Current Psychiatry

I believe the ridiculously brief inpatient stays and restrictions on available medications are the worst part of psychiatric practice. Reports of patients going berserk fail to note the restrictions placed on physicians in maintaining long-term care.

In New Zealand, inpatient commitment laws—although complex—allow a patient to be involuntarily committed when it is foreseeable that the patient will decompensate without medications or other treatments. This policy permits much better long-term treatment.

Scott A. Joseph, MD
Clinical director
Bemidji Community Behavioral Health Hospital
Bemidji, MN

I believe the ridiculously brief inpatient stays and restrictions on available medications are the worst part of psychiatric practice. Reports of patients going berserk fail to note the restrictions placed on physicians in maintaining long-term care.

In New Zealand, inpatient commitment laws—although complex—allow a patient to be involuntarily committed when it is foreseeable that the patient will decompensate without medications or other treatments. This policy permits much better long-term treatment.

Scott A. Joseph, MD
Clinical director
Bemidji Community Behavioral Health Hospital
Bemidji, MN

I believe the ridiculously brief inpatient stays and restrictions on available medications are the worst part of psychiatric practice. Reports of patients going berserk fail to note the restrictions placed on physicians in maintaining long-term care.

In New Zealand, inpatient commitment laws—although complex—allow a patient to be involuntarily committed when it is foreseeable that the patient will decompensate without medications or other treatments. This policy permits much better long-term treatment.

Scott A. Joseph, MD
Clinical director
Bemidji Community Behavioral Health Hospital
Bemidji, MN

I was surprised that I did not see my first choice of challenges to psychiatry on Dr. Nasrallah’s list: psychiatrists doing “med checks” and ignoring psychotherapy. This trend is bad for patients and psychiatrists.

Our relationship with patients is what allows healing to begin. Medications are fertilizer for the barren soil, and psychotherapy is the hard work of planting and tending the fields. We kid ourselves when we think medications are going to “fix” people.

Craig Heacock, MD
Fort Collins, CO

I was surprised that I did not see my first choice of challenges to psychiatry on Dr. Nasrallah’s list: psychiatrists doing “med checks” and ignoring psychotherapy. This trend is bad for patients and psychiatrists.

Our relationship with patients is what allows healing to begin. Medications are fertilizer for the barren soil, and psychotherapy is the hard work of planting and tending the fields. We kid ourselves when we think medications are going to “fix” people.

Craig Heacock, MD
Fort Collins, CO

I was surprised that I did not see my first choice of challenges to psychiatry on Dr. Nasrallah’s list: psychiatrists doing “med checks” and ignoring psychotherapy. This trend is bad for patients and psychiatrists.

Our relationship with patients is what allows healing to begin. Medications are fertilizer for the barren soil, and psychotherapy is the hard work of planting and tending the fields. We kid ourselves when we think medications are going to “fix” people.

Craig Heacock, MD
Fort Collins, CO

I agree with Dr. Nasrallah’s observation that “As psychiatry’s promise grows, however, so do its frustrations.” In addition to Dr. Nasrallah’s list of 17 challenges to psychiatry, I propose adding the proliferation of industry-sponsored continuing medical education, unpublished unfavorable industry-sponsored research, and potential conflicts of interest when physicians are compensated by industry for conducting educational symposia.

Steven Singer, MD
Madison, WI

I agree with Dr. Nasrallah’s observation that “As psychiatry’s promise grows, however, so do its frustrations.” In addition to Dr. Nasrallah’s list of 17 challenges to psychiatry, I propose adding the proliferation of industry-sponsored continuing medical education, unpublished unfavorable industry-sponsored research, and potential conflicts of interest when physicians are compensated by industry for conducting educational symposia.

Steven Singer, MD
Madison, WI

I agree with Dr. Nasrallah’s observation that “As psychiatry’s promise grows, however, so do its frustrations.” In addition to Dr. Nasrallah’s list of 17 challenges to psychiatry, I propose adding the proliferation of industry-sponsored continuing medical education, unpublished unfavorable industry-sponsored research, and potential conflicts of interest when physicians are compensated by industry for conducting educational symposia.

Steven Singer, MD
Madison, WI

I thank my colleagues who responded to my survey about challenges facing psychiatry (“Your vote, please: What’s ailing psychiatry?” From the Editor, Current Psychiatry, June 2008).

Survey results indicate that psychiatrists care more about their patients than their pocketbooks. The 3 top-rated challenges address the “broken” public mental health system, lack of parity for mental illness, and the shortage of beds to hospitalize psychiatric patients. Close behind are inadequate philanthropy for psychiatric causes—such as education, research, and clinical programs—and dismal lack of adequate primary care for the seriously mentally ill. Unreimbursed time spent on paperwork, persistent stigma, and shrinking funds for research were tied, and low compensation for psychiatrists ranked after those ( Table ).

Among the lowest-ranked challenges, the high rate of off-label psychotropic use was considered least important, which makes sense given how many psychiatric disorders have no FDA-approved drugs. Similarly, the lack of evidence-based psychotherapy research may reflect the fact that a large portion of today’s psychiatric work is assessment, differential diagnosis, and medical management rather than psychotherapy. Other mental health professionals are doing the bulk of psychotherapeutic interventions.

Let me end by expressing my surprise that not one reader wrote about psychologists’ push for prescribing privileges as a threat to psychiatry—which I deliberately did not include on my list—even though it is a hot-button issue. This suggests to me that so many issues impact psychiatric practice that psychologists are under the radar. However, I expect this issue will reemerge in the future.

Henry A. Nasrallah, MD
Editor-in-Chief

I thank my colleagues who responded to my survey about challenges facing psychiatry (“Your vote, please: What’s ailing psychiatry?” From the Editor, Current Psychiatry, June 2008).

Survey results indicate that psychiatrists care more about their patients than their pocketbooks. The 3 top-rated challenges address the “broken” public mental health system, lack of parity for mental illness, and the shortage of beds to hospitalize psychiatric patients. Close behind are inadequate philanthropy for psychiatric causes—such as education, research, and clinical programs—and dismal lack of adequate primary care for the seriously mentally ill. Unreimbursed time spent on paperwork, persistent stigma, and shrinking funds for research were tied, and low compensation for psychiatrists ranked after those ( Table ).

Among the lowest-ranked challenges, the high rate of off-label psychotropic use was considered least important, which makes sense given how many psychiatric disorders have no FDA-approved drugs. Similarly, the lack of evidence-based psychotherapy research may reflect the fact that a large portion of today’s psychiatric work is assessment, differential diagnosis, and medical management rather than psychotherapy. Other mental health professionals are doing the bulk of psychotherapeutic interventions.

Let me end by expressing my surprise that not one reader wrote about psychologists’ push for prescribing privileges as a threat to psychiatry—which I deliberately did not include on my list—even though it is a hot-button issue. This suggests to me that so many issues impact psychiatric practice that psychologists are under the radar. However, I expect this issue will reemerge in the future.

Henry A. Nasrallah, MD
Editor-in-Chief

I thank my colleagues who responded to my survey about challenges facing psychiatry (“Your vote, please: What’s ailing psychiatry?” From the Editor, Current Psychiatry, June 2008).

Survey results indicate that psychiatrists care more about their patients than their pocketbooks. The 3 top-rated challenges address the “broken” public mental health system, lack of parity for mental illness, and the shortage of beds to hospitalize psychiatric patients. Close behind are inadequate philanthropy for psychiatric causes—such as education, research, and clinical programs—and dismal lack of adequate primary care for the seriously mentally ill. Unreimbursed time spent on paperwork, persistent stigma, and shrinking funds for research were tied, and low compensation for psychiatrists ranked after those ( Table ).

Among the lowest-ranked challenges, the high rate of off-label psychotropic use was considered least important, which makes sense given how many psychiatric disorders have no FDA-approved drugs. Similarly, the lack of evidence-based psychotherapy research may reflect the fact that a large portion of today’s psychiatric work is assessment, differential diagnosis, and medical management rather than psychotherapy. Other mental health professionals are doing the bulk of psychotherapeutic interventions.

Let me end by expressing my surprise that not one reader wrote about psychologists’ push for prescribing privileges as a threat to psychiatry—which I deliberately did not include on my list—even though it is a hot-button issue. This suggests to me that so many issues impact psychiatric practice that psychologists are under the radar. However, I expect this issue will reemerge in the future.

Henry A. Nasrallah, MD
Editor-in-Chief

The complex process by which psychiatric medications are discovered, developed, and tested culminates in “evidence-based medicine”—the backbone of psychopharmacology. Large controlled clinical trials are designed to demonstrate under highly controlled conditions that a newly synthesized molecule has sufficient efficacy and a reasonable side-effect profile to warrant FDA approval. Results are published, and the pharmaceutical company launches the approved medication in the community.

Not usually recognized is that a treasure trove of information may be buried in a preapproval clinical trial’s massive database. The pharmaceutical company might not “mine” this information without the likelihood of revenue enhancement, but the raw data may hold clinically useful revelations.

These may include clues about which patients are likely to respond (or not) or experience a serious side effect with the drug (or placebo). Some-times examining contrarian psychopharmacology—unexpected patterns of response or adverse effects—provides valuable insights with clinical applications. Here are some questions we could explore beyond the efficacy-safety-tolerability data published on atypical antipsychotics.

Drug efficacy

• What are the demographic, biologic, and clinical profiles of rapid responders vs delayed responders vs nonresponders?
• How do full responders differ from partial responders or complete nonresponders? Can we identify them in clinical settings?
• Can we predict who will respond or not to a particular antipsychotic? Why not report whether the nonresponders in a clinical trial responded to some other antipsychotic after the trial was completed? That information would be tremendously useful and cost-effective in clinical practice.

Placebo efficacy

• How do placebo responders differ from nonresponders?
• Are placebo nonresponders similar in some ways to drug nonresponders?
• Would placebo nonresponders respond to the active drug after the controlled trial is completed?

Side effects

Each atypical has common side effects, but we know little about patients who buck the trend. Consider the potentially useful insights from studying patients who:

• lose weight on olanzapine
• gain weight on ziprasidone
• get sedated with aripiprazole
• develop insomnia or extrapyramidal symptoms with quetiapine
• continue to menstruate regularly on risperidone.

Patients such as these are reported in clinical trials but not monitored or compared for their response rates.

Placebo

• What would we learn if we compared psychotic patients who developed sedation with those who developed insomnia while receiving placebo in a clinical trial? Would these 2 groups differ in their response to the antipsychotic?
• Some psychotic patients gain substantial weight (>7%) on placebo, whereas others lose quite a bit of weight. Do they differ in response rates or other traits?

Individualized therapy

Contrarian patients who develop unexpected responses (such as strong improvement on placebo or side effects the opposite of what is expected) represent missed opportunities for research to elucidate the heterogeneity of psychosis (as well as mania, depression, or anxiety). Understanding individual differences could enable practitioners to predict efficacy and tolerability and to match patients with the most suitable medications from the start. These insights could save time, reduce duration of illness, predict likely side effects, and ultimately reduce the costs of treatment.

The complex process by which psychiatric medications are discovered, developed, and tested culminates in “evidence-based medicine”—the backbone of psychopharmacology. Large controlled clinical trials are designed to demonstrate under highly controlled conditions that a newly synthesized molecule has sufficient efficacy and a reasonable side-effect profile to warrant FDA approval. Results are published, and the pharmaceutical company launches the approved medication in the community.

Not usually recognized is that a treasure trove of information may be buried in a preapproval clinical trial’s massive database. The pharmaceutical company might not “mine” this information without the likelihood of revenue enhancement, but the raw data may hold clinically useful revelations.

These may include clues about which patients are likely to respond (or not) or experience a serious side effect with the drug (or placebo). Some-times examining contrarian psychopharmacology—unexpected patterns of response or adverse effects—provides valuable insights with clinical applications. Here are some questions we could explore beyond the efficacy-safety-tolerability data published on atypical antipsychotics.

Drug efficacy

• What are the demographic, biologic, and clinical profiles of rapid responders vs delayed responders vs nonresponders?
• How do full responders differ from partial responders or complete nonresponders? Can we identify them in clinical settings?
• Can we predict who will respond or not to a particular antipsychotic? Why not report whether the nonresponders in a clinical trial responded to some other antipsychotic after the trial was completed? That information would be tremendously useful and cost-effective in clinical practice.

Placebo efficacy

• How do placebo responders differ from nonresponders?
• Are placebo nonresponders similar in some ways to drug nonresponders?
• Would placebo nonresponders respond to the active drug after the controlled trial is completed?

Side effects

Each atypical has common side effects, but we know little about patients who buck the trend. Consider the potentially useful insights from studying patients who:

• lose weight on olanzapine
• gain weight on ziprasidone
• get sedated with aripiprazole
• develop insomnia or extrapyramidal symptoms with quetiapine
• continue to menstruate regularly on risperidone.

Patients such as these are reported in clinical trials but not monitored or compared for their response rates.

Placebo

• What would we learn if we compared psychotic patients who developed sedation with those who developed insomnia while receiving placebo in a clinical trial? Would these 2 groups differ in their response to the antipsychotic?
• Some psychotic patients gain substantial weight (>7%) on placebo, whereas others lose quite a bit of weight. Do they differ in response rates or other traits?

Individualized therapy

Contrarian patients who develop unexpected responses (such as strong improvement on placebo or side effects the opposite of what is expected) represent missed opportunities for research to elucidate the heterogeneity of psychosis (as well as mania, depression, or anxiety). Understanding individual differences could enable practitioners to predict efficacy and tolerability and to match patients with the most suitable medications from the start. These insights could save time, reduce duration of illness, predict likely side effects, and ultimately reduce the costs of treatment.

The complex process by which psychiatric medications are discovered, developed, and tested culminates in “evidence-based medicine”—the backbone of psychopharmacology. Large controlled clinical trials are designed to demonstrate under highly controlled conditions that a newly synthesized molecule has sufficient efficacy and a reasonable side-effect profile to warrant FDA approval. Results are published, and the pharmaceutical company launches the approved medication in the community.

Not usually recognized is that a treasure trove of information may be buried in a preapproval clinical trial’s massive database. The pharmaceutical company might not “mine” this information without the likelihood of revenue enhancement, but the raw data may hold clinically useful revelations.

These may include clues about which patients are likely to respond (or not) or experience a serious side effect with the drug (or placebo). Some-times examining contrarian psychopharmacology—unexpected patterns of response or adverse effects—provides valuable insights with clinical applications. Here are some questions we could explore beyond the efficacy-safety-tolerability data published on atypical antipsychotics.

Drug efficacy

• What are the demographic, biologic, and clinical profiles of rapid responders vs delayed responders vs nonresponders?
• How do full responders differ from partial responders or complete nonresponders? Can we identify them in clinical settings?
• Can we predict who will respond or not to a particular antipsychotic? Why not report whether the nonresponders in a clinical trial responded to some other antipsychotic after the trial was completed? That information would be tremendously useful and cost-effective in clinical practice.

Placebo efficacy

• How do placebo responders differ from nonresponders?
• Are placebo nonresponders similar in some ways to drug nonresponders?
• Would placebo nonresponders respond to the active drug after the controlled trial is completed?

