Current Psychiatry

The risk of serious rash leaves many psychiatrists and patients reluctant use an anticonvulsant for bipolar disorder (Current Psychiatry, February 2006). When a minor rash develops, you must decide whether to stop the anticonvulsant and treat the allergy, or continue the offending agent lest bipolar symptoms resurface. Most physicians I know stop the anticonvulsant.

Early detection and treatment of skin problems and warning patients about the risk of rash are key to avoiding this adverse effect. I have treated the following types of rashes in patients taking anticonvulsants:

Drug rash with eosinophilia and systemic symptoms (DRESS) manifests as a delayed allergic reaction and often starts 2 weeks to 3 months after starting the anticonvulsant. It is often fatal if not detected early and treated promptly.

One patient with bipolar affective disorder, depressed type, was taking lamotrigine, 100 mg bid. She developed DRESS 7 months after starting the medication. I stopped lamotrigine and gave her diphenhydramine, 25 mg qid for 2 days, tid for 2 weeks, and bid for 1 week. The rash took approximately 4 weeks to clear.

Stevens-Johnson syndrome. A patient taking carbamazepine, 100 mg tid for bipolar affective disorder, presented with lesions of varying color, size, and shape throughout her body, including her mouth, palms, and soles. She did not have the classic “target lesion” that looks like a shooting target with several circles of varying colors. She had pain, cough, weakness, and generalized edematous joint swelling.

The patient received IV cortisone, IV fluids, antiallergic medications, and antibiotics for the skin infection. The rash subsided after 3 weeks and the skin discoloration resolved after approximately 3 months. She would not switch to lithium for fear it would sedate her but was maintained with IM fluphenazine, 37.5 mg every 4 weeks.

Surendran Nair, MD
Medical director, Easter Seals
Southfield, MI

The risk of serious rash leaves many psychiatrists and patients reluctant use an anticonvulsant for bipolar disorder (Current Psychiatry, February 2006). When a minor rash develops, you must decide whether to stop the anticonvulsant and treat the allergy, or continue the offending agent lest bipolar symptoms resurface. Most physicians I know stop the anticonvulsant.

Early detection and treatment of skin problems and warning patients about the risk of rash are key to avoiding this adverse effect. I have treated the following types of rashes in patients taking anticonvulsants:

Drug rash with eosinophilia and systemic symptoms (DRESS) manifests as a delayed allergic reaction and often starts 2 weeks to 3 months after starting the anticonvulsant. It is often fatal if not detected early and treated promptly.

One patient with bipolar affective disorder, depressed type, was taking lamotrigine, 100 mg bid. She developed DRESS 7 months after starting the medication. I stopped lamotrigine and gave her diphenhydramine, 25 mg qid for 2 days, tid for 2 weeks, and bid for 1 week. The rash took approximately 4 weeks to clear.

Stevens-Johnson syndrome. A patient taking carbamazepine, 100 mg tid for bipolar affective disorder, presented with lesions of varying color, size, and shape throughout her body, including her mouth, palms, and soles. She did not have the classic “target lesion” that looks like a shooting target with several circles of varying colors. She had pain, cough, weakness, and generalized edematous joint swelling.

The patient received IV cortisone, IV fluids, antiallergic medications, and antibiotics for the skin infection. The rash subsided after 3 weeks and the skin discoloration resolved after approximately 3 months. She would not switch to lithium for fear it would sedate her but was maintained with IM fluphenazine, 37.5 mg every 4 weeks.

Surendran Nair, MD
Medical director, Easter Seals
Southfield, MI

The risk of serious rash leaves many psychiatrists and patients reluctant use an anticonvulsant for bipolar disorder (Current Psychiatry, February 2006). When a minor rash develops, you must decide whether to stop the anticonvulsant and treat the allergy, or continue the offending agent lest bipolar symptoms resurface. Most physicians I know stop the anticonvulsant.

Early detection and treatment of skin problems and warning patients about the risk of rash are key to avoiding this adverse effect. I have treated the following types of rashes in patients taking anticonvulsants:

Drug rash with eosinophilia and systemic symptoms (DRESS) manifests as a delayed allergic reaction and often starts 2 weeks to 3 months after starting the anticonvulsant. It is often fatal if not detected early and treated promptly.

