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What to do when a patient makes you angry

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Improve sleep with group CBT for insomnia

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Cognitive-behavioral therapy for insomnia (CBT-I) can be effective, regardless of whether chronic insomnia is primary or secondary to psychiatric, substance dependence, or psychophysiologic causes.1 In fact, with a response rate of 70% to 80%,2 CBT-I can be as effective as medication in the short term and even more effective in the long term.3

Delivered in 4 to 10 sessions, CBT-I typically includes assessment and monitoring of insomnia and sleep patterns, sleep restriction, stimulus control, sleep hygiene education, relaxation training, cognitive therapy, and relapse prevention. Goals are to:

  • decrease the time spent awake in bed, thereby increasing sleep efficiency
  • strengthen the association between the bedroom and sleep
  • address maladaptive sleep habits and lifestyle factors that affect sleep
  • remove extraneous stimuli from the bedroom.

Group therapy with CBT-I

At our clinic, we have modified standard CBT-I techniques into a group format that includes patients with other sleep disorders, medical conditions, or psychiatric diagnoses. Also, CBT-I can benefit mentally ill out-patients with persistent secondary insomnia despite adequate hypnotic dosages.

Challenges to a CBT-I format include: member dropout, inconsistent attendance, disparate psychiatric diagnoses, and different forms of insomnia. In addition, motivating patients to change poor sleep habits that have been in place for decades can be difficult. Finally, CBT-I—although simple in concept—can be difficult to employ, particularly the behavioral components of stimulus control and sleep restriction. Many patients resist these behavioral interventions because they do not experience relief in the short term. Because improved sleep quality frequently is experienced toward the end of treatment, patient motivation and consistency are crucial for success.

For optimal results when leading group CBT-I, be consistent when teaching skills, checking homework, and gaining treatment compliance. Educate patients about CBT-I principles, and help them understand the rationale for what may seem like counterintuitive treatments, such as decreasing time spent in bed. Inform patients that they must practice these skills consistently and stick with the protocol until treatment ends. When patients know the treatment is time-limited and see others in the group begin to benefit, this commitment can seem less daunting.

References

1. Perlis ML, Sharpe M, Smith MT, et al. Behavioral treatment of insomnia: treatment outcome and the relevance of medical and psychiatric morbidity. J Behav Med. 2001;24(3):281-296.

2. Morin CM. Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics. 2006;1(3):375-386.

3. Smith MT, Perlis ML, Park A, et al. Comparative meta-analysis of pharmacotherapy and behavior therapy for persistent insomnia. Am J Psychiatry. 2002;159:5-11.

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Cognitive-behavioral therapy for insomnia (CBT-I) can be effective, regardless of whether chronic insomnia is primary or secondary to psychiatric, substance dependence, or psychophysiologic causes.1 In fact, with a response rate of 70% to 80%,2 CBT-I can be as effective as medication in the short term and even more effective in the long term.3

Delivered in 4 to 10 sessions, CBT-I typically includes assessment and monitoring of insomnia and sleep patterns, sleep restriction, stimulus control, sleep hygiene education, relaxation training, cognitive therapy, and relapse prevention. Goals are to:

  • decrease the time spent awake in bed, thereby increasing sleep efficiency
  • strengthen the association between the bedroom and sleep
  • address maladaptive sleep habits and lifestyle factors that affect sleep
  • remove extraneous stimuli from the bedroom.

Group therapy with CBT-I

At our clinic, we have modified standard CBT-I techniques into a group format that includes patients with other sleep disorders, medical conditions, or psychiatric diagnoses. Also, CBT-I can benefit mentally ill out-patients with persistent secondary insomnia despite adequate hypnotic dosages.

Challenges to a CBT-I format include: member dropout, inconsistent attendance, disparate psychiatric diagnoses, and different forms of insomnia. In addition, motivating patients to change poor sleep habits that have been in place for decades can be difficult. Finally, CBT-I—although simple in concept—can be difficult to employ, particularly the behavioral components of stimulus control and sleep restriction. Many patients resist these behavioral interventions because they do not experience relief in the short term. Because improved sleep quality frequently is experienced toward the end of treatment, patient motivation and consistency are crucial for success.

For optimal results when leading group CBT-I, be consistent when teaching skills, checking homework, and gaining treatment compliance. Educate patients about CBT-I principles, and help them understand the rationale for what may seem like counterintuitive treatments, such as decreasing time spent in bed. Inform patients that they must practice these skills consistently and stick with the protocol until treatment ends. When patients know the treatment is time-limited and see others in the group begin to benefit, this commitment can seem less daunting.

Cognitive-behavioral therapy for insomnia (CBT-I) can be effective, regardless of whether chronic insomnia is primary or secondary to psychiatric, substance dependence, or psychophysiologic causes.1 In fact, with a response rate of 70% to 80%,2 CBT-I can be as effective as medication in the short term and even more effective in the long term.3

Delivered in 4 to 10 sessions, CBT-I typically includes assessment and monitoring of insomnia and sleep patterns, sleep restriction, stimulus control, sleep hygiene education, relaxation training, cognitive therapy, and relapse prevention. Goals are to:

  • decrease the time spent awake in bed, thereby increasing sleep efficiency
  • strengthen the association between the bedroom and sleep
  • address maladaptive sleep habits and lifestyle factors that affect sleep
  • remove extraneous stimuli from the bedroom.

Group therapy with CBT-I

At our clinic, we have modified standard CBT-I techniques into a group format that includes patients with other sleep disorders, medical conditions, or psychiatric diagnoses. Also, CBT-I can benefit mentally ill out-patients with persistent secondary insomnia despite adequate hypnotic dosages.

Challenges to a CBT-I format include: member dropout, inconsistent attendance, disparate psychiatric diagnoses, and different forms of insomnia. In addition, motivating patients to change poor sleep habits that have been in place for decades can be difficult. Finally, CBT-I—although simple in concept—can be difficult to employ, particularly the behavioral components of stimulus control and sleep restriction. Many patients resist these behavioral interventions because they do not experience relief in the short term. Because improved sleep quality frequently is experienced toward the end of treatment, patient motivation and consistency are crucial for success.

For optimal results when leading group CBT-I, be consistent when teaching skills, checking homework, and gaining treatment compliance. Educate patients about CBT-I principles, and help them understand the rationale for what may seem like counterintuitive treatments, such as decreasing time spent in bed. Inform patients that they must practice these skills consistently and stick with the protocol until treatment ends. When patients know the treatment is time-limited and see others in the group begin to benefit, this commitment can seem less daunting.

References

1. Perlis ML, Sharpe M, Smith MT, et al. Behavioral treatment of insomnia: treatment outcome and the relevance of medical and psychiatric morbidity. J Behav Med. 2001;24(3):281-296.

2. Morin CM. Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics. 2006;1(3):375-386.

3. Smith MT, Perlis ML, Park A, et al. Comparative meta-analysis of pharmacotherapy and behavior therapy for persistent insomnia. Am J Psychiatry. 2002;159:5-11.

References

1. Perlis ML, Sharpe M, Smith MT, et al. Behavioral treatment of insomnia: treatment outcome and the relevance of medical and psychiatric morbidity. J Behav Med. 2001;24(3):281-296.

2. Morin CM. Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics. 2006;1(3):375-386.

3. Smith MT, Perlis ML, Park A, et al. Comparative meta-analysis of pharmacotherapy and behavior therapy for persistent insomnia. Am J Psychiatry. 2002;159:5-11.

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Is bipolar disorder overdiagnosed?

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I note with some dismay an increasing trend in Current Psychiatry to identify almost any mood disorder as bipolar disorder. I found the clinical logic expressed in the supplement “Diagnosing and managing psychotic and mood disorders” (Current Psychiatry, December 2008) especially confounding.

In the case “Bipolar depression and anxiety,” a clinician is implicitly criticized for “focusing on symptoms without giving due consideration to a patient’s history and family history (leading) to a snap misjudgment and inappropriate treatment.” These are harsh words. However, the only possible bipolar symptoms reported in the case study are “feeling over-stimulated and…tremendously irritable.” There also is a family history that “suggested” bipolar disorder. Although this history in the context of a poorly responsive, agitated depression certainly makes bipolar disorder a reasonable diagnosis, assuming that a patient is bipolar and starting mood stabilizers from treatment onset given the data seems like a leap of faith. If I diagnosed bipolar disorder in all my irritable, depressed patients with a vague family history of possible bipolar illness, then my rate of unipolar depression would drop to around 5%.

In addition, Dr. Henry Nasrallah’s suggestion that the chronically and severely psychotic man in “Treatment-resistant psychosis and schizophrenia” has bipolar disorder seems dubious. There is no history of lack of need for sleep, excessive psychomotor activity, grandiosity, or a stated episodic nature to his disturbance. Yes, he has been severely ill, psychotic, and violent, but all these factors are consistent with severe schizophrenia. Finally, to suggest that his tardive dyskinesia adds credibility to the bipolar argument is illogical. Almost all cats have fur but this does not mean that because a newly discovered species is furry, it must be a cat.

One would wonder if clinical judgment has been influenced in any way by the large number of pharmaceutical grants received by the expert panel.

Joshua O. Zimmerman, MD
Minneapolis, MN

Dr. Nasrallah responds

I thank Dr. Zimmerman for his letter regarding the December 2008 supplement to Current Psychiatry, which was based on a roundtable discussion of 4 cases from the 4 participating faculty’s clinical practices. Both diagnostic and treatment issues were discussed in a spontaneous and unrehearsed manner. The faculty submitted their challenging cases before they knew who sponsored the CME activity, so it is not fair to assume the clinicians were influenced by pharmaceutical industry involvement.

Whether or not you agree, studies have shown that bipolar depression is frequently misdiagnosed as unipolar depression if a patient has never had a manic episode.1,2 This is an important diagnostic issue because antidepressants—all approved by the FDA for unipolar depression only—may cause a switch to hypomania, mania, mixed states, or rapid cycling when used as monotherapy in some patients. The faculty agreed that the patient with bipolar depression and anxiety was 1 of those misdiagnosed bipolar depression cases that switched to a mixed state (irritable depression) when given venlafaxine, which was shown in a recent meta-analysis to have the highest switching rate among antidepressants.3

It would be an egregious oversight if a psychiatrist did not have a high index of suspicion about the possibility of a bipolar depression in a patient who presented with:

  • early-onset depression (in her early 20s in this case)
  • a first-degree family member diagnosed with bipolar disorder (her father)
  • a description of her depressed mood as “tremendously irritable.”
Also, there is a high rate of anxiety/obsessive-compulsive disorder comorbidity in bipolar depression when there is a history of high functioning prior to the onset of depression, as was the case in this patient.

I also would add that about a dozen published, controlled studies report significant improvement with the addition of lithium in “treatment-resistant depression” after numerous failures or worsening with antidepressants. Many of those cases likely are bipolar depression that worsened with antidepressant monotherapy because a mood stabilizer was needed.

As for the second case of “Treatment-resistant psychosis and schizophrenia,” numerous clues in the patient’s history point to severe psychotic bipolar disorder:

  • initial psychotic symptoms appeared in high school after age 17, but he completed his college degree, which is more typical of bipolar disorder than schizophrenia
  • very frequent hospitalizations (>50 admissions), which is consistent with bipolar cyclicity
  • assaultiveness, which is more consistent with irritable mania than schizophrenia
  • past and current treatment with mood stabilizers, which suggests that his psychiatrist noted manic symptoms
  • ability to get married early in his illness even after hospitalization
  • advanced vocabulary, which is characteristic of mania rather than schizophrenia
  • history of episodic depression and suicidal ideas
  • episodes of excitement, rapid speech, hypersexuality, and grandiose delusions, which can be found in schizophrenia but are consistent with psychotic mania in the context of these other bipolar disorder features.
 

 

Finally, I brought up the issue of tardive dyskinesia being consistent with bipolar disorder based on my many years researching tardive dyskinesia and extra-pyramidal symptoms. I found a higher occurrence of movement disorders in patients with bipolar disorder than in those with schizophrenia.

I welcome Dr. Zimmerman’s disagreement on diagnostic issues and hope that he sees that the faculty’s diagnostic formulations were driven by the historical facts in the presented cases as well as research findings, not due to any other reason or motive. All of the participants would have given the same diagnostic discussion to our medical students and residents on any morning rounds.

Henry A. Nasrallah, MD
Editor-in-Chief

References

1. Hirschfeld RM, Vornik LA. Recognition and diagnosis of bipolar disorder. J Clin Psychiatry. 2004;65(suppl 15):5-9.

2. Berk M, Dodd S, Callaly P, et al. History of illness prior to a diagnosis of bipolar disorder or schizoaffective disorder. J Affect Disord. 2007;103(1-3):181-186.

3. Post RM, Altshuler LL, Leverich GS, et al. Mood switch in bipolar depression: comparison of adjunctive venlafaxine, bupropion and sertraline. Br J Psychiatry. 2006;189:124-131.

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I note with some dismay an increasing trend in Current Psychiatry to identify almost any mood disorder as bipolar disorder. I found the clinical logic expressed in the supplement “Diagnosing and managing psychotic and mood disorders” (Current Psychiatry, December 2008) especially confounding.

In the case “Bipolar depression and anxiety,” a clinician is implicitly criticized for “focusing on symptoms without giving due consideration to a patient’s history and family history (leading) to a snap misjudgment and inappropriate treatment.” These are harsh words. However, the only possible bipolar symptoms reported in the case study are “feeling over-stimulated and…tremendously irritable.” There also is a family history that “suggested” bipolar disorder. Although this history in the context of a poorly responsive, agitated depression certainly makes bipolar disorder a reasonable diagnosis, assuming that a patient is bipolar and starting mood stabilizers from treatment onset given the data seems like a leap of faith. If I diagnosed bipolar disorder in all my irritable, depressed patients with a vague family history of possible bipolar illness, then my rate of unipolar depression would drop to around 5%.

In addition, Dr. Henry Nasrallah’s suggestion that the chronically and severely psychotic man in “Treatment-resistant psychosis and schizophrenia” has bipolar disorder seems dubious. There is no history of lack of need for sleep, excessive psychomotor activity, grandiosity, or a stated episodic nature to his disturbance. Yes, he has been severely ill, psychotic, and violent, but all these factors are consistent with severe schizophrenia. Finally, to suggest that his tardive dyskinesia adds credibility to the bipolar argument is illogical. Almost all cats have fur but this does not mean that because a newly discovered species is furry, it must be a cat.

One would wonder if clinical judgment has been influenced in any way by the large number of pharmaceutical grants received by the expert panel.

Joshua O. Zimmerman, MD
Minneapolis, MN

Dr. Nasrallah responds

I thank Dr. Zimmerman for his letter regarding the December 2008 supplement to Current Psychiatry, which was based on a roundtable discussion of 4 cases from the 4 participating faculty’s clinical practices. Both diagnostic and treatment issues were discussed in a spontaneous and unrehearsed manner. The faculty submitted their challenging cases before they knew who sponsored the CME activity, so it is not fair to assume the clinicians were influenced by pharmaceutical industry involvement.

Whether or not you agree, studies have shown that bipolar depression is frequently misdiagnosed as unipolar depression if a patient has never had a manic episode.1,2 This is an important diagnostic issue because antidepressants—all approved by the FDA for unipolar depression only—may cause a switch to hypomania, mania, mixed states, or rapid cycling when used as monotherapy in some patients. The faculty agreed that the patient with bipolar depression and anxiety was 1 of those misdiagnosed bipolar depression cases that switched to a mixed state (irritable depression) when given venlafaxine, which was shown in a recent meta-analysis to have the highest switching rate among antidepressants.3

It would be an egregious oversight if a psychiatrist did not have a high index of suspicion about the possibility of a bipolar depression in a patient who presented with:

  • early-onset depression (in her early 20s in this case)
  • a first-degree family member diagnosed with bipolar disorder (her father)
  • a description of her depressed mood as “tremendously irritable.”
Also, there is a high rate of anxiety/obsessive-compulsive disorder comorbidity in bipolar depression when there is a history of high functioning prior to the onset of depression, as was the case in this patient.

I also would add that about a dozen published, controlled studies report significant improvement with the addition of lithium in “treatment-resistant depression” after numerous failures or worsening with antidepressants. Many of those cases likely are bipolar depression that worsened with antidepressant monotherapy because a mood stabilizer was needed.

As for the second case of “Treatment-resistant psychosis and schizophrenia,” numerous clues in the patient’s history point to severe psychotic bipolar disorder:

  • initial psychotic symptoms appeared in high school after age 17, but he completed his college degree, which is more typical of bipolar disorder than schizophrenia
  • very frequent hospitalizations (>50 admissions), which is consistent with bipolar cyclicity
  • assaultiveness, which is more consistent with irritable mania than schizophrenia
  • past and current treatment with mood stabilizers, which suggests that his psychiatrist noted manic symptoms
  • ability to get married early in his illness even after hospitalization
  • advanced vocabulary, which is characteristic of mania rather than schizophrenia
  • history of episodic depression and suicidal ideas
  • episodes of excitement, rapid speech, hypersexuality, and grandiose delusions, which can be found in schizophrenia but are consistent with psychotic mania in the context of these other bipolar disorder features.
 

 

Finally, I brought up the issue of tardive dyskinesia being consistent with bipolar disorder based on my many years researching tardive dyskinesia and extra-pyramidal symptoms. I found a higher occurrence of movement disorders in patients with bipolar disorder than in those with schizophrenia.

I welcome Dr. Zimmerman’s disagreement on diagnostic issues and hope that he sees that the faculty’s diagnostic formulations were driven by the historical facts in the presented cases as well as research findings, not due to any other reason or motive. All of the participants would have given the same diagnostic discussion to our medical students and residents on any morning rounds.

Henry A. Nasrallah, MD
Editor-in-Chief

I note with some dismay an increasing trend in Current Psychiatry to identify almost any mood disorder as bipolar disorder. I found the clinical logic expressed in the supplement “Diagnosing and managing psychotic and mood disorders” (Current Psychiatry, December 2008) especially confounding.

In the case “Bipolar depression and anxiety,” a clinician is implicitly criticized for “focusing on symptoms without giving due consideration to a patient’s history and family history (leading) to a snap misjudgment and inappropriate treatment.” These are harsh words. However, the only possible bipolar symptoms reported in the case study are “feeling over-stimulated and…tremendously irritable.” There also is a family history that “suggested” bipolar disorder. Although this history in the context of a poorly responsive, agitated depression certainly makes bipolar disorder a reasonable diagnosis, assuming that a patient is bipolar and starting mood stabilizers from treatment onset given the data seems like a leap of faith. If I diagnosed bipolar disorder in all my irritable, depressed patients with a vague family history of possible bipolar illness, then my rate of unipolar depression would drop to around 5%.

In addition, Dr. Henry Nasrallah’s suggestion that the chronically and severely psychotic man in “Treatment-resistant psychosis and schizophrenia” has bipolar disorder seems dubious. There is no history of lack of need for sleep, excessive psychomotor activity, grandiosity, or a stated episodic nature to his disturbance. Yes, he has been severely ill, psychotic, and violent, but all these factors are consistent with severe schizophrenia. Finally, to suggest that his tardive dyskinesia adds credibility to the bipolar argument is illogical. Almost all cats have fur but this does not mean that because a newly discovered species is furry, it must be a cat.

One would wonder if clinical judgment has been influenced in any way by the large number of pharmaceutical grants received by the expert panel.

Joshua O. Zimmerman, MD
Minneapolis, MN

Dr. Nasrallah responds

I thank Dr. Zimmerman for his letter regarding the December 2008 supplement to Current Psychiatry, which was based on a roundtable discussion of 4 cases from the 4 participating faculty’s clinical practices. Both diagnostic and treatment issues were discussed in a spontaneous and unrehearsed manner. The faculty submitted their challenging cases before they knew who sponsored the CME activity, so it is not fair to assume the clinicians were influenced by pharmaceutical industry involvement.

Whether or not you agree, studies have shown that bipolar depression is frequently misdiagnosed as unipolar depression if a patient has never had a manic episode.1,2 This is an important diagnostic issue because antidepressants—all approved by the FDA for unipolar depression only—may cause a switch to hypomania, mania, mixed states, or rapid cycling when used as monotherapy in some patients. The faculty agreed that the patient with bipolar depression and anxiety was 1 of those misdiagnosed bipolar depression cases that switched to a mixed state (irritable depression) when given venlafaxine, which was shown in a recent meta-analysis to have the highest switching rate among antidepressants.3

It would be an egregious oversight if a psychiatrist did not have a high index of suspicion about the possibility of a bipolar depression in a patient who presented with:

  • early-onset depression (in her early 20s in this case)
  • a first-degree family member diagnosed with bipolar disorder (her father)
  • a description of her depressed mood as “tremendously irritable.”
Also, there is a high rate of anxiety/obsessive-compulsive disorder comorbidity in bipolar depression when there is a history of high functioning prior to the onset of depression, as was the case in this patient.

I also would add that about a dozen published, controlled studies report significant improvement with the addition of lithium in “treatment-resistant depression” after numerous failures or worsening with antidepressants. Many of those cases likely are bipolar depression that worsened with antidepressant monotherapy because a mood stabilizer was needed.

As for the second case of “Treatment-resistant psychosis and schizophrenia,” numerous clues in the patient’s history point to severe psychotic bipolar disorder:

  • initial psychotic symptoms appeared in high school after age 17, but he completed his college degree, which is more typical of bipolar disorder than schizophrenia
  • very frequent hospitalizations (>50 admissions), which is consistent with bipolar cyclicity
  • assaultiveness, which is more consistent with irritable mania than schizophrenia
  • past and current treatment with mood stabilizers, which suggests that his psychiatrist noted manic symptoms
  • ability to get married early in his illness even after hospitalization
  • advanced vocabulary, which is characteristic of mania rather than schizophrenia
  • history of episodic depression and suicidal ideas
  • episodes of excitement, rapid speech, hypersexuality, and grandiose delusions, which can be found in schizophrenia but are consistent with psychotic mania in the context of these other bipolar disorder features.
 

 

Finally, I brought up the issue of tardive dyskinesia being consistent with bipolar disorder based on my many years researching tardive dyskinesia and extra-pyramidal symptoms. I found a higher occurrence of movement disorders in patients with bipolar disorder than in those with schizophrenia.

I welcome Dr. Zimmerman’s disagreement on diagnostic issues and hope that he sees that the faculty’s diagnostic formulations were driven by the historical facts in the presented cases as well as research findings, not due to any other reason or motive. All of the participants would have given the same diagnostic discussion to our medical students and residents on any morning rounds.

Henry A. Nasrallah, MD
Editor-in-Chief

References

1. Hirschfeld RM, Vornik LA. Recognition and diagnosis of bipolar disorder. J Clin Psychiatry. 2004;65(suppl 15):5-9.

2. Berk M, Dodd S, Callaly P, et al. History of illness prior to a diagnosis of bipolar disorder or schizoaffective disorder. J Affect Disord. 2007;103(1-3):181-186.

3. Post RM, Altshuler LL, Leverich GS, et al. Mood switch in bipolar depression: comparison of adjunctive venlafaxine, bupropion and sertraline. Br J Psychiatry. 2006;189:124-131.

References

1. Hirschfeld RM, Vornik LA. Recognition and diagnosis of bipolar disorder. J Clin Psychiatry. 2004;65(suppl 15):5-9.

2. Berk M, Dodd S, Callaly P, et al. History of illness prior to a diagnosis of bipolar disorder or schizoaffective disorder. J Affect Disord. 2007;103(1-3):181-186.

3. Post RM, Altshuler LL, Leverich GS, et al. Mood switch in bipolar depression: comparison of adjunctive venlafaxine, bupropion and sertraline. Br J Psychiatry. 2006;189:124-131.

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Long overdue: Measurement-based psychiatric practice

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Can you imagine an internist starting insulin for a patient with diabetes without obtaining a baseline glucose level? How would that internist know from visit to visit whether treatment was working and to what extent? How would he or she know how and when to adjust the dose to achieve hyperglycemia remission and a normal serum level?

If our medical colleagues wouldn’t dream of treating patients without measuring the symptoms of illness, why should psychiatric practice be different? Why aren’t psychiatrists measuring patients’ depression, anxiety, mania, or psychosis before and after starting psychopharmacologic agents?

Standardized tools unused

I recently surveyed a sample of Current Psychiatry readers, asking about their use of standard measurement instruments in clinical practice. I conducted this online survey as part of the needs assessment for a CME workshop I am planning at the University of Cincinnati. As I expected, most of the respondents indicated that they do not utilize any of 4 clinical rating scales routinely used in the evidence-based controlled trials required for FDA approval of psychiatric medications. These scales—which most said they had heard of or read about—include:

 

  • Positive and Negative Syndrome Scale (PANSS) for schizophrenia
  • Young Mania Rating Scale (YMRS) for bipolar mania
  • Hamilton Depression Rating Scale (HAM-D) for unipolar depression
  • Montgomery-Åsberg Depression Rating Scale (MADRS) for bipolar depression.

Lack of time was the most common reason respondents cited for not using these tools. Many preferred that their patients complete self-rating scales instead. Although I agree that patient self-ratings can be useful, they lack the objectivity and comprehensiveness of a clinician’s observation.

Many good reasons

One of the most important goals in modern psychiatric practice is to achieve remission, not just partial symptomatic response. Remission of depression, bipolar disorder, or schizophrenia is defined by a quantitative threshold measured on a standard rating scale. Therefore, we must use the pertinent rating scales if we wish to document that our patients achieve remission, which is the gateway to recovery and return to social and vocational functioning.

I believe psychiatrists should use standardized clinical rating scales because it is good medical practice that our patients need. Standardized measurements would enable all psychiatrists to use the same language relating to severity of illness, response, or remission. Then, when we read records of patients referred to us or cover while a colleague is on vacation, the numerical assessment combined with clinical impressions in the notes will facilitate continuity of care and guide ongoing treatment.

Let’s face it: the contents of many psychiatric charts are too general (“patient is doing better”) or vague (“patient partially improved”). Very few practitioners have time to cite whether or not every sign and symptom persists at a mild, moderate, or severe degree. By adopting standard rating scales, busy practitioners could do more (through better documentation) in less time (such as by circling the severity number corresponding to the symptoms listed on the scale).

Coming soon: Electronic medical records

The Obama administration’s economic stimulus package includes $19 billion to incentivize the adoption of universal electronic medical records (a 10-year goal set in 2004 by President Bush). Clinicians in facilities that have adopted e-medical records can enter clinical ratings with the click of a mouse. Issues beyond symptoms—such as functioning, quality of life, relationships, coping with stresses, etc.—can be addressed in the handwritten progress note text. (By the way, standard rating scales exist for those issues, too.)

Let us not wait for the time when reimbursement may become linked to documenting PANSS, YMRS, or MADRS scores at initial evaluations and follow-up visits. The time has come for psychiatrists—like our medical colleagues—to upgrade to objective, measurement-based practice and documentation. Improving the quality of inadequately informative or outright deficient medical records would be good for the patient and the practitioner. The quality of psychiatric treatment in the clinical setting should be no less rigorous than the controlled research trials that led to approval of the treatments.

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Comment on this article

Can you imagine an internist starting insulin for a patient with diabetes without obtaining a baseline glucose level? How would that internist know from visit to visit whether treatment was working and to what extent? How would he or she know how and when to adjust the dose to achieve hyperglycemia remission and a normal serum level?

If our medical colleagues wouldn’t dream of treating patients without measuring the symptoms of illness, why should psychiatric practice be different? Why aren’t psychiatrists measuring patients’ depression, anxiety, mania, or psychosis before and after starting psychopharmacologic agents?

Standardized tools unused

I recently surveyed a sample of Current Psychiatry readers, asking about their use of standard measurement instruments in clinical practice. I conducted this online survey as part of the needs assessment for a CME workshop I am planning at the University of Cincinnati. As I expected, most of the respondents indicated that they do not utilize any of 4 clinical rating scales routinely used in the evidence-based controlled trials required for FDA approval of psychiatric medications. These scales—which most said they had heard of or read about—include:

 

  • Positive and Negative Syndrome Scale (PANSS) for schizophrenia
  • Young Mania Rating Scale (YMRS) for bipolar mania
  • Hamilton Depression Rating Scale (HAM-D) for unipolar depression
  • Montgomery-Åsberg Depression Rating Scale (MADRS) for bipolar depression.

Lack of time was the most common reason respondents cited for not using these tools. Many preferred that their patients complete self-rating scales instead. Although I agree that patient self-ratings can be useful, they lack the objectivity and comprehensiveness of a clinician’s observation.

Many good reasons

One of the most important goals in modern psychiatric practice is to achieve remission, not just partial symptomatic response. Remission of depression, bipolar disorder, or schizophrenia is defined by a quantitative threshold measured on a standard rating scale. Therefore, we must use the pertinent rating scales if we wish to document that our patients achieve remission, which is the gateway to recovery and return to social and vocational functioning.

I believe psychiatrists should use standardized clinical rating scales because it is good medical practice that our patients need. Standardized measurements would enable all psychiatrists to use the same language relating to severity of illness, response, or remission. Then, when we read records of patients referred to us or cover while a colleague is on vacation, the numerical assessment combined with clinical impressions in the notes will facilitate continuity of care and guide ongoing treatment.

Let’s face it: the contents of many psychiatric charts are too general (“patient is doing better”) or vague (“patient partially improved”). Very few practitioners have time to cite whether or not every sign and symptom persists at a mild, moderate, or severe degree. By adopting standard rating scales, busy practitioners could do more (through better documentation) in less time (such as by circling the severity number corresponding to the symptoms listed on the scale).

Coming soon: Electronic medical records

The Obama administration’s economic stimulus package includes $19 billion to incentivize the adoption of universal electronic medical records (a 10-year goal set in 2004 by President Bush). Clinicians in facilities that have adopted e-medical records can enter clinical ratings with the click of a mouse. Issues beyond symptoms—such as functioning, quality of life, relationships, coping with stresses, etc.—can be addressed in the handwritten progress note text. (By the way, standard rating scales exist for those issues, too.)

Let us not wait for the time when reimbursement may become linked to documenting PANSS, YMRS, or MADRS scores at initial evaluations and follow-up visits. The time has come for psychiatrists—like our medical colleagues—to upgrade to objective, measurement-based practice and documentation. Improving the quality of inadequately informative or outright deficient medical records would be good for the patient and the practitioner. The quality of psychiatric treatment in the clinical setting should be no less rigorous than the controlled research trials that led to approval of the treatments.

Comment on this article

Can you imagine an internist starting insulin for a patient with diabetes without obtaining a baseline glucose level? How would that internist know from visit to visit whether treatment was working and to what extent? How would he or she know how and when to adjust the dose to achieve hyperglycemia remission and a normal serum level?

If our medical colleagues wouldn’t dream of treating patients without measuring the symptoms of illness, why should psychiatric practice be different? Why aren’t psychiatrists measuring patients’ depression, anxiety, mania, or psychosis before and after starting psychopharmacologic agents?