Side effects

Each atypical has common side effects, but we know little about patients who buck the trend. Consider the potentially useful insights from studying patients who:

• lose weight on olanzapine
• gain weight on ziprasidone
• get sedated with aripiprazole
• develop insomnia or extrapyramidal symptoms with quetiapine
• continue to menstruate regularly on risperidone.

Patients such as these are reported in clinical trials but not monitored or compared for their response rates.

Placebo

• What would we learn if we compared psychotic patients who developed sedation with those who developed insomnia while receiving placebo in a clinical trial? Would these 2 groups differ in their response to the antipsychotic?
• Some psychotic patients gain substantial weight (>7%) on placebo, whereas others lose quite a bit of weight. Do they differ in response rates or other traits?

Individualized therapy

Contrarian patients who develop unexpected responses (such as strong improvement on placebo or side effects the opposite of what is expected) represent missed opportunities for research to elucidate the heterogeneity of psychosis (as well as mania, depression, or anxiety). Understanding individual differences could enable practitioners to predict efficacy and tolerability and to match patients with the most suitable medications from the start. These insights could save time, reduce duration of illness, predict likely side effects, and ultimately reduce the costs of treatment.

CASE: Unexplained unresponsiveness

One month after being hospitalized with E coli sepsis—and just after completing a course of ciprofloxacin—Mrs. D, a 79-year-old widow, becomes withdrawn and has several days of worsening fatigue, weakness, and somnolence. Within 2 hours of being admitted to the hospital, she becomes flaccid and unresponsive, although she seems to be awake. She has decreased respirations and is intubated.

The neurology team finds her unresponsive to verbal and noxious stimuli, with some resistance to eye opening. Neurologic exam is nonfocal. Cranial nerve testing is intact, muscle strength and reflexes are normal and symmetrical, and sensory function is intact to light touch. MRI, ECG, chest radiography, and laboratory tests—including metabolic and infectious screenings—do not reveal acute pathology. Within hours, Mrs. D becomes much more responsive and is successfully extubated. Her rapid improvement rules out locked-in syndrome.

The next day, Mrs. D has another episode of reduced responsiveness that lasts several minutes and resolves quickly. The neurologist observes this episode—which occurred when Mrs. D’s daughter entered the room—and recommends a psychiatric consultation.

For the past 3 weeks Mrs. D has experienced depressed mood, low energy, poor sleep, memory complaints, and feeling as if her mind was “scattered.” She has stopped attending church, is isolating to her home, and has been hiding valuables because of an irrational fear that she would lose possessions from her estate. Her primary care physician noted markedly reduced speech during recent office visits and agrees with the family that Mrs. D seems depressed.

On psychiatric exam, Mrs. D’s speech is quiet and slow but coherent. Her mood is depressed with a flat affect. Her thought process is goal-directed, and her Mini-Mental State Examination (MMSE) score is 27/30, indicating her cognition is grossly intact.

Mrs. D develops a low-grade fever. Although the physician does not suspect an infection, he prescribes a prophylactic course of levofloxacin, 500 mg/d. After 2 days of monitoring and assessments, the psychiatrist attributes Mrs. D’s presentation to depression, prescribes bupropion, 100 mg/d, and zolpidem, 5 mg at bedtime, and refers her for psychiatric follow-up.

Six days after discharge, Mrs. D’s family brings her to the psychiatric emergency room. They report that since discharge she has remained fatigued and seems confused intermittently. Her depressive symptoms—decreased appetite, anhedonia, poor sleep, and agitation—persist, and her personal care has deteriorated.

The authors’ observations

The psychiatrist attributes Mrs. D’s declining functioning to a worsening mood disorder. Major depression with psychotic features can include:

• fearfulness
  
• suspiciousness
  
• delusions of poverty.
  

Mrs. D’s cognitive and behavioral status fluctuated during her initial medical hospitalization, and on 1 occasion she required intubation. Her confusion worsened after discharge. These aspects of her history, along with worsening psychosis, can indicate seizures.

Psychiatric manifestations of seizures have been recognized for centuries. Partial complex seizures—one of the most common seizure types—have been called “psychosensory” or “psychomotor” seizures because they often include psychiatric symptoms.¹

Psychiatric symptoms most often occur with seizures involving the temporal lobe, and limbic system activation adds an affective dimension to perceptual data processed by the temporal neocortex.² Frontal and parietal lobe seizure foci also are associated with behavior change.

Psychiatric manifestations of seizures can include:

• cognitive problems
  
• anxiety
  
• mood/affect, psychotic, and dissociative symptoms
  
• personality changes (Table 1).^2-6
  

As many as 30% of patients with seizures experience prominent psychiatric symptoms.⁷ Approximately one-half have comorbid psychiatric syndromes.⁸

Table 1

Seizure-related psychiatric symptoms: What to look for

EVALUATION: Continuing decline

The emergency room staff learns Mrs. D has a history of vague auditory hallucinations and has developed more overt paranoia, including thoughts that police may be out to harm her. She has difficulty responding to questions and can not offer details of her history; her speech is soft and her thought process appears slowed.

Mrs. D is admitted to the inpatient psychiatry service. Her family reports that she has episodes of disorientation, poor memory, staring, and paranoia about the police that last minutes to 1 hour.

On a subsequent examination 1 hour later, her speech difficulties are variable. She cannot speak fluently, has limited ability to repeat phrases, and cannot follow simple verbal commands. These symptoms persist only minutes. Mrs. D slowly becomes more conversant but appears tired. During the next few hours she is disoriented and tries to walk into the nursing station. Other repetitive activity includes putting on/taking offmultiple layers of clothing.

The authors’ observations

• A normal EEG does not guarantee the absence of recent seizures; a standard scalp EEG can miss epileptiform changes that may occur earlier in the ictal phase.⁹
  
• EEG abnormalities may occur in normal subjects.
  

• visual, olfactory, or tactile hallucinations
  
• mutism
  
• catatonia
  
• poor memory not due to inattention
  
• episodic aphasia, apraxia, or agnosia.
  

Mrs. D’s confusion level and speech abnormalities varied over time. Her speech arrest early in the admission appeared to be a Broca’s or expressive aphasia because she comprehended commands but was unable to speak. Later, her speech exhibited a mixed transcortical aphasia pattern—she was unable to speak or comprehend, but retained some ability to repeat. The changing aphasia patterns and the often abrupt starting and stopping of these symptoms were the clues that an active process was occurring, suggesting that seizures should be considered.

DIAGNOSIS: Irrefutable EEG evidence

Mrs. D receives another neurology consult. An EEG shows spike and wave discharges in both frontal lobes consistent with nonconvulsive status epilepticus (NCSE). During these bursts, the neurologist notes speech arrest and altered alertness. Phenytoin loading is administered as a single 800-mg oral dose followed by 100 mg twice daily, and Mrs. D is transferred to the neurology unit for further stabilization.

The authors’ observations

When evaluating whether a psychiatric presentation reflects an underlying general medical or neurologic disorder—including seizures—consider the clinical features outlined in Table 2.¹²

In Mrs. D’s case, several factors supported the diagnosis of depression. She had numerous depressive symptoms, including depressed mood, social withdrawal, low energy, poor sleep, and “scattered mind,” which the psychiatrist interpreted as poor concentration. Interestingly, she attributed her dramatic episode of mutism and unresponsiveness in the hospital to being depressed. Mrs. D also had a personal and family history of depression; she had experienced a possible major depressive episode in her late 20s but was never treated, and her brother had depression.

Several features of her presentation were atypical, however, and suggested a medical etiology. Her family described the onset of her symptoms as abrupt, and she declined rapidly. Mrs. D’s concern about her estate had no connection with reality, and she became more psychotic. The dramatic episode of decreased responsiveness that led to her intubation was both peculiar and brief.

Mrs. D’s symptoms had an episodic quality with sudden onset, were repeatedly associated with aphasia, and included some automatic behavior (including dressing and undressing) suggestive of seizures. Symptoms of depression should not be surprising in this context because depression may be the most common comorbid psychiatric condition in elderly persons with epilepsy.¹³ Indeed, Mrs. D’s ultimate diagnosis—NCSE—is characterized by great variability in presentation, ranging from mildly impaired attention and orientation to mood disturbance, speech disturbance, and psychosis. All of these symptoms are seen with seizures.

Further, NCSE can have gradual or sudden onset, varying intensity and duration of symptoms, and fluctuating responsiveness.¹⁴ At least 10% of patients presenting with NCSE have no history of seizures.¹⁵ Precipitating factors include infection and drug toxicity.¹⁴

OUTCOME: Dual treatment

During a one-week neurology hospitalization, Mrs. D continues to receive phenytoin. Long-term EEG monitoring reveals she is no longer in status epilepticus. The patient is prescribed citalopram, 10 mg/d, and olanzapine, 2.5 mg at bedtime, to resolve mild depressive symptoms and hallucinosis. Mrs. D is referred for both neurology and psychiatry outpatient follow-up.

Table 2

Is the patient’s disorder psychiatric or medical/neurologic?

• Ettinger AB, Kanner AM, eds. Psychiatric issues in epilepsy: a practical guide to diagnosis and treatment. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
  

• Bupropion • Wellbutrin
  
• Ciprofloxacin • Cipro
  
• Citalopram • Celexa
  
• Levofloxacin • Levaquin
  
• Olanzapine • Zyprexa
  
• Phenytoin • Dilantin
  
• Zolpidem • Ambien
  

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

Dr. Maixner receives research/grant support from Neuronetics Inc., and is a speaker for Pfizer Inc., Bristol-Meyers Squibb, Janssen LP, and AstraZeneca.

CASE: Unexplained unresponsiveness

One month after being hospitalized with E coli sepsis—and just after completing a course of ciprofloxacin—Mrs. D, a 79-year-old widow, becomes withdrawn and has several days of worsening fatigue, weakness, and somnolence. Within 2 hours of being admitted to the hospital, she becomes flaccid and unresponsive, although she seems to be awake. She has decreased respirations and is intubated.

The neurology team finds her unresponsive to verbal and noxious stimuli, with some resistance to eye opening. Neurologic exam is nonfocal. Cranial nerve testing is intact, muscle strength and reflexes are normal and symmetrical, and sensory function is intact to light touch. MRI, ECG, chest radiography, and laboratory tests—including metabolic and infectious screenings—do not reveal acute pathology. Within hours, Mrs. D becomes much more responsive and is successfully extubated. Her rapid improvement rules out locked-in syndrome.

The next day, Mrs. D has another episode of reduced responsiveness that lasts several minutes and resolves quickly. The neurologist observes this episode—which occurred when Mrs. D’s daughter entered the room—and recommends a psychiatric consultation.

For the past 3 weeks Mrs. D has experienced depressed mood, low energy, poor sleep, memory complaints, and feeling as if her mind was “scattered.” She has stopped attending church, is isolating to her home, and has been hiding valuables because of an irrational fear that she would lose possessions from her estate. Her primary care physician noted markedly reduced speech during recent office visits and agrees with the family that Mrs. D seems depressed.

On psychiatric exam, Mrs. D’s speech is quiet and slow but coherent. Her mood is depressed with a flat affect. Her thought process is goal-directed, and her Mini-Mental State Examination (MMSE) score is 27/30, indicating her cognition is grossly intact.

Mrs. D develops a low-grade fever. Although the physician does not suspect an infection, he prescribes a prophylactic course of levofloxacin, 500 mg/d. After 2 days of monitoring and assessments, the psychiatrist attributes Mrs. D’s presentation to depression, prescribes bupropion, 100 mg/d, and zolpidem, 5 mg at bedtime, and refers her for psychiatric follow-up.

Six days after discharge, Mrs. D’s family brings her to the psychiatric emergency room. They report that since discharge she has remained fatigued and seems confused intermittently. Her depressive symptoms—decreased appetite, anhedonia, poor sleep, and agitation—persist, and her personal care has deteriorated.

The authors’ observations

The psychiatrist attributes Mrs. D’s declining functioning to a worsening mood disorder. Major depression with psychotic features can include:

• fearfulness
  
• suspiciousness
  
• delusions of poverty.
  

Mrs. D’s cognitive and behavioral status fluctuated during her initial medical hospitalization, and on 1 occasion she required intubation. Her confusion worsened after discharge. These aspects of her history, along with worsening psychosis, can indicate seizures.

Psychiatric manifestations of seizures have been recognized for centuries. Partial complex seizures—one of the most common seizure types—have been called “psychosensory” or “psychomotor” seizures because they often include psychiatric symptoms.¹

Psychiatric symptoms most often occur with seizures involving the temporal lobe, and limbic system activation adds an affective dimension to perceptual data processed by the temporal neocortex.² Frontal and parietal lobe seizure foci also are associated with behavior change.

Psychiatric manifestations of seizures can include:

• cognitive problems
  
• anxiety
  
• mood/affect, psychotic, and dissociative symptoms
  
• personality changes (Table 1).^2-6
  

As many as 30% of patients with seizures experience prominent psychiatric symptoms.⁷ Approximately one-half have comorbid psychiatric syndromes.⁸

Table 1

Seizure-related psychiatric symptoms: What to look for

EVALUATION: Continuing decline

The emergency room staff learns Mrs. D has a history of vague auditory hallucinations and has developed more overt paranoia, including thoughts that police may be out to harm her. She has difficulty responding to questions and can not offer details of her history; her speech is soft and her thought process appears slowed.

Mrs. D is admitted to the inpatient psychiatry service. Her family reports that she has episodes of disorientation, poor memory, staring, and paranoia about the police that last minutes to 1 hour.

On a subsequent examination 1 hour later, her speech difficulties are variable. She cannot speak fluently, has limited ability to repeat phrases, and cannot follow simple verbal commands. These symptoms persist only minutes. Mrs. D slowly becomes more conversant but appears tired. During the next few hours she is disoriented and tries to walk into the nursing station. Other repetitive activity includes putting on/taking offmultiple layers of clothing.

The authors’ observations

• A normal EEG does not guarantee the absence of recent seizures; a standard scalp EEG can miss epileptiform changes that may occur earlier in the ictal phase.⁹
  
• EEG abnormalities may occur in normal subjects.
  

• visual, olfactory, or tactile hallucinations
  
• mutism
  
• catatonia
  
• poor memory not due to inattention
  
• episodic aphasia, apraxia, or agnosia.
  

Mrs. D’s confusion level and speech abnormalities varied over time. Her speech arrest early in the admission appeared to be a Broca’s or expressive aphasia because she comprehended commands but was unable to speak. Later, her speech exhibited a mixed transcortical aphasia pattern—she was unable to speak or comprehend, but retained some ability to repeat. The changing aphasia patterns and the often abrupt starting and stopping of these symptoms were the clues that an active process was occurring, suggesting that seizures should be considered.

DIAGNOSIS: Irrefutable EEG evidence

Mrs. D receives another neurology consult. An EEG shows spike and wave discharges in both frontal lobes consistent with nonconvulsive status epilepticus (NCSE). During these bursts, the neurologist notes speech arrest and altered alertness. Phenytoin loading is administered as a single 800-mg oral dose followed by 100 mg twice daily, and Mrs. D is transferred to the neurology unit for further stabilization.

