’s (APA) practice guideline for treating bipolar disorder, published in 2002, advises against antidepressants as monotherapy for bipolar depression, recommending instead that lithium or lamotrigine be used first-line. A revised APA guideline is scheduled for publication this year.¹²

Why is BP II underdiagnosed?

Notwithstanding the limitations of DSMIV-TR criteria for hypomania, additional factors contribute to under-recognition of BP II in clinical practice.

Dominant depressive symptoms. The clinical course of bipolar disorders is dominated by low-grade depressive symptoms and recurrent depressive episodes rather than mania or hypomania. This is especially true for BP II disorder, where the ratio of time spent with depressive symptoms relative to time with hypomanic symptoms is approximately 30:1.¹³ The fact that BP II patients in general seek help only during depressive periods means that consultations inevitably focus on the diagnosis and treatment of depression, rather than long-term prophylaxis of both depressive and hypomanic episodes.

Indistinguishable symptoms? Bipolar depressions are generally thought to be clinically indistinguishable from unipolar depressions, but this might not be clear-cut. Although differentiating symptoms of unipolar and bipolar depression can be difficult in clinical practice, evidence suggests that certain symptoms may be more common in bipolar than unipolar depression:

• atypical depressive features such as mood reactivity, overeating, oversleeping, and excessive fatigue¹⁴
  
• depressive psychotic symptoms, especially in younger patients¹⁵
  
• “mixed” depressive episodes (depressive episodes with concurrent manic symptoms).¹⁶
  

How to recognize BP II disorder

To detect and diagnose BP II disorder, systematically assess hypomanic features in all patients who present with recurrent MDD, especially those who have an early age of onset or don’t seem to be responding well to antidepressant monotherapy. As noted, a corroborative history from a close relative is essential. Within a full clinical assessment, use the features listed in Table 2 to help differentiate bipolar depression from unipolar depression.

Screening instruments for hypomania are no substitute for a careful psychiatric history but can be very helpful in everyday clinical practice. The most well-known is the Mood Disorder Questionnaire (MDQ);¹⁷ other options include the Hypomania Checklist (HCL-32)¹⁸ and the Bipolar Spectrum Diagnostic Scale (BSDS).¹⁹ In general, the MDQ performs better at detecting BP I in psychiatric practice settings, whereas the HCL-32 and BSDS may be more useful in primary care and general population settings.²⁰

The BSDS has a particular focus on the softer end of the bipolar spectrum,¹⁹ and in my experience patients like its narrative structure. It can help prompt discussions about previous hypomania symptoms and mood instability. In this sense, the BSDS is a useful adjunct to the routine clinical assessment of patients with recurrent depressive disorders. Click here to view the BSDS.

Table 2

Possible indicators of bipolarity in apparently unipolar depression

Treatment strategies for BP II

As with all psychiatric disorders, treatment needs to multimodal and tailored to the individual. For a detailed assessment of pharmacologic and psychological options, see Goodwin and Jamison’s authoritative text, chapters 17 to 20.²¹

Pharmacologic options. Because few clinical trials have focused exclusively on BP II patients, much psychiatric practice has been extrapolated from trials involving BP I patients. Obviously, trials with BP II samples are needed, but these may be limited by the restrictive DSM-IV-TR definition of hypomania.

Lithium has the most supporting evidence, showing efficacy for all 3 phases of BP II—treatment of hypomania, treatment of bipolar depression, and prophylaxis against hypomanic and depressive relapses.²² Different medications used in bipolar disorder appear to have different efficacy profiles, however. For example, a systematic review of 14 randomized controlled trials with 2,526 patients found that although lithium, lamotrigine, olanzapine, and valproate were more effective than placebo at preventing relapse due to any mood episode:

• only lithium and olanzapine significantly reduced manic relapses
  
• only lamotrigine and valproate significantly reduced depressive relapses.²³
  

The Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) trial did not find any therapeutic benefit or increased risk of switching to mania for anti depressants plus mood stabilizer vs mood stabilizer alone.²⁶ Many trials of bipolar depression have recruited such heterogeneous groups of patients (including BP I, BP II, and BP NOS; schizoaffective disorder, bipolar type; and even recurrent MDD) that it is difficult to make firm recommendations about pharmacologic options for the depressive phase of BP II disorder.