Standardized tools unused

I recently surveyed a sample of Current Psychiatry readers, asking about their use of standard measurement instruments in clinical practice. I conducted this online survey as part of the needs assessment for a CME workshop I am planning at the University of Cincinnati. As I expected, most of the respondents indicated that they do not utilize any of 4 clinical rating scales routinely used in the evidence-based controlled trials required for FDA approval of psychiatric medications. These scales—which most said they had heard of or read about—include:

 

  • Positive and Negative Syndrome Scale (PANSS) for schizophrenia
  • Young Mania Rating Scale (YMRS) for bipolar mania
  • Hamilton Depression Rating Scale (HAM-D) for unipolar depression
  • Montgomery-Åsberg Depression Rating Scale (MADRS) for bipolar depression.

Lack of time was the most common reason respondents cited for not using these tools. Many preferred that their patients complete self-rating scales instead. Although I agree that patient self-ratings can be useful, they lack the objectivity and comprehensiveness of a clinician’s observation.

Many good reasons

One of the most important goals in modern psychiatric practice is to achieve remission, not just partial symptomatic response. Remission of depression, bipolar disorder, or schizophrenia is defined by a quantitative threshold measured on a standard rating scale. Therefore, we must use the pertinent rating scales if we wish to document that our patients achieve remission, which is the gateway to recovery and return to social and vocational functioning.

I believe psychiatrists should use standardized clinical rating scales because it is good medical practice that our patients need. Standardized measurements would enable all psychiatrists to use the same language relating to severity of illness, response, or remission. Then, when we read records of patients referred to us or cover while a colleague is on vacation, the numerical assessment combined with clinical impressions in the notes will facilitate continuity of care and guide ongoing treatment.

Let’s face it: the contents of many psychiatric charts are too general (“patient is doing better”) or vague (“patient partially improved”). Very few practitioners have time to cite whether or not every sign and symptom persists at a mild, moderate, or severe degree. By adopting standard rating scales, busy practitioners could do more (through better documentation) in less time (such as by circling the severity number corresponding to the symptoms listed on the scale).

Coming soon: Electronic medical records

The Obama administration’s economic stimulus package includes $19 billion to incentivize the adoption of universal electronic medical records (a 10-year goal set in 2004 by President Bush). Clinicians in facilities that have adopted e-medical records can enter clinical ratings with the click of a mouse. Issues beyond symptoms—such as functioning, quality of life, relationships, coping with stresses, etc.—can be addressed in the handwritten progress note text. (By the way, standard rating scales exist for those issues, too.)

Let us not wait for the time when reimbursement may become linked to documenting PANSS, YMRS, or MADRS scores at initial evaluations and follow-up visits. The time has come for psychiatrists—like our medical colleagues—to upgrade to objective, measurement-based practice and documentation. Improving the quality of inadequately informative or outright deficient medical records would be good for the patient and the practitioner. The quality of psychiatric treatment in the clinical setting should be no less rigorous than the controlled research trials that led to approval of the treatments.

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A mysterious loss of memory

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A mysterious loss of memory

Case: Worsening memory

Mrs. K, age 46, is being treated by a neurologist for stable relapsing-remitting multiple sclerosis (MS) and migraine headaches when she complains of worsening memory over the past 5 years. She reports having difficulty recalling details of recent events and conversations. She describes occasional word-finding difficulties and problems maintaining her train of thought. She forgets where she places things and has gotten lost while driving, even on familiar routes. Her husband reports she takes more time to process things in general.

Mrs. K’s cognitive decline has affected her daily life and ability to work. For 4 years, she has been an office assistant at a campground, where she takes phone reservations and keeps a site schedule. Formerly simple tasks—such as taking a phone number—have become increasingly difficult, and she cannot recall a list of 3 things to buy at the supermarket without writing them down.

Her psychiatric history is unremarkable for inpatient or outpatient treatment. She denies a history of head trauma or seizure disorder. Her medical history includes allergic rhinitis, hypothyroidism, mitral valve prolapse, fibrocystic breasts, endometriosis, and temporomandibular joint disorder. Mrs. K had a hysterectomy in 2006. She denies current alcohol or tobacco use.

As a teenager, Mrs. K suffered migraines but did not seek treatment, and her headaches remitted for about 10 years. At age 29, she started to experience tunnel vision. Three years later she reported bilateral foot numbness and was diagnosed with MS. She responded well to interferon beta-1b but her migraines returned, occurring several times a week. Her migraines are successfully treated with topiramate, 75 mg/d, for prophylactic therapy and rizatriptan, 10 mg, as needed for abortive therapy. Her medication regimen also includes:

  • eszopiclone, 2 mg/d, and amitriptyline, 10 mg/d, for insomnia
  • butalbital/aspirin/caffeine, 50/325/40 mg, as needed for tension headaches
  • fexofenadine, 12 mg/d, and budesonide, 32 mcg, 4 sprays/d, for allergy symptoms
  • esomeprazole, 80 mg/d, and famotidine, 20 mg/d, as needed for dyspepsia
  • propranolol, 120 mg/d, for hypertension
  • levothyroxine, 75 mcg/d, for hypothyroidism
  • conjugatedestrogens, 0.45 mg/d, for hypoestrogenemia
  • alprazolam, 0.25 mg/d, aspirin, 81 mg/d, vitamin E, 800 IU/d, and a multivitamin.
Her family history is remarkable for signs of neurocognitive degeneration in her father, age 75. She has 3 siblings with no known neurologic or neuropsychological symptoms.

The neurologist orders neuropsychological testing. Mrs. K demonstrates some depressive symptoms but is within normal limits across all aspects of neurocognition, including basic and complex attention, memory, bilateral motor functioning, expressive and receptive language, visuospatial/constructional function, and self-regulatory/executive functioning. The neurologist refers Mrs. K for psychiatric evaluation of her depressive symptoms.

The author’s observations

Many neuropsychiatric abnormalities may accompany MS (Table).1 These can be classified as cognitive dysfunction or disturbances in mood, affect, and behavior.

Although the cause of cognitive impairment in patients with MS is unclear, its extent and profound impact on functioning has become widely recognized over the past 20 years.2

An estimated 40% to 65% of patients with MS suffer from cognitive dysfunction.1,3 Testing indicates deficiencies most often in:

  • attention
  • information processing speed
  • working memory
  • verbal memory
  • visuospatial function
  • executive functions.4
Although in neuropsychological testing Mrs. K had scored within normal limits on memory, attention, and executive and visuospatial function, at the time of her psychiatric evaluation she is experiencing difficulties in all of these areas. Cognitive decline can occur early in the course of MS, but Mrs. K’s cognitive symptoms began approximately 10 years after she was diagnosed. The extent of the cognitive deficits commonly expands as the disease progresses.1 Cognitive dysfunction is the primary cause of MS patients’ withdrawal from the workplace5 and often leads to:

  • reduced social interactions
  • increased sexual dysfunction
  • greater difficulty with household tasks.6
When she first complained of memory loss, Mrs. K was taking topiramate for migraine prophylaxis. Multiple studies have demonstrated adverse cognitive effects from topiramate;7 however, Mrs. K had noticed substantial memory changes at least 2 years before starting topiramate. She denied experiencing worsening memory after starting topiramate and did not recall any major change after her dosage was increased to 75 mg/d. She chose to continue topiramate because it effectively prevented migraines and, in her mind, was unlikely related to her memory problems.

Long-term interferon beta-1b treatment prevents MS relapses, but a recent study found that interferon beta-1b had a negative impact on patients’ mental health composite score and in most quality-of-life subscales over 2 years.8 Nevertheless, Mrs. K received interferon beta-1b therapy for at least 9 years without noticing cognitive decline.

 

 

Table

Neuropsychiatric conditions associated with MS

DisorderPrevalence
Major depressionLifetime prevalence: 50%
Bipolar disorderEstimated prevalence is 10%, twice that of the general population
Euphoria25%
Pseudobulbar affectPathological laughing or crying, emotional incontinence; affects 10% of patients
Psychosis2% to 3% vs 0.5% to 1% in general population
Cognitive impairment40% to 60%
Source: Reference 1

EVALUATION: Dysthymia

Mrs. K reports memory problems as her chief complaint. She also complains of a depressed mood, irritability, distractibility, and insomnia since her memory problems began, and admits being readily tearful. Mrs. K has difficulty “turning off her thinking” at night, which leads to delayed sleep onset, but denies sleeplessness, racing thoughts, or feelings of euphoria.

During the mental status exam, she is cooperative, alert, and oriented to person, place, and time, but distractible. She is hypokinetic throughout the interview. Her speech is normal. She describes her mood as “empty” and scores 3 on a 1-to-5-point scale for depression severity. She demonstrates a constricted affect.

Her thought process is coherent and goal-directed, and she denies having auditory or visual hallucinations or active or passive suicidal or homicidal ideation. She scores 29/30 on the Mini-Mental State Exam, but by interview she appears to have impaired remote memory. Mrs. K demonstrates unimpaired judgment and good insight.

The author’s observations

Mrs. K meets DSM-IV-TR criteria for dysthymic disorder and agrees to start mirtazapine, 15 mg at bedtime. I chose this antidepressant because Mrs. K continues to complain of difficulty falling asleep, and mirtazapine is known to significantly decrease sleep latency and increase total sleep time. Approximately one-half of patients with MS will experience depression.1,9 In a recent study of 245 MS patients followed in a neurology clinic, two-thirds of those who met criteria for major depressive disorder did not receive antidepressants.10

TREATMENT: A new strategy

Mrs. K returns 2 months after starting mirtazapine and reports she is “doing the same.” Her mood is improved but still dysthymic. She again demonstrates irritability during her mental status examination and continues to complain of persistent memory problems. I titrate mirtazapine up to 30 mg/d.

After 2 more months Mrs. K’s mood is euthymic and she demonstrates a bright affect, but she experiences continued decline in short- and long-term memory and reports increasing frustration with simple tasks. The rest of her mental status exam is unremarkable. I instruct her to reduce the mirtazapine dosage to 15 mg/d.

At the next visit 10 weeks later, she again presents with a euthymic mood and a bright affect. She says she attempted to decrease mirtazapine but experienced increased irritability so she remained on the 30-mg dose, with a positive effect on her mood and reduced irritability. Unfortunately, her memory problems persist.

Approximately 2 years after Mrs. K’s first visit, I devise a new pharmacologic strategy. Mrs. K believes that she no longer is depressed and that her only problem is her inability to recall events. To address this, I decide to try memantine, which has been shown to cause modest improvement in clinical symptoms in severe stages of Alzheimer’s disease11 and also has been reported to be useful in the treatment of cognitive impairment in some bipolar disorder patients.12 I start memantine at 10 mg/d and titrate up to 20 mg/d in 3 months.

At 3 months, Mrs. K reports improvement that she describes as “life-changing.” She experiences improved memory in almost every aspect of daily functioning. She remembers daytime events and has stronger short-term memory. She can recall up to 4 items on a list several hours later, and no longer relies upon written lists to complete daily activities. Her husband and children also comment on her “remarkable” improvement.

The author’s observations

Mrs. K’s substantial memory improvement while receiving memantine warrants considering the drug for patients with cognitive dysfunction attributable to MS. Memantine is an uncompetitive NMDA receptor antagonist that the FDA approved in 2003 to treat moderate-to-severe Alzheimer’s disease (Box).11,13 It is generally well tolerated and safe, with a low potential for drug-drug interactions. In clinical trials of patients receiving memantine for Alzheimer’s disease and vascular dementia, the most commonly reported side effects were dizziness, headache, constipation, and confusion.14

A recent trial of memantine therapy for MS at the University of Navarra was suspended for reversible mild-to-moderate neurologic side effects.15 A phase II/phase III double-blind placebo-controlled trial at the University of Oregon designed to determine whether memantine is an effective treatment for memory and cognitive problems associated with MS is recruiting participants.16

 

 

Memantine has been reported to successfully treat other MS symptoms. A 1997 retrospective study found that 11 patients with acquired pendular nystagmus (APN) secondary to MS experienced complete resolution of APN when given memantine.17

Box

Memantine’s mechanism of action in dementia

Memantine was FDA-approved in 2003 to treat moderate-to-severe Alzheimer’s disease dementia. The drug also has been used off-label to treat vascular dementia, dementia of Wernicke-Korsakoff syndrome, and acquired pendular nystagmus.11

Although the neurobiologic basis for memantine’s therapeutic activity in patients with dementia is not fully understood, it is thought to reduce glutamatergic excitotoxicity. The mechanism of action is voltage-dependent, uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonism with low-to-moderate affinity and fast blocking/unblocking kinetics.12 Its kinetic profile is beneficial because it allows memantine to occupy the receptor for a sufficient time to prevent pathologic activation of glutamate receptors. However, it dissociates when the physiologic activation of glutamate receptors is necessary, thus preserving normal NMDA receptor activity required for learning and memory. By blocking the effects of abnormal glutamate activity, memantine may prevent abnormal neuronal cell death and cognitive dysfunction.

Related resources

  • Parsons CG, Stöffler A, Danysz W. Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system—too little activation is bad, too much is even worse. Neuropharmacology. 2007;53(6):699-723.
Drug brand names

  • Alprazolam • Xanax
  • Amitriptyline • Elavil
  • Budesonide • Rhinocort
  • Butalbital/Aspirin/Caffeine • Fiorinal
  • Conjugated Estrogens • Premarin
  • Esomeprazole • Nexium
  • Eszopiclone • Lunesta
  • Famotidine • Pepcid
  • Fexofenadine • Allegra
  • Interferon beta-1b • Betaseron
  • Levothyroxine • Synthroid
  • Memantine • Namenda
  • Propranolol • Inderal
  • Rizatriptan • Maxalt
  • Topiramate • Topamax
Disclosure

Dr. Rao is a speaker for Forest Pharmaceuticals.

Acknowledgement

The author thanks Alexander M. Timchak, MS-IV, Stritch School of Medicine, Loyola University, Chicago, for his assistance with this article.

References

1. Ghaffar O, Feinstein A. The neuropsychiatry of multiple sclerosis: a review of recent developments. Curr Opin Psychiatry. 2007;20(3):278-285.

2. Amato MP, Portaccio E, Zipoli V. Are there protective treatments for cognitive decline in MS? J Neurol Sci. 2006;245(1-2):183-186.

3. Bobholz JA, Rao SM. Cognitive dysfunction in multiple sclerosis: a review of recent developments. Curr Opin Neurol. 2003;16(3):283-288.

4. Hoffmann S, Tittgemeyer M, von Cramon DY. Cognitive impairment in multiple sclerosis. Curr Opin Neurol. 2007;20(3):275-280.

5. Pierson SH, Griffith N. Treatment of cognitive impairment in multiple sclerosis. Behav Neurol. 2006;17(1):53-67.

6. Bagert B, Camplair P, Bourdette D. Cognitive dysfunction in multiple sclerosis: natural history, pathophysiology and management. CNS Drugs. 2002;16(7):445-455.

7. Martin R, Kuzniecky R, Ho S, et al. Cognitive effects of topiramate, gabapentin, and lamotrigine in healthy young adults. Neurology. 1999;52(2):321-327.

8. Simone IL, Ceccarelli A, Tortorella C, et al. Influence of Interferon beta treatment on quality of life in multiple sclerosis patients. Health Qual Life Outcomes. 2006;4:96.-

9. Siegert RJ, Abernethy DA. Depression in multiple sclerosis: a review. J Neurol Neurosurg Psychiatry. 2005;76(4):469-475.

10. Mohr DC, Hart SL, Fonareva I, et al. Treatment of depression for patients with multiple sclerosis in neurology clinics. Mult Scler. 2006;12(2):204-208.

11. Kumar S. Memantine: pharmacological properties and clinical uses. Neurol India. 2004;52(3):307-309.

12. Teng CT, Demetrio FN. Memantine may acutely improve cognition and have a mood stabilizing effect in treatment-resistant bipolar disorder. Rev Bras Psiquiatr. 2006;28(3):252-4.

13. Danysz W, Parsons CG, Mobius HJ, et al. Neuroprotective and symptomatological action of memantine relevant for Alzheimer’s disease: a unified glutamatergic hypothesis on the mechanism of action. Neurotox Res. 2000;2(2-3):85-97.

14. Namenda [package insert] St. Louis, MO: Forest Pharmaceuticals; 2007.

15. Memantine therapy for multiple sclerosis (NCT00638833) Available at: http://www.clinicaltrials.gov/ct2/show/NCT00638833. Accessed February 17, 2009.

16. Trial of memantine for cognitive impairment in multiple sclerosis (NCT00300716) Available at: http://www.clinicaltrials.gov/ct2/show/NCT00300716. Accessed February 17, 2009.

17. Starck M, Albrecht H, Pöllmann W, et al. Drug therapy for acquired pendular nystagmus in multiple sclerosis. J Neurol. 1997;244(1):9-16.

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Case: Worsening memory

Mrs. K, age 46, is being treated by a neurologist for stable relapsing-remitting multiple sclerosis (MS) and migraine headaches when she complains of worsening memory over the past 5 years. She reports having difficulty recalling details of recent events and conversations. She describes occasional word-finding difficulties and problems maintaining her train of thought. She forgets where she places things and has gotten lost while driving, even on familiar routes. Her husband reports she takes more time to process things in general.

Mrs. K’s cognitive decline has affected her daily life and ability to work. For 4 years, she has been an office assistant at a campground, where she takes phone reservations and keeps a site schedule. Formerly simple tasks—such as taking a phone number—have become increasingly difficult, and she cannot recall a list of 3 things to buy at the supermarket without writing them down.

Her psychiatric history is unremarkable for inpatient or outpatient treatment. She denies a history of head trauma or seizure disorder. Her medical history includes allergic rhinitis, hypothyroidism, mitral valve prolapse, fibrocystic breasts, endometriosis, and temporomandibular joint disorder. Mrs. K had a hysterectomy in 2006. She denies current alcohol or tobacco use.

As a teenager, Mrs. K suffered migraines but did not seek treatment, and her headaches remitted for about 10 years. At age 29, she started to experience tunnel vision. Three years later she reported bilateral foot numbness and was diagnosed with MS. She responded well to interferon beta-1b but her migraines returned, occurring several times a week. Her migraines are successfully treated with topiramate, 75 mg/d, for prophylactic therapy and rizatriptan, 10 mg, as needed for abortive therapy. Her medication regimen also includes:

  • eszopiclone, 2 mg/d, and amitriptyline, 10 mg/d, for insomnia
  • butalbital/aspirin/caffeine, 50/325/40 mg, as needed for tension headaches
  • fexofenadine, 12 mg/d, and budesonide, 32 mcg, 4 sprays/d, for allergy symptoms
  • esomeprazole, 80 mg/d, and famotidine, 20 mg/d, as needed for dyspepsia
  • propranolol, 120 mg/d, for hypertension
  • levothyroxine, 75 mcg/d, for hypothyroidism
  • conjugatedestrogens, 0.45 mg/d, for hypoestrogenemia
  • alprazolam, 0.25 mg/d, aspirin, 81 mg/d, vitamin E, 800 IU/d, and a multivitamin.
Her family history is remarkable for signs of neurocognitive degeneration in her father, age 75. She has 3 siblings with no known neurologic or neuropsychological symptoms.

The neurologist orders neuropsychological testing. Mrs. K demonstrates some depressive symptoms but is within normal limits across all aspects of neurocognition, including basic and complex attention, memory, bilateral motor functioning, expressive and receptive language, visuospatial/constructional function, and self-regulatory/executive functioning. The neurologist refers Mrs. K for psychiatric evaluation of her depressive symptoms.

The author’s observations

Many neuropsychiatric abnormalities may accompany MS (Table).1 These can be classified as cognitive dysfunction or disturbances in mood, affect, and behavior.

Although the cause of cognitive impairment in patients with MS is unclear, its extent and profound impact on functioning has become widely recognized over the past 20 years.2

An estimated 40% to 65% of patients with MS suffer from cognitive dysfunction.1,3 Testing indicates deficiencies most often in:

  • attention
  • information processing speed
  • working memory
  • verbal memory
  • visuospatial function
  • executive functions.4
Although in neuropsychological testing Mrs. K had scored within normal limits on memory, attention, and executive and visuospatial function, at the time of her psychiatric evaluation she is experiencing difficulties in all of these areas. Cognitive decline can occur early in the course of MS, but Mrs. K’s cognitive symptoms began approximately 10 years after she was diagnosed. The extent of the cognitive deficits commonly expands as the disease progresses.1 Cognitive dysfunction is the primary cause of MS patients’ withdrawal from the workplace5 and often leads to:

  • reduced social interactions
  • increased sexual dysfunction
  • greater difficulty with household tasks.6
When she first complained of memory loss, Mrs. K was taking topiramate for migraine prophylaxis. Multiple studies have demonstrated adverse cognitive effects from topiramate;7 however, Mrs. K had noticed substantial memory changes at least 2 years before starting topiramate. She denied experiencing worsening memory after starting topiramate and did not recall any major change after her dosage was increased to 75 mg/d. She chose to continue topiramate because it effectively prevented migraines and, in her mind, was unlikely related to her memory problems.

Long-term interferon beta-1b treatment prevents MS relapses, but a recent study found that interferon beta-1b had a negative impact on patients’ mental health composite score and in most quality-of-life subscales over 2 years.8 Nevertheless, Mrs. K received interferon beta-1b therapy for at least 9 years without noticing cognitive decline.

 

 

Table

Neuropsychiatric conditions associated with MS

DisorderPrevalence
Major depressionLifetime prevalence: 50%
Bipolar disorderEstimated prevalence is 10%, twice that of the general population
Euphoria25%
Pseudobulbar affectPathological laughing or crying, emotional incontinence; affects 10% of patients
Psychosis2% to 3% vs 0.5% to 1% in general population
Cognitive impairment40% to 60%
Source: Reference 1

EVALUATION: Dysthymia

Mrs. K reports memory problems as her chief complaint. She also complains of a depressed mood, irritability, distractibility, and insomnia since her memory problems began, and admits being readily tearful. Mrs. K has difficulty “turning off her thinking” at night, which leads to delayed sleep onset, but denies sleeplessness, racing thoughts, or feelings of euphoria.

During the mental status exam, she is cooperative, alert, and oriented to person, place, and time, but distractible. She is hypokinetic throughout the interview. Her speech is normal. She describes her mood as “empty” and scores 3 on a 1-to-5-point scale for depression severity. She demonstrates a constricted affect.

Her thought process is coherent and goal-directed, and she denies having auditory or visual hallucinations or active or passive suicidal or homicidal ideation. She scores 29/30 on the Mini-Mental State Exam, but by interview she appears to have impaired remote memory. Mrs. K demonstrates unimpaired judgment and good insight.

The author’s observations

Mrs. K meets DSM-IV-TR criteria for dysthymic disorder and agrees to start mirtazapine, 15 mg at bedtime. I chose this antidepressant because Mrs. K continues to complain of difficulty falling asleep, and mirtazapine is known to significantly decrease sleep latency and increase total sleep time. Approximately one-half of patients with MS will experience depression.1,9 In a recent study of 245 MS patients followed in a neurology clinic, two-thirds of those who met criteria for major depressive disorder did not receive antidepressants.10

TREATMENT: A new strategy

Mrs. K returns 2 months after starting mirtazapine and reports she is “doing the same.” Her mood is improved but still dysthymic. She again demonstrates irritability during her mental status examination and continues to complain of persistent memory problems. I titrate mirtazapine up to 30 mg/d.

After 2 more months Mrs. K’s mood is euthymic and she demonstrates a bright affect, but she experiences continued decline in short- and long-term memory and reports increasing frustration with simple tasks. The rest of her mental status exam is unremarkable. I instruct her to reduce the mirtazapine dosage to 15 mg/d.

At the next visit 10 weeks later, she again presents with a euthymic mood and a bright affect. She says she attempted to decrease mirtazapine but experienced increased irritability so she remained on the 30-mg dose, with a positive effect on her mood and reduced irritability. Unfortunately, her memory problems persist.

Approximately 2 years after Mrs. K’s first visit, I devise a new pharmacologic strategy. Mrs. K believes that she no longer is depressed and that her only problem is her inability to recall events. To address this, I decide to try memantine, which has been shown to cause modest improvement in clinical symptoms in severe stages of Alzheimer’s disease11 and also has been reported to be useful in the treatment of cognitive impairment in some bipolar disorder patients.12 I start memantine at 10 mg/d and titrate up to 20 mg/d in 3 months.

At 3 months, Mrs. K reports improvement that she describes as “life-changing.” She experiences improved memory in almost every aspect of daily functioning. She remembers daytime events and has stronger short-term memory. She can recall up to 4 items on a list several hours later, and no longer relies upon written lists to complete daily activities. Her husband and children also comment on her “remarkable” improvement.

The author’s observations

Mrs. K’s substantial memory improvement while receiving memantine warrants considering the drug for patients with cognitive dysfunction attributable to MS. Memantine is an uncompetitive NMDA receptor antagonist that the FDA approved in 2003 to treat moderate-to-severe Alzheimer’s disease (Box).11,13 It is generally well tolerated and safe, with a low potential for drug-drug interactions. In clinical trials of patients receiving memantine for Alzheimer’s disease and vascular dementia, the most commonly reported side effects were dizziness, headache, constipation, and confusion.14

A recent trial of memantine therapy for MS at the University of Navarra was suspended for reversible mild-to-moderate neurologic side effects.15 A phase II/phase III double-blind placebo-controlled trial at the University of Oregon designed to determine whether memantine is an effective treatment for memory and cognitive problems associated with MS is recruiting participants.16

 

 

Memantine has been reported to successfully treat other MS symptoms. A 1997 retrospective study found that 11 patients with acquired pendular nystagmus (APN) secondary to MS experienced complete resolution of APN when given memantine.17

Box

Memantine’s mechanism of action in dementia

Memantine was FDA-approved in 2003 to treat moderate-to-severe Alzheimer’s disease dementia. The drug also has been used off-label to treat vascular dementia, dementia of Wernicke-Korsakoff syndrome, and acquired pendular nystagmus.11

Although the neurobiologic basis for memantine’s therapeutic activity in patients with dementia is not fully understood, it is thought to reduce glutamatergic excitotoxicity. The mechanism of action is voltage-dependent, uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonism with low-to-moderate affinity and fast blocking/unblocking kinetics.12 Its kinetic profile is beneficial because it allows memantine to occupy the receptor for a sufficient time to prevent pathologic activation of glutamate receptors. However, it dissociates when the physiologic activation of glutamate receptors is necessary, thus preserving normal NMDA receptor activity required for learning and memory. By blocking the effects of abnormal glutamate activity, memantine may prevent abnormal neuronal cell death and cognitive dysfunction.

Related resources

  • Parsons CG, Stöffler A, Danysz W. Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system—too little activation is bad, too much is even worse. Neuropharmacology. 2007;53(6):699-723.
Drug brand names

  • Alprazolam • Xanax
  • Amitriptyline • Elavil
  • Budesonide • Rhinocort
  • Butalbital/Aspirin/Caffeine • Fiorinal
  • Conjugated Estrogens • Premarin
  • Esomeprazole • Nexium
  • Eszopiclone • Lunesta
  • Famotidine • Pepcid
  • Fexofenadine • Allegra
  • Interferon beta-1b • Betaseron
  • Levothyroxine • Synthroid
  • Memantine • Namenda
  • Propranolol • Inderal
  • Rizatriptan • Maxalt
  • Topiramate • Topamax
Disclosure

Dr. Rao is a speaker for Forest Pharmaceuticals.

Acknowledgement

The author thanks Alexander M. Timchak, MS-IV, Stritch School of Medicine, Loyola University, Chicago, for his assistance with this article.

Case: Worsening memory

Mrs. K, age 46, is being treated by a neurologist for stable relapsing-remitting multiple sclerosis (MS) and migraine headaches when she complains of worsening memory over the past 5 years. She reports having difficulty recalling details of recent events and conversations. She describes occasional word-finding difficulties and problems maintaining her train of thought. She forgets where she places things and has gotten lost while driving, even on familiar routes. Her husband reports she takes more time to process things in general.

Mrs. K’s cognitive decline has affected her daily life and ability to work. For 4 years, she has been an office assistant at a campground, where she takes phone reservations and keeps a site schedule. Formerly simple tasks—such as taking a phone number—have become increasingly difficult, and she cannot recall a list of 3 things to buy at the supermarket without writing them down.

Her psychiatric history is unremarkable for inpatient or outpatient treatment. She denies a history of head trauma or seizure disorder. Her medical history includes allergic rhinitis, hypothyroidism, mitral valve prolapse, fibrocystic breasts, endometriosis, and temporomandibular joint disorder. Mrs. K had a hysterectomy in 2006. She denies current alcohol or tobacco use.

As a teenager, Mrs. K suffered migraines but did not seek treatment, and her headaches remitted for about 10 years. At age 29, she started to experience tunnel vision. Three years later she reported bilateral foot numbness and was diagnosed with MS. She responded well to interferon beta-1b but her migraines returned, occurring several times a week. Her migraines are successfully treated with topiramate, 75 mg/d, for prophylactic therapy and rizatriptan, 10 mg, as needed for abortive therapy. Her medication regimen also includes:

  • eszopiclone, 2 mg/d, and amitriptyline, 10 mg/d, for insomnia
  • butalbital/aspirin/caffeine, 50/325/40 mg, as needed for tension headaches
  • fexofenadine, 12 mg/d, and budesonide, 32 mcg, 4 sprays/d, for allergy symptoms
  • esomeprazole, 80 mg/d, and famotidine, 20 mg/d, as needed for dyspepsia
  • propranolol, 120 mg/d, for hypertension
  • levothyroxine, 75 mcg/d, for hypothyroidism
  • conjugatedestrogens, 0.45 mg/d, for hypoestrogenemia
  • alprazolam, 0.25 mg/d, aspirin, 81 mg/d, vitamin E, 800 IU/d, and a multivitamin.
Her family history is remarkable for signs of neurocognitive degeneration in her father, age 75. She has 3 siblings with no known neurologic or neuropsychological symptoms.

The neurologist orders neuropsychological testing. Mrs. K demonstrates some depressive symptoms but is within normal limits across all aspects of neurocognition, including basic and complex attention, memory, bilateral motor functioning, expressive and receptive language, visuospatial/constructional function, and self-regulatory/executive functioning. The neurologist refers Mrs. K for psychiatric evaluation of her depressive symptoms.

The author’s observations

Many neuropsychiatric abnormalities may accompany MS (Table).1 These can be classified as cognitive dysfunction or disturbances in mood, affect, and behavior.

Although the cause of cognitive impairment in patients with MS is unclear, its extent and profound impact on functioning has become widely recognized over the past 20 years.2

An estimated 40% to 65% of patients with MS suffer from cognitive dysfunction.1,3 Testing indicates deficiencies most often in:

  • attention
  • information processing speed
  • working memory
  • verbal memory
  • visuospatial function
  • executive functions.4
Although in neuropsychological testing Mrs. K had scored within normal limits on memory, attention, and executive and visuospatial function, at the time of her psychiatric evaluation she is experiencing difficulties in all of these areas. Cognitive decline can occur early in the course of MS, but Mrs. K’s cognitive symptoms began approximately 10 years after she was diagnosed. The extent of the cognitive deficits commonly expands as the disease progresses.1 Cognitive dysfunction is the primary cause of MS patients’ withdrawal from the workplace5 and often leads to:

  • reduced social interactions
  • increased sexual dysfunction
  • greater difficulty with household tasks.6
When she first complained of memory loss, Mrs. K was taking topiramate for migraine prophylaxis. Multiple studies have demonstrated adverse cognitive effects from topiramate;7 however, Mrs. K had noticed substantial memory changes at least 2 years before starting topiramate. She denied experiencing worsening memory after starting topiramate and did not recall any major change after her dosage was increased to 75 mg/d. She chose to continue topiramate because it effectively prevented migraines and, in her mind, was unlikely related to her memory problems.