The authors’ observations

When evaluating whether a psychiatric presentation reflects an underlying general medical or neurologic disorder—including seizures—consider the clinical features outlined in Table 2.¹²

In Mrs. D’s case, several factors supported the diagnosis of depression. She had numerous depressive symptoms, including depressed mood, social withdrawal, low energy, poor sleep, and “scattered mind,” which the psychiatrist interpreted as poor concentration. Interestingly, she attributed her dramatic episode of mutism and unresponsiveness in the hospital to being depressed. Mrs. D also had a personal and family history of depression; she had experienced a possible major depressive episode in her late 20s but was never treated, and her brother had depression.

Several features of her presentation were atypical, however, and suggested a medical etiology. Her family described the onset of her symptoms as abrupt, and she declined rapidly. Mrs. D’s concern about her estate had no connection with reality, and she became more psychotic. The dramatic episode of decreased responsiveness that led to her intubation was both peculiar and brief.

Mrs. D’s symptoms had an episodic quality with sudden onset, were repeatedly associated with aphasia, and included some automatic behavior (including dressing and undressing) suggestive of seizures. Symptoms of depression should not be surprising in this context because depression may be the most common comorbid psychiatric condition in elderly persons with epilepsy.¹³ Indeed, Mrs. D’s ultimate diagnosis—NCSE—is characterized by great variability in presentation, ranging from mildly impaired attention and orientation to mood disturbance, speech disturbance, and psychosis. All of these symptoms are seen with seizures.

Further, NCSE can have gradual or sudden onset, varying intensity and duration of symptoms, and fluctuating responsiveness.¹⁴ At least 10% of patients presenting with NCSE have no history of seizures.¹⁵ Precipitating factors include infection and drug toxicity.¹⁴

OUTCOME: Dual treatment

During a one-week neurology hospitalization, Mrs. D continues to receive phenytoin. Long-term EEG monitoring reveals she is no longer in status epilepticus. The patient is prescribed citalopram, 10 mg/d, and olanzapine, 2.5 mg at bedtime, to resolve mild depressive symptoms and hallucinosis. Mrs. D is referred for both neurology and psychiatry outpatient follow-up.

Table 2

Is the patient’s disorder psychiatric or medical/neurologic?

• Ettinger AB, Kanner AM, eds. Psychiatric issues in epilepsy: a practical guide to diagnosis and treatment. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
  

• Bupropion • Wellbutrin
  
• Ciprofloxacin • Cipro
  
• Citalopram • Celexa
  
• Levofloxacin • Levaquin
  
• Olanzapine • Zyprexa
  
• Phenytoin • Dilantin
  
• Zolpidem • Ambien
  

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

Dr. Maixner receives research/grant support from Neuronetics Inc., and is a speaker for Pfizer Inc., Bristol-Meyers Squibb, Janssen LP, and AstraZeneca.

CASE: Unexplained unresponsiveness

One month after being hospitalized with E coli sepsis—and just after completing a course of ciprofloxacin—Mrs. D, a 79-year-old widow, becomes withdrawn and has several days of worsening fatigue, weakness, and somnolence. Within 2 hours of being admitted to the hospital, she becomes flaccid and unresponsive, although she seems to be awake. She has decreased respirations and is intubated.

The neurology team finds her unresponsive to verbal and noxious stimuli, with some resistance to eye opening. Neurologic exam is nonfocal. Cranial nerve testing is intact, muscle strength and reflexes are normal and symmetrical, and sensory function is intact to light touch. MRI, ECG, chest radiography, and laboratory tests—including metabolic and infectious screenings—do not reveal acute pathology. Within hours, Mrs. D becomes much more responsive and is successfully extubated. Her rapid improvement rules out locked-in syndrome.

The next day, Mrs. D has another episode of reduced responsiveness that lasts several minutes and resolves quickly. The neurologist observes this episode—which occurred when Mrs. D’s daughter entered the room—and recommends a psychiatric consultation.

For the past 3 weeks Mrs. D has experienced depressed mood, low energy, poor sleep, memory complaints, and feeling as if her mind was “scattered.” She has stopped attending church, is isolating to her home, and has been hiding valuables because of an irrational fear that she would lose possessions from her estate. Her primary care physician noted markedly reduced speech during recent office visits and agrees with the family that Mrs. D seems depressed.

On psychiatric exam, Mrs. D’s speech is quiet and slow but coherent. Her mood is depressed with a flat affect. Her thought process is goal-directed, and her Mini-Mental State Examination (MMSE) score is 27/30, indicating her cognition is grossly intact.

Mrs. D develops a low-grade fever. Although the physician does not suspect an infection, he prescribes a prophylactic course of levofloxacin, 500 mg/d. After 2 days of monitoring and assessments, the psychiatrist attributes Mrs. D’s presentation to depression, prescribes bupropion, 100 mg/d, and zolpidem, 5 mg at bedtime, and refers her for psychiatric follow-up.

Six days after discharge, Mrs. D’s family brings her to the psychiatric emergency room. They report that since discharge she has remained fatigued and seems confused intermittently. Her depressive symptoms—decreased appetite, anhedonia, poor sleep, and agitation—persist, and her personal care has deteriorated.

The authors’ observations

The psychiatrist attributes Mrs. D’s declining functioning to a worsening mood disorder. Major depression with psychotic features can include:

• fearfulness
  
• suspiciousness
  
• delusions of poverty.
  

Mrs. D’s cognitive and behavioral status fluctuated during her initial medical hospitalization, and on 1 occasion she required intubation. Her confusion worsened after discharge. These aspects of her history, along with worsening psychosis, can indicate seizures.

Psychiatric manifestations of seizures have been recognized for centuries. Partial complex seizures—one of the most common seizure types—have been called “psychosensory” or “psychomotor” seizures because they often include psychiatric symptoms.¹

Psychiatric symptoms most often occur with seizures involving the temporal lobe, and limbic system activation adds an affective dimension to perceptual data processed by the temporal neocortex.² Frontal and parietal lobe seizure foci also are associated with behavior change.

Psychiatric manifestations of seizures can include:

• cognitive problems
  
• anxiety
  
• mood/affect, psychotic, and dissociative symptoms
  
• personality changes (Table 1).^2-6
  

As many as 30% of patients with seizures experience prominent psychiatric symptoms.⁷ Approximately one-half have comorbid psychiatric syndromes.⁸

Table 1

Seizure-related psychiatric symptoms: What to look for

EVALUATION: Continuing decline

The emergency room staff learns Mrs. D has a history of vague auditory hallucinations and has developed more overt paranoia, including thoughts that police may be out to harm her. She has difficulty responding to questions and can not offer details of her history; her speech is soft and her thought process appears slowed.

Mrs. D is admitted to the inpatient psychiatry service. Her family reports that she has episodes of disorientation, poor memory, staring, and paranoia about the police that last minutes to 1 hour.

On a subsequent examination 1 hour later, her speech difficulties are variable. She cannot speak fluently, has limited ability to repeat phrases, and cannot follow simple verbal commands. These symptoms persist only minutes. Mrs. D slowly becomes more conversant but appears tired. During the next few hours she is disoriented and tries to walk into the nursing station. Other repetitive activity includes putting on/taking offmultiple layers of clothing.

The authors’ observations

• A normal EEG does not guarantee the absence of recent seizures; a standard scalp EEG can miss epileptiform changes that may occur earlier in the ictal phase.⁹
  
• EEG abnormalities may occur in normal subjects.
  

• visual, olfactory, or tactile hallucinations
  
• mutism
  
• catatonia
  
• poor memory not due to inattention
  
• episodic aphasia, apraxia, or agnosia.
  

Mrs. D’s confusion level and speech abnormalities varied over time. Her speech arrest early in the admission appeared to be a Broca’s or expressive aphasia because she comprehended commands but was unable to speak. Later, her speech exhibited a mixed transcortical aphasia pattern—she was unable to speak or comprehend, but retained some ability to repeat. The changing aphasia patterns and the often abrupt starting and stopping of these symptoms were the clues that an active process was occurring, suggesting that seizures should be considered.

DIAGNOSIS: Irrefutable EEG evidence

Mrs. D receives another neurology consult. An EEG shows spike and wave discharges in both frontal lobes consistent with nonconvulsive status epilepticus (NCSE). During these bursts, the neurologist notes speech arrest and altered alertness. Phenytoin loading is administered as a single 800-mg oral dose followed by 100 mg twice daily, and Mrs. D is transferred to the neurology unit for further stabilization.

The authors’ observations

When evaluating whether a psychiatric presentation reflects an underlying general medical or neurologic disorder—including seizures—consider the clinical features outlined in Table 2.¹²

In Mrs. D’s case, several factors supported the diagnosis of depression. She had numerous depressive symptoms, including depressed mood, social withdrawal, low energy, poor sleep, and “scattered mind,” which the psychiatrist interpreted as poor concentration. Interestingly, she attributed her dramatic episode of mutism and unresponsiveness in the hospital to being depressed. Mrs. D also had a personal and family history of depression; she had experienced a possible major depressive episode in her late 20s but was never treated, and her brother had depression.

Several features of her presentation were atypical, however, and suggested a medical etiology. Her family described the onset of her symptoms as abrupt, and she declined rapidly. Mrs. D’s concern about her estate had no connection with reality, and she became more psychotic. The dramatic episode of decreased responsiveness that led to her intubation was both peculiar and brief.

Mrs. D’s symptoms had an episodic quality with sudden onset, were repeatedly associated with aphasia, and included some automatic behavior (including dressing and undressing) suggestive of seizures. Symptoms of depression should not be surprising in this context because depression may be the most common comorbid psychiatric condition in elderly persons with epilepsy.¹³ Indeed, Mrs. D’s ultimate diagnosis—NCSE—is characterized by great variability in presentation, ranging from mildly impaired attention and orientation to mood disturbance, speech disturbance, and psychosis. All of these symptoms are seen with seizures.

Further, NCSE can have gradual or sudden onset, varying intensity and duration of symptoms, and fluctuating responsiveness.¹⁴ At least 10% of patients presenting with NCSE have no history of seizures.¹⁵ Precipitating factors include infection and drug toxicity.¹⁴

OUTCOME: Dual treatment

During a one-week neurology hospitalization, Mrs. D continues to receive phenytoin. Long-term EEG monitoring reveals she is no longer in status epilepticus. The patient is prescribed citalopram, 10 mg/d, and olanzapine, 2.5 mg at bedtime, to resolve mild depressive symptoms and hallucinosis. Mrs. D is referred for both neurology and psychiatry outpatient follow-up.

Table 2

Is the patient’s disorder psychiatric or medical/neurologic?

• Ettinger AB, Kanner AM, eds. Psychiatric issues in epilepsy: a practical guide to diagnosis and treatment. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
  

• Bupropion • Wellbutrin
  
• Ciprofloxacin • Cipro
  
• Citalopram • Celexa
  
• Levofloxacin • Levaquin
  
• Olanzapine • Zyprexa
  
• Phenytoin • Dilantin
  
• Zolpidem • Ambien
  

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

Dr. Maixner receives research/grant support from Neuronetics Inc., and is a speaker for Pfizer Inc., Bristol-Meyers Squibb, Janssen LP, and AstraZeneca.

Dr. M is facing financial challenges with his fledgling private practice and begins consulting at a weight loss clinic to supplement his income. He finds him-self attracted to Ms. Y, a weight-loss patient he is treating. They seem to click interpersonally, and he extends his office visits with her. Ms. Y clearly enjoys this extra attention, and Dr. M begins including personal disclosures in his conversations with her.

In his residency training, Dr. M was taught never to date a current or former patient, but he views this situation as different. Ms. Y is seeing him only for weight loss, and he rationalizes that he is providing her with medical care, not “psychiatric” care. On 2 occasions he gives her a limited quantity of benzodiazepines for mild anxiety, which he considers a transitory stress-related condition and not an “official” DSM-IV-TR disorder.

Eventually, Dr. M asks Ms. Y to dinner and she accepts. After they begin dating, he decides to transfer her to another clinic physician “just to be safe.”

Although many psychiatrists assume that psychiatrist/patient boundaries are well defined by ethical and legal standards, boundary issues are a complex and controversial aspect of clinical practice. Psychoanalysts initially defined psychiatrist/patient boundaries as a way of structuring the unique and intimate relationship that evolves during analysis.^1,2 The introduction of other therapeutic techniques and changes in health care funding have combined to make psychiatrist/patient boundaries far more complex.

Boundary violations are about exploitation. Both the American Medical Association (AMA) and the Canadian Medical Association warn members to “scrupulously avoid using the physician/patient relationship to gratify their own emotional, financial, and sexual needs.”³

Boundaries represent the edge of appropriate behavior and serve 2 important purposes:

• They separate the therapeutic relationship from social, sexual, romantic, and business relationships and from relationships that transform into caretaking of the psychiatrist by the patient.
• They structure the professional relationship in ways that maintain the identity and roles of the patient and the professional.⁴

Psychiatry’s unique dilemmas

As are all physicians, psychiatrists are governed by the 9 biomedical ethics set forth in the AMA’s Principles of Medical Ethics. The American Psychiatric Association (APA), however, acknowledges that psychiatry has a “broader set of moral and ethical problems and dilemmas” that are unique to and magnified by the mental health setting.⁵ The APA has adopted 39 standards in addition to those set forth by the AMA. The first standard captures the unique responsibilities inherent in the psychiatrist/ patient relationship: A psychiatrist shall not gratify his or her own needs by exploiting the patient (Box).⁶

Sexual contact with patients is inherently harmful to patients, always unethical, and usually illegal.⁷ The rate of sexual misconduct among psychiatrists is unknown. National Practitioner Data Bank information is not available to the general public.⁸ Based on literature reviews and data from individual states^9,10 and government agencies,¹¹ an estimated 6% to10% of psychiatrists have had inappropriate sexual relations with patients.¹² Estimates of sexual misconduct by psychiatrists:

BOX

• increase if misconduct is based on patient complaints
• decrease if self-reports are used
• decrease even further if based on official investigations.⁴

American psychoanalyst Frieda Fromm-Reichman reportedly offered her colleagues a not-so-humorous admonition: “Don’t have sex with your patients; you will only disappoint them.”⁴

Nonsexual boundary violations—such as accepting gifts, entering into business arrangements, or trying to influence a patient’s political or religious beliefs or sexual orientation—occur more frequently than sexual misconduct.¹² Although the impact of nonsexual violations generally is less serious, any relationship that coexists with the therapeutic relationship has the potential to impair your judgment and contaminate your ability to focus exclusively on your patient’s well-being.¹³ Be cautious about any decision that could affect the treatment relationship.¹⁴

Triangle relationships.Originally, this term referred to the patient/therapist/psychiatrist triad. The term now has a broader meaning that includes:

• encroachments into care by managed care companies and government regulatory agencies
• interactions with the patient’s family members
• providing psychiatric care in non-traditional settings such as schools or prisons
• serving as an expert witness.¹⁵

The framework of trust once considered a core feature of the psychiatrist/patient relationship is being undermined by a funding system that demands efficiency and economy.¹⁶ Recognizing that some settings sacrifice patients’ clinical needs to the interests of the organization, the APA’s Guidelines for Ethical Practice in Organized Settings stipulate that the psychiatrist must “strive to resolve these conflicts in a manner that is likely to be of greatest benefit to the patient” by (for example):

• informing a patient of financial incentives or penalties that limit your ability to provide appropriate treatment
• not with holding information the patient could use to make informed treatment decisions, including treatment options not provided by you.⁶

Psychiatrists who doubt that the system—such as a mental health clinic, hospital, or managed care contract provider or reviewer—upholds the standard of acceptable care have the “ethical responsibility” to improve the system.⁶

Another change in mental health care attempts to limit psychiatrists to “medication management” so that less expensive professionals can provide adjunctive therapies. The treating psychiatrist bears some responsibility, however, for the appropriateness of the patient’s therapeutic options.⁶ According to Reid,¹⁷ psychiatrists are responsible for knowing something about the care, treatment style, credentials, and even ethics of those with whom they share treatment or to whom they refer patients.