One patient with bipolar affective disorder, depressed type, was taking lamotrigine, 100 mg bid. She developed DRESS 7 months after starting the medication. I stopped lamotrigine and gave her diphenhydramine, 25 mg qid for 2 days, tid for 2 weeks, and bid for 1 week. The rash took approximately 4 weeks to clear.

Stevens-Johnson syndrome. A patient taking carbamazepine, 100 mg tid for bipolar affective disorder, presented with lesions of varying color, size, and shape throughout her body, including her mouth, palms, and soles. She did not have the classic “target lesion” that looks like a shooting target with several circles of varying colors. She had pain, cough, weakness, and generalized edematous joint swelling.

The patient received IV cortisone, IV fluids, antiallergic medications, and antibiotics for the skin infection. The rash subsided after 3 weeks and the skin discoloration resolved after approximately 3 months. She would not switch to lithium for fear it would sedate her but was maintained with IM fluphenazine, 37.5 mg every 4 weeks.

Surendran Nair, MD
Medical director, Easter Seals
Southfield, MI

The dramatic mental status changes shown by Dr. Lake’s and Dr. Hurwitz’ sample patient (Current Psychiatry, March 2006) speak to the blurred boundaries between major illness categories in DSM-IV-TR. Discovering demonstrable brain pathology or a causative systemic medical disorder clarifies these boundaries.

Dr. Randy Hillard notes that psychiatry is evolving as a specialty (Current Psychiatry, March 2006), but use of atypical antipsychotics to control mood and thought symptoms accounts for much of this evolution. Bipolar disorder and schizophrenia are not biologically different mental illnesses, but rather varying abnormal manifestations of a severe mental process.

Drs. Lake and Hurwitz write that correct initial diagnosis is essential for effective psychiatric treatment. When possible, we must also consider psychodynamic causes of hallucinations, delusional behavior, or mood swings—such as unresolved conflicts and stressors—as well as the patient’s acquired insight before we can make a diagnosis.

Although psychotropics can control thought and mood symptoms, psychotherapy that delves into the psychosocial nuances at the root of the disturbance is crucial to restoring a patient with a major mental illness to sustained life activity. Unfortunately, such psychotherapy is time-consuming, and managed care restricts reimbursement for psychotherapy. In this sense, psychiatry is regressing rather than evolving.

We need to classify functional mental illnesses into major and minor entities instead of a myriad of disorders—as DSM-IV-TR has done—and focus on psychodynamic causes of psychopathology instead of speculative biological differences between mental illness presentations. This will restore sense and meaning to psychiatry as a medical discipline.

Theodore Pearlman, MD
Houston, TX

The dramatic mental status changes shown by Dr. Lake’s and Dr. Hurwitz’ sample patient (Current Psychiatry, March 2006) speak to the blurred boundaries between major illness categories in DSM-IV-TR. Discovering demonstrable brain pathology or a causative systemic medical disorder clarifies these boundaries.

Dr. Randy Hillard notes that psychiatry is evolving as a specialty (Current Psychiatry, March 2006), but use of atypical antipsychotics to control mood and thought symptoms accounts for much of this evolution. Bipolar disorder and schizophrenia are not biologically different mental illnesses, but rather varying abnormal manifestations of a severe mental process.

Drs. Lake and Hurwitz write that correct initial diagnosis is essential for effective psychiatric treatment. When possible, we must also consider psychodynamic causes of hallucinations, delusional behavior, or mood swings—such as unresolved conflicts and stressors—as well as the patient’s acquired insight before we can make a diagnosis.

Although psychotropics can control thought and mood symptoms, psychotherapy that delves into the psychosocial nuances at the root of the disturbance is crucial to restoring a patient with a major mental illness to sustained life activity. Unfortunately, such psychotherapy is time-consuming, and managed care restricts reimbursement for psychotherapy. In this sense, psychiatry is regressing rather than evolving.