In my experience, approximately one-third of BP II patients have a history of poor response to antidepressants or adverse effects from antidepressants (extreme irritability, activation, and antidepressant-induced hypomania). In the long term, these patients often do much better on mood stabilizer monotherapy or a combination of mood stabilizers such as lithium plus lamotrigine. The key is to be flexible with treatment options within recommended guidelines and to tailor treatment choices to the individual’s pattern of illness and treatment preferences.

Psychological interventions. Some evidence supports cognitive-behavioral therapy (CBT) and interpersonal and social rhythm therapy (IPSRT) in long-term treatment of bipolar disorders, although—as with medication trials—we need to be careful about extrapolating these findings to BP II disorder.²⁹ For example, a recent large-scale randomized controlled trial of CBT for bipolar disorder was largely negative.³⁰ Psychoeducation given in families and groups can be effective long-term options when used as adjuncts to medications.³¹

Table 3

Recommendations for treating patients with BP II disorder

• Goodwin GM and the Consensus Group of the British Association for Psychopharmacology. Evidence-based guidelines for treating bipolar disorder: revised second edition—recommendations from the British Association for Psychopharmacology. J Psychopharmacol. 2009;23(4):346-388. www.bap.org.uk/pdfs/Bipolar_guidelines.pdf.
  
• Goodwin FK, Jamison KR. Manic-depressive illness: bipolar disorders and recurrent depression. 2nd ed. New York, NY: Oxford University Press; 2007.
  
• Phelps J. Bipolar psychoeducation. www.psycheducation.org.
  
• Mood Disorders Treatment Team, Cardiff University. Interactive online psychoeducational treatment for bipolar disorder. www.BeatingBipolar.org.
  
• Goodwin GM, Geddes JR. What is the heartland of psychiatry? Br J Psychiatry. 2007;191(3):189-191.
  

• Lamotrigine • Lamictal
  
• Lithium • Various
  
• Olanzapine • Zyprexa
  
• Quetiapine • Seroquel
  
• Valproate • Depakon
  

Dr. Smith receives research funding from the National Institute of Health Research UK, the MRC/Welsh Assembly Government, NARSAD, and the American Psychiatric Institute for Research and Education. He is a speaker for Eli Lilly and Company, AstraZeneca, and Bristol-Myers Squibb and is a consultant to Shire Pharmaceuticals.

Comment on this article

Police take Ms. L, age 23, to the emergency room (ER) after her fiancé called them. He told the police that after a “night of drinking” they argued about a girl he had flirted with. Ms. L took out a loaded gun and threatened to shoot herself. She eventually handed the gun over to the police.

In the ER, Ms. L’s blood alcohol level is 0.20%. She tells the admitting emergency room nurse, “I would never hurt myself. I drank too much and was acting stupid. I just want to go home and sleep it off. I promise not to harm myself.” Emergency room staff observe Ms. L smile and giggle while waiting for a psychiatric evaluation.

What would you do? Hospitalize Ms. L for safety, or accept her promise not to hurt herself and send her home? What criteria would you use?

Knowing how to assess patients such as Ms. L is an essential psychiatric skill, whether or not you trained in forensic psychiatry. This article includes case reports that illustrate techniques for evaluating patients who may harbor suicidal or homicidal thoughts.