Long-term interferon beta-1b treatment prevents MS relapses, but a recent study found that interferon beta-1b had a negative impact on patients’ mental health composite score and in most quality-of-life subscales over 2 years.8 Nevertheless, Mrs. K received interferon beta-1b therapy for at least 9 years without noticing cognitive decline.

 

 

Table

Neuropsychiatric conditions associated with MS

DisorderPrevalence
Major depressionLifetime prevalence: 50%
Bipolar disorderEstimated prevalence is 10%, twice that of the general population
Euphoria25%
Pseudobulbar affectPathological laughing or crying, emotional incontinence; affects 10% of patients
Psychosis2% to 3% vs 0.5% to 1% in general population
Cognitive impairment40% to 60%
Source: Reference 1

EVALUATION: Dysthymia

Mrs. K reports memory problems as her chief complaint. She also complains of a depressed mood, irritability, distractibility, and insomnia since her memory problems began, and admits being readily tearful. Mrs. K has difficulty “turning off her thinking” at night, which leads to delayed sleep onset, but denies sleeplessness, racing thoughts, or feelings of euphoria.

During the mental status exam, she is cooperative, alert, and oriented to person, place, and time, but distractible. She is hypokinetic throughout the interview. Her speech is normal. She describes her mood as “empty” and scores 3 on a 1-to-5-point scale for depression severity. She demonstrates a constricted affect.

Her thought process is coherent and goal-directed, and she denies having auditory or visual hallucinations or active or passive suicidal or homicidal ideation. She scores 29/30 on the Mini-Mental State Exam, but by interview she appears to have impaired remote memory. Mrs. K demonstrates unimpaired judgment and good insight.

The author’s observations

Mrs. K meets DSM-IV-TR criteria for dysthymic disorder and agrees to start mirtazapine, 15 mg at bedtime. I chose this antidepressant because Mrs. K continues to complain of difficulty falling asleep, and mirtazapine is known to significantly decrease sleep latency and increase total sleep time. Approximately one-half of patients with MS will experience depression.1,9 In a recent study of 245 MS patients followed in a neurology clinic, two-thirds of those who met criteria for major depressive disorder did not receive antidepressants.10

TREATMENT: A new strategy

Mrs. K returns 2 months after starting mirtazapine and reports she is “doing the same.” Her mood is improved but still dysthymic. She again demonstrates irritability during her mental status examination and continues to complain of persistent memory problems. I titrate mirtazapine up to 30 mg/d.

After 2 more months Mrs. K’s mood is euthymic and she demonstrates a bright affect, but she experiences continued decline in short- and long-term memory and reports increasing frustration with simple tasks. The rest of her mental status exam is unremarkable. I instruct her to reduce the mirtazapine dosage to 15 mg/d.

At the next visit 10 weeks later, she again presents with a euthymic mood and a bright affect. She says she attempted to decrease mirtazapine but experienced increased irritability so she remained on the 30-mg dose, with a positive effect on her mood and reduced irritability. Unfortunately, her memory problems persist.

Approximately 2 years after Mrs. K’s first visit, I devise a new pharmacologic strategy. Mrs. K believes that she no longer is depressed and that her only problem is her inability to recall events. To address this, I decide to try memantine, which has been shown to cause modest improvement in clinical symptoms in severe stages of Alzheimer’s disease11 and also has been reported to be useful in the treatment of cognitive impairment in some bipolar disorder patients.12 I start memantine at 10 mg/d and titrate up to 20 mg/d in 3 months.

At 3 months, Mrs. K reports improvement that she describes as “life-changing.” She experiences improved memory in almost every aspect of daily functioning. She remembers daytime events and has stronger short-term memory. She can recall up to 4 items on a list several hours later, and no longer relies upon written lists to complete daily activities. Her husband and children also comment on her “remarkable” improvement.

The author’s observations

Mrs. K’s substantial memory improvement while receiving memantine warrants considering the drug for patients with cognitive dysfunction attributable to MS. Memantine is an uncompetitive NMDA receptor antagonist that the FDA approved in 2003 to treat moderate-to-severe Alzheimer’s disease (Box).11,13 It is generally well tolerated and safe, with a low potential for drug-drug interactions. In clinical trials of patients receiving memantine for Alzheimer’s disease and vascular dementia, the most commonly reported side effects were dizziness, headache, constipation, and confusion.14

A recent trial of memantine therapy for MS at the University of Navarra was suspended for reversible mild-to-moderate neurologic side effects.15 A phase II/phase III double-blind placebo-controlled trial at the University of Oregon designed to determine whether memantine is an effective treatment for memory and cognitive problems associated with MS is recruiting participants.16

 

 

Memantine has been reported to successfully treat other MS symptoms. A 1997 retrospective study found that 11 patients with acquired pendular nystagmus (APN) secondary to MS experienced complete resolution of APN when given memantine.17

Box

Memantine’s mechanism of action in dementia

Memantine was FDA-approved in 2003 to treat moderate-to-severe Alzheimer’s disease dementia. The drug also has been used off-label to treat vascular dementia, dementia of Wernicke-Korsakoff syndrome, and acquired pendular nystagmus.11

Although the neurobiologic basis for memantine’s therapeutic activity in patients with dementia is not fully understood, it is thought to reduce glutamatergic excitotoxicity. The mechanism of action is voltage-dependent, uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonism with low-to-moderate affinity and fast blocking/unblocking kinetics.12 Its kinetic profile is beneficial because it allows memantine to occupy the receptor for a sufficient time to prevent pathologic activation of glutamate receptors. However, it dissociates when the physiologic activation of glutamate receptors is necessary, thus preserving normal NMDA receptor activity required for learning and memory. By blocking the effects of abnormal glutamate activity, memantine may prevent abnormal neuronal cell death and cognitive dysfunction.

Related resources

  • Parsons CG, Stöffler A, Danysz W. Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system—too little activation is bad, too much is even worse. Neuropharmacology. 2007;53(6):699-723.
Drug brand names

  • Alprazolam • Xanax
  • Amitriptyline • Elavil
  • Budesonide • Rhinocort
  • Butalbital/Aspirin/Caffeine • Fiorinal
  • Conjugated Estrogens • Premarin
  • Esomeprazole • Nexium
  • Eszopiclone • Lunesta
  • Famotidine • Pepcid
  • Fexofenadine • Allegra
  • Interferon beta-1b • Betaseron
  • Levothyroxine • Synthroid
  • Memantine • Namenda
  • Propranolol • Inderal
  • Rizatriptan • Maxalt
  • Topiramate • Topamax
Disclosure

Dr. Rao is a speaker for Forest Pharmaceuticals.

Acknowledgement

The author thanks Alexander M. Timchak, MS-IV, Stritch School of Medicine, Loyola University, Chicago, for his assistance with this article.

References

1. Ghaffar O, Feinstein A. The neuropsychiatry of multiple sclerosis: a review of recent developments. Curr Opin Psychiatry. 2007;20(3):278-285.

2. Amato MP, Portaccio E, Zipoli V. Are there protective treatments for cognitive decline in MS? J Neurol Sci. 2006;245(1-2):183-186.

3. Bobholz JA, Rao SM. Cognitive dysfunction in multiple sclerosis: a review of recent developments. Curr Opin Neurol. 2003;16(3):283-288.

4. Hoffmann S, Tittgemeyer M, von Cramon DY. Cognitive impairment in multiple sclerosis. Curr Opin Neurol. 2007;20(3):275-280.

5. Pierson SH, Griffith N. Treatment of cognitive impairment in multiple sclerosis. Behav Neurol. 2006;17(1):53-67.

6. Bagert B, Camplair P, Bourdette D. Cognitive dysfunction in multiple sclerosis: natural history, pathophysiology and management. CNS Drugs. 2002;16(7):445-455.

7. Martin R, Kuzniecky R, Ho S, et al. Cognitive effects of topiramate, gabapentin, and lamotrigine in healthy young adults. Neurology. 1999;52(2):321-327.

8. Simone IL, Ceccarelli A, Tortorella C, et al. Influence of Interferon beta treatment on quality of life in multiple sclerosis patients. Health Qual Life Outcomes. 2006;4:96.-

9. Siegert RJ, Abernethy DA. Depression in multiple sclerosis: a review. J Neurol Neurosurg Psychiatry. 2005;76(4):469-475.

10. Mohr DC, Hart SL, Fonareva I, et al. Treatment of depression for patients with multiple sclerosis in neurology clinics. Mult Scler. 2006;12(2):204-208.

11. Kumar S. Memantine: pharmacological properties and clinical uses. Neurol India. 2004;52(3):307-309.

12. Teng CT, Demetrio FN. Memantine may acutely improve cognition and have a mood stabilizing effect in treatment-resistant bipolar disorder. Rev Bras Psiquiatr. 2006;28(3):252-4.

13. Danysz W, Parsons CG, Mobius HJ, et al. Neuroprotective and symptomatological action of memantine relevant for Alzheimer’s disease: a unified glutamatergic hypothesis on the mechanism of action. Neurotox Res. 2000;2(2-3):85-97.

14. Namenda [package insert] St. Louis, MO: Forest Pharmaceuticals; 2007.

15. Memantine therapy for multiple sclerosis (NCT00638833) Available at: http://www.clinicaltrials.gov/ct2/show/NCT00638833. Accessed February 17, 2009.

16. Trial of memantine for cognitive impairment in multiple sclerosis (NCT00300716) Available at: http://www.clinicaltrials.gov/ct2/show/NCT00300716. Accessed February 17, 2009.

17. Starck M, Albrecht H, Pöllmann W, et al. Drug therapy for acquired pendular nystagmus in multiple sclerosis. J Neurol. 1997;244(1):9-16.

References

1. Ghaffar O, Feinstein A. The neuropsychiatry of multiple sclerosis: a review of recent developments. Curr Opin Psychiatry. 2007;20(3):278-285.

2. Amato MP, Portaccio E, Zipoli V. Are there protective treatments for cognitive decline in MS? J Neurol Sci. 2006;245(1-2):183-186.

3. Bobholz JA, Rao SM. Cognitive dysfunction in multiple sclerosis: a review of recent developments. Curr Opin Neurol. 2003;16(3):283-288.

4. Hoffmann S, Tittgemeyer M, von Cramon DY. Cognitive impairment in multiple sclerosis. Curr Opin Neurol. 2007;20(3):275-280.

5. Pierson SH, Griffith N. Treatment of cognitive impairment in multiple sclerosis. Behav Neurol. 2006;17(1):53-67.

6. Bagert B, Camplair P, Bourdette D. Cognitive dysfunction in multiple sclerosis: natural history, pathophysiology and management. CNS Drugs. 2002;16(7):445-455.

7. Martin R, Kuzniecky R, Ho S, et al. Cognitive effects of topiramate, gabapentin, and lamotrigine in healthy young adults. Neurology. 1999;52(2):321-327.

8. Simone IL, Ceccarelli A, Tortorella C, et al. Influence of Interferon beta treatment on quality of life in multiple sclerosis patients. Health Qual Life Outcomes. 2006;4:96.-

9. Siegert RJ, Abernethy DA. Depression in multiple sclerosis: a review. J Neurol Neurosurg Psychiatry. 2005;76(4):469-475.

10. Mohr DC, Hart SL, Fonareva I, et al. Treatment of depression for patients with multiple sclerosis in neurology clinics. Mult Scler. 2006;12(2):204-208.

11. Kumar S. Memantine: pharmacological properties and clinical uses. Neurol India. 2004;52(3):307-309.

12. Teng CT, Demetrio FN. Memantine may acutely improve cognition and have a mood stabilizing effect in treatment-resistant bipolar disorder. Rev Bras Psiquiatr. 2006;28(3):252-4.

13. Danysz W, Parsons CG, Mobius HJ, et al. Neuroprotective and symptomatological action of memantine relevant for Alzheimer’s disease: a unified glutamatergic hypothesis on the mechanism of action. Neurotox Res. 2000;2(2-3):85-97.

14. Namenda [package insert] St. Louis, MO: Forest Pharmaceuticals; 2007.

15. Memantine therapy for multiple sclerosis (NCT00638833) Available at: http://www.clinicaltrials.gov/ct2/show/NCT00638833. Accessed February 17, 2009.

16. Trial of memantine for cognitive impairment in multiple sclerosis (NCT00300716) Available at: http://www.clinicaltrials.gov/ct2/show/NCT00300716. Accessed February 17, 2009.

17. Starck M, Albrecht H, Pöllmann W, et al. Drug therapy for acquired pendular nystagmus in multiple sclerosis. J Neurol. 1997;244(1):9-16.

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Workplace mobbing: Are they really out to get your patient?

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Mr. G, age 46, works for a large federal government agency in a middle-management position. He presents seeking treatment for insomnia. He says, “I just need a sleeping pill. I haven’t been able to sleep for the last 3 months because everybody at work is talking behind my back and spreading rumors about how I’m crazy. My boss is in on it, too. She is always trying to undermine me and makes a big deal out of every little mistake I make.”

Mr. G is suspicious, asking questions about the confidentiality of medical records. His speech is rapid, and he is anxious but exhibits a full range of affect and no pressured speech or flight of ideas. Mr. G describes early, middle, and late insomnia, decreased energy and interest, and gaining 10 pounds over the past 3 months.

He admits owning a gun and having frequent thoughts of suicide and fantasies of killing his boss, although Mr. G repeatedly affirms he would never act on these thoughts. A week ago, his wife moved in with her parents because, he says, “she just couldn’t stand to be around me any longer.”

I consider involuntary hospitalization for Mr. G. Ultimately I contact his wife, who agrees to pick him up, stay with him overnight, and return with him the next morning. Because the only medication Mr. G is willing to consider is sleeping pills, I prescribe flurazepam, 30 mg qhs.

Mr. G was apparently paranoid, thinking of killing his boss, and had a gun. If his wife had not answered the phone and been willing to stay with him, he might have been involuntarily committed. As it was, further interviews with him revealed that Mr. G had been a target of workplace “mobbing,” and that his insomnia and paranoia developed because of a deliberate campaign by coworkers.

This article discusses how to recognize symptoms of workplace mobbing, using Mr. G’s experience to illustrate the dynamics of this group behavior. An informed mental health professional can be of enormous help to a mobbing victim, but an uninformed professional can unwittingly make the situation much worse.

What is ‘mobbing’?

Initiated most often by a person in a position of power or influence, mobbing has been described as “a desperate urge to crush and eliminate the target…. As the campaign proceeds, a steadily larger range of hostile ploys and communications comes to be seen as legitimate.”1 This behavior pattern has been recognized in Europe since the 1980s but is not well recognized in the United States.

Davenport et al2 brought the phenomenon and its consequences to the U.S. public’s attention in 1999 with the publication of Mobbing: emotional abuse in the American workplace. Otherwise, little professional literature on workplace mobbing has been produced in the United States.

A PubMed search on the term “mobbing” limited to 1982 through October 2008 returned 95 listings, excluding those dealing purely with ethology, but only 1 report from the United States. Studies from outside the United States indicate that mobbing is relatively common (Box).

Mobbing, bullying, and harassment. The term “workplace mobbing” was coined by Leymann,3 an occupational psychologist who investigated the psychology of workers who had suffered severe trauma. He observed that some of the most severe reactions were among workers who had been the target of “an impassioned collective campaign by coworkers to exclude, punish, or humiliate” them.

Many researchers use the term mobbing to describe a negative work environment created by several individuals working together.13 However, some researchers such as Namie et al4 use the term workplace bullying to describe the creation of a hostile work environment by either a single individual—usually a boss—or a number of individuals.

Box

Workplace mobbing: How often does it occur?

In 1990 Leymann3 estimated that 3.5% of the Swedish workforce had been victims of significant mobbing. Studies from various other European countries have estimated prevalence of mobbing at 4% to 15% of the total workforce.10

Studies from Europe have shown that all age groups can be affected, but that posttraumatic stress disorder among mobbing victims is more common in patients age >40. Both genders are equally at risk.6

CASE CONTINUED: Why I first thought ‘paranoia’

During our first interview, Mr. G said that 6 months before he sought treatment he had reported misuse of government property by his supervisor’s boss. The case was investigated and dismissed. Mr. G’s supervisor never confronted him about the complaint, but shortly afterwards Mr. G started to notice disturbing changes in the workplace.

 

 

His supervisor avoided Mr. G’s phone calls and e-mails and stopped meeting with him. Instead, she met with Mr. G’s subordinates. The subordinates started to ignore Mr. G’s instructions and would roll their eyes or be inattentive when he spoke. Coworkers stopped talking when Mr. G approached, and he started receiving anonymous e-mails questioning his ability and sanity. He was reprimanded in writing for having made a $9 mathematical error in an expense reimbursement request.

Mr. G said when he approached his superior about the work environment, she stated that he was “just paranoid” and needed to see a psychiatrist.

When Mr. G’s wife accompanies him to the second interview, she confirms his impressions of ostracism and gossip at work. She also relates her experiences with people from Mr. G’s office who previously had been friendly but now were distant or hostile. Mr. G shows me copies of harassing work e-mails and memos. I tell Mr. G I believe his story and diagnose him as suffering from posttraumatic stress disorder (PTSD). He begins supportive/cognitive therapy and continues flurazepam.

Mobbing syndrome

As it turns out, Mr. G was not paranoid; his coworkers really were trying to get him. Leymann5 divided 45 types of mobbing behaviors into 5 categories. These were organized as attacks on:

  • self-expression and ability to communicate (victim is silenced, given no opportunity to communicate, subject to verbal attacks)
  • social relationships (colleagues do not talk to the victim, victim is physically isolated from others)
  • reputation (victim is the target of gossip and ridicule)
  • occupational situation (victim is given meaningless tasks or no work at all)
  • physical health (victim is assigned dangerous tasks, threatened with bodily harm, or physically attacked).
Davenport et al2 distilled this list into 10 key factors of the mobbing syndrome (Table 1); identified 5 phases in the mobbing process (Table 2); and defined 3 “degrees” of mobbing analogous to first-, second-, and third-degree burns (Table 3).

Table 1

Mobbing syndrome: 10 factors

Assaults on dignity, integrity, credibility, and competence
Negative, humiliating, intimidating, abusive, malevolent, and controlling communication
Committed directly or indirectly in subtle or obvious ways
Perpetrated by ≥1 staff members*
Occurring in a continual, multiple, and systematic fashion over time
Portraying the victim as being at fault
Engineered to discredit, confuse, intimidate, isolate, and force the person into submission
Committed with the intent to force the person out
Representing the removal as the victim’s choice
Unrecognized, misinterpreted, ignored, tolerated, encouraged, or even instigated by management
*Some researchers limit their definition of mobbing to acts committed by >1 person
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:41
Mobbing risk factors. According to Leymann,5 no specific personality factors predispose workers to being mobbed. Westhues1 and others, however, identify a variety of social risk factors. These include any factors that make an individual different from other members of his or her work environment, such as:

  • different ethnicity
  • an “odd” personality
  • high achievement.
Table 2

Phases of mobbing

Conflict, often characterized by a ‘critical incident’
Aggressive acts, such as those in Table 1
Management involvement
Branding as difficult or mentally ill
Expulsion or resignation from the workplace
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:38
Whistleblowers or union organizers also run a risk of stigmatization and mobbing. Organizations with unclear goals or extensive recent turnover in senior leadership can be conducive to mobbing. Three industries identified as at special risk for mobbing are academia, government, and religious organizations.5

Secondary morbidity. Victims of workplace mobbing frequently suffer from:

  • adjustment disorders
  • somatic symptoms (eg, headaches or irritable bowel syndrome)
  • PTSD6,7
  • major depression.8
In mobbing targets with PTSD, Leymann notes that the “mental effects were fully comparable with PTSD from war or prison camp experiences.”3 Some patients may develop alcoholism or other substance abuse disorders. Family relationships routinely suffer.9 Some targets may even develop brief psychotic episodes, generally with paranoid symptoms.

Leymann3 estimated that 15% of suicides in Sweden could be directly attributed to workplace mobbing. Although no other researcher has reported such a dramatic proportion, others have reported increased risk of suicidal behavior among mobbing victims.10

Table 3

Degrees of mobbing

First degree: Victim manages to resist, escapes at an early stage, or is fully rehabilitated in the original workplace or elsewhere
Second degree: Victim cannot resist or escape immediately and suffers temporary or prolonged mental and/or physical disability and has difficulty reentering the workforce
Third degree: Victim is unable to reenter the workforce and suffers serious, long-lasting mental or physical disability
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:39
 

 

CASE CONTINUED: Redirecting energy into a job search

As I met with Mr. G over the next 3 months, the pattern of malicious communication and actions continued at his office. For example, he received a written reprimand for being 10 minutes late after having overslept when starting flurazepam, which he continued to take for about 6 weeks without further tardiness. I encouraged Mr. G to withdraw energy from work by keeping a low profile and trying not to react to provocations. Instead, I counseled him to put energy into family activities and try to find a new job.

Within 3 months, Mr. G found a new position in the private sector at a similar salary, although with lower benefits. Six months later, he was still with his wife, had been promoted at his new job, lost the 10 pounds he gained, discontinued psychotherapy, and was sleeping well without medication. He reported that he still thinks “almost every day” about what happened in his previous job but keeps telling himself “everything did work out OK after all.”

Mr. G experienced relatively mild, first-degree workplace mobbing, but it had a substantial effect on his quality of life and that of his wife for almost 1 year. If I had followed my first impulse and had Mr. G involuntarily hospitalized after our first interview, it would have confirmed rumors at his office and probably would have escalated the mobbing behavior.

Diagnostic recommendations

Consider the possibility that seemingly paranoid individuals could be the target of mobbing at work, and don’t underestimate the psychological stress of being mobbed. Other forms of workplace harassment can be extremely stressful but do not have the “paranoidogenic” potential of mobbing. Patients may be so distressed that it is difficult to figure out what is going on in their work environment.

Ask patients to present physical evidence of conspiracy or harassment. Mobbing patients usually are willing to bring in large quantities of material. Keep in mind that when subjected to mobbing behavior over time, a person who is not initially paranoid is likely to develop some secondary suspiciousness and even frank paranoia.

Also consider the possibility of “pseudomobbing,” in which an individual falsely believes he or she is a mobbing victim. Cases of pseudomobbing have been reported in European literature11 and may represent a negative side effect of greater public awareness of the mobbing phenomenon (and of legal remedies to mobbing available in various European countries).

Mobbing is a serious stressor that can lead to psychiatric and medical morbidity and even suicide. Major depressive disorder—often with suicidal ideation—is frequently associated with being mobbed.12

A diagnosis of PTSD can be missed if the mobbing victim does not seem to have been subjected to a severe enough stress to meet PTSD criteria.

Treatment recommendations

First, do no harm: Do not allow yourself to be used by the mob. This process can be direct—as in the Mr. G’s case, where the patient was almost involuntarily committed—or subtle. For example, a person you know may describe the behavior of “someone at work,” and you may be tempted to respond, “Well, I have not examined this person, but from what you say, it sounds like maybe…” You could then be quoted as a psychiatrist who agrees that the person is paranoid.

Giving your patient a name for what is happening to him or her may be the most therapeutic intervention. Generally, patients have not heard of mobbing. They typically are confused about what is happening and may blame themselves.

Treat the patient’s family. Giving a patient’s spouse or partner a name for what is happening is almost always helpful. One-third of mobbing victims suffer breakup of their marriages or relationships during the course of a mobbing, which can create a vicious cycle of stress, leading to isolation, leading to more stress.3 Encourage the patient not to subject the spouse to repeated ruminations about insults at work.

Treat secondary symptoms of depression, anxiety, PTSD, or other sequelae with pharmacotherapy, psychotherapy, or a combination as appropriate. Refer patients with somatic symptoms to primary care if you feel that they need further evaluation.

Encourage your patient to visualize choices and ways to escape the situation. Frequently, patients will be locked into “fighting for justice” or putting up with the situation because they see no options.

 

 

Encourage your patient to withdraw energy from work and invest it in family, social life, or anything else. At the appropriate time, encourage him or her to grieve losses experienced as a result of the mobbing.

Related resources

Drug brand name

  • Flurazepam • Dalmane
Disclosure

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

References

1. Westhues K. At the mercy of the mob: a summary of research on workplace mobbing. Canada’s Occupational Health and Safety Magazine. 2002;18:30-36.

2. Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999.

3. Leymann H. Mobbing and psychological terror at workplaces. Violence Vict. 1990;5:119-125.

4. Namie G, Namie R. The bully at work: what you can do to stop the hurt and reclaim your dignity on the job. Naperville, IL: Sourcebooks, Inc; 2003.

5. Leymann H. The content and development of mobbing at work. European Journal of Work and Organizational Psychology. 1996;5:165-184.

6. Leymann H, Gustafsson A. Mobbing at work and the development of post-traumatic stress disorders. European Journal of Work and Organizational Psychology. 1996;5:251-275.

7. Bonafons C, Jehel L, Coroller-Bequet A. Specificity of the links between workplace harassment and PTSD: primary results using court decisions, a pilot study in France. Int Arch Occup Environ Health. 2008 Oct 25 (Epub ahead of print).

8. Girardi P, Monaco C, Prestigiacomo C, et al. Personality and psychopathological profiles in individuals exposed to mobbing. Violence Vict. 2007;22:172-188.

9. Duffy M. Workplace mobbing: individual and family health consequences. The Family Journal. 2007;15:398-404.

10. Pompili M, Lester D, Innamorati M, et al. Suicide risk and exposure to mobbing. Work. 2008;31:237-243.

11. Jarreta BM. Medico-legal implications of mobbing. A false accusation of psychological harassment at the workplace. Forensic Sci Int. 2004;146(suppl):S17-S18.

12. Girardi P, Monaco E, Prestigiacomo C, et al. Personality and psychopathological profiles in individuals exposed to mobbing. Violence Vict. 2007;22(2):172-188.

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Comment on this article

Mr. G, age 46, works for a large federal government agency in a middle-management position. He presents seeking treatment for insomnia. He says, “I just need a sleeping pill. I haven’t been able to sleep for the last 3 months because everybody at work is talking behind my back and spreading rumors about how I’m crazy. My boss is in on it, too. She is always trying to undermine me and makes a big deal out of every little mistake I make.”

Mr. G is suspicious, asking questions about the confidentiality of medical records. His speech is rapid, and he is anxious but exhibits a full range of affect and no pressured speech or flight of ideas. Mr. G describes early, middle, and late insomnia, decreased energy and interest, and gaining 10 pounds over the past 3 months.

He admits owning a gun and having frequent thoughts of suicide and fantasies of killing his boss, although Mr. G repeatedly affirms he would never act on these thoughts. A week ago, his wife moved in with her parents because, he says, “she just couldn’t stand to be around me any longer.”

I consider involuntary hospitalization for Mr. G. Ultimately I contact his wife, who agrees to pick him up, stay with him overnight, and return with him the next morning. Because the only medication Mr. G is willing to consider is sleeping pills, I prescribe flurazepam, 30 mg qhs.

Mr. G was apparently paranoid, thinking of killing his boss, and had a gun. If his wife had not answered the phone and been willing to stay with him, he might have been involuntarily committed. As it was, further interviews with him revealed that Mr. G had been a target of workplace “mobbing,” and that his insomnia and paranoia developed because of a deliberate campaign by coworkers.

This article discusses how to recognize symptoms of workplace mobbing, using Mr. G’s experience to illustrate the dynamics of this group behavior. An informed mental health professional can be of enormous help to a mobbing victim, but an uninformed professional can unwittingly make the situation much worse.

What is ‘mobbing’?

Initiated most often by a person in a position of power or influence, mobbing has been described as “a desperate urge to crush and eliminate the target…. As the campaign proceeds, a steadily larger range of hostile ploys and communications comes to be seen as legitimate.”1 This behavior pattern has been recognized in Europe since the 1980s but is not well recognized in the United States.

Davenport et al2 brought the phenomenon and its consequences to the U.S. public’s attention in 1999 with the publication of Mobbing: emotional abuse in the American workplace. Otherwise, little professional literature on workplace mobbing has been produced in the United States.

A PubMed search on the term “mobbing” limited to 1982 through October 2008 returned 95 listings, excluding those dealing purely with ethology, but only 1 report from the United States. Studies from outside the United States indicate that mobbing is relatively common (Box).

Mobbing, bullying, and harassment. The term “workplace mobbing” was coined by Leymann,3 an occupational psychologist who investigated the psychology of workers who had suffered severe trauma. He observed that some of the most severe reactions were among workers who had been the target of “an impassioned collective campaign by coworkers to exclude, punish, or humiliate” them.

Many researchers use the term mobbing to describe a negative work environment created by several individuals working together.13 However, some researchers such as Namie et al4 use the term workplace bullying to describe the creation of a hostile work environment by either a single individual—usually a boss—or a number of individuals.

Box

Workplace mobbing: How often does it occur?

In 1990 Leymann3 estimated that 3.5% of the Swedish workforce had been victims of significant mobbing. Studies from various other European countries have estimated prevalence of mobbing at 4% to 15% of the total workforce.10

Studies from Europe have shown that all age groups can be affected, but that posttraumatic stress disorder among mobbing victims is more common in patients age >40. Both genders are equally at risk.6

CASE CONTINUED: Why I first thought ‘paranoia’

During our first interview, Mr. G said that 6 months before he sought treatment he had reported misuse of government property by his supervisor’s boss. The case was investigated and dismissed. Mr. G’s supervisor never confronted him about the complaint, but shortly afterwards Mr. G started to notice disturbing changes in the workplace.

 

 

His supervisor avoided Mr. G’s phone calls and e-mails and stopped meeting with him. Instead, she met with Mr. G’s subordinates. The subordinates started to ignore Mr. G’s instructions and would roll their eyes or be inattentive when he spoke. Coworkers stopped talking when Mr. G approached, and he started receiving anonymous e-mails questioning his ability and sanity. He was reprimanded in writing for having made a $9 mathematical error in an expense reimbursement request.

Mr. G said when he approached his superior about the work environment, she stated that he was “just paranoid” and needed to see a psychiatrist.

When Mr. G’s wife accompanies him to the second interview, she confirms his impressions of ostracism and gossip at work. She also relates her experiences with people from Mr. G’s office who previously had been friendly but now were distant or hostile. Mr. G shows me copies of harassing work e-mails and memos. I tell Mr. G I believe his story and diagnose him as suffering from posttraumatic stress disorder (PTSD). He begins supportive/cognitive therapy and continues flurazepam.

Mobbing syndrome

As it turns out, Mr. G was not paranoid; his coworkers really were trying to get him. Leymann5 divided 45 types of mobbing behaviors into 5 categories. These were organized as attacks on:

  • self-expression and ability to communicate (victim is silenced, given no opportunity to communicate, subject to verbal attacks)
  • social relationships (colleagues do not talk to the victim, victim is physically isolated from others)
  • reputation (victim is the target of gossip and ridicule)
  • occupational situation (victim is given meaningless tasks or no work at all)
  • physical health (victim is assigned dangerous tasks, threatened with bodily harm, or physically attacked).
Davenport et al2 distilled this list into 10 key factors of the mobbing syndrome (Table 1); identified 5 phases in the mobbing process (Table 2); and defined 3 “degrees” of mobbing analogous to first-, second-, and third-degree burns (Table 3).