We need to classify functional mental illnesses into major and minor entities instead of a myriad of disorders—as DSM-IV-TR has done—and focus on psychodynamic causes of psychopathology instead of speculative biological differences between mental illness presentations. This will restore sense and meaning to psychiatry as a medical discipline.

Theodore Pearlman, MD
Houston, TX

The dramatic mental status changes shown by Dr. Lake’s and Dr. Hurwitz’ sample patient (Current Psychiatry, March 2006) speak to the blurred boundaries between major illness categories in DSM-IV-TR. Discovering demonstrable brain pathology or a causative systemic medical disorder clarifies these boundaries.

Dr. Randy Hillard notes that psychiatry is evolving as a specialty (Current Psychiatry, March 2006), but use of atypical antipsychotics to control mood and thought symptoms accounts for much of this evolution. Bipolar disorder and schizophrenia are not biologically different mental illnesses, but rather varying abnormal manifestations of a severe mental process.

Drs. Lake and Hurwitz write that correct initial diagnosis is essential for effective psychiatric treatment. When possible, we must also consider psychodynamic causes of hallucinations, delusional behavior, or mood swings—such as unresolved conflicts and stressors—as well as the patient’s acquired insight before we can make a diagnosis.

Although psychotropics can control thought and mood symptoms, psychotherapy that delves into the psychosocial nuances at the root of the disturbance is crucial to restoring a patient with a major mental illness to sustained life activity. Unfortunately, such psychotherapy is time-consuming, and managed care restricts reimbursement for psychotherapy. In this sense, psychiatry is regressing rather than evolving.

We need to classify functional mental illnesses into major and minor entities instead of a myriad of disorders—as DSM-IV-TR has done—and focus on psychodynamic causes of psychopathology instead of speculative biological differences between mental illness presentations. This will restore sense and meaning to psychiatry as a medical discipline.

Theodore Pearlman, MD
Houston, TX

CATIE study Phase 1 (Current Psychiatry, February 2006) is controversial for good reason. Critical details are problematic, such as the relatively low dosage of perphenazine that might have artificially reduced tardive dyskinesia incidence among patients taking that drug.¹

A more fundamental limitation is the investigators’ use of “all-cause discontinuation” as the primary effectiveness measure. By contrast, an objective measure (Hamilton Rating Scale for Depression) was used in the STAR-D study to judge antidepressant effectiveness.

All-cause discontinuation measures are highly subjective, as patients stop taking medication for a variety of reasons:

• a spouse, parent, or friend pressured them into stopping
  
• they think the medication is making them weak, dependent, or vulnerable
  
• they don’t notice the drug’s therapeutic effects, or lack the mental skill to balance adverse and good effects
  
• or they are incapable of understanding that they might need to endure adverse effects to obtain a benefit.
  

These and other factors vary widely among patients and—in their decision process—could outweigh a medication’s objective effects on specific symptoms. These subjective factors probably obscured any objective differences among the five drugs studied in CATIE phase 1.

Other variables were uncontrolled, including:

• effects of other medications taken before and during the study. The authors state that 72% of subjects were taking other medications at base-line. Previous antipsychotics were washed out, but patients could remain on other medications. Did the investigators consider the effects of combining the study antipsychotics with these medications?
  

Even the washout periods seem to have been flexible (ie, not controlled) based on the study’s wording: “Overlap in the administration of (antipsychotics) that patients received before study entry was permitted for the first 4 weeks after randomization.”² In other words, some patients stayed on their previous antipsychotics for 4 weeks, and others stopped taking the previous medication sooner. Do we know enough about variations in drug metabolism and effect duration to be sure that the overlap variable did not affect the results?

• nonpharmacologic treatment. According to the study, “No care was mandated across all sites other than the drug study.”³
  

If other types of treatment—such as group or individual therapy—were uncontrolled across all sites, did some patients receive such care whereas others did not? If so, were the potential effects of these treatments figured into the findings?