Evaluating danger to self

Your role is to weigh an individual’s risk factors for suicide against potential protective factors and to make a judgment call. Potential risk factors for suicide include (but are not limited to):

• current suicidal thoughts
  
• prior suicide attempts
  
• presence of a comorbid psychiatric disorder (particularly depression)
  
• intoxication or ongoing substance use
  
• feelings of hopelessness
  
• marked anxiety
  
• recent stressors
  
• family history of suicide
  
• lack of psychosocial support.¹
  

Also review information that is reasonably available. In the ER, records from other facilities or private psychiatric treatment notes may not be accessed easily. However, in addition to conducting a suicide risk assessment and mental status examination, consider reviewing the collateral information outlined in Table 2.

Furthermore, do not rely on “no-suicide” contracts. They do not guarantee that a person won’t attempt suicide, and they will not provide legal protection if the patient commits suicide after being released from your care.²

What to document. After completing your evaluation, specifically document:

• that a suicide risk assessment was conducted
  
• what risk factors were present
  
• interventions to address those risk factors
  
• the level of risk determined (minimal, moderate, or high)
  
• factors that may protect the patient against suicide.
  

Table 1

Evaluating suicidality: Sample questions to ask

Table 2

Sources of information to assess suicidality in the ER

CASE REPORT: Paranoid and armed

Mr. J, age 21, is brought involuntarily to the psychiatric ER by police. His mother reports he was locked in his room with a gun, claiming “the FBI is going to kill me.”

Mr. J’s mother tells the ER psychiatrist that her son has schizophrenia, paranoid type, and stopped taking risperidone, 3 mg/d, 4 weeks ago. She explains that Mr. J sometimes “hears voices” whispering to him that his medications are poison and to not trust his family. She states that Mr. J also abuses alcohol and methamphetamine and has 2 prior arrests for assault with a deadly weapon.

She adds that Mr. J now believes his family is working with the FBI to have him placed in a “secret detention camp.” Mr. J’s mother found a loaded pistol in his room and is “scared of what might happen.” During your psychiatric interview, Mr. J appears frightened and paranoid and provides only minimal answers to your questions. He clenches his teeth while staring intently at you.

Evaluating danger to others

There is good reason to be concerned that Mr. J might behave violently, and you likely have sufficient information to hospitalize him. When creating a long-term violence risk prevention plan, divide the concept of dangerousness into 5 components:

• magnitude of potential harm
  
• likelihood that harm will occur
  
• imminence of harm
  
• frequency of dangerous behavior
  
• situational variables that promote or protect against aggressive behavior.
  

Drugs and alcohol are strongly associated with violent behavior.⁵ Most persons involved in violent crimes are under the influence of alcohol or drugs at the time of their aggression.⁶ Stimulants such as cocaine, crack, amphetamines, and phencyclidine are of special concern. These drugs often are associated with feelings of disinhibition, a sense of power, and paranoia. The violence linked with cocaine use differs by gender: men are more likely to perpetrate violent crimes, whereas women are more likely to be the victims of violence.⁷

Table 3

10 questions to ask patients about a history of violence

Mental illness and violence

Studies examining whether individuals with mental illness are more violent than the non-mentally ill have yielded mixed results.^8,9 In a study of civilly committed psychiatric patients released into the community, most mentally ill individuals were not violent.¹⁰ Although researchers noted a weak relationship between mental illness and violence, violent conduct was greater only when the person was experiencing acute psychiatric symptoms. Subsequent research suggests that individuals with schizophrenia may have increased rates of violence even when not experiencing active signs of their illness.¹¹

Psychosis. In paranoid psychotic patients, violence often is well planned and in line with their false beliefs.¹² These patients usually direct the violence at a specific person they perceive as a persecutor. Paranoid individuals often target relatives or friends. In addition, community-dwelling paranoid persons are more likely to be dangerous because they have greater access to weapons than institutionalized patients.¹²

Carefully inquire about hallucinations—particularly auditory ones—to determine whether their presence increases the person’s risk to commit a violent act. Patients with schizophrenia are more likely to be violent if their auditory hallucinations generate negative emotions (anger, anxiety, or sadness) and if the patients have not developed successful coping strategies.¹³ Although most patients ignore violent command hallucinations to harm others, the presence of command hallucinations may increase the likelihood of behaving violently,¹⁴ particularly if:

• the voice is familiar to the person,¹⁵ and
  
• the person has delusional beliefs associated with the hallucinations.¹⁶
  

In addition to DSM-IV-TR personality disorders, be familiar with the psychological construct known as psychopathy. Cleckley²⁰ used the term psychopath to describe a person who is superficially charming, lacks close relationships, is impulsive, and is primarily concerned with self-gratification. Hare et al²¹ developed the Psychopathy Checklist-Revised as a validated measure of psychopathy in adults. Psychopathy is a strong predictor of criminal behavior and violence among adults.²²

Affect. Individuals who are angry and lack empathy for others are at increased risk for violent behavior.²³ Also observe the patient for physical signs and symptoms of changes indicating incipient violence. Berg et al²⁴ noted that signs of imminent violence can include:

• chanting
  
• clenched jaw
  
• flared nostrils
  
• flushed face
  
• darting eyes
  
• close proximity to the clinician
  
• clenched or gripping hands.
  

Static vs dynamic factors. When organizing strategies to decrease risk factors for violence, distinguish static from dynamic factors. Static factors include demographic information and history of violence. Dynamic factors, which are subject to change with intervention, include access to weapons, psychotic symptoms, active substance use, and a person’s living situation.

Table 4

Sample violence risk management chart for Mr. J

Related resource

• Simon RI, Hales RE, eds. The American Psychiatric Publishing textbook of suicide assessment and management. Arlington, VA: American Psychiatric Publishing, Inc; 2006.
  
• Simon RI, Tardiff K, eds. Textbook of violence assessment and management. Arlington, VA: American Psychiatric Publishing, Inc; 2008.
  

• Risperidone • Risperdal
  

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

Comment on this article

Police take Ms. L, age 23, to the emergency room (ER) after her fiancé called them. He told the police that after a “night of drinking” they argued about a girl he had flirted with. Ms. L took out a loaded gun and threatened to shoot herself. She eventually handed the gun over to the police.

In the ER, Ms. L’s blood alcohol level is 0.20%. She tells the admitting emergency room nurse, “I would never hurt myself. I drank too much and was acting stupid. I just want to go home and sleep it off. I promise not to harm myself.” Emergency room staff observe Ms. L smile and giggle while waiting for a psychiatric evaluation.

What would you do? Hospitalize Ms. L for safety, or accept her promise not to hurt herself and send her home? What criteria would you use?

Knowing how to assess patients such as Ms. L is an essential psychiatric skill, whether or not you trained in forensic psychiatry. This article includes case reports that illustrate techniques for evaluating patients who may harbor suicidal or homicidal thoughts.

Evaluating danger to self

Your role is to weigh an individual’s risk factors for suicide against potential protective factors and to make a judgment call. Potential risk factors for suicide include (but are not limited to):

• current suicidal thoughts
  
• prior suicide attempts
  
• presence of a comorbid psychiatric disorder (particularly depression)
  
• intoxication or ongoing substance use
  
• feelings of hopelessness
  
• marked anxiety
  
• recent stressors
  
• family history of suicide
  
• lack of psychosocial support.¹
  

Also review information that is reasonably available. In the ER, records from other facilities or private psychiatric treatment notes may not be accessed easily. However, in addition to conducting a suicide risk assessment and mental status examination, consider reviewing the collateral information outlined in Table 2.

Furthermore, do not rely on “no-suicide” contracts. They do not guarantee that a person won’t attempt suicide, and they will not provide legal protection if the patient commits suicide after being released from your care.²

What to document. After completing your evaluation, specifically document:

• that a suicide risk assessment was conducted
  
• what risk factors were present
  
• interventions to address those risk factors
  
• the level of risk determined (minimal, moderate, or high)
  
• factors that may protect the patient against suicide.
  