Table 1

Mobbing syndrome: 10 factors

Assaults on dignity, integrity, credibility, and competence
Negative, humiliating, intimidating, abusive, malevolent, and controlling communication
Committed directly or indirectly in subtle or obvious ways
Perpetrated by ≥1 staff members*
Occurring in a continual, multiple, and systematic fashion over time
Portraying the victim as being at fault
Engineered to discredit, confuse, intimidate, isolate, and force the person into submission
Committed with the intent to force the person out
Representing the removal as the victim’s choice
Unrecognized, misinterpreted, ignored, tolerated, encouraged, or even instigated by management
*Some researchers limit their definition of mobbing to acts committed by >1 person
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:41
Mobbing risk factors. According to Leymann,5 no specific personality factors predispose workers to being mobbed. Westhues1 and others, however, identify a variety of social risk factors. These include any factors that make an individual different from other members of his or her work environment, such as:

  • different ethnicity
  • an “odd” personality
  • high achievement.
Table 2

Phases of mobbing

Conflict, often characterized by a ‘critical incident’
Aggressive acts, such as those in Table 1
Management involvement
Branding as difficult or mentally ill
Expulsion or resignation from the workplace
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:38
Whistleblowers or union organizers also run a risk of stigmatization and mobbing. Organizations with unclear goals or extensive recent turnover in senior leadership can be conducive to mobbing. Three industries identified as at special risk for mobbing are academia, government, and religious organizations.5

Secondary morbidity. Victims of workplace mobbing frequently suffer from:

  • adjustment disorders
  • somatic symptoms (eg, headaches or irritable bowel syndrome)
  • PTSD6,7
  • major depression.8
In mobbing targets with PTSD, Leymann notes that the “mental effects were fully comparable with PTSD from war or prison camp experiences.”3 Some patients may develop alcoholism or other substance abuse disorders. Family relationships routinely suffer.9 Some targets may even develop brief psychotic episodes, generally with paranoid symptoms.

Leymann3 estimated that 15% of suicides in Sweden could be directly attributed to workplace mobbing. Although no other researcher has reported such a dramatic proportion, others have reported increased risk of suicidal behavior among mobbing victims.10

Table 3

Degrees of mobbing

First degree: Victim manages to resist, escapes at an early stage, or is fully rehabilitated in the original workplace or elsewhere
Second degree: Victim cannot resist or escape immediately and suffers temporary or prolonged mental and/or physical disability and has difficulty reentering the workforce
Third degree: Victim is unable to reenter the workforce and suffers serious, long-lasting mental or physical disability
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:39
 

 

CASE CONTINUED: Redirecting energy into a job search

As I met with Mr. G over the next 3 months, the pattern of malicious communication and actions continued at his office. For example, he received a written reprimand for being 10 minutes late after having overslept when starting flurazepam, which he continued to take for about 6 weeks without further tardiness. I encouraged Mr. G to withdraw energy from work by keeping a low profile and trying not to react to provocations. Instead, I counseled him to put energy into family activities and try to find a new job.

Within 3 months, Mr. G found a new position in the private sector at a similar salary, although with lower benefits. Six months later, he was still with his wife, had been promoted at his new job, lost the 10 pounds he gained, discontinued psychotherapy, and was sleeping well without medication. He reported that he still thinks “almost every day” about what happened in his previous job but keeps telling himself “everything did work out OK after all.”

Mr. G experienced relatively mild, first-degree workplace mobbing, but it had a substantial effect on his quality of life and that of his wife for almost 1 year. If I had followed my first impulse and had Mr. G involuntarily hospitalized after our first interview, it would have confirmed rumors at his office and probably would have escalated the mobbing behavior.

Diagnostic recommendations

Consider the possibility that seemingly paranoid individuals could be the target of mobbing at work, and don’t underestimate the psychological stress of being mobbed. Other forms of workplace harassment can be extremely stressful but do not have the “paranoidogenic” potential of mobbing. Patients may be so distressed that it is difficult to figure out what is going on in their work environment.

Ask patients to present physical evidence of conspiracy or harassment. Mobbing patients usually are willing to bring in large quantities of material. Keep in mind that when subjected to mobbing behavior over time, a person who is not initially paranoid is likely to develop some secondary suspiciousness and even frank paranoia.

Also consider the possibility of “pseudomobbing,” in which an individual falsely believes he or she is a mobbing victim. Cases of pseudomobbing have been reported in European literature11 and may represent a negative side effect of greater public awareness of the mobbing phenomenon (and of legal remedies to mobbing available in various European countries).

Mobbing is a serious stressor that can lead to psychiatric and medical morbidity and even suicide. Major depressive disorder—often with suicidal ideation—is frequently associated with being mobbed.12

A diagnosis of PTSD can be missed if the mobbing victim does not seem to have been subjected to a severe enough stress to meet PTSD criteria.

Treatment recommendations

First, do no harm: Do not allow yourself to be used by the mob. This process can be direct—as in the Mr. G’s case, where the patient was almost involuntarily committed—or subtle. For example, a person you know may describe the behavior of “someone at work,” and you may be tempted to respond, “Well, I have not examined this person, but from what you say, it sounds like maybe…” You could then be quoted as a psychiatrist who agrees that the person is paranoid.

Giving your patient a name for what is happening to him or her may be the most therapeutic intervention. Generally, patients have not heard of mobbing. They typically are confused about what is happening and may blame themselves.

Treat the patient’s family. Giving a patient’s spouse or partner a name for what is happening is almost always helpful. One-third of mobbing victims suffer breakup of their marriages or relationships during the course of a mobbing, which can create a vicious cycle of stress, leading to isolation, leading to more stress.3 Encourage the patient not to subject the spouse to repeated ruminations about insults at work.

Treat secondary symptoms of depression, anxiety, PTSD, or other sequelae with pharmacotherapy, psychotherapy, or a combination as appropriate. Refer patients with somatic symptoms to primary care if you feel that they need further evaluation.

Encourage your patient to visualize choices and ways to escape the situation. Frequently, patients will be locked into “fighting for justice” or putting up with the situation because they see no options.

 

 

Encourage your patient to withdraw energy from work and invest it in family, social life, or anything else. At the appropriate time, encourage him or her to grieve losses experienced as a result of the mobbing.

Related resources

Drug brand name

  • Flurazepam • Dalmane
Disclosure

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

Comment on this article

Mr. G, age 46, works for a large federal government agency in a middle-management position. He presents seeking treatment for insomnia. He says, “I just need a sleeping pill. I haven’t been able to sleep for the last 3 months because everybody at work is talking behind my back and spreading rumors about how I’m crazy. My boss is in on it, too. She is always trying to undermine me and makes a big deal out of every little mistake I make.”

Mr. G is suspicious, asking questions about the confidentiality of medical records. His speech is rapid, and he is anxious but exhibits a full range of affect and no pressured speech or flight of ideas. Mr. G describes early, middle, and late insomnia, decreased energy and interest, and gaining 10 pounds over the past 3 months.

He admits owning a gun and having frequent thoughts of suicide and fantasies of killing his boss, although Mr. G repeatedly affirms he would never act on these thoughts. A week ago, his wife moved in with her parents because, he says, “she just couldn’t stand to be around me any longer.”

I consider involuntary hospitalization for Mr. G. Ultimately I contact his wife, who agrees to pick him up, stay with him overnight, and return with him the next morning. Because the only medication Mr. G is willing to consider is sleeping pills, I prescribe flurazepam, 30 mg qhs.

Mr. G was apparently paranoid, thinking of killing his boss, and had a gun. If his wife had not answered the phone and been willing to stay with him, he might have been involuntarily committed. As it was, further interviews with him revealed that Mr. G had been a target of workplace “mobbing,” and that his insomnia and paranoia developed because of a deliberate campaign by coworkers.

This article discusses how to recognize symptoms of workplace mobbing, using Mr. G’s experience to illustrate the dynamics of this group behavior. An informed mental health professional can be of enormous help to a mobbing victim, but an uninformed professional can unwittingly make the situation much worse.

What is ‘mobbing’?

Initiated most often by a person in a position of power or influence, mobbing has been described as “a desperate urge to crush and eliminate the target…. As the campaign proceeds, a steadily larger range of hostile ploys and communications comes to be seen as legitimate.”1 This behavior pattern has been recognized in Europe since the 1980s but is not well recognized in the United States.

Davenport et al2 brought the phenomenon and its consequences to the U.S. public’s attention in 1999 with the publication of Mobbing: emotional abuse in the American workplace. Otherwise, little professional literature on workplace mobbing has been produced in the United States.

A PubMed search on the term “mobbing” limited to 1982 through October 2008 returned 95 listings, excluding those dealing purely with ethology, but only 1 report from the United States. Studies from outside the United States indicate that mobbing is relatively common (Box).

Mobbing, bullying, and harassment. The term “workplace mobbing” was coined by Leymann,3 an occupational psychologist who investigated the psychology of workers who had suffered severe trauma. He observed that some of the most severe reactions were among workers who had been the target of “an impassioned collective campaign by coworkers to exclude, punish, or humiliate” them.

Many researchers use the term mobbing to describe a negative work environment created by several individuals working together.13 However, some researchers such as Namie et al4 use the term workplace bullying to describe the creation of a hostile work environment by either a single individual—usually a boss—or a number of individuals.

Box

Workplace mobbing: How often does it occur?

In 1990 Leymann3 estimated that 3.5% of the Swedish workforce had been victims of significant mobbing. Studies from various other European countries have estimated prevalence of mobbing at 4% to 15% of the total workforce.10

Studies from Europe have shown that all age groups can be affected, but that posttraumatic stress disorder among mobbing victims is more common in patients age >40. Both genders are equally at risk.6

CASE CONTINUED: Why I first thought ‘paranoia’

During our first interview, Mr. G said that 6 months before he sought treatment he had reported misuse of government property by his supervisor’s boss. The case was investigated and dismissed. Mr. G’s supervisor never confronted him about the complaint, but shortly afterwards Mr. G started to notice disturbing changes in the workplace.

 

 

His supervisor avoided Mr. G’s phone calls and e-mails and stopped meeting with him. Instead, she met with Mr. G’s subordinates. The subordinates started to ignore Mr. G’s instructions and would roll their eyes or be inattentive when he spoke. Coworkers stopped talking when Mr. G approached, and he started receiving anonymous e-mails questioning his ability and sanity. He was reprimanded in writing for having made a $9 mathematical error in an expense reimbursement request.

Mr. G said when he approached his superior about the work environment, she stated that he was “just paranoid” and needed to see a psychiatrist.

When Mr. G’s wife accompanies him to the second interview, she confirms his impressions of ostracism and gossip at work. She also relates her experiences with people from Mr. G’s office who previously had been friendly but now were distant or hostile. Mr. G shows me copies of harassing work e-mails and memos. I tell Mr. G I believe his story and diagnose him as suffering from posttraumatic stress disorder (PTSD). He begins supportive/cognitive therapy and continues flurazepam.

Mobbing syndrome

As it turns out, Mr. G was not paranoid; his coworkers really were trying to get him. Leymann5 divided 45 types of mobbing behaviors into 5 categories. These were organized as attacks on:

  • self-expression and ability to communicate (victim is silenced, given no opportunity to communicate, subject to verbal attacks)
  • social relationships (colleagues do not talk to the victim, victim is physically isolated from others)
  • reputation (victim is the target of gossip and ridicule)
  • occupational situation (victim is given meaningless tasks or no work at all)
  • physical health (victim is assigned dangerous tasks, threatened with bodily harm, or physically attacked).
Davenport et al2 distilled this list into 10 key factors of the mobbing syndrome (Table 1); identified 5 phases in the mobbing process (Table 2); and defined 3 “degrees” of mobbing analogous to first-, second-, and third-degree burns (Table 3).

Table 1

Mobbing syndrome: 10 factors

Assaults on dignity, integrity, credibility, and competence
Negative, humiliating, intimidating, abusive, malevolent, and controlling communication
Committed directly or indirectly in subtle or obvious ways
Perpetrated by ≥1 staff members*
Occurring in a continual, multiple, and systematic fashion over time
Portraying the victim as being at fault
Engineered to discredit, confuse, intimidate, isolate, and force the person into submission
Committed with the intent to force the person out
Representing the removal as the victim’s choice
Unrecognized, misinterpreted, ignored, tolerated, encouraged, or even instigated by management
*Some researchers limit their definition of mobbing to acts committed by >1 person
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:41
Mobbing risk factors. According to Leymann,5 no specific personality factors predispose workers to being mobbed. Westhues1 and others, however, identify a variety of social risk factors. These include any factors that make an individual different from other members of his or her work environment, such as:

  • different ethnicity
  • an “odd” personality
  • high achievement.
Table 2

Phases of mobbing

Conflict, often characterized by a ‘critical incident’
Aggressive acts, such as those in Table 1
Management involvement
Branding as difficult or mentally ill
Expulsion or resignation from the workplace
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:38
Whistleblowers or union organizers also run a risk of stigmatization and mobbing. Organizations with unclear goals or extensive recent turnover in senior leadership can be conducive to mobbing. Three industries identified as at special risk for mobbing are academia, government, and religious organizations.5

Secondary morbidity. Victims of workplace mobbing frequently suffer from:

  • adjustment disorders
  • somatic symptoms (eg, headaches or irritable bowel syndrome)
  • PTSD6,7
  • major depression.8
In mobbing targets with PTSD, Leymann notes that the “mental effects were fully comparable with PTSD from war or prison camp experiences.”3 Some patients may develop alcoholism or other substance abuse disorders. Family relationships routinely suffer.9 Some targets may even develop brief psychotic episodes, generally with paranoid symptoms.

Leymann3 estimated that 15% of suicides in Sweden could be directly attributed to workplace mobbing. Although no other researcher has reported such a dramatic proportion, others have reported increased risk of suicidal behavior among mobbing victims.10

Table 3

Degrees of mobbing

First degree: Victim manages to resist, escapes at an early stage, or is fully rehabilitated in the original workplace or elsewhere
Second degree: Victim cannot resist or escape immediately and suffers temporary or prolonged mental and/or physical disability and has difficulty reentering the workforce
Third degree: Victim is unable to reenter the workforce and suffers serious, long-lasting mental or physical disability
Source: Adapted with permission from Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999:39
 

 

CASE CONTINUED: Redirecting energy into a job search

As I met with Mr. G over the next 3 months, the pattern of malicious communication and actions continued at his office. For example, he received a written reprimand for being 10 minutes late after having overslept when starting flurazepam, which he continued to take for about 6 weeks without further tardiness. I encouraged Mr. G to withdraw energy from work by keeping a low profile and trying not to react to provocations. Instead, I counseled him to put energy into family activities and try to find a new job.

Within 3 months, Mr. G found a new position in the private sector at a similar salary, although with lower benefits. Six months later, he was still with his wife, had been promoted at his new job, lost the 10 pounds he gained, discontinued psychotherapy, and was sleeping well without medication. He reported that he still thinks “almost every day” about what happened in his previous job but keeps telling himself “everything did work out OK after all.”

Mr. G experienced relatively mild, first-degree workplace mobbing, but it had a substantial effect on his quality of life and that of his wife for almost 1 year. If I had followed my first impulse and had Mr. G involuntarily hospitalized after our first interview, it would have confirmed rumors at his office and probably would have escalated the mobbing behavior.

Diagnostic recommendations

Consider the possibility that seemingly paranoid individuals could be the target of mobbing at work, and don’t underestimate the psychological stress of being mobbed. Other forms of workplace harassment can be extremely stressful but do not have the “paranoidogenic” potential of mobbing. Patients may be so distressed that it is difficult to figure out what is going on in their work environment.

Ask patients to present physical evidence of conspiracy or harassment. Mobbing patients usually are willing to bring in large quantities of material. Keep in mind that when subjected to mobbing behavior over time, a person who is not initially paranoid is likely to develop some secondary suspiciousness and even frank paranoia.

Also consider the possibility of “pseudomobbing,” in which an individual falsely believes he or she is a mobbing victim. Cases of pseudomobbing have been reported in European literature11 and may represent a negative side effect of greater public awareness of the mobbing phenomenon (and of legal remedies to mobbing available in various European countries).

Mobbing is a serious stressor that can lead to psychiatric and medical morbidity and even suicide. Major depressive disorder—often with suicidal ideation—is frequently associated with being mobbed.12

A diagnosis of PTSD can be missed if the mobbing victim does not seem to have been subjected to a severe enough stress to meet PTSD criteria.

Treatment recommendations

First, do no harm: Do not allow yourself to be used by the mob. This process can be direct—as in the Mr. G’s case, where the patient was almost involuntarily committed—or subtle. For example, a person you know may describe the behavior of “someone at work,” and you may be tempted to respond, “Well, I have not examined this person, but from what you say, it sounds like maybe…” You could then be quoted as a psychiatrist who agrees that the person is paranoid.

Giving your patient a name for what is happening to him or her may be the most therapeutic intervention. Generally, patients have not heard of mobbing. They typically are confused about what is happening and may blame themselves.

Treat the patient’s family. Giving a patient’s spouse or partner a name for what is happening is almost always helpful. One-third of mobbing victims suffer breakup of their marriages or relationships during the course of a mobbing, which can create a vicious cycle of stress, leading to isolation, leading to more stress.3 Encourage the patient not to subject the spouse to repeated ruminations about insults at work.

Treat secondary symptoms of depression, anxiety, PTSD, or other sequelae with pharmacotherapy, psychotherapy, or a combination as appropriate. Refer patients with somatic symptoms to primary care if you feel that they need further evaluation.

Encourage your patient to visualize choices and ways to escape the situation. Frequently, patients will be locked into “fighting for justice” or putting up with the situation because they see no options.

 

 

Encourage your patient to withdraw energy from work and invest it in family, social life, or anything else. At the appropriate time, encourage him or her to grieve losses experienced as a result of the mobbing.

Related resources

Drug brand name

  • Flurazepam • Dalmane
Disclosure

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

References

1. Westhues K. At the mercy of the mob: a summary of research on workplace mobbing. Canada’s Occupational Health and Safety Magazine. 2002;18:30-36.

2. Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999.

3. Leymann H. Mobbing and psychological terror at workplaces. Violence Vict. 1990;5:119-125.

4. Namie G, Namie R. The bully at work: what you can do to stop the hurt and reclaim your dignity on the job. Naperville, IL: Sourcebooks, Inc; 2003.

5. Leymann H. The content and development of mobbing at work. European Journal of Work and Organizational Psychology. 1996;5:165-184.

6. Leymann H, Gustafsson A. Mobbing at work and the development of post-traumatic stress disorders. European Journal of Work and Organizational Psychology. 1996;5:251-275.

7. Bonafons C, Jehel L, Coroller-Bequet A. Specificity of the links between workplace harassment and PTSD: primary results using court decisions, a pilot study in France. Int Arch Occup Environ Health. 2008 Oct 25 (Epub ahead of print).

8. Girardi P, Monaco C, Prestigiacomo C, et al. Personality and psychopathological profiles in individuals exposed to mobbing. Violence Vict. 2007;22:172-188.

9. Duffy M. Workplace mobbing: individual and family health consequences. The Family Journal. 2007;15:398-404.

10. Pompili M, Lester D, Innamorati M, et al. Suicide risk and exposure to mobbing. Work. 2008;31:237-243.

11. Jarreta BM. Medico-legal implications of mobbing. A false accusation of psychological harassment at the workplace. Forensic Sci Int. 2004;146(suppl):S17-S18.

12. Girardi P, Monaco E, Prestigiacomo C, et al. Personality and psychopathological profiles in individuals exposed to mobbing. Violence Vict. 2007;22(2):172-188.

References

1. Westhues K. At the mercy of the mob: a summary of research on workplace mobbing. Canada’s Occupational Health and Safety Magazine. 2002;18:30-36.

2. Davenport N, Schwartz RD, Elliott GP. Mobbing: emotional abuse in the American workplace. Ames, IA: Civil Society Publishing; 1999.

3. Leymann H. Mobbing and psychological terror at workplaces. Violence Vict. 1990;5:119-125.

4. Namie G, Namie R. The bully at work: what you can do to stop the hurt and reclaim your dignity on the job. Naperville, IL: Sourcebooks, Inc; 2003.

5. Leymann H. The content and development of mobbing at work. European Journal of Work and Organizational Psychology. 1996;5:165-184.

6. Leymann H, Gustafsson A. Mobbing at work and the development of post-traumatic stress disorders. European Journal of Work and Organizational Psychology. 1996;5:251-275.

7. Bonafons C, Jehel L, Coroller-Bequet A. Specificity of the links between workplace harassment and PTSD: primary results using court decisions, a pilot study in France. Int Arch Occup Environ Health. 2008 Oct 25 (Epub ahead of print).

8. Girardi P, Monaco C, Prestigiacomo C, et al. Personality and psychopathological profiles in individuals exposed to mobbing. Violence Vict. 2007;22:172-188.

9. Duffy M. Workplace mobbing: individual and family health consequences. The Family Journal. 2007;15:398-404.

10. Pompili M, Lester D, Innamorati M, et al. Suicide risk and exposure to mobbing. Work. 2008;31:237-243.

11. Jarreta BM. Medico-legal implications of mobbing. A false accusation of psychological harassment at the workplace. Forensic Sci Int. 2004;146(suppl):S17-S18.

12. Girardi P, Monaco E, Prestigiacomo C, et al. Personality and psychopathological profiles in individuals exposed to mobbing. Violence Vict. 2007;22(2):172-188.

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Informed consent: Is your patient competent to refuse treatment?

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Mr. D, age 45 with a history of schizophrenia, is admitted to an inpatient psychiatric unit. The psychiatrist recommends an antipsychotic to help Mr. D with fears that the FBI has implanted a radio signal device into his tooth filling. She explains the risks and benefits of the proposed drug and alternate medications, as well as the risks of no treatment.

Mr. D calmly but consistently declines the treatment. He states that he recognizes the antipsychotic is used to treat psychotic symptoms, can help people who hear voices, and can have side effects such as tardive dyskinesia. His thoughts become disorganized and difficult to follow, however, as he explains that he does not believe the medication is needed for his situation because the FBI is involved in tracking his behavior.

Informed consent in clinical settings is designed to allow patients to make rational choices about their treatment before it begins. When a psychiatric patient such as Mr. D declines a treatment you recommend, how can you balance the 2 ethical principles in medicine: beneficence toward the patient and respect for individual autonomy?1

Some authors have raised concerns that informed consent in physician-patient interactions are at times an empty exercise undertaken solely to satisfy a legal expectation.2 If executed properly, however, informed consent can enhance the therapeutic alliance and help improve treatment adherence.

Patient-centered treatment

As patients have become more informed consumers, the “doctor knows best” model of care has given way to an expectation that patients know best what they would want done regarding their health. Lawsuits related to informed consent generally allege that physicians failed to provide appropriate informed consent for treatment the plaintiffs received. These complaints suggest that had the patient been more appropriately informed, he or she might have made a different choice and would not have suffered harm related to treatment.

In a patient-centered approach to treatment, informed consent allows the patient to make an autonomous decision with the appropriate information. Providing treatment without the patient’s expressed consent could be viewed more seriously, potentially even as battery.3 Recent informed consent cases tend to rely on negligence theories, however, rather than on claims of battery. Negligence cases helped set the stage of evolving expectations—first seen with surgical procedures, then medical interventions, then medication treatment, and now even with psychotherapy (Box 1)—that informed consent should be obtained in clinical settings.4

Box 1

How to reduce risk when obtaining informed consent

Because failure to provide informed consent can be grounds for a negligence claim, consider strategies to reduce the chance of successful litigation.

Although a written form can provide some proof that informed consent occurred, it may not prove that you conveyed adequate information or that your patient understood the information. Overly simplistic or complex forms can pose other difficulties in malpractice claims. Documenting aspects of the informed consent dialogue often provides the best “proof” that such a conversation occurred.

In retrospect, helpful evidence that adequate informed consent was obtained may include information related to the disclosed information and the patient’s response to the information (such as might be seen in a quote that indicated his or her understanding of a particular side effect). Although a full accounting of the conversation would not be a reasonable expectation for documentation, you might wish to consider the risks and benefits inherent to the particular treatment and tailor the note related to the informed consent accordingly.

3 components of informed consent

Informed consent includes 3 components: voluntariness, disclosure, and competence.5

Voluntariness implies that the patient must make treatment-related choices of his or her own free will and without coercion. In Kaimowitz v Michigan Department of Mental Health,6 the court ruled that involuntarily committed persons living in what was considered an inherently coercive institutional environment were not capable of providing voluntary consent to a high-risk experimental procedure. This case had a major impact on prison research.

In treatment settings as well, a patient’s circumstances might be considered coercive. Historically, civilly committed patients did not have the right to refuse treatment. A movement in the 1980s helped to separate civil commitment and the right to refuse treatment, which is well-established in most jurisdictions today.7 In psychiatric inpatient settings, even an involuntarily committed patient generally has a right to refuse recommended medications unless a legally permissible mechanism overrides the refusal.

Disclosure means that a person requires certain information to make a rational decision to accept or reject treatment. The question is: How much information needs to be disclosed for a patient to be adequately informed?

 

 

Disclosure requirements vary across jurisdictions. In 1960, Natanson v Kline supported the standard that disclosure required that which a “reasonable practitioner” might disclose to patients about their treatment in similar circumstances.8 Although some jurisdictions have maintained that standard,5 subsequent cases identified a more patient-centered approach to disclosure called the “reasonable person” standard (Box 2).5,9

Competence. In many settings, clinicians use the construct of “capacity” rather than “competence” because competence is a legal term that can be determined only by a judge. When an individual is deemed incompetent, his or her right to make autonomous decisions can be overridden. Children are not competent by virtue of their status as minors, although exceptions may be made for certain older youth. Adults are presumed competent unless adjudicated otherwise.

Box 2

Typical elements of disclosure to meet the ‘reasonable person’ standard

The “reasonable person” standard endorses the obligation of the professional to disclose information that a reasonable person would want to know about a proposed treatment. This standard evolved in part from Canterbury v Spence,9 in which a plaintiff who had become paralyzed alleged that he was not informed of the risks of a laminectomy. The court found that the patient must be able to rely on information that the physician holds that would be material to the patient in making an informed treatment decision in his or her best interest.

The typically required elements of disclosure include:

  • diagnosis, if known
  • nature and purpose of proposed treatment
  • risks and benefits of proposed treatment
  • alternatives to treatment and their risks and benefits
  • risks and benefits of no treatment.

Disclosing information that is uniquely relevant to an individual’s situation and would be generally unknown to the clinician might not be required. For example, a clinician might not realize that it is important for a particular patient to be able to make small art objects as a hobby, so the clinician might not reveal that a medication very rarely causes a tremor. Nevertheless, when you are aware of a need for such nuanced information, the usual general disclosure can be modified to include whatever details are relevant to that patient.5

Adult patients with psychotic disorders are not automatically or always incompetent. Research has shown that most inpatients with mental illness have capacities to make treatment decisions similar to persons with medical illness.10 Patients with schizophrenia, however, have deficits relevant to capacity to make treatment decisions more often than patients with medical illnesses and depressive disorders. Patients with depressive disorders also are more likely to have some decision-making impairment compared with persons with medical illnesses.10 Thus, in psychiatric settings, a heightened awareness of a patient’s potential deficits related to competence is important.

Competence can be broken down into 4 component capacities (Box 3).11 The degree of incapacity required for a finding of incompetence is complicated and difficult to codify. Instruments designed to standardize competence assessment are available12 but not routinely used in clinical settings. Even with these instruments, no threshold of capacity clearly defines competence. Some authors have argued for a sliding scale of competence, with standards becoming more stringent as the degree of risk related to the treatment decision increases.13,14

Box 3

4 abilities patients must have to be considered legally competent

Express and sustain a choice. To be considered competent to give informed consent, a person must be able to evidence a choice regarding the decision at hand. The choice need not be expressed verbally, but a patient must be able to communicate in some fashion (such as eye blinking or handwritten communication). The patient also must be able to maintain that choice over time, long enough for treatment to be implemented.

Understand presented information. A person must have a factual understanding of the information presented about the treatment. A full scientific understanding of diagnosis and subtleties of treatment likely would be an excessive expectation. For example, a patient would not be expected to understand the nuances of the serotonin neurotransmitter system. A physician should, however, assess whether the patient understands—in the patient’s words—that a selective serotonin reuptake inhibitor could induce manic-type symptoms and that the patient should bring these symptoms to the prescribing physician’s attention if they occur.

Appreciate one’s situation. Individuals who are competent must have a realistic appreciation of their situation. Though a patient may understand the facts you have presented, he may fail to fully integrate why the information is relevant to him. Persons with schizophrenia who do not believe they are ill—such as Mr. D—might have a limited appreciation of why an antipsychotic would help them.

Rationally manipulate information. A person also must be able to rationally manipulate the information in a way that is not impaired by symptoms of illness. Patients faced with a treatment decision should be able to use reason to reach a logical and rational decision that they see as being in their best interest. This might not be the same decision you would make. For example, a patient with thought disorganization or one who psychotically believes that the color of a recommended medication signals that someone tampered with the pills might not be able to rationally manipulate information presented about treatment options.

Source: Reference 11

 

 

Exceptions to informed consent

Emergencies. Informed consent is not required under some circumstances.5 Consider the patient who is brought to the emergency room unconscious after a fall, with no family contact information. A neurosurgeon might need to intervene immediately to save the patient’s life, using the emergency exception to informed consent.

In an emergency, when a person is unable to give informed consent or time does not allow for a full informed consent process, the clinician generally follows the principle of doing no harm. Treatment may be started in an emergency without full informed consent on the assumption that most competent people would consent to treatment, especially where life or limb was at risk. If time and circumstances permit in an emergency, obtaining the consent of available family members may be prudent.

Treating psychosis when no associated behavioral disturbance is placing a patient or others at risk might not constitute an emergency that would negate the need for informed consent. Thus, given Mr. D’s calm demeanor in talking with the clinician about his treatment, an emergency exception probably would not apply in his case.

Incompetence. If a judge determines that a patient is incompetent to make his or her own treatment decisions, a substitute decision-maker—such as a guardian—could be appointed. In these cases, respect would suggest that to the extent possible and appropriate you would inform the incompetent ward about treatment in a way that he or she may understand.

In other circumstances, such as when a healthcare proxy has been invoked, previously designated surrogate decision-makers provide informed consent on behalf of the patient who clinically is found to lack the capacity to make healthcare decisions.

Waivers. Sometimes a competent patient decides to waive the right to further information and may turn the decision over to the clinician. To rely upon this exception, some documented assessment—even if brief—of the patient’s capacity to waive information may be important.

Therapeutic privilege often is cited in the literature but should be an infrequently used exception to informed consent. In very limited situations, a physician might decide to not engage in an informed consent discussion, believing the information to be disclosed would be so damaging that it would directly harm the patient or so emotionally distressing as to foreclose the possibility of the patient making a rational decision.