Arthur Mode, MD
Falls Church, VA

CATIE study Phase 1 (Current Psychiatry, February 2006) is controversial for good reason. Critical details are problematic, such as the relatively low dosage of perphenazine that might have artificially reduced tardive dyskinesia incidence among patients taking that drug.¹

A more fundamental limitation is the investigators’ use of “all-cause discontinuation” as the primary effectiveness measure. By contrast, an objective measure (Hamilton Rating Scale for Depression) was used in the STAR-D study to judge antidepressant effectiveness.

All-cause discontinuation measures are highly subjective, as patients stop taking medication for a variety of reasons:

• a spouse, parent, or friend pressured them into stopping
  
• they think the medication is making them weak, dependent, or vulnerable
  
• they don’t notice the drug’s therapeutic effects, or lack the mental skill to balance adverse and good effects
  
• or they are incapable of understanding that they might need to endure adverse effects to obtain a benefit.
  

These and other factors vary widely among patients and—in their decision process—could outweigh a medication’s objective effects on specific symptoms. These subjective factors probably obscured any objective differences among the five drugs studied in CATIE phase 1.

Other variables were uncontrolled, including:

• effects of other medications taken before and during the study. The authors state that 72% of subjects were taking other medications at base-line. Previous antipsychotics were washed out, but patients could remain on other medications. Did the investigators consider the effects of combining the study antipsychotics with these medications?
  

Even the washout periods seem to have been flexible (ie, not controlled) based on the study’s wording: “Overlap in the administration of (antipsychotics) that patients received before study entry was permitted for the first 4 weeks after randomization.”² In other words, some patients stayed on their previous antipsychotics for 4 weeks, and others stopped taking the previous medication sooner. Do we know enough about variations in drug metabolism and effect duration to be sure that the overlap variable did not affect the results?

• nonpharmacologic treatment. According to the study, “No care was mandated across all sites other than the drug study.”³
  

If other types of treatment—such as group or individual therapy—were uncontrolled across all sites, did some patients receive such care whereas others did not? If so, were the potential effects of these treatments figured into the findings?

Arthur Mode, MD
Falls Church, VA

CATIE study Phase 1 (Current Psychiatry, February 2006) is controversial for good reason. Critical details are problematic, such as the relatively low dosage of perphenazine that might have artificially reduced tardive dyskinesia incidence among patients taking that drug.¹

A more fundamental limitation is the investigators’ use of “all-cause discontinuation” as the primary effectiveness measure. By contrast, an objective measure (Hamilton Rating Scale for Depression) was used in the STAR-D study to judge antidepressant effectiveness.

All-cause discontinuation measures are highly subjective, as patients stop taking medication for a variety of reasons:

• a spouse, parent, or friend pressured them into stopping
  
• they think the medication is making them weak, dependent, or vulnerable
  
• they don’t notice the drug’s therapeutic effects, or lack the mental skill to balance adverse and good effects
  
• or they are incapable of understanding that they might need to endure adverse effects to obtain a benefit.
  

These and other factors vary widely among patients and—in their decision process—could outweigh a medication’s objective effects on specific symptoms. These subjective factors probably obscured any objective differences among the five drugs studied in CATIE phase 1.

Other variables were uncontrolled, including:

• effects of other medications taken before and during the study. The authors state that 72% of subjects were taking other medications at base-line. Previous antipsychotics were washed out, but patients could remain on other medications. Did the investigators consider the effects of combining the study antipsychotics with these medications?
  

Even the washout periods seem to have been flexible (ie, not controlled) based on the study’s wording: “Overlap in the administration of (antipsychotics) that patients received before study entry was permitted for the first 4 weeks after randomization.”² In other words, some patients stayed on their previous antipsychotics for 4 weeks, and others stopped taking the previous medication sooner. Do we know enough about variations in drug metabolism and effect duration to be sure that the overlap variable did not affect the results?

• nonpharmacologic treatment. According to the study, “No care was mandated across all sites other than the drug study.”³
  

If other types of treatment—such as group or individual therapy—were uncontrolled across all sites, did some patients receive such care whereas others did not? If so, were the potential effects of these treatments figured into the findings?

Arthur Mode, MD
Falls Church, VA

Jane Pauley is well-known for hosting NBC television’s Today Show but also for developing manic symptoms from corticosteroid therapy. Dr. Michael Cerullo (page 43) mentions her case in his excellent discussion of how to treat steroid-induced mania or mixed bipolar symptoms and reduce the risk in patients who require sustained corticosteroids.