The American Academy of Child and Adolescent Psychiatry (AACAP) Code of Ethics addresses the unique challenges encountered when a patient’s opinions differ from those of parents and other authority figures, such as school staff. The AACAP standards consistently direct the psychiatrist to keep the child’s interest primary, explaining that “the child and adolescent psychiatrist may be called upon to participate in attempts to control or change the behavior of children or adolescents…[but] the child and adolescent psychiatrist will avoid acting solely as an agent of the parents, guardians, or agencies.”¹⁸

Another triangle can occur when a treating psychiatrist serves as an expert witness or other evaluator for forensic or disability purposes. The American Academy of Psychiatry and the Law (AAPL) recommends that psychiatrists avoid acting as expert witnesses for their patients or performing patient evaluations for legal purposes.¹⁹ While recognizing that certain situations may require a psychiatrist to serve a dual role, the AAPL stresses that sensitivity to differences between clinical and legal obligations remains important.

Avoid serving as an expert witness for your patient. The intrusion of another role into the doctor/patient relationship can alter the treatment process and permanently color future inter actions. Likewise, treating an individual whom you previously evaluated for forensic purposes raises similar concerns, including the possibility of a mercenary motivation. Even when no such motivation exists, these situations can create the appearance that you have conscripted a vulnerable individual into your practice.

Emerging trends

Crossings vs violations. Efforts to distinguish when an action is unethical or illegal have led some to differentiate boundary crossings from boundary violations. Unfortunately, the 2 terms continue to be used synonymously, which confuses rather than clarifies the issue:

• Boundary crossings are aimed at enhancing the therapist’s treatment efforts—such as a hug instead of a hand shake at the end of a particularly difficult treatment session.
• Boundary violations are invariably harmful and unethical because they serve the therapist’s needs rather than the patient’s needs or the therapeutic process.²⁰

Rather than trying to differentiate between crossings and violations or to determine under what circumstances changing boundaries is acceptable, Sheets²¹ conceptualizes a boundary not as a line to cross, but as a continuum of behavior. Under-involvement is at one end, over-involvement at the other, and a “zone of helpfulness” is in the middle.

Glass uses a Venn diagram to illustrate that although most boundary crossings probably fall within the realm of ethical practice, gray areas alert therapists that they are approaching a violation (Figure).²⁰ Five factors have been found to increase psychiatrists’ vulnerability to boundary violations (Table 1).²²

Figure Beware the ‘gray areas’ between boundary crossings, violations
Source: Glass L. The gray areas of boundary crossings and violations. Am J Psychother 2003;57(4):429-44. Republished with permission of the Association for the Advancement of PsychotherapyTable 1

Boundary violations: Factors that increase your vulnerability

CASE CONTINUED: Board investigation

Dr. M’s relationship with Ms. Y grows intense, and he becomes increasingly concerned about her “clinginess.” After several months, Dr. M feels emotionally suffocated and ends the relationship. Despondent and suicidal, she seeks treatment in the local emergency room. Ms. Y tells the ER psychiatrist about her relationship with Dr. M and that she cannot go on without him in her life. The ER psychiatrist refers her to another psychiatrist for outpatient care, and, with Ms. Y’s permission, files a complaint about Dr. M with the state medical board and the district branch ethics committee.

The state medical board investigates Dr. M. He is contrite about his actions and their effect on Ms. Y. The state board refers Dr. M to an impaired physician’s program. He is required to attend a boundary violations course and undergo 1 year of practice supervision by a local psychiatrist. Several years later, Dr. M is doing well in his practice and has had no further complaints lodged against him.

Boundaries vs relationships. Using boundaries as a metaphor for maintaining the separation of therapist and patient was intended to serve the analytic process and to protect the patient’s welfare.² Clearly, certain boundaries—such as sexual contact between psychiatrist and patient—must remain sacrosanct. Yet certain practices avoided in analysis may be appropriate for other therapeutic interventions. For example, whereas psychoanalysis has strict prohibitions against seeing patients anywhere except in the office, cognitive-behavioral therapists may find it useful to conduct sessions in public, or—under carefully arranged circumstances—even in a patient’s home. Other examples include accompanying a patient with agoraphobia to a public gathering or dining with a patient with anorexia.

Exercise caution when you decide to alter traditional boundaries. Even minor crossings that are not likely to progress to violations have the potential to contaminate the therapeutic relationship and place the psychiatrist on a “slippery slope” to patient exploitation.^22,23 Some boundary issues are ambiguous, and extenuating circumstances can create a context that temporarily stretches a boundary beyond its normal limits,²⁴ especially in small communities and rural settings where patients and treating psychiatrists are likely to know and encounter each other in social settings.²⁵ Our recommendations for avoiding boundary violations appear in Table 2.

Except in clear cases of malfeasance, determining whether or not you have crossed a boundary is not a straightforward decision based on a single theoretical perspective or absolute standard.²⁶ Regardless of whether a given boundary’s edge is well defined, 2 things are clear:

• unlike patients, psychiatrists have a professional code to honor²⁷
• harm is determined by the meaning of the behavior to the patient and not the psychiatrist’s intentions.⁴

Table 2

Simple steps help avoid boundary violations

Related Resources

• American Medical Association. Principles of medical ethics. www.ama-assn.org/ama/pub/category/2512.html.
• American Psychiatric Association. The principles of medical ethics with annotations especially applicable to psychiatry. Washington, DC: American Psychiatric Association; 2008.

Disclosures

Drs. Marshall and Myers report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Teston is a speaker for Shire US, Inc.

Dr. M is facing financial challenges with his fledgling private practice and begins consulting at a weight loss clinic to supplement his income. He finds him-self attracted to Ms. Y, a weight-loss patient he is treating. They seem to click interpersonally, and he extends his office visits with her. Ms. Y clearly enjoys this extra attention, and Dr. M begins including personal disclosures in his conversations with her.

In his residency training, Dr. M was taught never to date a current or former patient, but he views this situation as different. Ms. Y is seeing him only for weight loss, and he rationalizes that he is providing her with medical care, not “psychiatric” care. On 2 occasions he gives her a limited quantity of benzodiazepines for mild anxiety, which he considers a transitory stress-related condition and not an “official” DSM-IV-TR disorder.

Eventually, Dr. M asks Ms. Y to dinner and she accepts. After they begin dating, he decides to transfer her to another clinic physician “just to be safe.”

Although many psychiatrists assume that psychiatrist/patient boundaries are well defined by ethical and legal standards, boundary issues are a complex and controversial aspect of clinical practice. Psychoanalysts initially defined psychiatrist/patient boundaries as a way of structuring the unique and intimate relationship that evolves during analysis.^1,2 The introduction of other therapeutic techniques and changes in health care funding have combined to make psychiatrist/patient boundaries far more complex.

Boundary violations are about exploitation. Both the American Medical Association (AMA) and the Canadian Medical Association warn members to “scrupulously avoid using the physician/patient relationship to gratify their own emotional, financial, and sexual needs.”³

Boundaries represent the edge of appropriate behavior and serve 2 important purposes:

• They separate the therapeutic relationship from social, sexual, romantic, and business relationships and from relationships that transform into caretaking of the psychiatrist by the patient.
• They structure the professional relationship in ways that maintain the identity and roles of the patient and the professional.⁴

Psychiatry’s unique dilemmas

As are all physicians, psychiatrists are governed by the 9 biomedical ethics set forth in the AMA’s Principles of Medical Ethics. The American Psychiatric Association (APA), however, acknowledges that psychiatry has a “broader set of moral and ethical problems and dilemmas” that are unique to and magnified by the mental health setting.⁵ The APA has adopted 39 standards in addition to those set forth by the AMA. The first standard captures the unique responsibilities inherent in the psychiatrist/ patient relationship: A psychiatrist shall not gratify his or her own needs by exploiting the patient (Box).⁶

Sexual contact with patients is inherently harmful to patients, always unethical, and usually illegal.⁷ The rate of sexual misconduct among psychiatrists is unknown. National Practitioner Data Bank information is not available to the general public.⁸ Based on literature reviews and data from individual states^9,10 and government agencies,¹¹ an estimated 6% to10% of psychiatrists have had inappropriate sexual relations with patients.¹² Estimates of sexual misconduct by psychiatrists:

BOX

• increase if misconduct is based on patient complaints
• decrease if self-reports are used
• decrease even further if based on official investigations.⁴

American psychoanalyst Frieda Fromm-Reichman reportedly offered her colleagues a not-so-humorous admonition: “Don’t have sex with your patients; you will only disappoint them.”⁴

Nonsexual boundary violations—such as accepting gifts, entering into business arrangements, or trying to influence a patient’s political or religious beliefs or sexual orientation—occur more frequently than sexual misconduct.¹² Although the impact of nonsexual violations generally is less serious, any relationship that coexists with the therapeutic relationship has the potential to impair your judgment and contaminate your ability to focus exclusively on your patient’s well-being.¹³ Be cautious about any decision that could affect the treatment relationship.¹⁴

Triangle relationships.Originally, this term referred to the patient/therapist/psychiatrist triad. The term now has a broader meaning that includes:

• encroachments into care by managed care companies and government regulatory agencies
• interactions with the patient’s family members
• providing psychiatric care in non-traditional settings such as schools or prisons
• serving as an expert witness.¹⁵

The framework of trust once considered a core feature of the psychiatrist/patient relationship is being undermined by a funding system that demands efficiency and economy.¹⁶ Recognizing that some settings sacrifice patients’ clinical needs to the interests of the organization, the APA’s Guidelines for Ethical Practice in Organized Settings stipulate that the psychiatrist must “strive to resolve these conflicts in a manner that is likely to be of greatest benefit to the patient” by (for example):

• informing a patient of financial incentives or penalties that limit your ability to provide appropriate treatment
• not with holding information the patient could use to make informed treatment decisions, including treatment options not provided by you.⁶

Psychiatrists who doubt that the system—such as a mental health clinic, hospital, or managed care contract provider or reviewer—upholds the standard of acceptable care have the “ethical responsibility” to improve the system.⁶

Another change in mental health care attempts to limit psychiatrists to “medication management” so that less expensive professionals can provide adjunctive therapies. The treating psychiatrist bears some responsibility, however, for the appropriateness of the patient’s therapeutic options.⁶ According to Reid,¹⁷ psychiatrists are responsible for knowing something about the care, treatment style, credentials, and even ethics of those with whom they share treatment or to whom they refer patients.

The American Academy of Child and Adolescent Psychiatry (AACAP) Code of Ethics addresses the unique challenges encountered when a patient’s opinions differ from those of parents and other authority figures, such as school staff. The AACAP standards consistently direct the psychiatrist to keep the child’s interest primary, explaining that “the child and adolescent psychiatrist may be called upon to participate in attempts to control or change the behavior of children or adolescents…[but] the child and adolescent psychiatrist will avoid acting solely as an agent of the parents, guardians, or agencies.”¹⁸

Another triangle can occur when a treating psychiatrist serves as an expert witness or other evaluator for forensic or disability purposes. The American Academy of Psychiatry and the Law (AAPL) recommends that psychiatrists avoid acting as expert witnesses for their patients or performing patient evaluations for legal purposes.¹⁹ While recognizing that certain situations may require a psychiatrist to serve a dual role, the AAPL stresses that sensitivity to differences between clinical and legal obligations remains important.

Avoid serving as an expert witness for your patient. The intrusion of another role into the doctor/patient relationship can alter the treatment process and permanently color future inter actions. Likewise, treating an individual whom you previously evaluated for forensic purposes raises similar concerns, including the possibility of a mercenary motivation. Even when no such motivation exists, these situations can create the appearance that you have conscripted a vulnerable individual into your practice.

Emerging trends

Crossings vs violations. Efforts to distinguish when an action is unethical or illegal have led some to differentiate boundary crossings from boundary violations. Unfortunately, the 2 terms continue to be used synonymously, which confuses rather than clarifies the issue:

• Boundary crossings are aimed at enhancing the therapist’s treatment efforts—such as a hug instead of a hand shake at the end of a particularly difficult treatment session.
• Boundary violations are invariably harmful and unethical because they serve the therapist’s needs rather than the patient’s needs or the therapeutic process.²⁰

Rather than trying to differentiate between crossings and violations or to determine under what circumstances changing boundaries is acceptable, Sheets²¹ conceptualizes a boundary not as a line to cross, but as a continuum of behavior. Under-involvement is at one end, over-involvement at the other, and a “zone of helpfulness” is in the middle.

Glass uses a Venn diagram to illustrate that although most boundary crossings probably fall within the realm of ethical practice, gray areas alert therapists that they are approaching a violation (Figure).²⁰ Five factors have been found to increase psychiatrists’ vulnerability to boundary violations (Table 1).²²

Figure Beware the ‘gray areas’ between boundary crossings, violations
Source: Glass L. The gray areas of boundary crossings and violations. Am J Psychother 2003;57(4):429-44. Republished with permission of the Association for the Advancement of PsychotherapyTable 1

Boundary violations: Factors that increase your vulnerability

CASE CONTINUED: Board investigation

Dr. M’s relationship with Ms. Y grows intense, and he becomes increasingly concerned about her “clinginess.” After several months, Dr. M feels emotionally suffocated and ends the relationship. Despondent and suicidal, she seeks treatment in the local emergency room. Ms. Y tells the ER psychiatrist about her relationship with Dr. M and that she cannot go on without him in her life. The ER psychiatrist refers her to another psychiatrist for outpatient care, and, with Ms. Y’s permission, files a complaint about Dr. M with the state medical board and the district branch ethics committee.

The state medical board investigates Dr. M. He is contrite about his actions and their effect on Ms. Y. The state board refers Dr. M to an impaired physician’s program. He is required to attend a boundary violations course and undergo 1 year of practice supervision by a local psychiatrist. Several years later, Dr. M is doing well in his practice and has had no further complaints lodged against him.

Boundaries vs relationships. Using boundaries as a metaphor for maintaining the separation of therapist and patient was intended to serve the analytic process and to protect the patient’s welfare.² Clearly, certain boundaries—such as sexual contact between psychiatrist and patient—must remain sacrosanct. Yet certain practices avoided in analysis may be appropriate for other therapeutic interventions. For example, whereas psychoanalysis has strict prohibitions against seeing patients anywhere except in the office, cognitive-behavioral therapists may find it useful to conduct sessions in public, or—under carefully arranged circumstances—even in a patient’s home. Other examples include accompanying a patient with agoraphobia to a public gathering or dining with a patient with anorexia.