As noted, informing patients of their health situations is expected and accepted. Even in psychiatric settings, receiving information about potentially serious medication side effects has not necessarily led to patient harm or refusal of treatment.15 Therefore, use of this exception is only for very narrowly tailored circumstances, if used at all, and not simply because you believe a patient will refuse to consent if informed about a proposed treatment.

Some case law exists on the need to establish why the therapeutic privilege was justified as a rationale to not provide informed consent in a particular situation.16 Therefore, though it should be rarely invoked, if you use therapeutic privilege, document why you invoked this exception for that particular patient and in that particular circumstance.

Building the therapeutic alliance

Although it may meet policy or legal informed consent requirements, simply providing the patient with a form to sign before treatment begins does little to enhance patient-clinician communication.2 Providing detailed written information also might not be adequate to ensure that the patient understands the complexity of a treatment you have asked him to consider.17 Instead, an informed consent model that relies on active, ongoing dialogue about treatment can maximize patient autonomy while working for the good of the patient (Table).

Lidz and colleagues2 identified key conditions that must be present for such a process model of informed consent to work:

  • the patient’s role is understood as that of an inquisitive consumer who may challenge the physician’s authority in the quest for information
  • the clinician challenges the patient’s preconceived beliefs about his or her illness and educates the patient so that both parties approach the medical issue from common ground.
A patient also must be allowed to consider his or her own values in weighing medical decisions. These values may include the patient’s ability to tolerate side effects, willingness to take risks, and own sense of quality of life.
 

 

1 In this model of shared decision-making, the clinician reveals information material to the decision, and the patient helps the clinician understand the circumstances that make him or her prefer 1 treatment over another.1,18

By engaging in ongoing informed consent, you may achieve greater gains within the therapeutic alliance and reduce the risk of liability.19 Where uncertainties are related to treatment, share these ambiguities as an aspect of informed consent, especially when the patient plays an active role in treatment.4 Similarly, an expanded informed consent process may be needed when:

  • proposed treatments are particularly risky
  • several treatment alternatives could be acceptable and effective
  • evidence supports opposing views of a treatment’s effectiveness.4,20
Table

Using informed consent to build a therapeutic alliance

  • Use the informed consent dialogue to establish trust and openness with patients while demonstrating respect for patient autonomy
  • Allow patients to share their values and concerns as part of the risk/benefit analysis
  • Talk with patients to understand their preconceived ideas about their illnesses and to seek a common understanding of the illness and its prognosis, with and without treatment

CASE CONTINUED: A question of competence

Mr. D is calm in his discussions with the psychiatrist, and the information she presents does not seem to cause him further harm. Thus, the emergency and therapeutic privilege exceptions do not eliminate the need for an ongoing informed consent process at this time.

Mr. D has a factual understanding of the risks and benefits of the recommended antipsychotic and is able to express a consistent choice about starting this treatment. He lacks, however, an ability to appreciate his situation and has difficulty manipulating information rationally. Overall, he has deficits in aspects of his decision-making competence, which could signal the need for an exception to obtaining informed consent.

The psychiatrist should continue to build an alliance with Mr. D as she works with him toward accepting treatment. Meeting with him regularly, trying to understand his concerns, and trying to help him understand how his symptoms may be interfering with his functioning can help build the alliance. If he continues to show competence-related deficits, she could pursue guardianship or other legal avenues to address his ongoing inability to provide informed consent. This approach would allow for a legally authorized mechanism to administer treatment to this patient.

Related resources

Disclosure

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

References

1. King JS, Moulton BW. Rethinking informed consent: the case for shared medical decision-making. Am J Law Med. 2006;32(4):429-501.

2. Lidz CW, Appelbaum PS, Meisel A. Two models of implementing informed consent. Arch Intern Med. 1988;148(6):1385-1389.

3. Schloendorff v Society of New York Hospital, 105 NE 92 (1914).

4. Beahrs JO, Gutheil TG. Informed consent in psychotherapy. Am J Psychiatry. 2001;158(1):4-10.

5. Appelbaum PS, Gutheil TG. Clinical handbook of psychiatry and the law. Philadelphia, PA: Wolters Kluwer and Lippincott Williams & Wilkins; 2007.

6. Kaimowitz v Michigan, DMH 1 MDLR 147 (1976).

7. Pinals DA, Hoge SK. Treatment refusal in psychiatric practice. In: Rosner R, ed. Principles and practice of forensic psychiatry, 2nd ed. London, UK: Arnold Press; 2003:129-136.

8. Natanson v Kline, 350 P.2D 1093 (1960).

9. Canterbury v Spence, 464 F.2d 772 (1972).

10. Grisso T, Appelbaum PS. The MacArthur Treatment Competence Study: III. Abilities of patients to consent to psychiatric and medical treatment. Law Human Behav. 1995;19(2):149-174.

11. Appelbaum PS, Grisso T. Assessing patients’ capacities to consent to treatment. N Engl J Med. 1988;319(25):1635-1638.

12. Dunn LB, Nowrangi MA, Palmer BW, et al. Assessing decisional capacity for clinical research or treatment: a review of instruments. Am J Psychiatry. 2006;163(8):1323-1334.

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

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

15. Munetz MR, Roth LH. Informing patients about tardive dyskinesia. Arch Gen Psychiatry. 1985;42(9):866-871.

16. Barcai v Betwee MD, 50 P3d 946 (2002).

17. Hafeez A, Wiseman O, Hill JT. Informed consent: are we deluding ourselves? A randomized controlled study. BJU International. 2007;99(1):4-5.

18. Kaplan RM. Shared medical decision making: a new tool for preventative medicine. Am J Prev Med. 2004;26(1):81-83.

19. Gutheil TG, Bursztajn H, Brodsky A. Malpractice prevention through the sharing of uncertainty. Informed consent and the therapeutic alliance. N Engl J Med. 1984;311(1):49-51.

20. Packman WL, Cabot MG, Bongar B. Malpractice arising from negligent psychotherapy: ethical, legal, and clinical implications of Osheroff v Chestnut Lodge. Ethics Behav. 1994;4(3):175-197.

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Mr. D, age 45 with a history of schizophrenia, is admitted to an inpatient psychiatric unit. The psychiatrist recommends an antipsychotic to help Mr. D with fears that the FBI has implanted a radio signal device into his tooth filling. She explains the risks and benefits of the proposed drug and alternate medications, as well as the risks of no treatment.

Mr. D calmly but consistently declines the treatment. He states that he recognizes the antipsychotic is used to treat psychotic symptoms, can help people who hear voices, and can have side effects such as tardive dyskinesia. His thoughts become disorganized and difficult to follow, however, as he explains that he does not believe the medication is needed for his situation because the FBI is involved in tracking his behavior.

Informed consent in clinical settings is designed to allow patients to make rational choices about their treatment before it begins. When a psychiatric patient such as Mr. D declines a treatment you recommend, how can you balance the 2 ethical principles in medicine: beneficence toward the patient and respect for individual autonomy?1

Some authors have raised concerns that informed consent in physician-patient interactions are at times an empty exercise undertaken solely to satisfy a legal expectation.2 If executed properly, however, informed consent can enhance the therapeutic alliance and help improve treatment adherence.

Patient-centered treatment

As patients have become more informed consumers, the “doctor knows best” model of care has given way to an expectation that patients know best what they would want done regarding their health. Lawsuits related to informed consent generally allege that physicians failed to provide appropriate informed consent for treatment the plaintiffs received. These complaints suggest that had the patient been more appropriately informed, he or she might have made a different choice and would not have suffered harm related to treatment.

In a patient-centered approach to treatment, informed consent allows the patient to make an autonomous decision with the appropriate information. Providing treatment without the patient’s expressed consent could be viewed more seriously, potentially even as battery.3 Recent informed consent cases tend to rely on negligence theories, however, rather than on claims of battery. Negligence cases helped set the stage of evolving expectations—first seen with surgical procedures, then medical interventions, then medication treatment, and now even with psychotherapy (Box 1)—that informed consent should be obtained in clinical settings.4

Box 1

How to reduce risk when obtaining informed consent

Because failure to provide informed consent can be grounds for a negligence claim, consider strategies to reduce the chance of successful litigation.

Although a written form can provide some proof that informed consent occurred, it may not prove that you conveyed adequate information or that your patient understood the information. Overly simplistic or complex forms can pose other difficulties in malpractice claims. Documenting aspects of the informed consent dialogue often provides the best “proof” that such a conversation occurred.

In retrospect, helpful evidence that adequate informed consent was obtained may include information related to the disclosed information and the patient’s response to the information (such as might be seen in a quote that indicated his or her understanding of a particular side effect). Although a full accounting of the conversation would not be a reasonable expectation for documentation, you might wish to consider the risks and benefits inherent to the particular treatment and tailor the note related to the informed consent accordingly.

3 components of informed consent

Informed consent includes 3 components: voluntariness, disclosure, and competence.5

Voluntariness implies that the patient must make treatment-related choices of his or her own free will and without coercion. In Kaimowitz v Michigan Department of Mental Health,6 the court ruled that involuntarily committed persons living in what was considered an inherently coercive institutional environment were not capable of providing voluntary consent to a high-risk experimental procedure. This case had a major impact on prison research.

In treatment settings as well, a patient’s circumstances might be considered coercive. Historically, civilly committed patients did not have the right to refuse treatment. A movement in the 1980s helped to separate civil commitment and the right to refuse treatment, which is well-established in most jurisdictions today.7 In psychiatric inpatient settings, even an involuntarily committed patient generally has a right to refuse recommended medications unless a legally permissible mechanism overrides the refusal.

Disclosure means that a person requires certain information to make a rational decision to accept or reject treatment. The question is: How much information needs to be disclosed for a patient to be adequately informed?

 

 

Disclosure requirements vary across jurisdictions. In 1960, Natanson v Kline supported the standard that disclosure required that which a “reasonable practitioner” might disclose to patients about their treatment in similar circumstances.8 Although some jurisdictions have maintained that standard,5 subsequent cases identified a more patient-centered approach to disclosure called the “reasonable person” standard (Box 2).5,9

Competence. In many settings, clinicians use the construct of “capacity” rather than “competence” because competence is a legal term that can be determined only by a judge. When an individual is deemed incompetent, his or her right to make autonomous decisions can be overridden. Children are not competent by virtue of their status as minors, although exceptions may be made for certain older youth. Adults are presumed competent unless adjudicated otherwise.

Box 2

Typical elements of disclosure to meet the ‘reasonable person’ standard

The “reasonable person” standard endorses the obligation of the professional to disclose information that a reasonable person would want to know about a proposed treatment. This standard evolved in part from Canterbury v Spence,9 in which a plaintiff who had become paralyzed alleged that he was not informed of the risks of a laminectomy. The court found that the patient must be able to rely on information that the physician holds that would be material to the patient in making an informed treatment decision in his or her best interest.

The typically required elements of disclosure include:

  • diagnosis, if known
  • nature and purpose of proposed treatment
  • risks and benefits of proposed treatment
  • alternatives to treatment and their risks and benefits
  • risks and benefits of no treatment.

Disclosing information that is uniquely relevant to an individual’s situation and would be generally unknown to the clinician might not be required. For example, a clinician might not realize that it is important for a particular patient to be able to make small art objects as a hobby, so the clinician might not reveal that a medication very rarely causes a tremor. Nevertheless, when you are aware of a need for such nuanced information, the usual general disclosure can be modified to include whatever details are relevant to that patient.5

Adult patients with psychotic disorders are not automatically or always incompetent. Research has shown that most inpatients with mental illness have capacities to make treatment decisions similar to persons with medical illness.10 Patients with schizophrenia, however, have deficits relevant to capacity to make treatment decisions more often than patients with medical illnesses and depressive disorders. Patients with depressive disorders also are more likely to have some decision-making impairment compared with persons with medical illnesses.10 Thus, in psychiatric settings, a heightened awareness of a patient’s potential deficits related to competence is important.

Competence can be broken down into 4 component capacities (Box 3).11 The degree of incapacity required for a finding of incompetence is complicated and difficult to codify. Instruments designed to standardize competence assessment are available12 but not routinely used in clinical settings. Even with these instruments, no threshold of capacity clearly defines competence. Some authors have argued for a sliding scale of competence, with standards becoming more stringent as the degree of risk related to the treatment decision increases.13,14

Box 3

4 abilities patients must have to be considered legally competent

Express and sustain a choice. To be considered competent to give informed consent, a person must be able to evidence a choice regarding the decision at hand. The choice need not be expressed verbally, but a patient must be able to communicate in some fashion (such as eye blinking or handwritten communication). The patient also must be able to maintain that choice over time, long enough for treatment to be implemented.

Understand presented information. A person must have a factual understanding of the information presented about the treatment. A full scientific understanding of diagnosis and subtleties of treatment likely would be an excessive expectation. For example, a patient would not be expected to understand the nuances of the serotonin neurotransmitter system. A physician should, however, assess whether the patient understands—in the patient’s words—that a selective serotonin reuptake inhibitor could induce manic-type symptoms and that the patient should bring these symptoms to the prescribing physician’s attention if they occur.

Appreciate one’s situation. Individuals who are competent must have a realistic appreciation of their situation. Though a patient may understand the facts you have presented, he may fail to fully integrate why the information is relevant to him. Persons with schizophrenia who do not believe they are ill—such as Mr. D—might have a limited appreciation of why an antipsychotic would help them.

Rationally manipulate information. A person also must be able to rationally manipulate the information in a way that is not impaired by symptoms of illness. Patients faced with a treatment decision should be able to use reason to reach a logical and rational decision that they see as being in their best interest. This might not be the same decision you would make. For example, a patient with thought disorganization or one who psychotically believes that the color of a recommended medication signals that someone tampered with the pills might not be able to rationally manipulate information presented about treatment options.

Source: Reference 11

 

 

Exceptions to informed consent

Emergencies. Informed consent is not required under some circumstances.5 Consider the patient who is brought to the emergency room unconscious after a fall, with no family contact information. A neurosurgeon might need to intervene immediately to save the patient’s life, using the emergency exception to informed consent.

In an emergency, when a person is unable to give informed consent or time does not allow for a full informed consent process, the clinician generally follows the principle of doing no harm. Treatment may be started in an emergency without full informed consent on the assumption that most competent people would consent to treatment, especially where life or limb was at risk. If time and circumstances permit in an emergency, obtaining the consent of available family members may be prudent.

Treating psychosis when no associated behavioral disturbance is placing a patient or others at risk might not constitute an emergency that would negate the need for informed consent. Thus, given Mr. D’s calm demeanor in talking with the clinician about his treatment, an emergency exception probably would not apply in his case.

Incompetence. If a judge determines that a patient is incompetent to make his or her own treatment decisions, a substitute decision-maker—such as a guardian—could be appointed. In these cases, respect would suggest that to the extent possible and appropriate you would inform the incompetent ward about treatment in a way that he or she may understand.

In other circumstances, such as when a healthcare proxy has been invoked, previously designated surrogate decision-makers provide informed consent on behalf of the patient who clinically is found to lack the capacity to make healthcare decisions.

Waivers. Sometimes a competent patient decides to waive the right to further information and may turn the decision over to the clinician. To rely upon this exception, some documented assessment—even if brief—of the patient’s capacity to waive information may be important.

Therapeutic privilege often is cited in the literature but should be an infrequently used exception to informed consent. In very limited situations, a physician might decide to not engage in an informed consent discussion, believing the information to be disclosed would be so damaging that it would directly harm the patient or so emotionally distressing as to foreclose the possibility of the patient making a rational decision.

As noted, informing patients of their health situations is expected and accepted. Even in psychiatric settings, receiving information about potentially serious medication side effects has not necessarily led to patient harm or refusal of treatment.15 Therefore, use of this exception is only for very narrowly tailored circumstances, if used at all, and not simply because you believe a patient will refuse to consent if informed about a proposed treatment.

Some case law exists on the need to establish why the therapeutic privilege was justified as a rationale to not provide informed consent in a particular situation.16 Therefore, though it should be rarely invoked, if you use therapeutic privilege, document why you invoked this exception for that particular patient and in that particular circumstance.

Building the therapeutic alliance

Although it may meet policy or legal informed consent requirements, simply providing the patient with a form to sign before treatment begins does little to enhance patient-clinician communication.2 Providing detailed written information also might not be adequate to ensure that the patient understands the complexity of a treatment you have asked him to consider.17 Instead, an informed consent model that relies on active, ongoing dialogue about treatment can maximize patient autonomy while working for the good of the patient (Table).

Lidz and colleagues2 identified key conditions that must be present for such a process model of informed consent to work:

  • the patient’s role is understood as that of an inquisitive consumer who may challenge the physician’s authority in the quest for information
  • the clinician challenges the patient’s preconceived beliefs about his or her illness and educates the patient so that both parties approach the medical issue from common ground.
A patient also must be allowed to consider his or her own values in weighing medical decisions. These values may include the patient’s ability to tolerate side effects, willingness to take risks, and own sense of quality of life.
 

 

1 In this model of shared decision-making, the clinician reveals information material to the decision, and the patient helps the clinician understand the circumstances that make him or her prefer 1 treatment over another.1,18

By engaging in ongoing informed consent, you may achieve greater gains within the therapeutic alliance and reduce the risk of liability.19 Where uncertainties are related to treatment, share these ambiguities as an aspect of informed consent, especially when the patient plays an active role in treatment.4 Similarly, an expanded informed consent process may be needed when:

  • proposed treatments are particularly risky
  • several treatment alternatives could be acceptable and effective
  • evidence supports opposing views of a treatment’s effectiveness.4,20
Table

Using informed consent to build a therapeutic alliance

  • Use the informed consent dialogue to establish trust and openness with patients while demonstrating respect for patient autonomy
  • Allow patients to share their values and concerns as part of the risk/benefit analysis
  • Talk with patients to understand their preconceived ideas about their illnesses and to seek a common understanding of the illness and its prognosis, with and without treatment

CASE CONTINUED: A question of competence

Mr. D is calm in his discussions with the psychiatrist, and the information she presents does not seem to cause him further harm. Thus, the emergency and therapeutic privilege exceptions do not eliminate the need for an ongoing informed consent process at this time.

Mr. D has a factual understanding of the risks and benefits of the recommended antipsychotic and is able to express a consistent choice about starting this treatment. He lacks, however, an ability to appreciate his situation and has difficulty manipulating information rationally. Overall, he has deficits in aspects of his decision-making competence, which could signal the need for an exception to obtaining informed consent.

The psychiatrist should continue to build an alliance with Mr. D as she works with him toward accepting treatment. Meeting with him regularly, trying to understand his concerns, and trying to help him understand how his symptoms may be interfering with his functioning can help build the alliance. If he continues to show competence-related deficits, she could pursue guardianship or other legal avenues to address his ongoing inability to provide informed consent. This approach would allow for a legally authorized mechanism to administer treatment to this patient.

Related resources

Disclosure

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

Comment on this article

Mr. D, age 45 with a history of schizophrenia, is admitted to an inpatient psychiatric unit. The psychiatrist recommends an antipsychotic to help Mr. D with fears that the FBI has implanted a radio signal device into his tooth filling. She explains the risks and benefits of the proposed drug and alternate medications, as well as the risks of no treatment.

Mr. D calmly but consistently declines the treatment. He states that he recognizes the antipsychotic is used to treat psychotic symptoms, can help people who hear voices, and can have side effects such as tardive dyskinesia. His thoughts become disorganized and difficult to follow, however, as he explains that he does not believe the medication is needed for his situation because the FBI is involved in tracking his behavior.

Informed consent in clinical settings is designed to allow patients to make rational choices about their treatment before it begins. When a psychiatric patient such as Mr. D declines a treatment you recommend, how can you balance the 2 ethical principles in medicine: beneficence toward the patient and respect for individual autonomy?1

Some authors have raised concerns that informed consent in physician-patient interactions are at times an empty exercise undertaken solely to satisfy a legal expectation.2 If executed properly, however, informed consent can enhance the therapeutic alliance and help improve treatment adherence.

Patient-centered treatment

As patients have become more informed consumers, the “doctor knows best” model of care has given way to an expectation that patients know best what they would want done regarding their health. Lawsuits related to informed consent generally allege that physicians failed to provide appropriate informed consent for treatment the plaintiffs received. These complaints suggest that had the patient been more appropriately informed, he or she might have made a different choice and would not have suffered harm related to treatment.

In a patient-centered approach to treatment, informed consent allows the patient to make an autonomous decision with the appropriate information. Providing treatment without the patient’s expressed consent could be viewed more seriously, potentially even as battery.3 Recent informed consent cases tend to rely on negligence theories, however, rather than on claims of battery. Negligence cases helped set the stage of evolving expectations—first seen with surgical procedures, then medical interventions, then medication treatment, and now even with psychotherapy (Box 1)—that informed consent should be obtained in clinical settings.4

Box 1

How to reduce risk when obtaining informed consent

Because failure to provide informed consent can be grounds for a negligence claim, consider strategies to reduce the chance of successful litigation.

Although a written form can provide some proof that informed consent occurred, it may not prove that you conveyed adequate information or that your patient understood the information. Overly simplistic or complex forms can pose other difficulties in malpractice claims. Documenting aspects of the informed consent dialogue often provides the best “proof” that such a conversation occurred.

In retrospect, helpful evidence that adequate informed consent was obtained may include information related to the disclosed information and the patient’s response to the information (such as might be seen in a quote that indicated his or her understanding of a particular side effect). Although a full accounting of the conversation would not be a reasonable expectation for documentation, you might wish to consider the risks and benefits inherent to the particular treatment and tailor the note related to the informed consent accordingly.

3 components of informed consent

Informed consent includes 3 components: voluntariness, disclosure, and competence.5

Voluntariness implies that the patient must make treatment-related choices of his or her own free will and without coercion. In Kaimowitz v Michigan Department of Mental Health,6 the court ruled that involuntarily committed persons living in what was considered an inherently coercive institutional environment were not capable of providing voluntary consent to a high-risk experimental procedure. This case had a major impact on prison research.

In treatment settings as well, a patient’s circumstances might be considered coercive. Historically, civilly committed patients did not have the right to refuse treatment. A movement in the 1980s helped to separate civil commitment and the right to refuse treatment, which is well-established in most jurisdictions today.7 In psychiatric inpatient settings, even an involuntarily committed patient generally has a right to refuse recommended medications unless a legally permissible mechanism overrides the refusal.

Disclosure means that a person requires certain information to make a rational decision to accept or reject treatment. The question is: How much information needs to be disclosed for a patient to be adequately informed?

 

 

Disclosure requirements vary across jurisdictions. In 1960, Natanson v Kline supported the standard that disclosure required that which a “reasonable practitioner” might disclose to patients about their treatment in similar circumstances.8 Although some jurisdictions have maintained that standard,5 subsequent cases identified a more patient-centered approach to disclosure called the “reasonable person” standard (Box 2).5,9

Competence. In many settings, clinicians use the construct of “capacity” rather than “competence” because competence is a legal term that can be determined only by a judge. When an individual is deemed incompetent, his or her right to make autonomous decisions can be overridden. Children are not competent by virtue of their status as minors, although exceptions may be made for certain older youth. Adults are presumed competent unless adjudicated otherwise.

Box 2

Typical elements of disclosure to meet the ‘reasonable person’ standard

The “reasonable person” standard endorses the obligation of the professional to disclose information that a reasonable person would want to know about a proposed treatment. This standard evolved in part from Canterbury v Spence,9 in which a plaintiff who had become paralyzed alleged that he was not informed of the risks of a laminectomy. The court found that the patient must be able to rely on information that the physician holds that would be material to the patient in making an informed treatment decision in his or her best interest.

The typically required elements of disclosure include:

  • diagnosis, if known
  • nature and purpose of proposed treatment
  • risks and benefits of proposed treatment
  • alternatives to treatment and their risks and benefits
  • risks and benefits of no treatment.

Disclosing information that is uniquely relevant to an individual’s situation and would be generally unknown to the clinician might not be required. For example, a clinician might not realize that it is important for a particular patient to be able to make small art objects as a hobby, so the clinician might not reveal that a medication very rarely causes a tremor. Nevertheless, when you are aware of a need for such nuanced information, the usual general disclosure can be modified to include whatever details are relevant to that patient.5

Adult patients with psychotic disorders are not automatically or always incompetent. Research has shown that most inpatients with mental illness have capacities to make treatment decisions similar to persons with medical illness.10 Patients with schizophrenia, however, have deficits relevant to capacity to make treatment decisions more often than patients with medical illnesses and depressive disorders. Patients with depressive disorders also are more likely to have some decision-making impairment compared with persons with medical illnesses.10 Thus, in psychiatric settings, a heightened awareness of a patient’s potential deficits related to competence is important.

Competence can be broken down into 4 component capacities (Box 3).11 The degree of incapacity required for a finding of incompetence is complicated and difficult to codify. Instruments designed to standardize competence assessment are available12 but not routinely used in clinical settings. Even with these instruments, no threshold of capacity clearly defines competence. Some authors have argued for a sliding scale of competence, with standards becoming more stringent as the degree of risk related to the treatment decision increases.13,14

Box 3

4 abilities patients must have to be considered legally competent

Express and sustain a choice. To be considered competent to give informed consent, a person must be able to evidence a choice regarding the decision at hand. The choice need not be expressed verbally, but a patient must be able to communicate in some fashion (such as eye blinking or handwritten communication). The patient also must be able to maintain that choice over time, long enough for treatment to be implemented.

Understand presented information. A person must have a factual understanding of the information presented about the treatment. A full scientific understanding of diagnosis and subtleties of treatment likely would be an excessive expectation. For example, a patient would not be expected to understand the nuances of the serotonin neurotransmitter system. A physician should, however, assess whether the patient understands—in the patient’s words—that a selective serotonin reuptake inhibitor could induce manic-type symptoms and that the patient should bring these symptoms to the prescribing physician’s attention if they occur.

Appreciate one’s situation. Individuals who are competent must have a realistic appreciation of their situation. Though a patient may understand the facts you have presented, he may fail to fully integrate why the information is relevant to him. Persons with schizophrenia who do not believe they are ill—such as Mr. D—might have a limited appreciation of why an antipsychotic would help them.

Rationally manipulate information. A person also must be able to rationally manipulate the information in a way that is not impaired by symptoms of illness. Patients faced with a treatment decision should be able to use reason to reach a logical and rational decision that they see as being in their best interest. This might not be the same decision you would make. For example, a patient with thought disorganization or one who psychotically believes that the color of a recommended medication signals that someone tampered with the pills might not be able to rationally manipulate information presented about treatment options.

Source: Reference 11

 

 

Exceptions to informed consent

Emergencies. Informed consent is not required under some circumstances.5 Consider the patient who is brought to the emergency room unconscious after a fall, with no family contact information. A neurosurgeon might need to intervene immediately to save the patient’s life, using the emergency exception to informed consent.

In an emergency, when a person is unable to give informed consent or time does not allow for a full informed consent process, the clinician generally follows the principle of doing no harm. Treatment may be started in an emergency without full informed consent on the assumption that most competent people would consent to treatment, especially where life or limb was at risk. If time and circumstances permit in an emergency, obtaining the consent of available family members may be prudent.

Treating psychosis when no associated behavioral disturbance is placing a patient or others at risk might not constitute an emergency that would negate the need for informed consent. Thus, given Mr. D’s calm demeanor in talking with the clinician about his treatment, an emergency exception probably would not apply in his case.

Incompetence. If a judge determines that a patient is incompetent to make his or her own treatment decisions, a substitute decision-maker—such as a guardian—could be appointed. In these cases, respect would suggest that to the extent possible and appropriate you would inform the incompetent ward about treatment in a way that he or she may understand.

In other circumstances, such as when a healthcare proxy has been invoked, previously designated surrogate decision-makers provide informed consent on behalf of the patient who clinically is found to lack the capacity to make healthcare decisions.

Waivers. Sometimes a competent patient decides to waive the right to further information and may turn the decision over to the clinician. To rely upon this exception, some documented assessment—even if brief—of the patient’s capacity to waive information may be important.

Therapeutic privilege often is cited in the literature but should be an infrequently used exception to informed consent. In very limited situations, a physician might decide to not engage in an informed consent discussion, believing the information to be disclosed would be so damaging that it would directly harm the patient or so emotionally distressing as to foreclose the possibility of the patient making a rational decision.

As noted, informing patients of their health situations is expected and accepted. Even in psychiatric settings, receiving information about potentially serious medication side effects has not necessarily led to patient harm or refusal of treatment.15 Therefore, use of this exception is only for very narrowly tailored circumstances, if used at all, and not simply because you believe a patient will refuse to consent if informed about a proposed treatment.

Some case law exists on the need to establish why the therapeutic privilege was justified as a rationale to not provide informed consent in a particular situation.16 Therefore, though it should be rarely invoked, if you use therapeutic privilege, document why you invoked this exception for that particular patient and in that particular circumstance.

Building the therapeutic alliance

Although it may meet policy or legal informed consent requirements, simply providing the patient with a form to sign before treatment begins does little to enhance patient-clinician communication.2 Providing detailed written information also might not be adequate to ensure that the patient understands the complexity of a treatment you have asked him to consider.17 Instead, an informed consent model that relies on active, ongoing dialogue about treatment can maximize patient autonomy while working for the good of the patient (Table).

Lidz and colleagues2 identified key conditions that must be present for such a process model of informed consent to work:

  • the patient’s role is understood as that of an inquisitive consumer who may challenge the physician’s authority in the quest for information
  • the clinician challenges the patient’s preconceived beliefs about his or her illness and educates the patient so that both parties approach the medical issue from common ground.
A patient also must be allowed to consider his or her own values in weighing medical decisions. These values may include the patient’s ability to tolerate side effects, willingness to take risks, and own sense of quality of life.
 

 

1 In this model of shared decision-making, the clinician reveals information material to the decision, and the patient helps the clinician understand the circumstances that make him or her prefer 1 treatment over another.1,18

By engaging in ongoing informed consent, you may achieve greater gains within the therapeutic alliance and reduce the risk of liability.19 Where uncertainties are related to treatment, share these ambiguities as an aspect of informed consent, especially when the patient plays an active role in treatment.4 Similarly, an expanded informed consent process may be needed when:

  • proposed treatments are particularly risky
  • several treatment alternatives could be acceptable and effective
  • evidence supports opposing views of a treatment’s effectiveness.4,20
Table

Using informed consent to build a therapeutic alliance

  • Use the informed consent dialogue to establish trust and openness with patients while demonstrating respect for patient autonomy
  • Allow patients to share their values and concerns as part of the risk/benefit analysis
  • Talk with patients to understand their preconceived ideas about their illnesses and to seek a common understanding of the illness and its prognosis, with and without treatment

CASE CONTINUED: A question of competence

Mr. D is calm in his discussions with the psychiatrist, and the information she presents does not seem to cause him further harm. Thus, the emergency and therapeutic privilege exceptions do not eliminate the need for an ongoing informed consent process at this time.

Mr. D has a factual understanding of the risks and benefits of the recommended antipsychotic and is able to express a consistent choice about starting this treatment. He lacks, however, an ability to appreciate his situation and has difficulty manipulating information rationally. Overall, he has deficits in aspects of his decision-making competence, which could signal the need for an exception to obtaining informed consent.