Jane (we are on a first-name basis, aren’t we?) revealed in her autobiography¹ that she developed mania after taking corticosteroids for urticaria. In this case, a widely admired broadcaster’s revelation probably helped reduce the stigma of psychiatric illness.

But last year Hollywood celebs Tom Cruise and Brooke Shields debated the merits of antidepressant therapy for postpartum depression. That highly publicized exchange—he on the “con” side, she on the “pro”—certainly raised public awareness of depression in new mothers, but its effects on psychiatry’s image might have been more negative than positive.

And what do we make of actress Lorraine Bracco, who plays a psychiatrist on the HBO TV series, The Sopranos? Her character, Dr. Jennifer Melfi, treats mobster Tony Soprano’s panic attacks but not his, well, antisocial traits. Speaking at last year’s American Psychiatric Association meeting, Bracco stated that “in real life, I’m actually someone who has suffered from depression and had to seek the help of a psychiatrist.”

So we have a real patient portraying a psychiatrist treating an imaginary patient and then lecturing to real psychiatrists. That seems ironic, but I think The Sopranos’ popularity and Bracco’s acknowledgment that she sought treatment for depression make psychiatry look pretty good.

Jane Pauley is well-known for hosting NBC television’s Today Show but also for developing manic symptoms from corticosteroid therapy. Dr. Michael Cerullo (page 43) mentions her case in his excellent discussion of how to treat steroid-induced mania or mixed bipolar symptoms and reduce the risk in patients who require sustained corticosteroids.

Jane (we are on a first-name basis, aren’t we?) revealed in her autobiography¹ that she developed mania after taking corticosteroids for urticaria. In this case, a widely admired broadcaster’s revelation probably helped reduce the stigma of psychiatric illness.

But last year Hollywood celebs Tom Cruise and Brooke Shields debated the merits of antidepressant therapy for postpartum depression. That highly publicized exchange—he on the “con” side, she on the “pro”—certainly raised public awareness of depression in new mothers, but its effects on psychiatry’s image might have been more negative than positive.

And what do we make of actress Lorraine Bracco, who plays a psychiatrist on the HBO TV series, The Sopranos? Her character, Dr. Jennifer Melfi, treats mobster Tony Soprano’s panic attacks but not his, well, antisocial traits. Speaking at last year’s American Psychiatric Association meeting, Bracco stated that “in real life, I’m actually someone who has suffered from depression and had to seek the help of a psychiatrist.”

So we have a real patient portraying a psychiatrist treating an imaginary patient and then lecturing to real psychiatrists. That seems ironic, but I think The Sopranos’ popularity and Bracco’s acknowledgment that she sought treatment for depression make psychiatry look pretty good.

Jane Pauley is well-known for hosting NBC television’s Today Show but also for developing manic symptoms from corticosteroid therapy. Dr. Michael Cerullo (page 43) mentions her case in his excellent discussion of how to treat steroid-induced mania or mixed bipolar symptoms and reduce the risk in patients who require sustained corticosteroids.

Jane (we are on a first-name basis, aren’t we?) revealed in her autobiography¹ that she developed mania after taking corticosteroids for urticaria. In this case, a widely admired broadcaster’s revelation probably helped reduce the stigma of psychiatric illness.

But last year Hollywood celebs Tom Cruise and Brooke Shields debated the merits of antidepressant therapy for postpartum depression. That highly publicized exchange—he on the “con” side, she on the “pro”—certainly raised public awareness of depression in new mothers, but its effects on psychiatry’s image might have been more negative than positive.

And what do we make of actress Lorraine Bracco, who plays a psychiatrist on the HBO TV series, The Sopranos? Her character, Dr. Jennifer Melfi, treats mobster Tony Soprano’s panic attacks but not his, well, antisocial traits. Speaking at last year’s American Psychiatric Association meeting, Bracco stated that “in real life, I’m actually someone who has suffered from depression and had to seek the help of a psychiatrist.”