Exercise caution when you decide to alter traditional boundaries. Even minor crossings that are not likely to progress to violations have the potential to contaminate the therapeutic relationship and place the psychiatrist on a “slippery slope” to patient exploitation.^22,23 Some boundary issues are ambiguous, and extenuating circumstances can create a context that temporarily stretches a boundary beyond its normal limits,²⁴ especially in small communities and rural settings where patients and treating psychiatrists are likely to know and encounter each other in social settings.²⁵ Our recommendations for avoiding boundary violations appear in Table 2.

Except in clear cases of malfeasance, determining whether or not you have crossed a boundary is not a straightforward decision based on a single theoretical perspective or absolute standard.²⁶ Regardless of whether a given boundary’s edge is well defined, 2 things are clear:

• unlike patients, psychiatrists have a professional code to honor²⁷
• harm is determined by the meaning of the behavior to the patient and not the psychiatrist’s intentions.⁴

Table 2

Simple steps help avoid boundary violations

Related Resources

• American Medical Association. Principles of medical ethics. www.ama-assn.org/ama/pub/category/2512.html.
• American Psychiatric Association. The principles of medical ethics with annotations especially applicable to psychiatry. Washington, DC: American Psychiatric Association; 2008.

Disclosures

Drs. Marshall and Myers report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Teston is a speaker for Shire US, Inc.

Dr. M is facing financial challenges with his fledgling private practice and begins consulting at a weight loss clinic to supplement his income. He finds him-self attracted to Ms. Y, a weight-loss patient he is treating. They seem to click interpersonally, and he extends his office visits with her. Ms. Y clearly enjoys this extra attention, and Dr. M begins including personal disclosures in his conversations with her.

In his residency training, Dr. M was taught never to date a current or former patient, but he views this situation as different. Ms. Y is seeing him only for weight loss, and he rationalizes that he is providing her with medical care, not “psychiatric” care. On 2 occasions he gives her a limited quantity of benzodiazepines for mild anxiety, which he considers a transitory stress-related condition and not an “official” DSM-IV-TR disorder.

Eventually, Dr. M asks Ms. Y to dinner and she accepts. After they begin dating, he decides to transfer her to another clinic physician “just to be safe.”

Although many psychiatrists assume that psychiatrist/patient boundaries are well defined by ethical and legal standards, boundary issues are a complex and controversial aspect of clinical practice. Psychoanalysts initially defined psychiatrist/patient boundaries as a way of structuring the unique and intimate relationship that evolves during analysis.^1,2 The introduction of other therapeutic techniques and changes in health care funding have combined to make psychiatrist/patient boundaries far more complex.

Boundary violations are about exploitation. Both the American Medical Association (AMA) and the Canadian Medical Association warn members to “scrupulously avoid using the physician/patient relationship to gratify their own emotional, financial, and sexual needs.”³

Boundaries represent the edge of appropriate behavior and serve 2 important purposes:

• They separate the therapeutic relationship from social, sexual, romantic, and business relationships and from relationships that transform into caretaking of the psychiatrist by the patient.
• They structure the professional relationship in ways that maintain the identity and roles of the patient and the professional.⁴

Psychiatry’s unique dilemmas

As are all physicians, psychiatrists are governed by the 9 biomedical ethics set forth in the AMA’s Principles of Medical Ethics. The American Psychiatric Association (APA), however, acknowledges that psychiatry has a “broader set of moral and ethical problems and dilemmas” that are unique to and magnified by the mental health setting.⁵ The APA has adopted 39 standards in addition to those set forth by the AMA. The first standard captures the unique responsibilities inherent in the psychiatrist/ patient relationship: A psychiatrist shall not gratify his or her own needs by exploiting the patient (Box).⁶

Sexual contact with patients is inherently harmful to patients, always unethical, and usually illegal.⁷ The rate of sexual misconduct among psychiatrists is unknown. National Practitioner Data Bank information is not available to the general public.⁸ Based on literature reviews and data from individual states^9,10 and government agencies,¹¹ an estimated 6% to10% of psychiatrists have had inappropriate sexual relations with patients.¹² Estimates of sexual misconduct by psychiatrists:

BOX

• increase if misconduct is based on patient complaints
• decrease if self-reports are used
• decrease even further if based on official investigations.⁴

American psychoanalyst Frieda Fromm-Reichman reportedly offered her colleagues a not-so-humorous admonition: “Don’t have sex with your patients; you will only disappoint them.”⁴

Nonsexual boundary violations—such as accepting gifts, entering into business arrangements, or trying to influence a patient’s political or religious beliefs or sexual orientation—occur more frequently than sexual misconduct.¹² Although the impact of nonsexual violations generally is less serious, any relationship that coexists with the therapeutic relationship has the potential to impair your judgment and contaminate your ability to focus exclusively on your patient’s well-being.¹³ Be cautious about any decision that could affect the treatment relationship.¹⁴

Triangle relationships.Originally, this term referred to the patient/therapist/psychiatrist triad. The term now has a broader meaning that includes:

• encroachments into care by managed care companies and government regulatory agencies
• interactions with the patient’s family members
• providing psychiatric care in non-traditional settings such as schools or prisons
• serving as an expert witness.¹⁵

The framework of trust once considered a core feature of the psychiatrist/patient relationship is being undermined by a funding system that demands efficiency and economy.¹⁶ Recognizing that some settings sacrifice patients’ clinical needs to the interests of the organization, the APA’s Guidelines for Ethical Practice in Organized Settings stipulate that the psychiatrist must “strive to resolve these conflicts in a manner that is likely to be of greatest benefit to the patient” by (for example):

• informing a patient of financial incentives or penalties that limit your ability to provide appropriate treatment
• not with holding information the patient could use to make informed treatment decisions, including treatment options not provided by you.⁶

Psychiatrists who doubt that the system—such as a mental health clinic, hospital, or managed care contract provider or reviewer—upholds the standard of acceptable care have the “ethical responsibility” to improve the system.⁶

Another change in mental health care attempts to limit psychiatrists to “medication management” so that less expensive professionals can provide adjunctive therapies. The treating psychiatrist bears some responsibility, however, for the appropriateness of the patient’s therapeutic options.⁶ According to Reid,¹⁷ psychiatrists are responsible for knowing something about the care, treatment style, credentials, and even ethics of those with whom they share treatment or to whom they refer patients.

The American Academy of Child and Adolescent Psychiatry (AACAP) Code of Ethics addresses the unique challenges encountered when a patient’s opinions differ from those of parents and other authority figures, such as school staff. The AACAP standards consistently direct the psychiatrist to keep the child’s interest primary, explaining that “the child and adolescent psychiatrist may be called upon to participate in attempts to control or change the behavior of children or adolescents…[but] the child and adolescent psychiatrist will avoid acting solely as an agent of the parents, guardians, or agencies.”¹⁸

Another triangle can occur when a treating psychiatrist serves as an expert witness or other evaluator for forensic or disability purposes. The American Academy of Psychiatry and the Law (AAPL) recommends that psychiatrists avoid acting as expert witnesses for their patients or performing patient evaluations for legal purposes.¹⁹ While recognizing that certain situations may require a psychiatrist to serve a dual role, the AAPL stresses that sensitivity to differences between clinical and legal obligations remains important.

Avoid serving as an expert witness for your patient. The intrusion of another role into the doctor/patient relationship can alter the treatment process and permanently color future inter actions. Likewise, treating an individual whom you previously evaluated for forensic purposes raises similar concerns, including the possibility of a mercenary motivation. Even when no such motivation exists, these situations can create the appearance that you have conscripted a vulnerable individual into your practice.

Emerging trends

Crossings vs violations. Efforts to distinguish when an action is unethical or illegal have led some to differentiate boundary crossings from boundary violations. Unfortunately, the 2 terms continue to be used synonymously, which confuses rather than clarifies the issue:

• Boundary crossings are aimed at enhancing the therapist’s treatment efforts—such as a hug instead of a hand shake at the end of a particularly difficult treatment session.
• Boundary violations are invariably harmful and unethical because they serve the therapist’s needs rather than the patient’s needs or the therapeutic process.²⁰

Rather than trying to differentiate between crossings and violations or to determine under what circumstances changing boundaries is acceptable, Sheets²¹ conceptualizes a boundary not as a line to cross, but as a continuum of behavior. Under-involvement is at one end, over-involvement at the other, and a “zone of helpfulness” is in the middle.

Glass uses a Venn diagram to illustrate that although most boundary crossings probably fall within the realm of ethical practice, gray areas alert therapists that they are approaching a violation (Figure).²⁰ Five factors have been found to increase psychiatrists’ vulnerability to boundary violations (Table 1).²²

Figure Beware the ‘gray areas’ between boundary crossings, violations
Source: Glass L. The gray areas of boundary crossings and violations. Am J Psychother 2003;57(4):429-44. Republished with permission of the Association for the Advancement of PsychotherapyTable 1

Boundary violations: Factors that increase your vulnerability

CASE CONTINUED: Board investigation

Dr. M’s relationship with Ms. Y grows intense, and he becomes increasingly concerned about her “clinginess.” After several months, Dr. M feels emotionally suffocated and ends the relationship. Despondent and suicidal, she seeks treatment in the local emergency room. Ms. Y tells the ER psychiatrist about her relationship with Dr. M and that she cannot go on without him in her life. The ER psychiatrist refers her to another psychiatrist for outpatient care, and, with Ms. Y’s permission, files a complaint about Dr. M with the state medical board and the district branch ethics committee.

The state medical board investigates Dr. M. He is contrite about his actions and their effect on Ms. Y. The state board refers Dr. M to an impaired physician’s program. He is required to attend a boundary violations course and undergo 1 year of practice supervision by a local psychiatrist. Several years later, Dr. M is doing well in his practice and has had no further complaints lodged against him.

Boundaries vs relationships. Using boundaries as a metaphor for maintaining the separation of therapist and patient was intended to serve the analytic process and to protect the patient’s welfare.² Clearly, certain boundaries—such as sexual contact between psychiatrist and patient—must remain sacrosanct. Yet certain practices avoided in analysis may be appropriate for other therapeutic interventions. For example, whereas psychoanalysis has strict prohibitions against seeing patients anywhere except in the office, cognitive-behavioral therapists may find it useful to conduct sessions in public, or—under carefully arranged circumstances—even in a patient’s home. Other examples include accompanying a patient with agoraphobia to a public gathering or dining with a patient with anorexia.

Exercise caution when you decide to alter traditional boundaries. Even minor crossings that are not likely to progress to violations have the potential to contaminate the therapeutic relationship and place the psychiatrist on a “slippery slope” to patient exploitation.^22,23 Some boundary issues are ambiguous, and extenuating circumstances can create a context that temporarily stretches a boundary beyond its normal limits,²⁴ especially in small communities and rural settings where patients and treating psychiatrists are likely to know and encounter each other in social settings.²⁵ Our recommendations for avoiding boundary violations appear in Table 2.

Except in clear cases of malfeasance, determining whether or not you have crossed a boundary is not a straightforward decision based on a single theoretical perspective or absolute standard.²⁶ Regardless of whether a given boundary’s edge is well defined, 2 things are clear:

• unlike patients, psychiatrists have a professional code to honor²⁷
• harm is determined by the meaning of the behavior to the patient and not the psychiatrist’s intentions.⁴

Table 2

Simple steps help avoid boundary violations

Related Resources

• American Medical Association. Principles of medical ethics. www.ama-assn.org/ama/pub/category/2512.html.
• American Psychiatric Association. The principles of medical ethics with annotations especially applicable to psychiatry. Washington, DC: American Psychiatric Association; 2008.

Disclosures

Drs. Marshall and Myers report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Teston is a speaker for Shire US, Inc.

Mr. W, a 53-year-old divorced entrepreneur, presents to you for evaluation of poor concentration, decreased self-esteem, and difficulty making decisions that are interfering with his work. A longtime patient of another psychiatrist, Mr. W has a 26-year history of bipolar I disorder. He has not had a manic episode for 5 years but has had several depressive episodes.

During his last manic episode, Mr. W was hospitalized with expansive and irritable mood, racing thoughts, impulsive sexual behavior, psychomotor agitation, elevated self-esteem, marked distractibility, and paranoid ideas about his business partners. His discharge regimen included lithium titrated to 0.9 mEq/L and divalproex sodium, 1,500 mg/d, with lamotrigine, 200 mg/d, added to reduce depressive relapse risk. After several years of stable treatment, Mr. W complained of cognitive impairment. His psychiatrist discontinued lithium and added a low-dose stimulant—methylphenidate, 20 mg bid—to address Mr. W’s complaints of poor concentration.

Mr. W also is taking zolpidem, 10 mg as needed for onset insomnia, and receives weekly psychodynamic psychotherapy. His work performance problems persist despite these treatments, and his company is failing.

A poor course in bipolar disorder—as in Mr. W’s case—is frequently characterized by persistent or relapsing depression. Bipolar disorder is diagnosed by a manic, mixed, or hypomanic episode, but depression and depressive symptoms are most prominent in clinical practice. Likewise, major observational studies blame depression for most of the time spent ill in bipolar types I and II.^1-8

A good deal of bipolar symptom burden is associated with subsyndromal depression—defined as having >2 but 5 and depressive symptoms are disproportionately responsible—compared with manic symptoms—for the impact of bipolar illness on patients and their families.⁹

This article offers clinically useful strategies to minimize subsyndromal depression in patients with bipolar disorder (Table 1). These strategies include an evidence-based approach to medication, the use of validated psychotherapies, regular sleep and socialization schedules, and careful monitoring of mood symptoms.

Table 1

How to minimize bipolar subsyndromal depression

Persistent depression

Randomized, controlled trials designed to obtain FDA approval of bipolar medications inadequately reflect the disabling, confounding nature of bipolar illness. Nearly all of these large studies of acute treatments for mood episodes are placebo-controlled trials with narrow inclusion and broad exclusion criteria. Eliminating subsyndromal symptoms is not their goal, and they are of little help in understanding how to manage residual symptoms.

A more realistic view of bipolar disorder comes from large observational studies that have examined its longitudinal course in outpatients under more or less ideal treatment conditions.¹⁰ These studies show that bipolar disorder is almost always recurrent and relapsing, but full recovery and functioning between episodes is not the norm. Most patients never achieve prolonged recovery, complete symptom relief, or return to full functioning.^5,8,11

STEP-BD. Most patients in the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) never recovered from a depressed episode during 2 years of prospective follow-up under optimal care. Only 58% of patients who entered the study during an episode of illness achieved 8 consecutive weeks of euthymia.⁵

Collaborative Depression study. Longitudinal data from the National Institute of Mental Health’s Collaborative Depression Study^6,7 showed:

• patients with bipolar I disorder had depressive symptoms in approximately three-quarters of the weeks in which they reported significant symptoms
  
• patients with bipolar II disorder were depressed in nearly all sick weeks.
  

The Stanley Foundation Bipolar Network had similar findings, with bipolar disorder patients reporting 3 times as much time spent with depressed mood as with elevated mood.⁸ Poor social and occupational functioning predicted poor outcomes, suggesting an interplay between subsyndromal depression, poor functioning, and relapse.

Risk factors

Rapid cycling may be a marker for persistent, subsyndromal symptoms. Rapid cycling is defined clinically as 4 distinct mood episodes—switching to the opposite pole or 2 episodes of the same pole separated by ≥8 weeks of partial or full recovery—in the previous 12 months. Rapid cycling usually is diagnosed retrospectively—introducing patients’ recall bias—but may be more of a marker for symptom persistence than for defined episodes.