The psychiatrist should continue to build an alliance with Mr. D as she works with him toward accepting treatment. Meeting with him regularly, trying to understand his concerns, and trying to help him understand how his symptoms may be interfering with his functioning can help build the alliance. If he continues to show competence-related deficits, she could pursue guardianship or other legal avenues to address his ongoing inability to provide informed consent. This approach would allow for a legally authorized mechanism to administer treatment to this patient.

Related resources

Disclosure

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

References

1. King JS, Moulton BW. Rethinking informed consent: the case for shared medical decision-making. Am J Law Med. 2006;32(4):429-501.

2. Lidz CW, Appelbaum PS, Meisel A. Two models of implementing informed consent. Arch Intern Med. 1988;148(6):1385-1389.

3. Schloendorff v Society of New York Hospital, 105 NE 92 (1914).

4. Beahrs JO, Gutheil TG. Informed consent in psychotherapy. Am J Psychiatry. 2001;158(1):4-10.

5. Appelbaum PS, Gutheil TG. Clinical handbook of psychiatry and the law. Philadelphia, PA: Wolters Kluwer and Lippincott Williams & Wilkins; 2007.

6. Kaimowitz v Michigan, DMH 1 MDLR 147 (1976).

7. Pinals DA, Hoge SK. Treatment refusal in psychiatric practice. In: Rosner R, ed. Principles and practice of forensic psychiatry, 2nd ed. London, UK: Arnold Press; 2003:129-136.

8. Natanson v Kline, 350 P.2D 1093 (1960).

9. Canterbury v Spence, 464 F.2d 772 (1972).

10. Grisso T, Appelbaum PS. The MacArthur Treatment Competence Study: III. Abilities of patients to consent to psychiatric and medical treatment. Law Human Behav. 1995;19(2):149-174.

11. Appelbaum PS, Grisso T. Assessing patients’ capacities to consent to treatment. N Engl J Med. 1988;319(25):1635-1638.

12. Dunn LB, Nowrangi MA, Palmer BW, et al. Assessing decisional capacity for clinical research or treatment: a review of instruments. Am J Psychiatry. 2006;163(8):1323-1334.

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

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

15. Munetz MR, Roth LH. Informing patients about tardive dyskinesia. Arch Gen Psychiatry. 1985;42(9):866-871.

16. Barcai v Betwee MD, 50 P3d 946 (2002).

17. Hafeez A, Wiseman O, Hill JT. Informed consent: are we deluding ourselves? A randomized controlled study. BJU International. 2007;99(1):4-5.

18. Kaplan RM. Shared medical decision making: a new tool for preventative medicine. Am J Prev Med. 2004;26(1):81-83.

19. Gutheil TG, Bursztajn H, Brodsky A. Malpractice prevention through the sharing of uncertainty. Informed consent and the therapeutic alliance. N Engl J Med. 1984;311(1):49-51.

20. Packman WL, Cabot MG, Bongar B. Malpractice arising from negligent psychotherapy: ethical, legal, and clinical implications of Osheroff v Chestnut Lodge. Ethics Behav. 1994;4(3):175-197.

References

1. King JS, Moulton BW. Rethinking informed consent: the case for shared medical decision-making. Am J Law Med. 2006;32(4):429-501.

2. Lidz CW, Appelbaum PS, Meisel A. Two models of implementing informed consent. Arch Intern Med. 1988;148(6):1385-1389.

3. Schloendorff v Society of New York Hospital, 105 NE 92 (1914).

4. Beahrs JO, Gutheil TG. Informed consent in psychotherapy. Am J Psychiatry. 2001;158(1):4-10.

5. Appelbaum PS, Gutheil TG. Clinical handbook of psychiatry and the law. Philadelphia, PA: Wolters Kluwer and Lippincott Williams & Wilkins; 2007.

6. Kaimowitz v Michigan, DMH 1 MDLR 147 (1976).

7. Pinals DA, Hoge SK. Treatment refusal in psychiatric practice. In: Rosner R, ed. Principles and practice of forensic psychiatry, 2nd ed. London, UK: Arnold Press; 2003:129-136.

8. Natanson v Kline, 350 P.2D 1093 (1960).

9. Canterbury v Spence, 464 F.2d 772 (1972).

10. Grisso T, Appelbaum PS. The MacArthur Treatment Competence Study: III. Abilities of patients to consent to psychiatric and medical treatment. Law Human Behav. 1995;19(2):149-174.

11. Appelbaum PS, Grisso T. Assessing patients’ capacities to consent to treatment. N Engl J Med. 1988;319(25):1635-1638.

12. Dunn LB, Nowrangi MA, Palmer BW, et al. Assessing decisional capacity for clinical research or treatment: a review of instruments. Am J Psychiatry. 2006;163(8):1323-1334.

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

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

15. Munetz MR, Roth LH. Informing patients about tardive dyskinesia. Arch Gen Psychiatry. 1985;42(9):866-871.

16. Barcai v Betwee MD, 50 P3d 946 (2002).

17. Hafeez A, Wiseman O, Hill JT. Informed consent: are we deluding ourselves? A randomized controlled study. BJU International. 2007;99(1):4-5.

18. Kaplan RM. Shared medical decision making: a new tool for preventative medicine. Am J Prev Med. 2004;26(1):81-83.

19. Gutheil TG, Bursztajn H, Brodsky A. Malpractice prevention through the sharing of uncertainty. Informed consent and the therapeutic alliance. N Engl J Med. 1984;311(1):49-51.

20. Packman WL, Cabot MG, Bongar B. Malpractice arising from negligent psychotherapy: ethical, legal, and clinical implications of Osheroff v Chestnut Lodge. Ethics Behav. 1994;4(3):175-197.

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Clinical guide to countertransference: Help medical colleagues deal with ‘difficult’ patients

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WEB AUDIO
Listen to Dr. Muskin discuss the patient-physician dynamic

Two strangers meet in the hospital cafeteria. Mrs. R, an elderly woman, asks Dr. W, a first-year medical resident, for help in getting a bottle of soda from the cooler. Afterward, Dr. W comments to a colleague with whom she is having lunch, “That woman reminds me of my grandmother.”

What does that comment reflect about Dr. W? It is a statement about the doctor’s transference. That is, she is aware of elements about Mrs. R that evoke internal responses appropriate to a prior important relationship.

What if Mrs. R was to subsequently faint, require admission to the hospital, and become Dr. W’s patient? If Dr. W’s comment indicates transference, would the same reaction to Mrs. R now be countertransference? Does that change if the doctor is unaware of emotions Mrs. R evokes? Is it still countertransference whether Dr. W is caring and compassionate, overly involved with Mrs. R, or—unaware of negative feelings associated with “grandmothers”—avoids the patient?

This article explores how complex internal experiences play out in the general medical setting and discusses how psychiatric consultants can help medical/surgical colleagues understand and manage difficult patient-physician relationships.

The therapeutic dyad

Countertransference and transference are concepts embedded in psychodynamic thinking. They are part of how many people think about interpersonal relations, whether or not they use these terms. Countertransference and transference may be conscious, but they always have an unconscious component. Factors that influence what will be transference and countertransference in adult life have both:

  • a biological component because part of personality is genetic
  • a psychological component based upon experiences throughout life ( Box 1 ).1
Box 1

Roots of transference: From a child’s experience of the world

Genetic factors play a role in personality formation. A child’s personality, which emerges early in life, shapes interactions with people who are significant during childhood. Predispositions shape those experiences and influence what people internalize from those relationships.

In adults, many aspects of what we understand as transference—the experience someone has of a figure from the past—originate from the limitations with which children perceive and interpret their experiences. Transference is not truth about a significant past relationship; it is truth as the person experienced other people and now remembers or reacts to individuals who are reminiscent of those from the past.1

Not all psychotherapeutic treatments—and thus not all therapists—use the concept of transference as a therapeutic component. Some therapists who employ transference in treatment will discuss how the patient interacts with the therapist only when the phenomenon interferes with therapy. Interpretation of transference is a therapeutic modality of psychoanalysis and psychodynamic psychotherapy. Discussion of how the patient interacts with the therapist is not the same as a transference interpretation. Because transference exists in all human relationships, transferential aspects in a relationship may have positive or negative effects on interactions outside the therapeutic environment. Whether acknowledged or ignored, transference—and thus countertransference—is present.

Transference is experiencing and/or relating to someone in the present as if that person was a significant individual from the past. The concept implies that all personal relationships contain elements of transference(s). That is, we all have the potential to displace or transfer to current situations infantile and internal conflicts that are out of place and thus not appropriate to the present person and/or situation.

Countertransference is a dimensional concept, not an all-or-nothing experience. Some reactions to patients are based entirely upon their transference to us and have nothing to do with us (therapists) as people. Others derive mostly from psychodynamics within the therapist ( Box 2 ). Countertransference has evolved to incorporate responses evoked by a combination of:

  • the patient’s transference
  • the therapist’s unique psychodynamics
  • the real relationship in the therapeutic dyad.2
Box 2

Reactions to other people: When are they countertransference?

In the therapeutic setting, some reactions to the patient are experienced as unusually powerful, out of keeping with our self-image, or as consciously disturbing. Such reactions to a patient—while still countertransference—might result from projective identification. This type of countertransference is most commonly, but not exclusively, encountered in therapy of patients with borderline personality organization.3

We suggest that the term countertransference be restricted to therapeutic situations (any relationship in which one person has the role of treating or helping the other person), including all patient-physician or patient-provider relationships. They have a transferential component because the physician occupies a role of authority/knowledge/power from which the patient seeks to benefit.

Outside of therapeutic situations, reactions to other people are our transferences to them, evoked by our internalized past relationships. We may have an emotional response to how someone behaves toward us (their transference), but that is a counter-transference, not countertransference.

 

 

Patients with medical illness

Psychiatrists think of countertransference as a psychological situation occurring in the office or on an inpatient psychiatric unit. We focus our attention on how we feel and what we think while working with patients. We talk about our reactions to patients in supervision, rounds, case conferences, and other situations where mental health professionals discuss patients.

Our medical/surgical colleagues’ reactions to patients often correlate with certain patient presentations and may have little to do with the actual person who is the patient.4 The medical setting provides an opportunity for countertransference to occur in the absence of apparent transference.

Somatic illness imposes on patients some degree of regression. This regression and attempts to cope with it are inherent to somatic illness and hospitalization. Several schemas5 describe basic coping mechanisms common to most patients ( Table ).6,7 Recognizing a patient’s character style or personality type may help clinicians predict their countertransference when interacting with that patient. Uncooperative patients and those perceived as “difficult” are particularly likely to evoke negative countertransference.8

Table

Patients’ response to illness,
with common countertransference by medical staff

Patient’s coping mechanismsStaff’s countertransference
Dependent personality
• Unconsciously wishes for unlimited care
• Depends on others to feel secure
• May make excessive requests of staff
• Gratification at being able to take care of patient’s needs
• Resentment if patient’s needs seem insatiable
Obsessional personality
• Meticulous self-discipline
• Illness represents loss of control
• Will try to gain mastery over illness by focusing on details, information
• Relief at patient’s willingness to actively participate
• Power struggle is possible
Histrionic personality
• Outgoing, colorful, lively
• Attractiveness and sexuality important
• Needs to feel the center of attention
• Illness represents defect, loss of physical beauty
• Warm initial engagement
• Fear of crossing boundaries
• Wonder about veracity of complaints
Masochistic personality
• Satisfies unconscious needs by suffering
• Needs to play victim role
• Frustration when reassurance does not help
• May unconsciously play into patient’s need for punishment
Paranoid personality
• Pervasive doubt of others’ motivations
• Often questions motives for interventions
• Illness represents threat to safety
• Wary of lack of alliance
• Anger that patient questions treatment motives
• Frustrated at inability to form a trusting relationship with patient
• Unsettled by lack of connection
Narcissistic personality
• Grandiose sense of self, which protects against shame, humiliation
• May demand superior care, insult junior team members
• May feel flattered by ability to treat patient as VIP
• May alternately feel devalued, wonder about competence
Source: References 6,7

CASE CONTINUED: No longer ‘grandmotherly’

Mrs. R and Dr. W are now in a patient-physician relationship. Dr. W is no longer handing Mrs. R a bottle of soda but is inquiring about her life, use of alcohol and other drugs, intimate activities, etc. Mrs. R reacts with anger at the “personal questions.” In addition, Dr. W orders tests that are uncomfortable for Mrs. R, who refuses to cooperate with some procedures.

Dr. W’s memories of her grandmother (who was encouraging, supportive, and loving) color her experience of Mrs. R. She ignores nursing staff’s complaints about Mrs. R being demanding and difficult as the patient becomes aggressive and increasingly confused.

Unable to see the patient as she really is, Dr. W becomes angry and defends Mrs. R’s behavior. The nurses feel Dr. W is unrealistic and ignore her at the nursing station. Late on a Friday night, Mrs. R becomes paranoid, hallucinating that “demons” are in her room. She tries to elope from the hospital. Dr. W is off for the weekend, and the staff requests an emergency psychiatric consultation.

Mrs. R evokes a reaction from the nurses because of how she interacts with them. Dr. W’s response—based on her experience of her grandmother—has nothing to do with the way Mrs. R relates interpersonally but reflects a reaction to the patient’s gender and age. Both reactions would be countertransference, using the modern definition.

If reactions to a patient such as Mrs. R are positive, no one seems to notice and the reactions might or might not influence her care. If the reactions are negative, they might influence her care and generate a request for a psychiatric consultation.

Countertransference might have a negative effect on patient care. For example, if a physician were to avoid Mrs. R because she is uncooperative, and if the nursing staff is intolerant of the patient’s confusion and agitation, she might be labeled as “demented” and be given medication without anyone exploring the etiology of her behavior.
 

 


Some patients cannot communicate because of neurologic disorders, intubation, language barriers, or because they are unconscious when admitted. Without information from the patient, medical staff may form ideas about the patient based on their unconscious fantasies. These fantasies may influence the patient’s care.9 Psychiatric consultants are not immune to countertransference, but we come into situations with the opportunity to experience all participants from the outside.

CASE CONTINUED: The psychiatric consultation

During the interview, the psychiatrist asks Mrs. R if she takes any medications. She retorts that she always takes “Centrum” at bed-time and demands to know why she is not getting her “vitamins.” She is given oxazepam and falls asleep.

The psychiatrist recommends benzodiazepine detoxification, suspecting Mrs. R is taking prazepam at home from an old prescription (when the medication was a brand called “Centrax”). This suspicion is confirmed when Mrs. R’s family brings in a large shopping bag of medications she has collected over decades, and Mrs. R identifies her nighttime “vitamin.”

A full evaluation for delirium is completed over the next 2 days. Mrs. R’s confusion and aggressive behavior respond to oxazepam.

Patients with particular character styles evoke predictable reactions from others, including psychotherapists. Discussing these reactions has been a part of psychiatric training for decades. A subset of patients has been described as “hateful,” as they routinely evoke extremely negative responses.10 Whether their primary disorder is psychiatric, medical, or some of both, these patients evoke strong countertransference reactions.

Psychiatrists may be comfortable discussing a “narcissistic patient, a dependent clinger with borderline features,” but our medical colleagues might not share our comfort with psychiatric jargon.11 It may be more useful to say to medical staff that the patient “thinks of himself as very important, cannot accept his need to be taken care of, and tends to see things in black and white.”

Managing difficult patients

The characterizations that follow describe unconscious reactions to types of individuals who are routinely experienced as “difficult” patients. Some patients may exhibit a mixture of character styles ( Table ) and do not easily fall into 1 category. The concepts can be useful in clarifying the reactions that patients evoke in medical staff.

‘Dependent’ patients. Some patients demand continuous attention but are unaware of their insatiable neediness. Early in treatment, they may evoke positive countertransference because they are intensely grateful for attention. They can be enticing, unconsciously seductive, and gratifying to their doctors. Over time, they drain and exhaust their physicians, who resort to avoidance and wish to get rid of these patients.

Recommendation. Set limits to prevent the patient from feeling rejected or an actual rejection when he or she is transferred to another doctor’s care. Coach physicians to:

  • ask patients to “Tell me what is most important for us to discuss today”
  • be clear how long the visit will last.
Reassuring the patient that other issues will be addressed in the next visit prevents the physician from feeling overwhelmed by the patient consuming too much time.

‘Entitled’ patients. Another type of “difficult” patient projects an air of entitlement, which typically reflects an underlying insatiable neediness. They may use intimidation, guilt, and threats of punishment to get their doctors to provide the care they demand. These patients appear powerful (even though they may possess no special status), and they may be overtly devaluing of the physician while simultaneously demanding special attention.

The doctor resents the patient’s entitlement but develops an expectable countertransference fear that he or she will get in trouble if the demands are not met. Wishes to retaliate and “put the patient in his or her place” are common.

Recommendation. Saying, “It is understandable that you want the best care, and I plan to give you the best care,” makes it clear to the patient that the physician hears the patient’s concerns. Advise the physician to request the patient’s “understanding and compassion” for other patients who also need the physician’s time and attention.

‘Help-rejecting’ patients. “Help-rejecting” patients demand care but show little faith in treatment and do not follow treatment plans. The harder the physician tries to help, the less likely the plan will succeed. For these patients, treatment success evokes a fear of abandonment; thus, treatment must fail to maintain the relationship.

Common countertransference reactions are initial anxiety that the treatment plan was not adequate, followed by anger and depression as the physician feels stuck with a patient for whom nothing works.

 

 

Recommendation. Setting realistic goals for treatment helps the physician guide the patient, who expects to be told not to return the moment he or she gets better. Telling the patient that medical care does not stop when a particular malady is treated speaks to the patient’s fear of being abandoned.

When the patient adheres only partially to the plan and a psychiatric consultant is called for an “uncooperative” patient, help the doctor understand how the patient sees the world. It is the patient’s psychological needs—not the physician’s failure—that control the outcome of the care.

‘Self-destructive’ patients may appear unaware of their dangerous actions. They evoke malice from their doctors, who feel the patients are purposely engaging in life-threatening behaviors. The patients’ unconscious dependence remains unknown as their denial of the consequences of their behavior frightens and angers those involved in their care. Some of these patients cannot be stopped before their actions cause them permanent harm or death.

Recommendation. You might remind the physician that we all are entitled to live our lives as we choose. To decompress intense feelings, advise the physician to share, without blaming the patient, what medical staff can realistically do. Saying “We’ll do the best we can” (rather than “Treatment is useless for someone like you”) permits the patient to receive the degree of care he or she can accept without the physician feeling helpless. Understanding our limitations and obligations is part of using our countertransference to aid in patient care.

CASE CONTINUED: Feeling better

When Dr. W returns on Monday, she angrily calls the psychiatrist to complain that her patient has been placed on a benzodiazepine and at the “implication” that Mrs. R was abusing medication. When they talk in person, the psychiatrist explains the situation to Dr. W and suggests they meet with Mrs. R together.

Mrs. R is embarrassed when told about her behavior, identifies the pill, and admits taking prazepam for several weeks prior to hospitalization. She says she never understood how a vitamin could help her sleep so well. No longer delirious, Mrs. R is pleasant and asks many questions. She is surprised that “so young” a doctor was assigned to her case and asks if the chief of medicine could be brought in, as she is on the board of directors of another hospital. “No offense, dear,” she says to Dr. W; “I’m sure you did an excellent job, but usually only senior doctors take care of me.”

Later, Dr. W talks with the psychiatric consultant about her chance meeting with Mrs. R in the cafeteria and the discord with the nursing staff. She notes that she was doing an elective in another country when her grandmother died. She realizes that her feelings about her grandmother are superimposed on the patient, resulting in an inability to see the patient as she really is.

Dr. W accepts the psychiatrist’s suggestion to repair her relationship with the nurses with an apology. She now notes that Mrs. R is nothing like her grandmother and seems “pretty stuck up.” She is glad to be off the case and accepts the psychiatrist’s idea that Mrs. R’s need to feel important should not make Dr. W feel bad about herself.

Related resources

  • Gabbard GO, ed. Countertransference issues in psychiatric treatment. In: Oldham JM, Riba MB, eds. Review of psychiatry series. Washington, DC: American Psychiatric Publishing, Inc.; 1999.
  • Blumenfield M, Strain JJ, Grossman S. Psychodynamic approach. In: Blumenfield M, Strain JJ, eds. Psychosomatic medicine. Philadelphia, PA: Lippincott, Williams and Wilkins; 2006:817-828.
Drug brand names

  • Oxazepam • Serax
  • Prazepam • Centrax
Disclosure

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

References

1. Gabbard GO. Basic principles of psychodynamic psychotherapy. In: Gabbard GO, ed. Psychodynamic psychiatry in clinical practice. Washington, DC: American Psychiatric Publishing, Inc.; 2005:1-30.

2. Harris A. Transference, countertransference, and the real relationship. In: Person ES, Cooper AM, Gabbard GO, eds. Textbook of psychoanalysis. Washington, DC: American Psychiatric Publishing, Inc.; 2005:201-216.

3. Goldstein WN. Clarification of projective identification. Am J Psychiatry. 1991;148:153-161.

4. Kuchariski A, Groves JE. The so-called “inappropriate” psychiatric consultation request on a medical or surgical ward. Int J Psychiatry Med. 1976;7(3):209-220.

5. Groves MA, Muskin PR. Psychological responses to illness. In: Levenson JL, ed. Textbook of psychosomatic medicine. Washington, DC: American Psychiatric Publishing, Inc.; 2005:67-90.

6. Kahana RJ, Bibring GL. Personality types in medical management. In: Zinberg N, ed. Psychiatry and medical practice in a general hospital. New York, NY: International Universities Press; 1964:108-123.

7. Geringer ES, Stern TA. Coping with medical illness: the impact of personality types. Psychosomatics. 1986;27:251-261.

8. Mozian SA, Muskin PR. The difficult patient. In: Barnhill JW, ed. The approach to the psychiatric patient. Washington, DC: American Psychiatric Publishing, Inc.; 2008:192-196.

9. Groves JE. Management of the borderline patient on a medical or surgical ward: the psychiatric consultant’s role. Int J Psychiatry Med. 1975;6:337-348.

10. Groves JE. Taking care of the hateful patient. N Engl J Med. 1978;298:883-887.

11. Pasnau RO. Ten Commandments of medical etiquette for psychiatrists. Psychosomatics. 1985;26(2):128-132.

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Philip R. Muskin, MD
Professor of clinical psychiatry, Columbia University College of Physicians and Surgeons, chief, consultation-liaison psychiatry, Columbia University Medical Center, faculty, Columbia University Psychoanalytic Center for Training and Research, New York, NY

Lucy A. Epstein, MD
Postdoctoral clinical fellow in psychosomatic medicine, Columbia University College of Physicians and Surgeons, New York, NY

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Postdoctoral clinical fellow in psychosomatic medicine, Columbia University College of Physicians and Surgeons, New York, NY

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Professor of clinical psychiatry, Columbia University College of Physicians and Surgeons, chief, consultation-liaison psychiatry, Columbia University Medical Center, faculty, Columbia University Psychoanalytic Center for Training and Research, New York, NY

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Postdoctoral clinical fellow in psychosomatic medicine, Columbia University College of Physicians and Surgeons, New York, NY

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WEB AUDIO
Listen to Dr. Muskin discuss the patient-physician dynamic

Two strangers meet in the hospital cafeteria. Mrs. R, an elderly woman, asks Dr. W, a first-year medical resident, for help in getting a bottle of soda from the cooler. Afterward, Dr. W comments to a colleague with whom she is having lunch, “That woman reminds me of my grandmother.”

What does that comment reflect about Dr. W? It is a statement about the doctor’s transference. That is, she is aware of elements about Mrs. R that evoke internal responses appropriate to a prior important relationship.

What if Mrs. R was to subsequently faint, require admission to the hospital, and become Dr. W’s patient? If Dr. W’s comment indicates transference, would the same reaction to Mrs. R now be countertransference? Does that change if the doctor is unaware of emotions Mrs. R evokes? Is it still countertransference whether Dr. W is caring and compassionate, overly involved with Mrs. R, or—unaware of negative feelings associated with “grandmothers”—avoids the patient?

This article explores how complex internal experiences play out in the general medical setting and discusses how psychiatric consultants can help medical/surgical colleagues understand and manage difficult patient-physician relationships.

The therapeutic dyad

Countertransference and transference are concepts embedded in psychodynamic thinking. They are part of how many people think about interpersonal relations, whether or not they use these terms. Countertransference and transference may be conscious, but they always have an unconscious component. Factors that influence what will be transference and countertransference in adult life have both:

  • a biological component because part of personality is genetic
  • a psychological component based upon experiences throughout life ( Box 1 ).1
Box 1

Roots of transference: From a child’s experience of the world

Genetic factors play a role in personality formation. A child’s personality, which emerges early in life, shapes interactions with people who are significant during childhood. Predispositions shape those experiences and influence what people internalize from those relationships.

In adults, many aspects of what we understand as transference—the experience someone has of a figure from the past—originate from the limitations with which children perceive and interpret their experiences. Transference is not truth about a significant past relationship; it is truth as the person experienced other people and now remembers or reacts to individuals who are reminiscent of those from the past.1

Not all psychotherapeutic treatments—and thus not all therapists—use the concept of transference as a therapeutic component. Some therapists who employ transference in treatment will discuss how the patient interacts with the therapist only when the phenomenon interferes with therapy. Interpretation of transference is a therapeutic modality of psychoanalysis and psychodynamic psychotherapy. Discussion of how the patient interacts with the therapist is not the same as a transference interpretation. Because transference exists in all human relationships, transferential aspects in a relationship may have positive or negative effects on interactions outside the therapeutic environment. Whether acknowledged or ignored, transference—and thus countertransference—is present.

Transference is experiencing and/or relating to someone in the present as if that person was a significant individual from the past. The concept implies that all personal relationships contain elements of transference(s). That is, we all have the potential to displace or transfer to current situations infantile and internal conflicts that are out of place and thus not appropriate to the present person and/or situation.

Countertransference is a dimensional concept, not an all-or-nothing experience. Some reactions to patients are based entirely upon their transference to us and have nothing to do with us (therapists) as people. Others derive mostly from psychodynamics within the therapist ( Box 2 ). Countertransference has evolved to incorporate responses evoked by a combination of:

  • the patient’s transference
  • the therapist’s unique psychodynamics
  • the real relationship in the therapeutic dyad.2
Box 2

Reactions to other people: When are they countertransference?

In the therapeutic setting, some reactions to the patient are experienced as unusually powerful, out of keeping with our self-image, or as consciously disturbing. Such reactions to a patient—while still countertransference—might result from projective identification. This type of countertransference is most commonly, but not exclusively, encountered in therapy of patients with borderline personality organization.3

We suggest that the term countertransference be restricted to therapeutic situations (any relationship in which one person has the role of treating or helping the other person), including all patient-physician or patient-provider relationships. They have a transferential component because the physician occupies a role of authority/knowledge/power from which the patient seeks to benefit.

Outside of therapeutic situations, reactions to other people are our transferences to them, evoked by our internalized past relationships. We may have an emotional response to how someone behaves toward us (their transference), but that is a counter-transference, not countertransference.

 

 

Patients with medical illness

Psychiatrists think of countertransference as a psychological situation occurring in the office or on an inpatient psychiatric unit. We focus our attention on how we feel and what we think while working with patients. We talk about our reactions to patients in supervision, rounds, case conferences, and other situations where mental health professionals discuss patients.

Our medical/surgical colleagues’ reactions to patients often correlate with certain patient presentations and may have little to do with the actual person who is the patient.4 The medical setting provides an opportunity for countertransference to occur in the absence of apparent transference.

Somatic illness imposes on patients some degree of regression. This regression and attempts to cope with it are inherent to somatic illness and hospitalization. Several schemas5 describe basic coping mechanisms common to most patients ( Table ).6,7 Recognizing a patient’s character style or personality type may help clinicians predict their countertransference when interacting with that patient. Uncooperative patients and those perceived as “difficult” are particularly likely to evoke negative countertransference.8

Table

Patients’ response to illness,
with common countertransference by medical staff

Patient’s coping mechanismsStaff’s countertransference
Dependent personality
• Unconsciously wishes for unlimited care
• Depends on others to feel secure
• May make excessive requests of staff
• Gratification at being able to take care of patient’s needs
• Resentment if patient’s needs seem insatiable
Obsessional personality
• Meticulous self-discipline
• Illness represents loss of control
• Will try to gain mastery over illness by focusing on details, information
• Relief at patient’s willingness to actively participate
• Power struggle is possible
Histrionic personality
• Outgoing, colorful, lively
• Attractiveness and sexuality important
• Needs to feel the center of attention
• Illness represents defect, loss of physical beauty
• Warm initial engagement
• Fear of crossing boundaries
• Wonder about veracity of complaints
Masochistic personality
• Satisfies unconscious needs by suffering
• Needs to play victim role
• Frustration when reassurance does not help
• May unconsciously play into patient’s need for punishment
Paranoid personality
• Pervasive doubt of others’ motivations
• Often questions motives for interventions
• Illness represents threat to safety
• Wary of lack of alliance
• Anger that patient questions treatment motives
• Frustrated at inability to form a trusting relationship with patient
• Unsettled by lack of connection
Narcissistic personality
• Grandiose sense of self, which protects against shame, humiliation
• May demand superior care, insult junior team members
• May feel flattered by ability to treat patient as VIP
• May alternately feel devalued, wonder about competence
Source: References 6,7

CASE CONTINUED: No longer ‘grandmotherly’

Mrs. R and Dr. W are now in a patient-physician relationship. Dr. W is no longer handing Mrs. R a bottle of soda but is inquiring about her life, use of alcohol and other drugs, intimate activities, etc. Mrs. R reacts with anger at the “personal questions.” In addition, Dr. W orders tests that are uncomfortable for Mrs. R, who refuses to cooperate with some procedures.

Dr. W’s memories of her grandmother (who was encouraging, supportive, and loving) color her experience of Mrs. R. She ignores nursing staff’s complaints about Mrs. R being demanding and difficult as the patient becomes aggressive and increasingly confused.

Unable to see the patient as she really is, Dr. W becomes angry and defends Mrs. R’s behavior. The nurses feel Dr. W is unrealistic and ignore her at the nursing station. Late on a Friday night, Mrs. R becomes paranoid, hallucinating that “demons” are in her room. She tries to elope from the hospital. Dr. W is off for the weekend, and the staff requests an emergency psychiatric consultation.

Mrs. R evokes a reaction from the nurses because of how she interacts with them. Dr. W’s response—based on her experience of her grandmother—has nothing to do with the way Mrs. R relates interpersonally but reflects a reaction to the patient’s gender and age. Both reactions would be countertransference, using the modern definition.

If reactions to a patient such as Mrs. R are positive, no one seems to notice and the reactions might or might not influence her care. If the reactions are negative, they might influence her care and generate a request for a psychiatric consultation.

Countertransference might have a negative effect on patient care. For example, if a physician were to avoid Mrs. R because she is uncooperative, and if the nursing staff is intolerant of the patient’s confusion and agitation, she might be labeled as “demented” and be given medication without anyone exploring the etiology of her behavior.
 

 


Some patients cannot communicate because of neurologic disorders, intubation, language barriers, or because they are unconscious when admitted. Without information from the patient, medical staff may form ideas about the patient based on their unconscious fantasies. These fantasies may influence the patient’s care.9 Psychiatric consultants are not immune to countertransference, but we come into situations with the opportunity to experience all participants from the outside.