Table 1

Evaluating suicidality: Sample questions to ask

Table 2

Sources of information to assess suicidality in the ER

CASE REPORT: Paranoid and armed

Mr. J, age 21, is brought involuntarily to the psychiatric ER by police. His mother reports he was locked in his room with a gun, claiming “the FBI is going to kill me.”

Mr. J’s mother tells the ER psychiatrist that her son has schizophrenia, paranoid type, and stopped taking risperidone, 3 mg/d, 4 weeks ago. She explains that Mr. J sometimes “hears voices” whispering to him that his medications are poison and to not trust his family. She states that Mr. J also abuses alcohol and methamphetamine and has 2 prior arrests for assault with a deadly weapon.

She adds that Mr. J now believes his family is working with the FBI to have him placed in a “secret detention camp.” Mr. J’s mother found a loaded pistol in his room and is “scared of what might happen.” During your psychiatric interview, Mr. J appears frightened and paranoid and provides only minimal answers to your questions. He clenches his teeth while staring intently at you.

Evaluating danger to others

There is good reason to be concerned that Mr. J might behave violently, and you likely have sufficient information to hospitalize him. When creating a long-term violence risk prevention plan, divide the concept of dangerousness into 5 components:

• magnitude of potential harm
  
• likelihood that harm will occur
  
• imminence of harm
  
• frequency of dangerous behavior
  
• situational variables that promote or protect against aggressive behavior.
  

Drugs and alcohol are strongly associated with violent behavior.⁵ Most persons involved in violent crimes are under the influence of alcohol or drugs at the time of their aggression.⁶ Stimulants such as cocaine, crack, amphetamines, and phencyclidine are of special concern. These drugs often are associated with feelings of disinhibition, a sense of power, and paranoia. The violence linked with cocaine use differs by gender: men are more likely to perpetrate violent crimes, whereas women are more likely to be the victims of violence.⁷

Table 3

10 questions to ask patients about a history of violence

Mental illness and violence

Studies examining whether individuals with mental illness are more violent than the non-mentally ill have yielded mixed results.^8,9 In a study of civilly committed psychiatric patients released into the community, most mentally ill individuals were not violent.¹⁰ Although researchers noted a weak relationship between mental illness and violence, violent conduct was greater only when the person was experiencing acute psychiatric symptoms. Subsequent research suggests that individuals with schizophrenia may have increased rates of violence even when not experiencing active signs of their illness.¹¹

Psychosis. In paranoid psychotic patients, violence often is well planned and in line with their false beliefs.¹² These patients usually direct the violence at a specific person they perceive as a persecutor. Paranoid individuals often target relatives or friends. In addition, community-dwelling paranoid persons are more likely to be dangerous because they have greater access to weapons than institutionalized patients.¹²

Carefully inquire about hallucinations—particularly auditory ones—to determine whether their presence increases the person’s risk to commit a violent act. Patients with schizophrenia are more likely to be violent if their auditory hallucinations generate negative emotions (anger, anxiety, or sadness) and if the patients have not developed successful coping strategies.¹³ Although most patients ignore violent command hallucinations to harm others, the presence of command hallucinations may increase the likelihood of behaving violently,¹⁴ particularly if:

• the voice is familiar to the person,¹⁵ and
  
• the person has delusional beliefs associated with the hallucinations.¹⁶
  

In addition to DSM-IV-TR personality disorders, be familiar with the psychological construct known as psychopathy. Cleckley²⁰ used the term psychopath to describe a person who is superficially charming, lacks close relationships, is impulsive, and is primarily concerned with self-gratification. Hare et al²¹ developed the Psychopathy Checklist-Revised as a validated measure of psychopathy in adults. Psychopathy is a strong predictor of criminal behavior and violence among adults.²²

Affect. Individuals who are angry and lack empathy for others are at increased risk for violent behavior.²³ Also observe the patient for physical signs and symptoms of changes indicating incipient violence. Berg et al²⁴ noted that signs of imminent violence can include:

• chanting
  
• clenched jaw
  
• flared nostrils
  
• flushed face
  
• darting eyes
  
• close proximity to the clinician
  
• clenched or gripping hands.
  