In STEP-BD, 32% of study entrants reported ≥4 mood episodes in the previous year, yet only 6% of that subgroup had ≥4 episodes after 1 year of prospective follow-up.¹² This suggests:

• patients who retrospectively report rapid cycling may be chronically and persistently ill, rather than experiencing multiple discrete episodes
  
• rapid cycling is a marker for symptom persistence, subsyndromal depression, and lack of sustained remission.
  

• comorbid anxiety disorders (present in ≤50% of patients with bipolar I and II disorder)
  
• active and past substance use disorders (including nicotine dependence)
  
• early age of onset of the mood disorder.^13-16
  

CASE CONTINUED: Restoring the cornerstone

You review Mr. W’s records. Recent lab values were essentially normal, with thyroid stimulating hormone 2.3 mIU/mL and stable renal function. He scores 11 on the Quick Inventory of Depressive Symptoms–self-rated version (QIDS-SR), indicating mild to moderate depressive symptom burden.

His mood chart and interview reveal that he has been depressed and anhedonic most of the day for 4 of the last 10 days. By systematically asking the depression questions in the DSM-IV-TR, you find that he does not meet criteria for depressed mood or anhedonia but has difficulty concentrating most of the day, persistent low self-esteem, and feeling “slowed.”

After you discuss lithium’s pros and cons with Mr. W, he agrees to try this mood stabilizer again. You explain the importance of preventing relapse to mania and of monitoring his cognitive performance at work.

Over time, you titrate lithium to a moderate serum level (0.5 to 0.7 mEq/L) and treat a resulting mild tremor with propranolol, 20 to 40 mg/d. Mr. W is tolerating lamotrigine well, so you continue this medication because of its potential to decrease the probability of relapse to depression. You also continue zolpidem, as needed, but discontinue methylphenidate because you think it may be contributing to sleep difficulties.

Managing medication

Nine drugs are FDA-approved for acute bipolar mania, but treatments for bipolar depression, maintenance treatment, and relapse prevention are far fewer, often partially effective, or effective for a limited number of patients. When depressive symptoms fail to resolve, a reasonable approach is to review patients’ medications and suggest alternatives with proven efficacy for bipolar disorder (Table 2). Patients can then accept or reject various options based on personal preference.

Combination strategies. Antimanic treatment is the cornerstone of treating bipolar I disorder, and preventing manic episodes should be a primary treatment goal. Thus, consider continuing treatments that have prevented mania for your patient—as lithium did in Mr. W’s case—while adding treatments aimed at depression. For example, adding lamotrigine to any antimanic agent is reasonable, especially if doing so does not add substantially to your patient’s side-effect burden.

Minimize antidepressants. Given the predominance and persistence of depressive symptoms in bipolar disorder, one can understand why clinicians and patients might try standard antidepressants without clear evidence supporting this practice. Antidepressants—especially venlafaxine and tricyclic antidepressants—are the most common and likely suspects when patients experience switching to mania, rapid cycling, and symptom persistence.¹⁷ Antidepressants’ negative effect has not been clearly defined, however, and may be patient-specific (related to patient factors rather than intrinsic to the compound).

In my clinical experience, minimizing antidepressant use in bipolar depression hastens rather than delays patients’ recovery. A prudent approach would be to use the minimum dose necessary and discontinue the antidepressant if possible. Also minimize medical pharmacotherapies—including corticosteroids and oral contraceptives—that may worsen mood symptoms, especially in patients with this history.

Avoid under-dosing. Inadequate dosing and duration often are overlooked as causes of treatment resistance in bipolar disorder and other illnesses.¹⁸ Bipolar disorder medications are hardly benign; every drug approved for any phase of bipolar disorder has a black-box warning. Understandably, clinicians and patients try to choose medications and dosages perceived to be most tolerable. Full-dose treatment trials may be warranted, however, given the high probability of incomplete recovery, impaired functioning, and risk of relapse with ineffective dosing.

Address iatrogenic causes. In addition, identify and eliminate medications and treatments that may be perpetuating patients’ bipolar symptoms. Stimulants such as methylphenidate and amphetamines may contribute to sleep disturbance and manic relapse and might be minimized or eliminated in a patient with continued symptoms and sleep disturbance.¹⁹

• Two trials of aripiprazole for bipolar depression failed to show benefit.²⁰
  
• A trial that compared risperidone with lamotrigine and inositol for treatment-resistant bipolar depression suggested that risperidone may have hindered recovery.²¹
  

Table 2

Subsyndromal bipolar depression: Recommended medications*

CASE CONTINUED: Distressed by psychotherapy

You ask Mr. W about his psychodynamic psychotherapy, and he says that exploring his early life experiences and his work difficulty is increasing his anxiety. You recommend switching to cognitive-behavioral therapy (CBT) to work on delegating tasks that are not his strong areas and focusing on his marketing talents. You also encourage him to maintain regular sleep-wake cycles.

Some psychodynamic psychotherapies are thought to increase anxiety and mood instability in bipolar disorder patients. Examine the form and content of psychosocial approaches for their role in worsening your patients’ symptoms. As with medications, validated psychotherapeutic interventions—such as CBT for bipolar disorder, family-focused treatment, interpersonal social rhythm therapy, and long-term group psychotherapy^23,24—are preferred over those not specifically studied in bipolar disorder.

• Establish a social rhythm that includes a regularized sleep-wake cycle and predictable daily schedules, with planned contact with people and organized activities.
  
• Decrease behaviors associated with mood fluctuation, such as substance use, irregular hours of sleep, conflicts in relationships and work, poor adherence to medications, and lack of regard for physical health.
  

CASE CONTINUED: Changes for the better

After several months of CBT and medication changes, Mr. W is continuing to work and shows some symptom improvement. His QIDS-SR scores have decreased to 6, indicating minimal to mild depressive symptom burden. He reports that most weeks he has no depressive symptoms, but he remains unable to focus on specific tasks for long periods. He continues to have difficulties when his work requires detailed, intensive activities.

Mr. W has developed a new relationship but gives high priority to keeping a regular schedule. Before going to sleep most nights, he records his mood in a diary to monitor his progress.

Mr. W may show additional improvement in work performance with continued daily mood monitoring and a regularized routine. The care of most patients with bipolar disorder must be systematically optimized over years, not weeks or months.²⁶ Because medication adherence during well periods is essential, discuss and address adverse effects such as weight gain or urinary symptoms.

• minimize or eliminate ineffective and harmful treatments
  
• continue effective treatments, whether psychopharmacologic or psychosocial.
  

Tools for monitoring subsyndromal symptoms

• Otto M, Reilly-Harrington N, Kogan JN, Henin A. Managing bipolar disorder: a cognitive behavior treatment program therapist guide (treatments that work). Oxford, UK: Oxford University Press; 2008.
  
• Inventory of Depressive Symptomatology (IDS) and Quick Inventory of Depressive Symptomatology (QIDS). Validity, reliability, administration, and scoring. www.ids-qids.org.
  
• Bipolar Clinic and Research Program, Massachusetts General Hospital. Resources for clinicians and patients, plus links to information on bipolar disorder. www.manicdepressive.org.
  

• Aripiprazole • Abilify
  
• Carbamazepine • Tegretol
  
• Divalproex • Depakote
  
• Lamotrigine • Lamictal
  
• Lithium • various
  
• Methylphenidate • various
  
• Modafinil • Provigil
  
• Olanzapine • Zyprexa
  
• Olanzapine/fluoxetine • Symbyax
  
• Propranolol • Inderal
  
• Quetiapine • Seroquel
  
• Valproate • Depacon
  
• Venlafaxine • Effexor
  
• Zolpidem • Ambien
  

Dr. Ostacher is a speaker for AstraZeneca, Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, and Pfizer Inc.

Mr. W, a 53-year-old divorced entrepreneur, presents to you for evaluation of poor concentration, decreased self-esteem, and difficulty making decisions that are interfering with his work. A longtime patient of another psychiatrist, Mr. W has a 26-year history of bipolar I disorder. He has not had a manic episode for 5 years but has had several depressive episodes.

During his last manic episode, Mr. W was hospitalized with expansive and irritable mood, racing thoughts, impulsive sexual behavior, psychomotor agitation, elevated self-esteem, marked distractibility, and paranoid ideas about his business partners. His discharge regimen included lithium titrated to 0.9 mEq/L and divalproex sodium, 1,500 mg/d, with lamotrigine, 200 mg/d, added to reduce depressive relapse risk. After several years of stable treatment, Mr. W complained of cognitive impairment. His psychiatrist discontinued lithium and added a low-dose stimulant—methylphenidate, 20 mg bid—to address Mr. W’s complaints of poor concentration.

Mr. W also is taking zolpidem, 10 mg as needed for onset insomnia, and receives weekly psychodynamic psychotherapy. His work performance problems persist despite these treatments, and his company is failing.

A poor course in bipolar disorder—as in Mr. W’s case—is frequently characterized by persistent or relapsing depression. Bipolar disorder is diagnosed by a manic, mixed, or hypomanic episode, but depression and depressive symptoms are most prominent in clinical practice. Likewise, major observational studies blame depression for most of the time spent ill in bipolar types I and II.^1-8

A good deal of bipolar symptom burden is associated with subsyndromal depression—defined as having >2 but 5 and depressive symptoms are disproportionately responsible—compared with manic symptoms—for the impact of bipolar illness on patients and their families.⁹

This article offers clinically useful strategies to minimize subsyndromal depression in patients with bipolar disorder (Table 1). These strategies include an evidence-based approach to medication, the use of validated psychotherapies, regular sleep and socialization schedules, and careful monitoring of mood symptoms.

Table 1

How to minimize bipolar subsyndromal depression

Persistent depression

Randomized, controlled trials designed to obtain FDA approval of bipolar medications inadequately reflect the disabling, confounding nature of bipolar illness. Nearly all of these large studies of acute treatments for mood episodes are placebo-controlled trials with narrow inclusion and broad exclusion criteria. Eliminating subsyndromal symptoms is not their goal, and they are of little help in understanding how to manage residual symptoms.

A more realistic view of bipolar disorder comes from large observational studies that have examined its longitudinal course in outpatients under more or less ideal treatment conditions.¹⁰ These studies show that bipolar disorder is almost always recurrent and relapsing, but full recovery and functioning between episodes is not the norm. Most patients never achieve prolonged recovery, complete symptom relief, or return to full functioning.^5,8,11

STEP-BD. Most patients in the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) never recovered from a depressed episode during 2 years of prospective follow-up under optimal care. Only 58% of patients who entered the study during an episode of illness achieved 8 consecutive weeks of euthymia.⁵

Collaborative Depression study. Longitudinal data from the National Institute of Mental Health’s Collaborative Depression Study^6,7 showed:

• patients with bipolar I disorder had depressive symptoms in approximately three-quarters of the weeks in which they reported significant symptoms
  
• patients with bipolar II disorder were depressed in nearly all sick weeks.
  

The Stanley Foundation Bipolar Network had similar findings, with bipolar disorder patients reporting 3 times as much time spent with depressed mood as with elevated mood.⁸ Poor social and occupational functioning predicted poor outcomes, suggesting an interplay between subsyndromal depression, poor functioning, and relapse.

Risk factors

Rapid cycling may be a marker for persistent, subsyndromal symptoms. Rapid cycling is defined clinically as 4 distinct mood episodes—switching to the opposite pole or 2 episodes of the same pole separated by ≥8 weeks of partial or full recovery—in the previous 12 months. Rapid cycling usually is diagnosed retrospectively—introducing patients’ recall bias—but may be more of a marker for symptom persistence than for defined episodes.

In STEP-BD, 32% of study entrants reported ≥4 mood episodes in the previous year, yet only 6% of that subgroup had ≥4 episodes after 1 year of prospective follow-up.¹² This suggests:

• patients who retrospectively report rapid cycling may be chronically and persistently ill, rather than experiencing multiple discrete episodes
  
• rapid cycling is a marker for symptom persistence, subsyndromal depression, and lack of sustained remission.
  

• comorbid anxiety disorders (present in ≤50% of patients with bipolar I and II disorder)
  
• active and past substance use disorders (including nicotine dependence)
  
• early age of onset of the mood disorder.^13-16
  

CASE CONTINUED: Restoring the cornerstone

You review Mr. W’s records. Recent lab values were essentially normal, with thyroid stimulating hormone 2.3 mIU/mL and stable renal function. He scores 11 on the Quick Inventory of Depressive Symptoms–self-rated version (QIDS-SR), indicating mild to moderate depressive symptom burden.

His mood chart and interview reveal that he has been depressed and anhedonic most of the day for 4 of the last 10 days. By systematically asking the depression questions in the DSM-IV-TR, you find that he does not meet criteria for depressed mood or anhedonia but has difficulty concentrating most of the day, persistent low self-esteem, and feeling “slowed.”

After you discuss lithium’s pros and cons with Mr. W, he agrees to try this mood stabilizer again. You explain the importance of preventing relapse to mania and of monitoring his cognitive performance at work.

Over time, you titrate lithium to a moderate serum level (0.5 to 0.7 mEq/L) and treat a resulting mild tremor with propranolol, 20 to 40 mg/d. Mr. W is tolerating lamotrigine well, so you continue this medication because of its potential to decrease the probability of relapse to depression. You also continue zolpidem, as needed, but discontinue methylphenidate because you think it may be contributing to sleep difficulties.

Managing medication

Nine drugs are FDA-approved for acute bipolar mania, but treatments for bipolar depression, maintenance treatment, and relapse prevention are far fewer, often partially effective, or effective for a limited number of patients. When depressive symptoms fail to resolve, a reasonable approach is to review patients’ medications and suggest alternatives with proven efficacy for bipolar disorder (Table 2). Patients can then accept or reject various options based on personal preference.

Combination strategies. Antimanic treatment is the cornerstone of treating bipolar I disorder, and preventing manic episodes should be a primary treatment goal. Thus, consider continuing treatments that have prevented mania for your patient—as lithium did in Mr. W’s case—while adding treatments aimed at depression. For example, adding lamotrigine to any antimanic agent is reasonable, especially if doing so does not add substantially to your patient’s side-effect burden.

Minimize antidepressants. Given the predominance and persistence of depressive symptoms in bipolar disorder, one can understand why clinicians and patients might try standard antidepressants without clear evidence supporting this practice. Antidepressants—especially venlafaxine and tricyclic antidepressants—are the most common and likely suspects when patients experience switching to mania, rapid cycling, and symptom persistence.¹⁷ Antidepressants’ negative effect has not been clearly defined, however, and may be patient-specific (related to patient factors rather than intrinsic to the compound).

In my clinical experience, minimizing antidepressant use in bipolar depression hastens rather than delays patients’ recovery. A prudent approach would be to use the minimum dose necessary and discontinue the antidepressant if possible. Also minimize medical pharmacotherapies—including corticosteroids and oral contraceptives—that may worsen mood symptoms, especially in patients with this history.

Avoid under-dosing. Inadequate dosing and duration often are overlooked as causes of treatment resistance in bipolar disorder and other illnesses.¹⁸ Bipolar disorder medications are hardly benign; every drug approved for any phase of bipolar disorder has a black-box warning. Understandably, clinicians and patients try to choose medications and dosages perceived to be most tolerable. Full-dose treatment trials may be warranted, however, given the high probability of incomplete recovery, impaired functioning, and risk of relapse with ineffective dosing.