CASE CONTINUED: The psychiatric consultation

During the interview, the psychiatrist asks Mrs. R if she takes any medications. She retorts that she always takes “Centrum” at bed-time and demands to know why she is not getting her “vitamins.” She is given oxazepam and falls asleep.

The psychiatrist recommends benzodiazepine detoxification, suspecting Mrs. R is taking prazepam at home from an old prescription (when the medication was a brand called “Centrax”). This suspicion is confirmed when Mrs. R’s family brings in a large shopping bag of medications she has collected over decades, and Mrs. R identifies her nighttime “vitamin.”

A full evaluation for delirium is completed over the next 2 days. Mrs. R’s confusion and aggressive behavior respond to oxazepam.

Patients with particular character styles evoke predictable reactions from others, including psychotherapists. Discussing these reactions has been a part of psychiatric training for decades. A subset of patients has been described as “hateful,” as they routinely evoke extremely negative responses.10 Whether their primary disorder is psychiatric, medical, or some of both, these patients evoke strong countertransference reactions.

Psychiatrists may be comfortable discussing a “narcissistic patient, a dependent clinger with borderline features,” but our medical colleagues might not share our comfort with psychiatric jargon.11 It may be more useful to say to medical staff that the patient “thinks of himself as very important, cannot accept his need to be taken care of, and tends to see things in black and white.”

Managing difficult patients

The characterizations that follow describe unconscious reactions to types of individuals who are routinely experienced as “difficult” patients. Some patients may exhibit a mixture of character styles ( Table ) and do not easily fall into 1 category. The concepts can be useful in clarifying the reactions that patients evoke in medical staff.

‘Dependent’ patients. Some patients demand continuous attention but are unaware of their insatiable neediness. Early in treatment, they may evoke positive countertransference because they are intensely grateful for attention. They can be enticing, unconsciously seductive, and gratifying to their doctors. Over time, they drain and exhaust their physicians, who resort to avoidance and wish to get rid of these patients.

Recommendation. Set limits to prevent the patient from feeling rejected or an actual rejection when he or she is transferred to another doctor’s care. Coach physicians to:

  • ask patients to “Tell me what is most important for us to discuss today”
  • be clear how long the visit will last.
Reassuring the patient that other issues will be addressed in the next visit prevents the physician from feeling overwhelmed by the patient consuming too much time.

‘Entitled’ patients. Another type of “difficult” patient projects an air of entitlement, which typically reflects an underlying insatiable neediness. They may use intimidation, guilt, and threats of punishment to get their doctors to provide the care they demand. These patients appear powerful (even though they may possess no special status), and they may be overtly devaluing of the physician while simultaneously demanding special attention.

The doctor resents the patient’s entitlement but develops an expectable countertransference fear that he or she will get in trouble if the demands are not met. Wishes to retaliate and “put the patient in his or her place” are common.

Recommendation. Saying, “It is understandable that you want the best care, and I plan to give you the best care,” makes it clear to the patient that the physician hears the patient’s concerns. Advise the physician to request the patient’s “understanding and compassion” for other patients who also need the physician’s time and attention.

‘Help-rejecting’ patients. “Help-rejecting” patients demand care but show little faith in treatment and do not follow treatment plans. The harder the physician tries to help, the less likely the plan will succeed. For these patients, treatment success evokes a fear of abandonment; thus, treatment must fail to maintain the relationship.

Common countertransference reactions are initial anxiety that the treatment plan was not adequate, followed by anger and depression as the physician feels stuck with a patient for whom nothing works.

 

 

Recommendation. Setting realistic goals for treatment helps the physician guide the patient, who expects to be told not to return the moment he or she gets better. Telling the patient that medical care does not stop when a particular malady is treated speaks to the patient’s fear of being abandoned.

When the patient adheres only partially to the plan and a psychiatric consultant is called for an “uncooperative” patient, help the doctor understand how the patient sees the world. It is the patient’s psychological needs—not the physician’s failure—that control the outcome of the care.

‘Self-destructive’ patients may appear unaware of their dangerous actions. They evoke malice from their doctors, who feel the patients are purposely engaging in life-threatening behaviors. The patients’ unconscious dependence remains unknown as their denial of the consequences of their behavior frightens and angers those involved in their care. Some of these patients cannot be stopped before their actions cause them permanent harm or death.

Recommendation. You might remind the physician that we all are entitled to live our lives as we choose. To decompress intense feelings, advise the physician to share, without blaming the patient, what medical staff can realistically do. Saying “We’ll do the best we can” (rather than “Treatment is useless for someone like you”) permits the patient to receive the degree of care he or she can accept without the physician feeling helpless. Understanding our limitations and obligations is part of using our countertransference to aid in patient care.

CASE CONTINUED: Feeling better

When Dr. W returns on Monday, she angrily calls the psychiatrist to complain that her patient has been placed on a benzodiazepine and at the “implication” that Mrs. R was abusing medication. When they talk in person, the psychiatrist explains the situation to Dr. W and suggests they meet with Mrs. R together.

Mrs. R is embarrassed when told about her behavior, identifies the pill, and admits taking prazepam for several weeks prior to hospitalization. She says she never understood how a vitamin could help her sleep so well. No longer delirious, Mrs. R is pleasant and asks many questions. She is surprised that “so young” a doctor was assigned to her case and asks if the chief of medicine could be brought in, as she is on the board of directors of another hospital. “No offense, dear,” she says to Dr. W; “I’m sure you did an excellent job, but usually only senior doctors take care of me.”

Later, Dr. W talks with the psychiatric consultant about her chance meeting with Mrs. R in the cafeteria and the discord with the nursing staff. She notes that she was doing an elective in another country when her grandmother died. She realizes that her feelings about her grandmother are superimposed on the patient, resulting in an inability to see the patient as she really is.

Dr. W accepts the psychiatrist’s suggestion to repair her relationship with the nurses with an apology. She now notes that Mrs. R is nothing like her grandmother and seems “pretty stuck up.” She is glad to be off the case and accepts the psychiatrist’s idea that Mrs. R’s need to feel important should not make Dr. W feel bad about herself.

Related resources

  • Gabbard GO, ed. Countertransference issues in psychiatric treatment. In: Oldham JM, Riba MB, eds. Review of psychiatry series. Washington, DC: American Psychiatric Publishing, Inc.; 1999.
  • Blumenfield M, Strain JJ, Grossman S. Psychodynamic approach. In: Blumenfield M, Strain JJ, eds. Psychosomatic medicine. Philadelphia, PA: Lippincott, Williams and Wilkins; 2006:817-828.
Drug brand names

  • Oxazepam • Serax
  • Prazepam • Centrax
Disclosure

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

WEB AUDIO
Listen to Dr. Muskin discuss the patient-physician dynamic

Two strangers meet in the hospital cafeteria. Mrs. R, an elderly woman, asks Dr. W, a first-year medical resident, for help in getting a bottle of soda from the cooler. Afterward, Dr. W comments to a colleague with whom she is having lunch, “That woman reminds me of my grandmother.”

What does that comment reflect about Dr. W? It is a statement about the doctor’s transference. That is, she is aware of elements about Mrs. R that evoke internal responses appropriate to a prior important relationship.

What if Mrs. R was to subsequently faint, require admission to the hospital, and become Dr. W’s patient? If Dr. W’s comment indicates transference, would the same reaction to Mrs. R now be countertransference? Does that change if the doctor is unaware of emotions Mrs. R evokes? Is it still countertransference whether Dr. W is caring and compassionate, overly involved with Mrs. R, or—unaware of negative feelings associated with “grandmothers”—avoids the patient?

This article explores how complex internal experiences play out in the general medical setting and discusses how psychiatric consultants can help medical/surgical colleagues understand and manage difficult patient-physician relationships.

The therapeutic dyad

Countertransference and transference are concepts embedded in psychodynamic thinking. They are part of how many people think about interpersonal relations, whether or not they use these terms. Countertransference and transference may be conscious, but they always have an unconscious component. Factors that influence what will be transference and countertransference in adult life have both:

  • a biological component because part of personality is genetic
  • a psychological component based upon experiences throughout life ( Box 1 ).1
Box 1

Roots of transference: From a child’s experience of the world

Genetic factors play a role in personality formation. A child’s personality, which emerges early in life, shapes interactions with people who are significant during childhood. Predispositions shape those experiences and influence what people internalize from those relationships.

In adults, many aspects of what we understand as transference—the experience someone has of a figure from the past—originate from the limitations with which children perceive and interpret their experiences. Transference is not truth about a significant past relationship; it is truth as the person experienced other people and now remembers or reacts to individuals who are reminiscent of those from the past.1

Not all psychotherapeutic treatments—and thus not all therapists—use the concept of transference as a therapeutic component. Some therapists who employ transference in treatment will discuss how the patient interacts with the therapist only when the phenomenon interferes with therapy. Interpretation of transference is a therapeutic modality of psychoanalysis and psychodynamic psychotherapy. Discussion of how the patient interacts with the therapist is not the same as a transference interpretation. Because transference exists in all human relationships, transferential aspects in a relationship may have positive or negative effects on interactions outside the therapeutic environment. Whether acknowledged or ignored, transference—and thus countertransference—is present.

Transference is experiencing and/or relating to someone in the present as if that person was a significant individual from the past. The concept implies that all personal relationships contain elements of transference(s). That is, we all have the potential to displace or transfer to current situations infantile and internal conflicts that are out of place and thus not appropriate to the present person and/or situation.

Countertransference is a dimensional concept, not an all-or-nothing experience. Some reactions to patients are based entirely upon their transference to us and have nothing to do with us (therapists) as people. Others derive mostly from psychodynamics within the therapist ( Box 2 ). Countertransference has evolved to incorporate responses evoked by a combination of:

  • the patient’s transference
  • the therapist’s unique psychodynamics
  • the real relationship in the therapeutic dyad.2
Box 2

Reactions to other people: When are they countertransference?

In the therapeutic setting, some reactions to the patient are experienced as unusually powerful, out of keeping with our self-image, or as consciously disturbing. Such reactions to a patient—while still countertransference—might result from projective identification. This type of countertransference is most commonly, but not exclusively, encountered in therapy of patients with borderline personality organization.3

We suggest that the term countertransference be restricted to therapeutic situations (any relationship in which one person has the role of treating or helping the other person), including all patient-physician or patient-provider relationships. They have a transferential component because the physician occupies a role of authority/knowledge/power from which the patient seeks to benefit.

Outside of therapeutic situations, reactions to other people are our transferences to them, evoked by our internalized past relationships. We may have an emotional response to how someone behaves toward us (their transference), but that is a counter-transference, not countertransference.

 

 

Patients with medical illness

Psychiatrists think of countertransference as a psychological situation occurring in the office or on an inpatient psychiatric unit. We focus our attention on how we feel and what we think while working with patients. We talk about our reactions to patients in supervision, rounds, case conferences, and other situations where mental health professionals discuss patients.

Our medical/surgical colleagues’ reactions to patients often correlate with certain patient presentations and may have little to do with the actual person who is the patient.4 The medical setting provides an opportunity for countertransference to occur in the absence of apparent transference.

Somatic illness imposes on patients some degree of regression. This regression and attempts to cope with it are inherent to somatic illness and hospitalization. Several schemas5 describe basic coping mechanisms common to most patients ( Table ).6,7 Recognizing a patient’s character style or personality type may help clinicians predict their countertransference when interacting with that patient. Uncooperative patients and those perceived as “difficult” are particularly likely to evoke negative countertransference.8

Table

Patients’ response to illness,
with common countertransference by medical staff

Patient’s coping mechanismsStaff’s countertransference
Dependent personality
• Unconsciously wishes for unlimited care
• Depends on others to feel secure
• May make excessive requests of staff
• Gratification at being able to take care of patient’s needs
• Resentment if patient’s needs seem insatiable
Obsessional personality
• Meticulous self-discipline
• Illness represents loss of control
• Will try to gain mastery over illness by focusing on details, information
• Relief at patient’s willingness to actively participate
• Power struggle is possible
Histrionic personality
• Outgoing, colorful, lively
• Attractiveness and sexuality important
• Needs to feel the center of attention
• Illness represents defect, loss of physical beauty
• Warm initial engagement
• Fear of crossing boundaries
• Wonder about veracity of complaints
Masochistic personality
• Satisfies unconscious needs by suffering
• Needs to play victim role
• Frustration when reassurance does not help
• May unconsciously play into patient’s need for punishment
Paranoid personality
• Pervasive doubt of others’ motivations
• Often questions motives for interventions
• Illness represents threat to safety
• Wary of lack of alliance
• Anger that patient questions treatment motives
• Frustrated at inability to form a trusting relationship with patient
• Unsettled by lack of connection
Narcissistic personality
• Grandiose sense of self, which protects against shame, humiliation
• May demand superior care, insult junior team members
• May feel flattered by ability to treat patient as VIP
• May alternately feel devalued, wonder about competence
Source: References 6,7

CASE CONTINUED: No longer ‘grandmotherly’

Mrs. R and Dr. W are now in a patient-physician relationship. Dr. W is no longer handing Mrs. R a bottle of soda but is inquiring about her life, use of alcohol and other drugs, intimate activities, etc. Mrs. R reacts with anger at the “personal questions.” In addition, Dr. W orders tests that are uncomfortable for Mrs. R, who refuses to cooperate with some procedures.

Dr. W’s memories of her grandmother (who was encouraging, supportive, and loving) color her experience of Mrs. R. She ignores nursing staff’s complaints about Mrs. R being demanding and difficult as the patient becomes aggressive and increasingly confused.

Unable to see the patient as she really is, Dr. W becomes angry and defends Mrs. R’s behavior. The nurses feel Dr. W is unrealistic and ignore her at the nursing station. Late on a Friday night, Mrs. R becomes paranoid, hallucinating that “demons” are in her room. She tries to elope from the hospital. Dr. W is off for the weekend, and the staff requests an emergency psychiatric consultation.

Mrs. R evokes a reaction from the nurses because of how she interacts with them. Dr. W’s response—based on her experience of her grandmother—has nothing to do with the way Mrs. R relates interpersonally but reflects a reaction to the patient’s gender and age. Both reactions would be countertransference, using the modern definition.

If reactions to a patient such as Mrs. R are positive, no one seems to notice and the reactions might or might not influence her care. If the reactions are negative, they might influence her care and generate a request for a psychiatric consultation.

Countertransference might have a negative effect on patient care. For example, if a physician were to avoid Mrs. R because she is uncooperative, and if the nursing staff is intolerant of the patient’s confusion and agitation, she might be labeled as “demented” and be given medication without anyone exploring the etiology of her behavior.
 

 


Some patients cannot communicate because of neurologic disorders, intubation, language barriers, or because they are unconscious when admitted. Without information from the patient, medical staff may form ideas about the patient based on their unconscious fantasies. These fantasies may influence the patient’s care.9 Psychiatric consultants are not immune to countertransference, but we come into situations with the opportunity to experience all participants from the outside.

CASE CONTINUED: The psychiatric consultation

During the interview, the psychiatrist asks Mrs. R if she takes any medications. She retorts that she always takes “Centrum” at bed-time and demands to know why she is not getting her “vitamins.” She is given oxazepam and falls asleep.

The psychiatrist recommends benzodiazepine detoxification, suspecting Mrs. R is taking prazepam at home from an old prescription (when the medication was a brand called “Centrax”). This suspicion is confirmed when Mrs. R’s family brings in a large shopping bag of medications she has collected over decades, and Mrs. R identifies her nighttime “vitamin.”

A full evaluation for delirium is completed over the next 2 days. Mrs. R’s confusion and aggressive behavior respond to oxazepam.

Patients with particular character styles evoke predictable reactions from others, including psychotherapists. Discussing these reactions has been a part of psychiatric training for decades. A subset of patients has been described as “hateful,” as they routinely evoke extremely negative responses.10 Whether their primary disorder is psychiatric, medical, or some of both, these patients evoke strong countertransference reactions.

Psychiatrists may be comfortable discussing a “narcissistic patient, a dependent clinger with borderline features,” but our medical colleagues might not share our comfort with psychiatric jargon.11 It may be more useful to say to medical staff that the patient “thinks of himself as very important, cannot accept his need to be taken care of, and tends to see things in black and white.”

Managing difficult patients

The characterizations that follow describe unconscious reactions to types of individuals who are routinely experienced as “difficult” patients. Some patients may exhibit a mixture of character styles ( Table ) and do not easily fall into 1 category. The concepts can be useful in clarifying the reactions that patients evoke in medical staff.

‘Dependent’ patients. Some patients demand continuous attention but are unaware of their insatiable neediness. Early in treatment, they may evoke positive countertransference because they are intensely grateful for attention. They can be enticing, unconsciously seductive, and gratifying to their doctors. Over time, they drain and exhaust their physicians, who resort to avoidance and wish to get rid of these patients.

Recommendation. Set limits to prevent the patient from feeling rejected or an actual rejection when he or she is transferred to another doctor’s care. Coach physicians to:

  • ask patients to “Tell me what is most important for us to discuss today”
  • be clear how long the visit will last.
Reassuring the patient that other issues will be addressed in the next visit prevents the physician from feeling overwhelmed by the patient consuming too much time.

‘Entitled’ patients. Another type of “difficult” patient projects an air of entitlement, which typically reflects an underlying insatiable neediness. They may use intimidation, guilt, and threats of punishment to get their doctors to provide the care they demand. These patients appear powerful (even though they may possess no special status), and they may be overtly devaluing of the physician while simultaneously demanding special attention.

The doctor resents the patient’s entitlement but develops an expectable countertransference fear that he or she will get in trouble if the demands are not met. Wishes to retaliate and “put the patient in his or her place” are common.

Recommendation. Saying, “It is understandable that you want the best care, and I plan to give you the best care,” makes it clear to the patient that the physician hears the patient’s concerns. Advise the physician to request the patient’s “understanding and compassion” for other patients who also need the physician’s time and attention.

‘Help-rejecting’ patients. “Help-rejecting” patients demand care but show little faith in treatment and do not follow treatment plans. The harder the physician tries to help, the less likely the plan will succeed. For these patients, treatment success evokes a fear of abandonment; thus, treatment must fail to maintain the relationship.

Common countertransference reactions are initial anxiety that the treatment plan was not adequate, followed by anger and depression as the physician feels stuck with a patient for whom nothing works.

 

 

Recommendation. Setting realistic goals for treatment helps the physician guide the patient, who expects to be told not to return the moment he or she gets better. Telling the patient that medical care does not stop when a particular malady is treated speaks to the patient’s fear of being abandoned.

When the patient adheres only partially to the plan and a psychiatric consultant is called for an “uncooperative” patient, help the doctor understand how the patient sees the world. It is the patient’s psychological needs—not the physician’s failure—that control the outcome of the care.

‘Self-destructive’ patients may appear unaware of their dangerous actions. They evoke malice from their doctors, who feel the patients are purposely engaging in life-threatening behaviors. The patients’ unconscious dependence remains unknown as their denial of the consequences of their behavior frightens and angers those involved in their care. Some of these patients cannot be stopped before their actions cause them permanent harm or death.

Recommendation. You might remind the physician that we all are entitled to live our lives as we choose. To decompress intense feelings, advise the physician to share, without blaming the patient, what medical staff can realistically do. Saying “We’ll do the best we can” (rather than “Treatment is useless for someone like you”) permits the patient to receive the degree of care he or she can accept without the physician feeling helpless. Understanding our limitations and obligations is part of using our countertransference to aid in patient care.

CASE CONTINUED: Feeling better

When Dr. W returns on Monday, she angrily calls the psychiatrist to complain that her patient has been placed on a benzodiazepine and at the “implication” that Mrs. R was abusing medication. When they talk in person, the psychiatrist explains the situation to Dr. W and suggests they meet with Mrs. R together.

Mrs. R is embarrassed when told about her behavior, identifies the pill, and admits taking prazepam for several weeks prior to hospitalization. She says she never understood how a vitamin could help her sleep so well. No longer delirious, Mrs. R is pleasant and asks many questions. She is surprised that “so young” a doctor was assigned to her case and asks if the chief of medicine could be brought in, as she is on the board of directors of another hospital. “No offense, dear,” she says to Dr. W; “I’m sure you did an excellent job, but usually only senior doctors take care of me.”

Later, Dr. W talks with the psychiatric consultant about her chance meeting with Mrs. R in the cafeteria and the discord with the nursing staff. She notes that she was doing an elective in another country when her grandmother died. She realizes that her feelings about her grandmother are superimposed on the patient, resulting in an inability to see the patient as she really is.

Dr. W accepts the psychiatrist’s suggestion to repair her relationship with the nurses with an apology. She now notes that Mrs. R is nothing like her grandmother and seems “pretty stuck up.” She is glad to be off the case and accepts the psychiatrist’s idea that Mrs. R’s need to feel important should not make Dr. W feel bad about herself.

Related resources

  • Gabbard GO, ed. Countertransference issues in psychiatric treatment. In: Oldham JM, Riba MB, eds. Review of psychiatry series. Washington, DC: American Psychiatric Publishing, Inc.; 1999.
  • Blumenfield M, Strain JJ, Grossman S. Psychodynamic approach. In: Blumenfield M, Strain JJ, eds. Psychosomatic medicine. Philadelphia, PA: Lippincott, Williams and Wilkins; 2006:817-828.
Drug brand names

  • Oxazepam • Serax
  • Prazepam • Centrax
Disclosure

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

References

1. Gabbard GO. Basic principles of psychodynamic psychotherapy. In: Gabbard GO, ed. Psychodynamic psychiatry in clinical practice. Washington, DC: American Psychiatric Publishing, Inc.; 2005:1-30.

2. Harris A. Transference, countertransference, and the real relationship. In: Person ES, Cooper AM, Gabbard GO, eds. Textbook of psychoanalysis. Washington, DC: American Psychiatric Publishing, Inc.; 2005:201-216.

3. Goldstein WN. Clarification of projective identification. Am J Psychiatry. 1991;148:153-161.

4. Kuchariski A, Groves JE. The so-called “inappropriate” psychiatric consultation request on a medical or surgical ward. Int J Psychiatry Med. 1976;7(3):209-220.

5. Groves MA, Muskin PR. Psychological responses to illness. In: Levenson JL, ed. Textbook of psychosomatic medicine. Washington, DC: American Psychiatric Publishing, Inc.; 2005:67-90.

6. Kahana RJ, Bibring GL. Personality types in medical management. In: Zinberg N, ed. Psychiatry and medical practice in a general hospital. New York, NY: International Universities Press; 1964:108-123.

7. Geringer ES, Stern TA. Coping with medical illness: the impact of personality types. Psychosomatics. 1986;27:251-261.

8. Mozian SA, Muskin PR. The difficult patient. In: Barnhill JW, ed. The approach to the psychiatric patient. Washington, DC: American Psychiatric Publishing, Inc.; 2008:192-196.

9. Groves JE. Management of the borderline patient on a medical or surgical ward: the psychiatric consultant’s role. Int J Psychiatry Med. 1975;6:337-348.

10. Groves JE. Taking care of the hateful patient. N Engl J Med. 1978;298:883-887.

11. Pasnau RO. Ten Commandments of medical etiquette for psychiatrists. Psychosomatics. 1985;26(2):128-132.

References

1. Gabbard GO. Basic principles of psychodynamic psychotherapy. In: Gabbard GO, ed. Psychodynamic psychiatry in clinical practice. Washington, DC: American Psychiatric Publishing, Inc.; 2005:1-30.

2. Harris A. Transference, countertransference, and the real relationship. In: Person ES, Cooper AM, Gabbard GO, eds. Textbook of psychoanalysis. Washington, DC: American Psychiatric Publishing, Inc.; 2005:201-216.

3. Goldstein WN. Clarification of projective identification. Am J Psychiatry. 1991;148:153-161.

4. Kuchariski A, Groves JE. The so-called “inappropriate” psychiatric consultation request on a medical or surgical ward. Int J Psychiatry Med. 1976;7(3):209-220.

5. Groves MA, Muskin PR. Psychological responses to illness. In: Levenson JL, ed. Textbook of psychosomatic medicine. Washington, DC: American Psychiatric Publishing, Inc.; 2005:67-90.

6. Kahana RJ, Bibring GL. Personality types in medical management. In: Zinberg N, ed. Psychiatry and medical practice in a general hospital. New York, NY: International Universities Press; 1964:108-123.

7. Geringer ES, Stern TA. Coping with medical illness: the impact of personality types. Psychosomatics. 1986;27:251-261.

8. Mozian SA, Muskin PR. The difficult patient. In: Barnhill JW, ed. The approach to the psychiatric patient. Washington, DC: American Psychiatric Publishing, Inc.; 2008:192-196.

9. Groves JE. Management of the borderline patient on a medical or surgical ward: the psychiatric consultant’s role. Int J Psychiatry Med. 1975;6:337-348.

10. Groves JE. Taking care of the hateful patient. N Engl J Med. 1978;298:883-887.

11. Pasnau RO. Ten Commandments of medical etiquette for psychiatrists. Psychosomatics. 1985;26(2):128-132.

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Worried about high-dose prescribing? Manage risk for you and your patient

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Comment on this article

Mr. B, age 35, is admitted for the fourth time to the inpatient service with hallucinations and delusions related to chronic schizophrenia. After appropriate attempts to control his symptoms, he has begun to respond to usual treatment with an atypical antipsychotic. He remains a “partial responder,” however, at the maximum FDA-approved dosage listed in the package insert (PI). What do you do next?

Because of this author’s (NSK) dual training in medicine and forensic psychiatry, other clinicians often ask me about patients such as Mr. B. Prescribing for patients who do not respond to standard dosages can create anxiety about going “off-label.” This article describes how to manage potential risk to yourself and your patient by communicating effectively and documenting informed consent.

What are the options?

To effectively treat Mr. B’s symptoms, you could:

  • change medications and start over
  • augment with a second atypical antipsychotic
  • stay with the antipsychotic to which he has shown partial response, but go above the PI dosing.
Each strategy could pose problems, but most psychopharmacologists would choose the third option—the most logical one.

Changing medications is attractive, but the choice of an atypical antipsychotic with relative metabolic neutrality is limited, and “switching” is time-consuming. When a drug begins to show efficacy, most clinicians won’t opt to “change horses midstream”—especially if managed care is pressuring for rapid discharge.

Augmentation introduces polypharmacy and potential drug-drug interactions. Very little evidence guides us in combining antipsychotics, as most manufacturers will never study the coadministration of 2 branded medications with the same indication.

Only a few case reports have described combining atypical antipsychotics.1-4 Moreover, many managed care providers and governmental payers/regulators will not pay for polypharmacy with 2 atypical antipsychotics or will allow it only during cross-tapering from one agent to another.

‘High-dose’ monotherapy is the choice most often taken by clinicians and experts. Pharmaceutical manufacturers study a wide range of doses during medication development. Two pivotal trials form the basis of the New Drug Application for FDA approval and largely dictate the PI language.

Don’t misconstrue the PI dosing as optimal for a specific medication or patient. Historically, FDA-approved dosing for atypical antipsychotics has been too high (risperidone, aripiprazole) or too low (ziprasidone, quetiapine) for many patients we treat, even when the medications are used as indicated. This problem is magnified when clinicians try to make individual patients (N=1) resemble the average pooled analysis of the clinical trial group (N>200) and find that the individual patient may be a low-dose, average-dose, or high-dose responder (Table 1).

Informed prescribing. Polypharmacy is a complex issue because essentially no pharmacokinetic or pharmacodynamic studies have examined the simultaneous use of ≥3 psychotropics. When a pharmacist or drug interaction computer alerts you to a potential drug-drug interaction, the warning is almost always theoretical. No real data exist about coadministering most medications.

Physicians may query a manufacturer about off-label, above-PI dosing data by contacting the company’s medical information department or asking a pharmaceutical representative. What you receive will vary by manufacturer, but in almost every case you will get the safety data you want. Occasionally you also will get efficacy data, which is nice but not crucial. An online literature search of MEDLINE is another way to obtain this information.

Table 1

Patient factors that influence response to medication

Patient body mass, age, race, ethnicity, and gender
Variability in medication absorption
Hepatic metabolizing factors
How ‘sick’ the patient is, compared with those in pivotal clinical trials
Patient’s behavior, lifestyle, habits, and diet
Comorbid medical conditions
Other psychiatric and nonpsychiatric pharmacotherapy

Liability risk?

Every clinician I’ve met prescribes drugs off-label, whether in terms of dose, indication, or age limits in the PI as published in the Physicians’ Desk Reference (PDR).5 Still, nearly all describe to me the following nightmare, in which they “violated” the PI and “something bad” happens.

They are sitting in court on the witness stand, white-knuckled and sweaty, as a plaintiff’s attorney strolls up to them, PDR in hand, and says: “Doctor, isn’t this the Bible, and you violated the Bible?” And thus is born the fear of a malpractice claim, predicated on off-label dosing.

Off-label prescribing is rarely the only issue in a lawsuit, according to Denny Rodriguez, assistant vice president, claims, Professional Risk Management Services (PRMS), Inc.—manager of The Psychiatrists’ Program endorsed by the American Psychiatric Association. When raised, allegations related to off-label prescribing are among many presented by the plaintiff under the rubric of treatment that violated the standard of care.

 

 

Contrary to the plaintiff’s allegations, off-label prescribing rarely violates the standard of care because it has valid clinical and scientific bases. And don’t acknowledge the PDR as “the Bible,” which it is not; it’s a compilation of PIs. The FDA affirms that once a product is approved for marketing, a physician may choose to prescribe it for off-label use (Box).5

Box

FDA statement on off-label prescribing

The FDA acknowledges that doctors need to treat patients and may prescribe medications off-label. As stated in the foreword to the Physicians’ Desk Reference:

The FDA has also recognized that the [Federal Food, Drug, and Cosmetic] Act does not, however, limit the manner in which a physician may use an approved drug. Once a product is approved for marketing, a physician may choose to prescribe it for uses or in treatment regimens or patient populations that are not included in approved drug labeling. The FDA also observes that accepted medical practice includes drug use that is not reflected in approved drug labeling.5

Standard of care

The real issue for practitioners is the “standard of care.” Violating the standard of care—what a similarly trained clinician would do under similar circumstances—is the first step on the slippery slope to malpractice. Here we can be quite sure that the standard of care and evidence-based medicine are in sync and support the use of off-label, high-dose monotherapy.

Properly documenting your reasoning helps to demonstrate that your prescribing meets the standard of care. Always document and obtain informed consent. Also stay up-to-date about:

  • medications you prescribe
  • emerging evidence and safety information
  • appropriate patient monitoring for clinical response and adverse effects.8

Black boxes and bold lettering

The FDA may mandate that a manufacturer highlight certain information on a PI in 3 ways—bold lettering, black-box warning, and red lettering, in order of presumed increasing seriousness. This system is meant to draw prescribers’ attention to potential safety problems with pharmaceutical agents. No psychiatric medications carry red-letter warnings, a classification usually reserved for antineoplastic agents.