So we have a real patient portraying a psychiatrist treating an imaginary patient and then lecturing to real psychiatrists. That seems ironic, but I think The Sopranos’ popularity and Bracco’s acknowledgment that she sought treatment for depression make psychiatry look pretty good.

History: ‘They’re making me crazy’

Ms. D, age 22, is brought to the emergency room by her older brother for psychiatric evaluation after a family argument. He tells us that his sister is out most nights, hanging out at nightclubs. When she’s home, he says, she locks herself in her room and avoids him and his younger brother, who also lives with them.

Recently, her brother says, Ms. D signed a contract to appear in pornographic videos. When he found out, he went to the studio’s producer and nullified the contract.

Ms. D, frustrated with her brother’s interference, tells us she dreams of becoming a movie star and going to college, but blames him for “holding me back” and keeping her unemployed.

Worse, she says, he and her two sisters are impostors who are “trying to hurt me” and are “making me go crazy.” She fears her “false brother” will take her house if she leaves, yet she feels unsafe at home because strangers—envious of “my beauty and intelligence”—peek into her windows and stalk her. She tells us her father is near and guards her—even though he died 4 years ago.

Ms. D, who lost her mother at age 2, began having psychotic episodes at age 19, a few months after her father’s death. At that time, she was hospitalized after insisting that her father had faked his death because of a conspiracy against him. A hospital psychiatrist diagnosed bipolar disorder and prescribed a mood stabilizer, but she did not take the medication and her psychosis has worsened.

Ms. D’s Mini-Mental State Examination score of 30 indicates that she is neither grossly confused nor has underlying dementia. However, she is emotionally labile with grossly disorganized thought processes and paranoid and grandiose delusions.

We could not locate other family members, so Ms. D’s family psychiatric history is unknown. She has casual relationships with men but does not have a boyfriend. She acknowledges that she frequents local nightclubs but denies using alcohol.

Blood work and other medical examination results are normal. Negative urine toxicology screen suggests she not abusing substances, and electrolytes and thyroid-stimulating hormone levels are normal. Negative rapid plasma reagin rules out tertiary syphilis. We do not order radiologic studies because her presentation does not suggest focal abnormality, and neurologic exam results are benign.

poll here

The authors’ observations

Patients with both paranoid delusions and manic features are challenging. Prognoses and treatment options for each group of symptoms differ substantially.

Ms. D’s grandiosity, pressured speech, tangential flight of ideas, and hypersexuality strongly suggest bipolar disorder. We could not rule out schizophrenia, however, because of her prominent hallucinations and paranoia.

Pharmacologic intoxication was not likely based on laboratory results and the longstanding, progressive course of Ms. D’s disorder. Organic pathology also was unlikely, given her normal neurologic examination and lack of other medical issues.

Treatment: Talk therapy

We tentatively diagnose Ms. D as having bipolar disorder type I with a manic episode and psychotic features. She does not meet DSM-IV-TR criteria for schizophrenia and lacks affective flattening, poverty of speech, avolition, and other negative symptoms typical of the disorder. We admit her to the inpatient psychiatric unit and prescribe lithium, 300 mg tid, and quetiapine, 50 mg bid.

An internal medicine (IM) resident visits Ms. D for 30 to 45 minutes daily during her hospitalization to check her medical status and to allow her to vent her frustration. A resident in psychiatry also interviews Ms. D for about one half-hour each day. The patient rarely interacts with other patients and speaks only with physicians and nurses.

Ms. D appears to trust the IM resident and confides in her about her brother. During their first meeting, she appears most disturbed that a man who “claims” to be her brother is sabotaging her life. She does not fear that this “impostor” will physically harm her but still distrusts him. She repeatedly reports that her late father is nearby or in the room above hers. She adds that she feels much safer in the hospital, where the “stalkers” cannot reach her.

At times, Ms. D tells the IM resident she has a twin. Other times, she believes her family is much larger than it is, and she sometimes laments that she is losing her identity. She often perseverates on Judgment Day, at which time she says her “fake” relatives will answer for their actions against her.