Address iatrogenic causes. In addition, identify and eliminate medications and treatments that may be perpetuating patients’ bipolar symptoms. Stimulants such as methylphenidate and amphetamines may contribute to sleep disturbance and manic relapse and might be minimized or eliminated in a patient with continued symptoms and sleep disturbance.¹⁹

• Two trials of aripiprazole for bipolar depression failed to show benefit.²⁰
  
• A trial that compared risperidone with lamotrigine and inositol for treatment-resistant bipolar depression suggested that risperidone may have hindered recovery.²¹
  

Table 2

Subsyndromal bipolar depression: Recommended medications*

CASE CONTINUED: Distressed by psychotherapy

You ask Mr. W about his psychodynamic psychotherapy, and he says that exploring his early life experiences and his work difficulty is increasing his anxiety. You recommend switching to cognitive-behavioral therapy (CBT) to work on delegating tasks that are not his strong areas and focusing on his marketing talents. You also encourage him to maintain regular sleep-wake cycles.

Some psychodynamic psychotherapies are thought to increase anxiety and mood instability in bipolar disorder patients. Examine the form and content of psychosocial approaches for their role in worsening your patients’ symptoms. As with medications, validated psychotherapeutic interventions—such as CBT for bipolar disorder, family-focused treatment, interpersonal social rhythm therapy, and long-term group psychotherapy^23,24—are preferred over those not specifically studied in bipolar disorder.

• Establish a social rhythm that includes a regularized sleep-wake cycle and predictable daily schedules, with planned contact with people and organized activities.
  
• Decrease behaviors associated with mood fluctuation, such as substance use, irregular hours of sleep, conflicts in relationships and work, poor adherence to medications, and lack of regard for physical health.
  

CASE CONTINUED: Changes for the better

After several months of CBT and medication changes, Mr. W is continuing to work and shows some symptom improvement. His QIDS-SR scores have decreased to 6, indicating minimal to mild depressive symptom burden. He reports that most weeks he has no depressive symptoms, but he remains unable to focus on specific tasks for long periods. He continues to have difficulties when his work requires detailed, intensive activities.

Mr. W has developed a new relationship but gives high priority to keeping a regular schedule. Before going to sleep most nights, he records his mood in a diary to monitor his progress.

Mr. W may show additional improvement in work performance with continued daily mood monitoring and a regularized routine. The care of most patients with bipolar disorder must be systematically optimized over years, not weeks or months.²⁶ Because medication adherence during well periods is essential, discuss and address adverse effects such as weight gain or urinary symptoms.

• minimize or eliminate ineffective and harmful treatments
  
• continue effective treatments, whether psychopharmacologic or psychosocial.
  

Tools for monitoring subsyndromal symptoms

• Otto M, Reilly-Harrington N, Kogan JN, Henin A. Managing bipolar disorder: a cognitive behavior treatment program therapist guide (treatments that work). Oxford, UK: Oxford University Press; 2008.
  
• Inventory of Depressive Symptomatology (IDS) and Quick Inventory of Depressive Symptomatology (QIDS). Validity, reliability, administration, and scoring. www.ids-qids.org.
  
• Bipolar Clinic and Research Program, Massachusetts General Hospital. Resources for clinicians and patients, plus links to information on bipolar disorder. www.manicdepressive.org.
  

• Aripiprazole • Abilify
  
• Carbamazepine • Tegretol
  
• Divalproex • Depakote
  
• Lamotrigine • Lamictal
  
• Lithium • various
  
• Methylphenidate • various
  
• Modafinil • Provigil
  
• Olanzapine • Zyprexa
  
• Olanzapine/fluoxetine • Symbyax
  
• Propranolol • Inderal
  
• Quetiapine • Seroquel
  
• Valproate • Depacon
  
• Venlafaxine • Effexor
  
• Zolpidem • Ambien
  

Dr. Ostacher is a speaker for AstraZeneca, Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, and Pfizer Inc.

Mr. W, a 53-year-old divorced entrepreneur, presents to you for evaluation of poor concentration, decreased self-esteem, and difficulty making decisions that are interfering with his work. A longtime patient of another psychiatrist, Mr. W has a 26-year history of bipolar I disorder. He has not had a manic episode for 5 years but has had several depressive episodes.

During his last manic episode, Mr. W was hospitalized with expansive and irritable mood, racing thoughts, impulsive sexual behavior, psychomotor agitation, elevated self-esteem, marked distractibility, and paranoid ideas about his business partners. His discharge regimen included lithium titrated to 0.9 mEq/L and divalproex sodium, 1,500 mg/d, with lamotrigine, 200 mg/d, added to reduce depressive relapse risk. After several years of stable treatment, Mr. W complained of cognitive impairment. His psychiatrist discontinued lithium and added a low-dose stimulant—methylphenidate, 20 mg bid—to address Mr. W’s complaints of poor concentration.

Mr. W also is taking zolpidem, 10 mg as needed for onset insomnia, and receives weekly psychodynamic psychotherapy. His work performance problems persist despite these treatments, and his company is failing.

A poor course in bipolar disorder—as in Mr. W’s case—is frequently characterized by persistent or relapsing depression. Bipolar disorder is diagnosed by a manic, mixed, or hypomanic episode, but depression and depressive symptoms are most prominent in clinical practice. Likewise, major observational studies blame depression for most of the time spent ill in bipolar types I and II.^1-8

A good deal of bipolar symptom burden is associated with subsyndromal depression—defined as having >2 but 5 and depressive symptoms are disproportionately responsible—compared with manic symptoms—for the impact of bipolar illness on patients and their families.⁹

This article offers clinically useful strategies to minimize subsyndromal depression in patients with bipolar disorder (Table 1). These strategies include an evidence-based approach to medication, the use of validated psychotherapies, regular sleep and socialization schedules, and careful monitoring of mood symptoms.

Table 1

How to minimize bipolar subsyndromal depression

Persistent depression

Randomized, controlled trials designed to obtain FDA approval of bipolar medications inadequately reflect the disabling, confounding nature of bipolar illness. Nearly all of these large studies of acute treatments for mood episodes are placebo-controlled trials with narrow inclusion and broad exclusion criteria. Eliminating subsyndromal symptoms is not their goal, and they are of little help in understanding how to manage residual symptoms.

A more realistic view of bipolar disorder comes from large observational studies that have examined its longitudinal course in outpatients under more or less ideal treatment conditions.¹⁰ These studies show that bipolar disorder is almost always recurrent and relapsing, but full recovery and functioning between episodes is not the norm. Most patients never achieve prolonged recovery, complete symptom relief, or return to full functioning.^5,8,11

STEP-BD. Most patients in the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) never recovered from a depressed episode during 2 years of prospective follow-up under optimal care. Only 58% of patients who entered the study during an episode of illness achieved 8 consecutive weeks of euthymia.⁵

Collaborative Depression study. Longitudinal data from the National Institute of Mental Health’s Collaborative Depression Study^6,7 showed:

• patients with bipolar I disorder had depressive symptoms in approximately three-quarters of the weeks in which they reported significant symptoms
  
• patients with bipolar II disorder were depressed in nearly all sick weeks.
  

The Stanley Foundation Bipolar Network had similar findings, with bipolar disorder patients reporting 3 times as much time spent with depressed mood as with elevated mood.⁸ Poor social and occupational functioning predicted poor outcomes, suggesting an interplay between subsyndromal depression, poor functioning, and relapse.

Risk factors

Rapid cycling may be a marker for persistent, subsyndromal symptoms. Rapid cycling is defined clinically as 4 distinct mood episodes—switching to the opposite pole or 2 episodes of the same pole separated by ≥8 weeks of partial or full recovery—in the previous 12 months. Rapid cycling usually is diagnosed retrospectively—introducing patients’ recall bias—but may be more of a marker for symptom persistence than for defined episodes.

In STEP-BD, 32% of study entrants reported ≥4 mood episodes in the previous year, yet only 6% of that subgroup had ≥4 episodes after 1 year of prospective follow-up.¹² This suggests:

• patients who retrospectively report rapid cycling may be chronically and persistently ill, rather than experiencing multiple discrete episodes
  
• rapid cycling is a marker for symptom persistence, subsyndromal depression, and lack of sustained remission.
  

• comorbid anxiety disorders (present in ≤50% of patients with bipolar I and II disorder)
  
• active and past substance use disorders (including nicotine dependence)
  
• early age of onset of the mood disorder.^13-16
  

CASE CONTINUED: Restoring the cornerstone

You review Mr. W’s records. Recent lab values were essentially normal, with thyroid stimulating hormone 2.3 mIU/mL and stable renal function. He scores 11 on the Quick Inventory of Depressive Symptoms–self-rated version (QIDS-SR), indicating mild to moderate depressive symptom burden.

His mood chart and interview reveal that he has been depressed and anhedonic most of the day for 4 of the last 10 days. By systematically asking the depression questions in the DSM-IV-TR, you find that he does not meet criteria for depressed mood or anhedonia but has difficulty concentrating most of the day, persistent low self-esteem, and feeling “slowed.”

After you discuss lithium’s pros and cons with Mr. W, he agrees to try this mood stabilizer again. You explain the importance of preventing relapse to mania and of monitoring his cognitive performance at work.

Over time, you titrate lithium to a moderate serum level (0.5 to 0.7 mEq/L) and treat a resulting mild tremor with propranolol, 20 to 40 mg/d. Mr. W is tolerating lamotrigine well, so you continue this medication because of its potential to decrease the probability of relapse to depression. You also continue zolpidem, as needed, but discontinue methylphenidate because you think it may be contributing to sleep difficulties.

Managing medication

Nine drugs are FDA-approved for acute bipolar mania, but treatments for bipolar depression, maintenance treatment, and relapse prevention are far fewer, often partially effective, or effective for a limited number of patients. When depressive symptoms fail to resolve, a reasonable approach is to review patients’ medications and suggest alternatives with proven efficacy for bipolar disorder (Table 2). Patients can then accept or reject various options based on personal preference.

Combination strategies. Antimanic treatment is the cornerstone of treating bipolar I disorder, and preventing manic episodes should be a primary treatment goal. Thus, consider continuing treatments that have prevented mania for your patient—as lithium did in Mr. W’s case—while adding treatments aimed at depression. For example, adding lamotrigine to any antimanic agent is reasonable, especially if doing so does not add substantially to your patient’s side-effect burden.

Minimize antidepressants. Given the predominance and persistence of depressive symptoms in bipolar disorder, one can understand why clinicians and patients might try standard antidepressants without clear evidence supporting this practice. Antidepressants—especially venlafaxine and tricyclic antidepressants—are the most common and likely suspects when patients experience switching to mania, rapid cycling, and symptom persistence.¹⁷ Antidepressants’ negative effect has not been clearly defined, however, and may be patient-specific (related to patient factors rather than intrinsic to the compound).

In my clinical experience, minimizing antidepressant use in bipolar depression hastens rather than delays patients’ recovery. A prudent approach would be to use the minimum dose necessary and discontinue the antidepressant if possible. Also minimize medical pharmacotherapies—including corticosteroids and oral contraceptives—that may worsen mood symptoms, especially in patients with this history.

Avoid under-dosing. Inadequate dosing and duration often are overlooked as causes of treatment resistance in bipolar disorder and other illnesses.¹⁸ Bipolar disorder medications are hardly benign; every drug approved for any phase of bipolar disorder has a black-box warning. Understandably, clinicians and patients try to choose medications and dosages perceived to be most tolerable. Full-dose treatment trials may be warranted, however, given the high probability of incomplete recovery, impaired functioning, and risk of relapse with ineffective dosing.

Address iatrogenic causes. In addition, identify and eliminate medications and treatments that may be perpetuating patients’ bipolar symptoms. Stimulants such as methylphenidate and amphetamines may contribute to sleep disturbance and manic relapse and might be minimized or eliminated in a patient with continued symptoms and sleep disturbance.¹⁹

• Two trials of aripiprazole for bipolar depression failed to show benefit.²⁰
  
• A trial that compared risperidone with lamotrigine and inositol for treatment-resistant bipolar depression suggested that risperidone may have hindered recovery.²¹
  

Table 2

Subsyndromal bipolar depression: Recommended medications*

CASE CONTINUED: Distressed by psychotherapy

You ask Mr. W about his psychodynamic psychotherapy, and he says that exploring his early life experiences and his work difficulty is increasing his anxiety. You recommend switching to cognitive-behavioral therapy (CBT) to work on delegating tasks that are not his strong areas and focusing on his marketing talents. You also encourage him to maintain regular sleep-wake cycles.

Some psychodynamic psychotherapies are thought to increase anxiety and mood instability in bipolar disorder patients. Examine the form and content of psychosocial approaches for their role in worsening your patients’ symptoms. As with medications, validated psychotherapeutic interventions—such as CBT for bipolar disorder, family-focused treatment, interpersonal social rhythm therapy, and long-term group psychotherapy^23,24—are preferred over those not specifically studied in bipolar disorder.

• Establish a social rhythm that includes a regularized sleep-wake cycle and predictable daily schedules, with planned contact with people and organized activities.
  
• Decrease behaviors associated with mood fluctuation, such as substance use, irregular hours of sleep, conflicts in relationships and work, poor adherence to medications, and lack of regard for physical health.
  

CASE CONTINUED: Changes for the better

After several months of CBT and medication changes, Mr. W is continuing to work and shows some symptom improvement. His QIDS-SR scores have decreased to 6, indicating minimal to mild depressive symptom burden. He reports that most weeks he has no depressive symptoms, but he remains unable to focus on specific tasks for long periods. He continues to have difficulties when his work requires detailed, intensive activities.

Mr. W has developed a new relationship but gives high priority to keeping a regular schedule. Before going to sleep most nights, he records his mood in a diary to monitor his progress.

Mr. W may show additional improvement in work performance with continued daily mood monitoring and a regularized routine. The care of most patients with bipolar disorder must be systematically optimized over years, not weeks or months.²⁶ Because medication adherence during well periods is essential, discuss and address adverse effects such as weight gain or urinary symptoms.

• minimize or eliminate ineffective and harmful treatments
  
• continue effective treatments, whether psychopharmacologic or psychosocial.
  

Tools for monitoring subsyndromal symptoms

• Otto M, Reilly-Harrington N, Kogan JN, Henin A. Managing bipolar disorder: a cognitive behavior treatment program therapist guide (treatments that work). Oxford, UK: Oxford University Press; 2008.
  
• Inventory of Depressive Symptomatology (IDS) and Quick Inventory of Depressive Symptomatology (QIDS). Validity, reliability, administration, and scoring. www.ids-qids.org.
  
• Bipolar Clinic and Research Program, Massachusetts General Hospital. Resources for clinicians and patients, plus links to information on bipolar disorder. www.manicdepressive.org.
  

• Aripiprazole • Abilify
  
• Carbamazepine • Tegretol
  
• Divalproex • Depakote
  
• Lamotrigine • Lamictal
  
• Lithium • various
  
• Methylphenidate • various
  
• Modafinil • Provigil
  
• Olanzapine • Zyprexa
  
• Olanzapine/fluoxetine • Symbyax
  
• Propranolol • Inderal
  
• Quetiapine • Seroquel
  
• Valproate • Depacon
  
• Venlafaxine • Effexor
  
• Zolpidem • Ambien
  

Dr. Ostacher is a speaker for AstraZeneca, Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, and Pfizer Inc.