At one time the FDA relied on evidenced-based data to determine the need for warnings. Recently, however, when a problem has been identified with one agent, the FDA has tended to require all drugs in that agent’s class to carry similar—if not identical—PI warnings. In psychiatry, the FDA has ordered suicide precautions on all antidepressants and metabolic syndrome/hyperglycemia warnings on all atypical antipsychotics, despite evidence of differences in potential risks associated with medications within classes. For example, clinical trials have shown a higher risk of obesity and diabetes among patients receiving olanzapine compared with those receiving ziprasidone.7

The FDA’s action appears to “level the playing field,” giving patients the misperception that any treatment would carry an equal risk. Therefore, when you prescribe a drug that carries a class-wide warning in its PI, present the evidence in a balanced, objective manner so that the patient can make an informed decision.

Managing risk

Your best protection against liability is to communicate effectively with the patient and document that communication—including informed consent—in the medical record.8 Obtain and document informed consent whenever:

  • you initiate a drug or other treatment
  • treatment extends beyond the PI-recommended maximum dose.
Similarly, when a new side-effect warning or safety information about a medication emerges, update the informed consent discussion and re-obtain and re-document the patient’s consent. When warnings are discussed on the nightly news or the Internet, patients prescribed that medication will expect you to address this. Informed consent discussions are an excellent way to discover and address patients’ concerns and ensure that they have realistic expectations about treatment.

Potential benefits for patients from updating informed consent include:

  • changes in medications or dosages based on the new information
  • closer monitoring of potential side effects and other actions
  • empowerment to make decisions about stopping a medication or trying alternate medications or treatments.
Documentation also reflects individualization of care, the patient’s involvement, and your clinical judgment and decision-making—all critical elements of a record that supports good patient care and protects both patient and clinician.

Documenting informed consent

What to include. View informed consent as an ongoing discussion, not a document that needs to be put into a chart to comply with a legal mandate. Documenting informed consent may be as simple as going through the process and then including pertinent points in the medical record (Table 2). The following is an example of a medical record entry used by one author (NSK) to document an initial informed consent discussion:

 

 

“I have explained to the patient the reasons for prescribing the above medication, the expected benefits and potential side effects, the treatment alternatives and possible risks and benefits of the alternatives, and the expected course w/o treatment. The patient asked appropriate questions and appeared to understand the answers. (I discussed off-label use.) I provided information from the manufacturer (or some other source). The patient has decided to try this medication and to be followed.”

Caveats. Avoid “cutting and pasting” language for each informed consent discussion into each medical record. Make your discussion and its documentation reflect each individual’s treatment plan. If you use a preprinted consent/medications side-effect form (as required by many institutions and clinics), consider entering a personalized notation into the progress notes as needed, such as when:

  • you prescribe medications with high risk for serious side effects
  • you use off-label prescribing that is not customary
  • a patient needs extra assistance to follow the treatment plan.8
The procedure’s formality helps a patient focus on the consent process, making it less likely that he/she will later believe he/she was not adequately informed. The signed form supports the assertion that the consent process took place and establishes at least some of what was disclosed. The signed form and the clinician’s entry in the record documenting the informed consent discussion will be beneficial should malpractice litigation allege consent issues.

Table 2

Informed consent: Pertinent points to document

Proposed treatment
Potential side effects (most common)
Potential side effects (most dangerous)
Potential side effects that might make a patient anxious, such as those included in recent FDA statements, changes in labeling, or advertisers’ consumer marketing messages
Alternatives, including their potential side effects
Course without treatment
Demonstration of patient’s comprehension of warnings and opportunity to ask questions
Preprinted forms. A disadvantage of preprinted forms is the difficulty in knowing what information to include. If the form’s content is very broad, then important information may not be disclosed. If the form is very specific and attempts to list all possible complications, one could presume that any complication not listed was not disclosed. If you incorporate an informed consent form into your practice:

  • include all significant and material risks on the form
  • state on the form that the risks “include, but are not limited to” those listed on the form
  • have thorough informed consent discussions with patients
  • enter into the medical record your discussion and a copy of the form signed by the patient.

What to disclose. Clinicians often struggle with how much information to disclose to patients. In general, include what a reasonable person would need to know to make an informed decision. A practical way to think about this is to ask yourself the following questions:

  • What information would I want a physician to disclose to my loved one (parent, child, spouse, etc.) if I was not present and my loved one needed to give consent to a treatment recommendation?
  • Is this information of the type that a reasonable person could say: “I wouldn’t have consented if the doctor had told me that”? If you think so, then provide this information to your patient.
Patient resources. Medication information sheets can enhance informed consent and patients’ understanding and retention of information about medications you prescribe. The FDA’s Web site (www.fda.gov) offers printable patient education sheets on hundreds of medications, medication guides, and other resources (see Related Resources).6 Many manufacturers also offer patient education information at their Web sites, via pharmaceutical representatives, and as part of the PI.

Related resources

Drug brand names

  • Aripiprazole • Abilify
  • Olanzapine • Zyprexa
  • Quetiapine • Seroquel
  • Risperidone • Risperdal
  • Ziprasidone • Geodon
Disclosures

Dr. Kaye receives research support from Pfizer Inc. and Takeda Pharmaceutical and is a consultant to and speaker for Pfizer Inc., AstraZeneca, and GlaxoSmithKline.

Jacqueline Melonas is a full-time employee of PRMS, Inc. PRMS, Inc. contracts with Eli Lilly and Company to provide risk management content related to the management of medical malpractice liability.

References

1. Kaye NS. Ziprasidone augmentation of clozapine in 11 patients. J Clin Psychiatry. 2003;64:215-216.

2. Freudenreich O, Goff DC. Antipsychotic combination therapy in schizophrenia: a review of efficacy and risks of current combinations. Acta Psychiatr Scand. 2002;106:323-330.

3. Pies R. Combining antipsychotics: risks and benefits. Psychopharm Rev. 2001;36(2):9-13.

4. Stahl SM. Antipsychotic polypharmacy, part 1: therapeutic option or dirty little secret? J Clin Psychiatry. 1999;60:425-426.

5. Physicians’ Desk Reference. 62nd ed. Montvale, NJ: Thompson Publishing, 2008.

6. Medwatch. Medical product safety information. Food and Drug Administration. Available at: http://www.fda.gov/medwatch/safety.htm. Accessed July 30, 2008.

7. American Diabetes Association, American Psychiatric Association, American Association of Clinical Endocrinologists, North American Association for the Study of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004;27:596-601.

8. Melonas JM. Preventing and reducing professional liability risk related to psychopharmacology. Psychiatric Times. 2005;23(14).-Available at http://www.psychiatrictimes.com/display/article/10168/48416. Accessed September 3, 2008.

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Jacqueline M. Melonas, RN, MS, JD
Vice president, risk management, Professional Risk Management Services, Inc., Arlington, VA

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Vice president, risk management, Professional Risk Management Services, Inc., Arlington, VA

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Comment on this article

Mr. B, age 35, is admitted for the fourth time to the inpatient service with hallucinations and delusions related to chronic schizophrenia. After appropriate attempts to control his symptoms, he has begun to respond to usual treatment with an atypical antipsychotic. He remains a “partial responder,” however, at the maximum FDA-approved dosage listed in the package insert (PI). What do you do next?

Because of this author’s (NSK) dual training in medicine and forensic psychiatry, other clinicians often ask me about patients such as Mr. B. Prescribing for patients who do not respond to standard dosages can create anxiety about going “off-label.” This article describes how to manage potential risk to yourself and your patient by communicating effectively and documenting informed consent.

What are the options?

To effectively treat Mr. B’s symptoms, you could:

  • change medications and start over
  • augment with a second atypical antipsychotic
  • stay with the antipsychotic to which he has shown partial response, but go above the PI dosing.
Each strategy could pose problems, but most psychopharmacologists would choose the third option—the most logical one.

Changing medications is attractive, but the choice of an atypical antipsychotic with relative metabolic neutrality is limited, and “switching” is time-consuming. When a drug begins to show efficacy, most clinicians won’t opt to “change horses midstream”—especially if managed care is pressuring for rapid discharge.

Augmentation introduces polypharmacy and potential drug-drug interactions. Very little evidence guides us in combining antipsychotics, as most manufacturers will never study the coadministration of 2 branded medications with the same indication.

Only a few case reports have described combining atypical antipsychotics.1-4 Moreover, many managed care providers and governmental payers/regulators will not pay for polypharmacy with 2 atypical antipsychotics or will allow it only during cross-tapering from one agent to another.

‘High-dose’ monotherapy is the choice most often taken by clinicians and experts. Pharmaceutical manufacturers study a wide range of doses during medication development. Two pivotal trials form the basis of the New Drug Application for FDA approval and largely dictate the PI language.

Don’t misconstrue the PI dosing as optimal for a specific medication or patient. Historically, FDA-approved dosing for atypical antipsychotics has been too high (risperidone, aripiprazole) or too low (ziprasidone, quetiapine) for many patients we treat, even when the medications are used as indicated. This problem is magnified when clinicians try to make individual patients (N=1) resemble the average pooled analysis of the clinical trial group (N>200) and find that the individual patient may be a low-dose, average-dose, or high-dose responder (Table 1).

Informed prescribing. Polypharmacy is a complex issue because essentially no pharmacokinetic or pharmacodynamic studies have examined the simultaneous use of ≥3 psychotropics. When a pharmacist or drug interaction computer alerts you to a potential drug-drug interaction, the warning is almost always theoretical. No real data exist about coadministering most medications.

Physicians may query a manufacturer about off-label, above-PI dosing data by contacting the company’s medical information department or asking a pharmaceutical representative. What you receive will vary by manufacturer, but in almost every case you will get the safety data you want. Occasionally you also will get efficacy data, which is nice but not crucial. An online literature search of MEDLINE is another way to obtain this information.

Table 1

Patient factors that influence response to medication

Patient body mass, age, race, ethnicity, and gender
Variability in medication absorption
Hepatic metabolizing factors
How ‘sick’ the patient is, compared with those in pivotal clinical trials
Patient’s behavior, lifestyle, habits, and diet
Comorbid medical conditions
Other psychiatric and nonpsychiatric pharmacotherapy

Liability risk?

Every clinician I’ve met prescribes drugs off-label, whether in terms of dose, indication, or age limits in the PI as published in the Physicians’ Desk Reference (PDR).5 Still, nearly all describe to me the following nightmare, in which they “violated” the PI and “something bad” happens.

They are sitting in court on the witness stand, white-knuckled and sweaty, as a plaintiff’s attorney strolls up to them, PDR in hand, and says: “Doctor, isn’t this the Bible, and you violated the Bible?” And thus is born the fear of a malpractice claim, predicated on off-label dosing.

Off-label prescribing is rarely the only issue in a lawsuit, according to Denny Rodriguez, assistant vice president, claims, Professional Risk Management Services (PRMS), Inc.—manager of The Psychiatrists’ Program endorsed by the American Psychiatric Association. When raised, allegations related to off-label prescribing are among many presented by the plaintiff under the rubric of treatment that violated the standard of care.

 

 

Contrary to the plaintiff’s allegations, off-label prescribing rarely violates the standard of care because it has valid clinical and scientific bases. And don’t acknowledge the PDR as “the Bible,” which it is not; it’s a compilation of PIs. The FDA affirms that once a product is approved for marketing, a physician may choose to prescribe it for off-label use (Box).5

Box

FDA statement on off-label prescribing

The FDA acknowledges that doctors need to treat patients and may prescribe medications off-label. As stated in the foreword to the Physicians’ Desk Reference:

The FDA has also recognized that the [Federal Food, Drug, and Cosmetic] Act does not, however, limit the manner in which a physician may use an approved drug. Once a product is approved for marketing, a physician may choose to prescribe it for uses or in treatment regimens or patient populations that are not included in approved drug labeling. The FDA also observes that accepted medical practice includes drug use that is not reflected in approved drug labeling.5

Standard of care

The real issue for practitioners is the “standard of care.” Violating the standard of care—what a similarly trained clinician would do under similar circumstances—is the first step on the slippery slope to malpractice. Here we can be quite sure that the standard of care and evidence-based medicine are in sync and support the use of off-label, high-dose monotherapy.

Properly documenting your reasoning helps to demonstrate that your prescribing meets the standard of care. Always document and obtain informed consent. Also stay up-to-date about:

  • medications you prescribe
  • emerging evidence and safety information
  • appropriate patient monitoring for clinical response and adverse effects.8

Black boxes and bold lettering

The FDA may mandate that a manufacturer highlight certain information on a PI in 3 ways—bold lettering, black-box warning, and red lettering, in order of presumed increasing seriousness. This system is meant to draw prescribers’ attention to potential safety problems with pharmaceutical agents. No psychiatric medications carry red-letter warnings, a classification usually reserved for antineoplastic agents.

At one time the FDA relied on evidenced-based data to determine the need for warnings. Recently, however, when a problem has been identified with one agent, the FDA has tended to require all drugs in that agent’s class to carry similar—if not identical—PI warnings. In psychiatry, the FDA has ordered suicide precautions on all antidepressants and metabolic syndrome/hyperglycemia warnings on all atypical antipsychotics, despite evidence of differences in potential risks associated with medications within classes. For example, clinical trials have shown a higher risk of obesity and diabetes among patients receiving olanzapine compared with those receiving ziprasidone.7

The FDA’s action appears to “level the playing field,” giving patients the misperception that any treatment would carry an equal risk. Therefore, when you prescribe a drug that carries a class-wide warning in its PI, present the evidence in a balanced, objective manner so that the patient can make an informed decision.

Managing risk

Your best protection against liability is to communicate effectively with the patient and document that communication—including informed consent—in the medical record.8 Obtain and document informed consent whenever:

  • you initiate a drug or other treatment
  • treatment extends beyond the PI-recommended maximum dose.
Similarly, when a new side-effect warning or safety information about a medication emerges, update the informed consent discussion and re-obtain and re-document the patient’s consent. When warnings are discussed on the nightly news or the Internet, patients prescribed that medication will expect you to address this. Informed consent discussions are an excellent way to discover and address patients’ concerns and ensure that they have realistic expectations about treatment.

Potential benefits for patients from updating informed consent include:

  • changes in medications or dosages based on the new information
  • closer monitoring of potential side effects and other actions
  • empowerment to make decisions about stopping a medication or trying alternate medications or treatments.
Documentation also reflects individualization of care, the patient’s involvement, and your clinical judgment and decision-making—all critical elements of a record that supports good patient care and protects both patient and clinician.

Documenting informed consent

What to include. View informed consent as an ongoing discussion, not a document that needs to be put into a chart to comply with a legal mandate. Documenting informed consent may be as simple as going through the process and then including pertinent points in the medical record (Table 2). The following is an example of a medical record entry used by one author (NSK) to document an initial informed consent discussion:

 

 

“I have explained to the patient the reasons for prescribing the above medication, the expected benefits and potential side effects, the treatment alternatives and possible risks and benefits of the alternatives, and the expected course w/o treatment. The patient asked appropriate questions and appeared to understand the answers. (I discussed off-label use.) I provided information from the manufacturer (or some other source). The patient has decided to try this medication and to be followed.”

Caveats. Avoid “cutting and pasting” language for each informed consent discussion into each medical record. Make your discussion and its documentation reflect each individual’s treatment plan. If you use a preprinted consent/medications side-effect form (as required by many institutions and clinics), consider entering a personalized notation into the progress notes as needed, such as when:

  • you prescribe medications with high risk for serious side effects
  • you use off-label prescribing that is not customary
  • a patient needs extra assistance to follow the treatment plan.8
The procedure’s formality helps a patient focus on the consent process, making it less likely that he/she will later believe he/she was not adequately informed. The signed form supports the assertion that the consent process took place and establishes at least some of what was disclosed. The signed form and the clinician’s entry in the record documenting the informed consent discussion will be beneficial should malpractice litigation allege consent issues.

Table 2

Informed consent: Pertinent points to document

Proposed treatment
Potential side effects (most common)
Potential side effects (most dangerous)
Potential side effects that might make a patient anxious, such as those included in recent FDA statements, changes in labeling, or advertisers’ consumer marketing messages
Alternatives, including their potential side effects
Course without treatment
Demonstration of patient’s comprehension of warnings and opportunity to ask questions
Preprinted forms. A disadvantage of preprinted forms is the difficulty in knowing what information to include. If the form’s content is very broad, then important information may not be disclosed. If the form is very specific and attempts to list all possible complications, one could presume that any complication not listed was not disclosed. If you incorporate an informed consent form into your practice:

  • include all significant and material risks on the form
  • state on the form that the risks “include, but are not limited to” those listed on the form
  • have thorough informed consent discussions with patients
  • enter into the medical record your discussion and a copy of the form signed by the patient.

What to disclose. Clinicians often struggle with how much information to disclose to patients. In general, include what a reasonable person would need to know to make an informed decision. A practical way to think about this is to ask yourself the following questions:

  • What information would I want a physician to disclose to my loved one (parent, child, spouse, etc.) if I was not present and my loved one needed to give consent to a treatment recommendation?
  • Is this information of the type that a reasonable person could say: “I wouldn’t have consented if the doctor had told me that”? If you think so, then provide this information to your patient.
Patient resources. Medication information sheets can enhance informed consent and patients’ understanding and retention of information about medications you prescribe. The FDA’s Web site (www.fda.gov) offers printable patient education sheets on hundreds of medications, medication guides, and other resources (see Related Resources).6 Many manufacturers also offer patient education information at their Web sites, via pharmaceutical representatives, and as part of the PI.

Related resources

Drug brand names

  • Aripiprazole • Abilify
  • Olanzapine • Zyprexa
  • Quetiapine • Seroquel
  • Risperidone • Risperdal
  • Ziprasidone • Geodon
Disclosures

Dr. Kaye receives research support from Pfizer Inc. and Takeda Pharmaceutical and is a consultant to and speaker for Pfizer Inc., AstraZeneca, and GlaxoSmithKline.

Jacqueline Melonas is a full-time employee of PRMS, Inc. PRMS, Inc. contracts with Eli Lilly and Company to provide risk management content related to the management of medical malpractice liability.

Comment on this article

Mr. B, age 35, is admitted for the fourth time to the inpatient service with hallucinations and delusions related to chronic schizophrenia. After appropriate attempts to control his symptoms, he has begun to respond to usual treatment with an atypical antipsychotic. He remains a “partial responder,” however, at the maximum FDA-approved dosage listed in the package insert (PI). What do you do next?

Because of this author’s (NSK) dual training in medicine and forensic psychiatry, other clinicians often ask me about patients such as Mr. B. Prescribing for patients who do not respond to standard dosages can create anxiety about going “off-label.” This article describes how to manage potential risk to yourself and your patient by communicating effectively and documenting informed consent.

What are the options?

To effectively treat Mr. B’s symptoms, you could:

  • change medications and start over
  • augment with a second atypical antipsychotic
  • stay with the antipsychotic to which he has shown partial response, but go above the PI dosing.
Each strategy could pose problems, but most psychopharmacologists would choose the third option—the most logical one.

Changing medications is attractive, but the choice of an atypical antipsychotic with relative metabolic neutrality is limited, and “switching” is time-consuming. When a drug begins to show efficacy, most clinicians won’t opt to “change horses midstream”—especially if managed care is pressuring for rapid discharge.

Augmentation introduces polypharmacy and potential drug-drug interactions. Very little evidence guides us in combining antipsychotics, as most manufacturers will never study the coadministration of 2 branded medications with the same indication.

Only a few case reports have described combining atypical antipsychotics.1-4 Moreover, many managed care providers and governmental payers/regulators will not pay for polypharmacy with 2 atypical antipsychotics or will allow it only during cross-tapering from one agent to another.

‘High-dose’ monotherapy is the choice most often taken by clinicians and experts. Pharmaceutical manufacturers study a wide range of doses during medication development. Two pivotal trials form the basis of the New Drug Application for FDA approval and largely dictate the PI language.

Don’t misconstrue the PI dosing as optimal for a specific medication or patient. Historically, FDA-approved dosing for atypical antipsychotics has been too high (risperidone, aripiprazole) or too low (ziprasidone, quetiapine) for many patients we treat, even when the medications are used as indicated. This problem is magnified when clinicians try to make individual patients (N=1) resemble the average pooled analysis of the clinical trial group (N>200) and find that the individual patient may be a low-dose, average-dose, or high-dose responder (Table 1).

Informed prescribing. Polypharmacy is a complex issue because essentially no pharmacokinetic or pharmacodynamic studies have examined the simultaneous use of ≥3 psychotropics. When a pharmacist or drug interaction computer alerts you to a potential drug-drug interaction, the warning is almost always theoretical. No real data exist about coadministering most medications.

Physicians may query a manufacturer about off-label, above-PI dosing data by contacting the company’s medical information department or asking a pharmaceutical representative. What you receive will vary by manufacturer, but in almost every case you will get the safety data you want. Occasionally you also will get efficacy data, which is nice but not crucial. An online literature search of MEDLINE is another way to obtain this information.

Table 1

Patient factors that influence response to medication

Patient body mass, age, race, ethnicity, and gender
Variability in medication absorption
Hepatic metabolizing factors
How ‘sick’ the patient is, compared with those in pivotal clinical trials
Patient’s behavior, lifestyle, habits, and diet
Comorbid medical conditions
Other psychiatric and nonpsychiatric pharmacotherapy

Liability risk?

Every clinician I’ve met prescribes drugs off-label, whether in terms of dose, indication, or age limits in the PI as published in the Physicians’ Desk Reference (PDR).5 Still, nearly all describe to me the following nightmare, in which they “violated” the PI and “something bad” happens.

They are sitting in court on the witness stand, white-knuckled and sweaty, as a plaintiff’s attorney strolls up to them, PDR in hand, and says: “Doctor, isn’t this the Bible, and you violated the Bible?” And thus is born the fear of a malpractice claim, predicated on off-label dosing.

Off-label prescribing is rarely the only issue in a lawsuit, according to Denny Rodriguez, assistant vice president, claims, Professional Risk Management Services (PRMS), Inc.—manager of The Psychiatrists’ Program endorsed by the American Psychiatric Association. When raised, allegations related to off-label prescribing are among many presented by the plaintiff under the rubric of treatment that violated the standard of care.

 

 

Contrary to the plaintiff’s allegations, off-label prescribing rarely violates the standard of care because it has valid clinical and scientific bases. And don’t acknowledge the PDR as “the Bible,” which it is not; it’s a compilation of PIs. The FDA affirms that once a product is approved for marketing, a physician may choose to prescribe it for off-label use (Box).5

Box

FDA statement on off-label prescribing

The FDA acknowledges that doctors need to treat patients and may prescribe medications off-label. As stated in the foreword to the Physicians’ Desk Reference:

The FDA has also recognized that the [Federal Food, Drug, and Cosmetic] Act does not, however, limit the manner in which a physician may use an approved drug. Once a product is approved for marketing, a physician may choose to prescribe it for uses or in treatment regimens or patient populations that are not included in approved drug labeling. The FDA also observes that accepted medical practice includes drug use that is not reflected in approved drug labeling.5

Standard of care

The real issue for practitioners is the “standard of care.” Violating the standard of care—what a similarly trained clinician would do under similar circumstances—is the first step on the slippery slope to malpractice. Here we can be quite sure that the standard of care and evidence-based medicine are in sync and support the use of off-label, high-dose monotherapy.

Properly documenting your reasoning helps to demonstrate that your prescribing meets the standard of care. Always document and obtain informed consent. Also stay up-to-date about:

  • medications you prescribe
  • emerging evidence and safety information
  • appropriate patient monitoring for clinical response and adverse effects.8

Black boxes and bold lettering

The FDA may mandate that a manufacturer highlight certain information on a PI in 3 ways—bold lettering, black-box warning, and red lettering, in order of presumed increasing seriousness. This system is meant to draw prescribers’ attention to potential safety problems with pharmaceutical agents. No psychiatric medications carry red-letter warnings, a classification usually reserved for antineoplastic agents.

At one time the FDA relied on evidenced-based data to determine the need for warnings. Recently, however, when a problem has been identified with one agent, the FDA has tended to require all drugs in that agent’s class to carry similar—if not identical—PI warnings. In psychiatry, the FDA has ordered suicide precautions on all antidepressants and metabolic syndrome/hyperglycemia warnings on all atypical antipsychotics, despite evidence of differences in potential risks associated with medications within classes. For example, clinical trials have shown a higher risk of obesity and diabetes among patients receiving olanzapine compared with those receiving ziprasidone.7

The FDA’s action appears to “level the playing field,” giving patients the misperception that any treatment would carry an equal risk. Therefore, when you prescribe a drug that carries a class-wide warning in its PI, present the evidence in a balanced, objective manner so that the patient can make an informed decision.

Managing risk

Your best protection against liability is to communicate effectively with the patient and document that communication—including informed consent—in the medical record.8 Obtain and document informed consent whenever:

  • you initiate a drug or other treatment
  • treatment extends beyond the PI-recommended maximum dose.
Similarly, when a new side-effect warning or safety information about a medication emerges, update the informed consent discussion and re-obtain and re-document the patient’s consent. When warnings are discussed on the nightly news or the Internet, patients prescribed that medication will expect you to address this. Informed consent discussions are an excellent way to discover and address patients’ concerns and ensure that they have realistic expectations about treatment.

Potential benefits for patients from updating informed consent include:

  • changes in medications or dosages based on the new information
  • closer monitoring of potential side effects and other actions
  • empowerment to make decisions about stopping a medication or trying alternate medications or treatments.
Documentation also reflects individualization of care, the patient’s involvement, and your clinical judgment and decision-making—all critical elements of a record that supports good patient care and protects both patient and clinician.

Documenting informed consent

What to include. View informed consent as an ongoing discussion, not a document that needs to be put into a chart to comply with a legal mandate. Documenting informed consent may be as simple as going through the process and then including pertinent points in the medical record (Table 2). The following is an example of a medical record entry used by one author (NSK) to document an initial informed consent discussion:

 

 

“I have explained to the patient the reasons for prescribing the above medication, the expected benefits and potential side effects, the treatment alternatives and possible risks and benefits of the alternatives, and the expected course w/o treatment. The patient asked appropriate questions and appeared to understand the answers. (I discussed off-label use.) I provided information from the manufacturer (or some other source). The patient has decided to try this medication and to be followed.”

Caveats. Avoid “cutting and pasting” language for each informed consent discussion into each medical record. Make your discussion and its documentation reflect each individual’s treatment plan. If you use a preprinted consent/medications side-effect form (as required by many institutions and clinics), consider entering a personalized notation into the progress notes as needed, such as when:

  • you prescribe medications with high risk for serious side effects
  • you use off-label prescribing that is not customary
  • a patient needs extra assistance to follow the treatment plan.8
The procedure’s formality helps a patient focus on the consent process, making it less likely that he/she will later believe he/she was not adequately informed. The signed form supports the assertion that the consent process took place and establishes at least some of what was disclosed. The signed form and the clinician’s entry in the record documenting the informed consent discussion will be beneficial should malpractice litigation allege consent issues.

Table 2

Informed consent: Pertinent points to document

Proposed treatment
Potential side effects (most common)
Potential side effects (most dangerous)
Potential side effects that might make a patient anxious, such as those included in recent FDA statements, changes in labeling, or advertisers’ consumer marketing messages
Alternatives, including their potential side effects
Course without treatment
Demonstration of patient’s comprehension of warnings and opportunity to ask questions
Preprinted forms. A disadvantage of preprinted forms is the difficulty in knowing what information to include. If the form’s content is very broad, then important information may not be disclosed. If the form is very specific and attempts to list all possible complications, one could presume that any complication not listed was not disclosed. If you incorporate an informed consent form into your practice:

  • include all significant and material risks on the form
  • state on the form that the risks “include, but are not limited to” those listed on the form
  • have thorough informed consent discussions with patients
  • enter into the medical record your discussion and a copy of the form signed by the patient.

What to disclose. Clinicians often struggle with how much information to disclose to patients. In general, include what a reasonable person would need to know to make an informed decision. A practical way to think about this is to ask yourself the following questions:

  • What information would I want a physician to disclose to my loved one (parent, child, spouse, etc.) if I was not present and my loved one needed to give consent to a treatment recommendation?
  • Is this information of the type that a reasonable person could say: “I wouldn’t have consented if the doctor had told me that”? If you think so, then provide this information to your patient.
Patient resources. Medication information sheets can enhance informed consent and patients’ understanding and retention of information about medications you prescribe. The FDA’s Web site (www.fda.gov) offers printable patient education sheets on hundreds of medications, medication guides, and other resources (see Related Resources).6 Many manufacturers also offer patient education information at their Web sites, via pharmaceutical representatives, and as part of the PI.

Related resources

Drug brand names

  • Aripiprazole • Abilify
  • Olanzapine • Zyprexa
  • Quetiapine • Seroquel
  • Risperidone • Risperdal
  • Ziprasidone • Geodon
Disclosures

Dr. Kaye receives research support from Pfizer Inc. and Takeda Pharmaceutical and is a consultant to and speaker for Pfizer Inc., AstraZeneca, and GlaxoSmithKline.

Jacqueline Melonas is a full-time employee of PRMS, Inc. PRMS, Inc. contracts with Eli Lilly and Company to provide risk management content related to the management of medical malpractice liability.

References

1. Kaye NS. Ziprasidone augmentation of clozapine in 11 patients. J Clin Psychiatry. 2003;64:215-216.

2. Freudenreich O, Goff DC. Antipsychotic combination therapy in schizophrenia: a review of efficacy and risks of current combinations. Acta Psychiatr Scand. 2002;106:323-330.

3. Pies R. Combining antipsychotics: risks and benefits. Psychopharm Rev. 2001;36(2):9-13.

4. Stahl SM. Antipsychotic polypharmacy, part 1: therapeutic option or dirty little secret? J Clin Psychiatry. 1999;60:425-426.

5. Physicians’ Desk Reference. 62nd ed. Montvale, NJ: Thompson Publishing, 2008.

6. Medwatch. Medical product safety information. Food and Drug Administration. Available at: http://www.fda.gov/medwatch/safety.htm. Accessed July 30, 2008.

7. American Diabetes Association, American Psychiatric Association, American Association of Clinical Endocrinologists, North American Association for the Study of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004;27:596-601.

8. Melonas JM. Preventing and reducing professional liability risk related to psychopharmacology. Psychiatric Times. 2005;23(14).-Available at http://www.psychiatrictimes.com/display/article/10168/48416. Accessed September 3, 2008.

References

1. Kaye NS. Ziprasidone augmentation of clozapine in 11 patients. J Clin Psychiatry. 2003;64:215-216.

2. Freudenreich O, Goff DC. Antipsychotic combination therapy in schizophrenia: a review of efficacy and risks of current combinations. Acta Psychiatr Scand. 2002;106:323-330.

3. Pies R. Combining antipsychotics: risks and benefits. Psychopharm Rev. 2001;36(2):9-13.

4. Stahl SM. Antipsychotic polypharmacy, part 1: therapeutic option or dirty little secret? J Clin Psychiatry. 1999;60:425-426.

5. Physicians’ Desk Reference. 62nd ed. Montvale, NJ: Thompson Publishing, 2008.

6. Medwatch. Medical product safety information. Food and Drug Administration. Available at: http://www.fda.gov/medwatch/safety.htm. Accessed July 30, 2008.

7. American Diabetes Association, American Psychiatric Association, American Association of Clinical Endocrinologists, North American Association for the Study of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004;27:596-601.

8. Melonas JM. Preventing and reducing professional liability risk related to psychopharmacology. Psychiatric Times. 2005;23(14).-Available at http://www.psychiatrictimes.com/display/article/10168/48416. Accessed September 3, 2008.

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