Ms. D’s delusions of grandiosity, tangentiality, circumferential speech, and flight of ideas persist through 4 days in the hospital. Her affect is extremely labile and occasionally inappropriate. She sometimes cries when discussing her father’s death, then stops, thinks a moment, and begins laughing. At this point, we increase lithium to 600 mg tid and quetiapine to 100 mg tid. She is suffering no side effects and infrequently requires haloperidol as a demand dose only.

poll here

The authors’ observations

A patient such as Ms. D who lives in a minimally supportive environment and has paranoid delusions could fabricate an explanation for what she perceives as family members’ incongruent behavior. She could create a reality in which these relatives are impostors.

Although this behavior is not unusual, Ms. D’s extreme reaction toward her siblings suggests Capgras syndrome, a rare misidentification disorder (Box). The syndrome is often missed in clinical practice, and its prevalence has not been quantified.

Capgras syndrome is seen most often in patients with paranoid schizophrenia—the highest functioning and most preserved schizophrenia patients. This association may indicate that both neurologic dysfunction and psychological background are necessary to produce the syndrome.

The belief that family members are impostors could point to a conspiracy theory or paranoid delusion. Ms. D’s suspicion and distrust toward her older brother indicate a paranoid state, and her other delusions—such as her belief that others are stalking her—suggest that her Capgras symptoms are another manifestation of paranoia.

Box

For Ms. D, structural brain deficits probably interacted with her psychosocial milieu to create Capgras delusions, though we did not perform confirmatory brain imaging or functional neurologic testing. Whereas right cortical lesions might impair recognition while preserving familiarity, Capgras syndrome preserves recognition but deadens the emotion that makes faces seem familiar. When focal lesions are found to cause Capgras delusion, however, the right hemisphere—specifically the frontal cortex—usually is affected.^2,3

Table

Proposed causes of Capgras syndrome

The authors’ observations

When interviewing a patient with paranoid delusions, get as much detail as possible about his or her close relationships. Try to interview one or two family members or friends. The information can help determine whether Capgras symptoms underlie paranoia.

Brain imaging might uncover pertinent abnormalities, but the cost could outweigh any benefit. No evidence supports use of CT to diagnose Capgras syndrome. Some evidence supports use of brain MRI, but more research is needed.

No specific treatment exists for Capgras delusions apart from using antipsychotics to treat the psychosis based on clinical suspicion and constellation of symptoms.

Studies have shown no difference in response to atypical antipsychotics between patients with schizophrenia and comcomitant Capgras symptoms and those with schizophrenia alone. In clinical practice, we have found that treating Capgras symptoms does improve schizophrenia’s course.

Adjunctive psychotherapy has not been studied in Capgras syndrome, and directed, insight-guided therapy might not resolve deeply rooted delusions for some patients. With Ms. D, however, “talk therapy” helped us build rapport and gave us insight into her strained familial relationships. Establishing a therapeutic alliance with the patient and encouraging healthy relationships with his or her family and friends can mitigate the effects of Capgras paranoia.

Continued treatment: Gradual change

Day by day Ms. D’s mania subsides gradually, though she still fears that a stranger posing as her brother is stalking her. She talks about her brother less frequently, though she is clearly holding fast to her delusional beliefs.

We discharge Ms. D after 10 days. Although her symptoms have not resolved, she is markedly less manic and less agitated than at admission. We arrange treatment with outpatient psychiatry. She does not follow up with her original psychiatrist and is lost to follow-up.

Related resources

• PsychNet-UK. Disorder information sheet: Capgras (delusion) syndrome. www.psychnet-uk.com/dsm_iv/capgras_syndrome.htm.
  
• Bourget D, Whitehurst L. Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence. Can J Psychiatry 2004;49:719-25. Available at: www.cpa-apc.org/Publications/Archives/CJP/2004/november/bourget.asp.
  
• Barton JJ. Disorders of face perception and recognition. Neurol Clin 2003;21:521-48.
  
• Lewis S. Brain imaging in a case of Capgras’ syndrome. Br J Psychiatry 1987;150:117-21.
  
• Christodoulou GN. The syndrome of Capgras. Br J Psychiatry 1977;130:556-64.
  