Static vs dynamic factors. When organizing strategies to decrease risk factors for violence, distinguish static from dynamic factors. Static factors include demographic information and history of violence. Dynamic factors, which are subject to change with intervention, include access to weapons, psychotic symptoms, active substance use, and a person’s living situation.

Table 4

Sample violence risk management chart for Mr. J

Related resource

• Simon RI, Hales RE, eds. The American Psychiatric Publishing textbook of suicide assessment and management. Arlington, VA: American Psychiatric Publishing, Inc; 2006.
  
• Simon RI, Tardiff K, eds. Textbook of violence assessment and management. Arlington, VA: American Psychiatric Publishing, Inc; 2008.
  

• Risperidone • Risperdal
  

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

Comment on this article

Police take Ms. L, age 23, to the emergency room (ER) after her fiancé called them. He told the police that after a “night of drinking” they argued about a girl he had flirted with. Ms. L took out a loaded gun and threatened to shoot herself. She eventually handed the gun over to the police.

In the ER, Ms. L’s blood alcohol level is 0.20%. She tells the admitting emergency room nurse, “I would never hurt myself. I drank too much and was acting stupid. I just want to go home and sleep it off. I promise not to harm myself.” Emergency room staff observe Ms. L smile and giggle while waiting for a psychiatric evaluation.

What would you do? Hospitalize Ms. L for safety, or accept her promise not to hurt herself and send her home? What criteria would you use?

Knowing how to assess patients such as Ms. L is an essential psychiatric skill, whether or not you trained in forensic psychiatry. This article includes case reports that illustrate techniques for evaluating patients who may harbor suicidal or homicidal thoughts.

Evaluating danger to self

Your role is to weigh an individual’s risk factors for suicide against potential protective factors and to make a judgment call. Potential risk factors for suicide include (but are not limited to):

• current suicidal thoughts
  
• prior suicide attempts
  
• presence of a comorbid psychiatric disorder (particularly depression)
  
• intoxication or ongoing substance use
  
• feelings of hopelessness
  
• marked anxiety
  
• recent stressors
  
• family history of suicide
  
• lack of psychosocial support.¹
  

Also review information that is reasonably available. In the ER, records from other facilities or private psychiatric treatment notes may not be accessed easily. However, in addition to conducting a suicide risk assessment and mental status examination, consider reviewing the collateral information outlined in Table 2.

Furthermore, do not rely on “no-suicide” contracts. They do not guarantee that a person won’t attempt suicide, and they will not provide legal protection if the patient commits suicide after being released from your care.²

What to document. After completing your evaluation, specifically document:

• that a suicide risk assessment was conducted
  
• what risk factors were present
  
• interventions to address those risk factors
  
• the level of risk determined (minimal, moderate, or high)
  
• factors that may protect the patient against suicide.
  

Table 1

Evaluating suicidality: Sample questions to ask

Table 2

Sources of information to assess suicidality in the ER

CASE REPORT: Paranoid and armed

Mr. J, age 21, is brought involuntarily to the psychiatric ER by police. His mother reports he was locked in his room with a gun, claiming “the FBI is going to kill me.”

Mr. J’s mother tells the ER psychiatrist that her son has schizophrenia, paranoid type, and stopped taking risperidone, 3 mg/d, 4 weeks ago. She explains that Mr. J sometimes “hears voices” whispering to him that his medications are poison and to not trust his family. She states that Mr. J also abuses alcohol and methamphetamine and has 2 prior arrests for assault with a deadly weapon.

She adds that Mr. J now believes his family is working with the FBI to have him placed in a “secret detention camp.” Mr. J’s mother found a loaded pistol in his room and is “scared of what might happen.” During your psychiatric interview, Mr. J appears frightened and paranoid and provides only minimal answers to your questions. He clenches his teeth while staring intently at you.