Mrs. A, age 50, reports recurrent headaches and neck pain from a motor vehicle accident in 1999. At the time, MRI revealed degenerative changes at the C5-C6 vertebrae without bony stenosis or spinal injury. Treatment consisted of conservative measures and physical therapy; she was not a candidate for surgical intervention.

Although Mrs. A can manage activities of daily living, pain prevents her from pastimes she previously enjoyed, including painting and pottery, and is causing problems in her marriage.

Mrs. A’s pain became much worse approximately 1 year ago. In the past year, its severity has lead to multiple clinical presentations and consultations. She uses transdermal fentanyl, 75 mcg/hr every 72 hours, and acetaminophen/ hydrocodone, 5 mg/500 mg every 4 hours up to 6 times a day for breakthrough pain. Even so, she still rates her pain as 7 on a 10-point scale.

Pain is a complex perception with psychological and sensory components. It is the most common reason patients seek treatment at ambulatory medical settings.¹ Most pain remits spontaneously or responds to simple treatment, but up to 25% of symptoms remain chronic.¹

Chronic pain—defined as pain at ≥1 anatomic sites for ≥6 months—can substantially impair adaptation and vocational and interpersonal functioning. Treatments that focus solely on analgesics are shortsighted and often of limited benefit. Patients with chronic pain need a rehabilitative approach that incorporates psychiatric and psychological intervention.

Complex chronic pain

Most individuals with chronic pain can maintain basic functioning, work, relationships, and interests. They work with healthcare providers and obtain relief from medications or other interventions.

Some, however, are preoccupied with—and entirely debilitated by—their pain. For them, life revolves around the pain and perceived disability. Many if not all aspects of this patient’s life are contingent on pain and fears it might worsen.² Preoccupation with pain can profoundly affect social activities and prevent employment. The patient may become dependent on others, and being a patient can become a primary psychosocial state. A chronic pain patient also may become increasingly preoccupied with medication use and possibly abuse.

• a general medical condition
  
• psychological factors
  
• both.
  

Pain disorder criteria often are perceived as insufficiently operationalized—there is no checklist of symptoms that collectively define the syndrome.^5,6 The clinician must infer whether—and to what extent—psychological factors are involved in the pain.⁵ There are no guidelines to help psychiatrists ascertain whether psychological factors “have an important role” in pain (criteria C) or if pain is “not better accounted for” by a mood disorder (criteria E).⁶ This distinction can be indecipherable because of frequent comorbidity of mood disturbances with pain.^7,8 Some clinicians have suggested that pain disorder be removed from the somato-form disorder classification and instead confined to Axis III.⁹

Table 1

DSM-IV-TR diagnostic criteria for pain disorder

What are the risk factors?

Psychological and social covariates play a substantial role in the chronic pain experience (Table 2). How patients experience chronic pain also is influenced by personality and premorbid, semi-dormant characteristics that become activated by the stress of unremitting pain.⁷

• mood
  
• thought patterns
  
• perceptions
  
• coping abilities
  
• personality.
  

Table 2

Patient factors that contribute to or perpetuate chronic pain

CASE CONTINUED: Underlying causes

Psychological and psychosocial factors appear to play an important role in Mrs. A’s pain. After her husband’s job was restructured, the couple moved away from Mrs. A’s mother, which she found distressing. Additionally, Mrs. A reports that her son has incurred substantial gambling debt.

Mrs. A admits she has “a hard time” accepting these events, but she cannot acknowledge anger or frustration. She avoids questions about such feelings and focuses on her pain. She reports, “The pain is always there and ruins my entire life. Absolutely nothing gives me relief.”

She does not endorse depressive or psychotic symptoms. She sometimes has passive thoughts of death when she feels hopeless about her persistent pain, but she vehemently denies suicidal ideas, intent, or plans. She has smoked 1 pack of cigarettes per day for 12 years but denies alcohol abuse or use of illicit substances.

Biopsychosocial assessment

Assessing a chronic pain patient includes evaluating somatic, psychological, and social factors (Table 3).³ A biopsychosocial approach recognizes that the patient’s experience of pain, presentation, and response to treatment are determined by the interaction of:

• biological factors
  
• the patient’s psychological makeup
  
• psychological comorbidities
  
• the extent of social support
  
• extenuating environmental circumstances.^3,10
  

Subsyndromal psychological factors—such as troubling affective states, problematic cognitive styles,¹⁴ and ineffective coping strategies and interpersonal skills—can accompany pain. If unattended, such factors can heighten the patient’s pain awareness and compromise rehabilitation.

For example, patients such as Mrs. A can aggravate pain by catastrophizing.¹⁵ Having a tendency to exaggerate pain and the significance of related life events interferes with their ability to attend to matters within their control and pursue productive activities.¹⁶ Catastrophizing is associated with increased pain and perceived disability, poor adjustment to pain, and marked emotional distress.^17,18

How pain shapes beliefs. Pain can shape the manner with which patients make sense of events in their lives by altering the way they perceive themselves and the world. Problematic beliefs of the self (inadequacy and helplessness), of the world (dangerousness), and of the future (hopelessness) can produce significant distress. A patient with such beliefs may experience a loss of self-esteem, self-efficacy, and connections with others and may experience marked disappointment and disillusionment.

• substance abuse
  
• nonadherence with treatment
  
• withdrawal from support systems
  
• incapacitating emotional states, such as marked dysphoria, anger, or anxiety.
  

Table 3

Biopsychosocial assessment of chronic pain patients: 3 components

CASE CONTINUED: Multifaceted treatment

You prescribe amitriptyline, 20 mg at bed-time, for pain and refer Mrs. A for cognitive-behavioral therapy (CBT). The emphasis of therapy is to identify affective states and cognitive distortions that are temporally related to pain exacerbations, to develop coping skills to deal with stressors, and to effectively express her anger. Mrs. A learns relaxation techniques and self-hypnosis to reduce distress. These measures help reduce her pain severity ratings to 3 on a 10-point scale. She also participates in physical therapy and yoga classes, which increase her endurance.

Psychiatrists’ role in treatment

Many chronic nonmalignant pain syndromes—including arthritic conditions, back pain, and fibromyalgia—are tenacious and not easily cured. Treatment goals are to relieve pain and maximize the patient’s functioning and quality of life while minimizing risks of iatrogenic harm. As part of a biopsychosocial approach to care:

• diagnose and treat psychiatric comorbidities
  
• assess responses to treatment interventions
  
• refine treatment measures when patients do not achieve functional and adaptational goals
  
• initiate pharmacologic interventions for pain
  
• address subsyndromal emotional and cognitive impediments to functional restoration.
  

In initial CBT sessions, the goal is to elicit the patient’s:

• perception of pain
  
• life situations
  
• beliefs about his or her life, relationships, and the future
  
• coping measures.
  

Self-regulatory techniques—including relaxation training, biofeedback, and hypnosis—can facilitate relaxation and “turn down” the physiologic triggers that cause and perpetuate pain.^25,26 Hypnosis can lead to dissociative states that modify how a patient experiences pain. There is modest evidence that self-regulatory techniques are effective for treating pain.^27,28

Pharmacotherapy. Multiple pathophysiologic mechanisms—including ion channel up-regulation, spinal hyperexcitability, and descending neurotransmitter pathway impairment—play a role in chronic pain states. Several classes of psychoactive agents can mitigate pain (Table 4), and some psychotropics are FDA-approved for specific pain conditions (Table 5).

Individualize medication selection, considering:

• cost
  
• ease of use
  
• tolerability
  
• interactions with coadministered medications
  
• clinical comorbidities.
  

• opioid therapy fails
  
• patients become dependent on escalating doses of opioids.
  

Antidepressants influence pain by blocking monoamine reuptake. Those that influence noradrenergic and serotonergic transmission may have greater analgesic effects than those that affect serotonin or norepinephrine reuptake alone.^31-33

Anticonvulsants mitigate pain by influencing sodium or calcium channel regulation, GABA activity, or combinations of the 3.

In randomized controlled trials that included patients with diabetic and postherpetic neuropathies:

• one-third of patients achieved ≥50% pain relief with tricyclic antidepressants (TCAs) or anticonvulsants
  
• adverse effects were slightly more common with TCAs.^34,35
  

Because antidepressants and anticonvulsants have different presumed mechanisms of action for pain relief, anticonvulsants might be useful for patients whose pain persists despite optimal antidepressant dosing or for whom antidepressants are in-tolerable. Alternately, coadministering antidepressants and anticonvulsants might capitalize on complimentary mechanisms of action. With coadministration, lower doses may be sufficiently analgesic and avoid adverse effects.

Benzodiazepines have been used short-term to mitigate muscle spasm pain as in fibromyalgia, phantom limb pain, and restless legs syndrome.^36,37 Long-term benzodiazepine use can lead to low activity levels, high use of ambulatory medical services, and high disability levels, however.³⁸ if required for muscle spasm or restless legs syndrome, benzodiazepines may best be confined to short-term use.

Antipsychotics. Limited studies have evaluated antipsychotics’ efficacy for chronic pain.^39,40 Some have been found to be useful in neuropathic pain.⁴⁰ Antipsychotics are seldom used to treat pain because of limited efficacy data, potential side effects, and an abundance of alternate agents. Because risks—most notably extrapyramidal side effects and tardive dyskinesia—appear to outweigh analgesic efficacy, I would confine antipsychotics to pain patients with delirium or psychosis. Antipsychotics’ potential role in treating refractory pain might warrant further investigation.⁴⁰

Stimulants may reduce sedation, dysphoria, and cognitive inefficiency that can accompany opioid use.

Table 4

Uses of psychotropics in patients with chronic pain

Psychotropics approved for managing pain

• International Association for the Study of Pain. www.iasp-pain.org.
  
• Leo RJ. Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing; 2007.
  
• Loeser JD, Butler SH, Chapman CR, Turk DC. Bonica’s management of pain. 3rd ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2001.
  

• Acetaminophen/hydrocodone • Lortab, others
  
• Amitriptyline • Elavil, Endep
  
• Carbamazepine • Tegretol
  
• Divalproex • Depakote
  
• Duloxetine • Cymbalta
  
• Fentanyl transdermal • Duragesic
  
• Gabapentin • Neurontin
  
• Lithium • Eskalith, Lithobid
  
• Pregabalin • Lyrica
  

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

Mrs. A, age 50, reports recurrent headaches and neck pain from a motor vehicle accident in 1999. At the time, MRI revealed degenerative changes at the C5-C6 vertebrae without bony stenosis or spinal injury. Treatment consisted of conservative measures and physical therapy; she was not a candidate for surgical intervention.

Although Mrs. A can manage activities of daily living, pain prevents her from pastimes she previously enjoyed, including painting and pottery, and is causing problems in her marriage.

Mrs. A’s pain became much worse approximately 1 year ago. In the past year, its severity has lead to multiple clinical presentations and consultations. She uses transdermal fentanyl, 75 mcg/hr every 72 hours, and acetaminophen/ hydrocodone, 5 mg/500 mg every 4 hours up to 6 times a day for breakthrough pain. Even so, she still rates her pain as 7 on a 10-point scale.

Pain is a complex perception with psychological and sensory components. It is the most common reason patients seek treatment at ambulatory medical settings.¹ Most pain remits spontaneously or responds to simple treatment, but up to 25% of symptoms remain chronic.¹

Chronic pain—defined as pain at ≥1 anatomic sites for ≥6 months—can substantially impair adaptation and vocational and interpersonal functioning. Treatments that focus solely on analgesics are shortsighted and often of limited benefit. Patients with chronic pain need a rehabilitative approach that incorporates psychiatric and psychological intervention.

Complex chronic pain

Most individuals with chronic pain can maintain basic functioning, work, relationships, and interests. They work with healthcare providers and obtain relief from medications or other interventions.

Some, however, are preoccupied with—and entirely debilitated by—their pain. For them, life revolves around the pain and perceived disability. Many if not all aspects of this patient’s life are contingent on pain and fears it might worsen.² Preoccupation with pain can profoundly affect social activities and prevent employment. The patient may become dependent on others, and being a patient can become a primary psychosocial state. A chronic pain patient also may become increasingly preoccupied with medication use and possibly abuse.

• a general medical condition
  
• psychological factors
  
• both.
  

Pain disorder criteria often are perceived as insufficiently operationalized—there is no checklist of symptoms that collectively define the syndrome.^5,6 The clinician must infer whether—and to what extent—psychological factors are involved in the pain.⁵ There are no guidelines to help psychiatrists ascertain whether psychological factors “have an important role” in pain (criteria C) or if pain is “not better accounted for” by a mood disorder (criteria E).⁶ This distinction can be indecipherable because of frequent comorbidity of mood disturbances with pain.^7,8 Some clinicians have suggested that pain disorder be removed from the somato-form disorder classification and instead confined to Axis III.⁹

Table 1

DSM-IV-TR diagnostic criteria for pain disorder

What are the risk factors?

Psychological and social covariates play a substantial role in the chronic pain experience (Table 2). How patients experience chronic pain also is influenced by personality and premorbid, semi-dormant characteristics that become activated by the stress of unremitting pain.⁷

• mood
  
• thought patterns
  
• perceptions
  
• coping abilities
  
• personality.
  

Table 2

Patient factors that contribute to or perpetuate chronic pain

CASE CONTINUED: Underlying causes

Psychological and psychosocial factors appear to play an important role in Mrs. A’s pain. After her husband’s job was restructured, the couple moved away from Mrs. A’s mother, which she found distressing. Additionally, Mrs. A reports that her son has incurred substantial gambling debt.

Mrs. A admits she has “a hard time” accepting these events, but she cannot acknowledge anger or frustration. She avoids questions about such feelings and focuses on her pain. She reports, “The pain is always there and ruins my entire life. Absolutely nothing gives me relief.”

She does not endorse depressive or psychotic symptoms. She sometimes has passive thoughts of death when she feels hopeless about her persistent pain, but she vehemently denies suicidal ideas, intent, or plans. She has smoked 1 pack of cigarettes per day for 12 years but denies alcohol abuse or use of illicit substances.

Biopsychosocial assessment

Assessing a chronic pain patient includes evaluating somatic, psychological, and social factors (Table 3).³ A biopsychosocial approach recognizes that the patient’s experience of pain, presentation, and response to treatment are determined by the interaction of:

• biological factors
  
• the patient’s psychological makeup
  
• psychological comorbidities
  
• the extent of social support
  
• extenuating environmental circumstances.^3,10
  

Subsyndromal psychological factors—such as troubling affective states, problematic cognitive styles,¹⁴ and ineffective coping strategies and interpersonal skills—can accompany pain. If unattended, such factors can heighten the patient’s pain awareness and compromise rehabilitation.

For example, patients such as Mrs. A can aggravate pain by catastrophizing.¹⁵ Having a tendency to exaggerate pain and the significance of related life events interferes with their ability to attend to matters within their control and pursue productive activities.¹⁶ Catastrophizing is associated with increased pain and perceived disability, poor adjustment to pain, and marked emotional distress.^17,18