Evaluating danger to others

There is good reason to be concerned that Mr. J might behave violently, and you likely have sufficient information to hospitalize him. When creating a long-term violence risk prevention plan, divide the concept of dangerousness into 5 components:

• magnitude of potential harm
  
• likelihood that harm will occur
  
• imminence of harm
  
• frequency of dangerous behavior
  
• situational variables that promote or protect against aggressive behavior.
  

Drugs and alcohol are strongly associated with violent behavior.⁵ Most persons involved in violent crimes are under the influence of alcohol or drugs at the time of their aggression.⁶ Stimulants such as cocaine, crack, amphetamines, and phencyclidine are of special concern. These drugs often are associated with feelings of disinhibition, a sense of power, and paranoia. The violence linked with cocaine use differs by gender: men are more likely to perpetrate violent crimes, whereas women are more likely to be the victims of violence.⁷

Table 3

10 questions to ask patients about a history of violence

Mental illness and violence

Studies examining whether individuals with mental illness are more violent than the non-mentally ill have yielded mixed results.^8,9 In a study of civilly committed psychiatric patients released into the community, most mentally ill individuals were not violent.¹⁰ Although researchers noted a weak relationship between mental illness and violence, violent conduct was greater only when the person was experiencing acute psychiatric symptoms. Subsequent research suggests that individuals with schizophrenia may have increased rates of violence even when not experiencing active signs of their illness.¹¹

Psychosis. In paranoid psychotic patients, violence often is well planned and in line with their false beliefs.¹² These patients usually direct the violence at a specific person they perceive as a persecutor. Paranoid individuals often target relatives or friends. In addition, community-dwelling paranoid persons are more likely to be dangerous because they have greater access to weapons than institutionalized patients.¹²

Carefully inquire about hallucinations—particularly auditory ones—to determine whether their presence increases the person’s risk to commit a violent act. Patients with schizophrenia are more likely to be violent if their auditory hallucinations generate negative emotions (anger, anxiety, or sadness) and if the patients have not developed successful coping strategies.¹³ Although most patients ignore violent command hallucinations to harm others, the presence of command hallucinations may increase the likelihood of behaving violently,¹⁴ particularly if:

• the voice is familiar to the person,¹⁵ and
  
• the person has delusional beliefs associated with the hallucinations.¹⁶
  

In addition to DSM-IV-TR personality disorders, be familiar with the psychological construct known as psychopathy. Cleckley²⁰ used the term psychopath to describe a person who is superficially charming, lacks close relationships, is impulsive, and is primarily concerned with self-gratification. Hare et al²¹ developed the Psychopathy Checklist-Revised as a validated measure of psychopathy in adults. Psychopathy is a strong predictor of criminal behavior and violence among adults.²²

Affect. Individuals who are angry and lack empathy for others are at increased risk for violent behavior.²³ Also observe the patient for physical signs and symptoms of changes indicating incipient violence. Berg et al²⁴ noted that signs of imminent violence can include:

• chanting
  
• clenched jaw
  
• flared nostrils
  
• flushed face
  
• darting eyes
  
• close proximity to the clinician
  
• clenched or gripping hands.
  

Static vs dynamic factors. When organizing strategies to decrease risk factors for violence, distinguish static from dynamic factors. Static factors include demographic information and history of violence. Dynamic factors, which are subject to change with intervention, include access to weapons, psychotic symptoms, active substance use, and a person’s living situation.

Table 4

Sample violence risk management chart for Mr. J

Related resource

• Simon RI, Hales RE, eds. The American Psychiatric Publishing textbook of suicide assessment and management. Arlington, VA: American Psychiatric Publishing, Inc; 2006.
  
• Simon RI, Tardiff K, eds. Textbook of violence assessment and management. Arlington, VA: American Psychiatric Publishing, Inc; 2008.
  

• Risperidone • Risperdal
  

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