• Haloperidol • Haldol
  
• Lithium • Eskalith, others
  
• Quetiapine • Seroquel
  

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

History: ‘They’re making me crazy’

Ms. D, age 22, is brought to the emergency room by her older brother for psychiatric evaluation after a family argument. He tells us that his sister is out most nights, hanging out at nightclubs. When she’s home, he says, she locks herself in her room and avoids him and his younger brother, who also lives with them.

Recently, her brother says, Ms. D signed a contract to appear in pornographic videos. When he found out, he went to the studio’s producer and nullified the contract.

Ms. D, frustrated with her brother’s interference, tells us she dreams of becoming a movie star and going to college, but blames him for “holding me back” and keeping her unemployed.

Worse, she says, he and her two sisters are impostors who are “trying to hurt me” and are “making me go crazy.” She fears her “false brother” will take her house if she leaves, yet she feels unsafe at home because strangers—envious of “my beauty and intelligence”—peek into her windows and stalk her. She tells us her father is near and guards her—even though he died 4 years ago.

Ms. D, who lost her mother at age 2, began having psychotic episodes at age 19, a few months after her father’s death. At that time, she was hospitalized after insisting that her father had faked his death because of a conspiracy against him. A hospital psychiatrist diagnosed bipolar disorder and prescribed a mood stabilizer, but she did not take the medication and her psychosis has worsened.

Ms. D’s Mini-Mental State Examination score of 30 indicates that she is neither grossly confused nor has underlying dementia. However, she is emotionally labile with grossly disorganized thought processes and paranoid and grandiose delusions.

We could not locate other family members, so Ms. D’s family psychiatric history is unknown. She has casual relationships with men but does not have a boyfriend. She acknowledges that she frequents local nightclubs but denies using alcohol.

Blood work and other medical examination results are normal. Negative urine toxicology screen suggests she not abusing substances, and electrolytes and thyroid-stimulating hormone levels are normal. Negative rapid plasma reagin rules out tertiary syphilis. We do not order radiologic studies because her presentation does not suggest focal abnormality, and neurologic exam results are benign.

poll here

The authors’ observations

Patients with both paranoid delusions and manic features are challenging. Prognoses and treatment options for each group of symptoms differ substantially.

Ms. D’s grandiosity, pressured speech, tangential flight of ideas, and hypersexuality strongly suggest bipolar disorder. We could not rule out schizophrenia, however, because of her prominent hallucinations and paranoia.

Pharmacologic intoxication was not likely based on laboratory results and the longstanding, progressive course of Ms. D’s disorder. Organic pathology also was unlikely, given her normal neurologic examination and lack of other medical issues.

Treatment: Talk therapy

We tentatively diagnose Ms. D as having bipolar disorder type I with a manic episode and psychotic features. She does not meet DSM-IV-TR criteria for schizophrenia and lacks affective flattening, poverty of speech, avolition, and other negative symptoms typical of the disorder. We admit her to the inpatient psychiatric unit and prescribe lithium, 300 mg tid, and quetiapine, 50 mg bid.

An internal medicine (IM) resident visits Ms. D for 30 to 45 minutes daily during her hospitalization to check her medical status and to allow her to vent her frustration. A resident in psychiatry also interviews Ms. D for about one half-hour each day. The patient rarely interacts with other patients and speaks only with physicians and nurses.

Ms. D appears to trust the IM resident and confides in her about her brother. During their first meeting, she appears most disturbed that a man who “claims” to be her brother is sabotaging her life. She does not fear that this “impostor” will physically harm her but still distrusts him. She repeatedly reports that her late father is nearby or in the room above hers. She adds that she feels much safer in the hospital, where the “stalkers” cannot reach her.

At times, Ms. D tells the IM resident she has a twin. Other times, she believes her family is much larger than it is, and she sometimes laments that she is losing her identity. She often perseverates on Judgment Day, at which time she says her “fake” relatives will answer for their actions against her.

Ms. D’s delusions of grandiosity, tangentiality, circumferential speech, and flight of ideas persist through 4 days in the hospital. Her affect is extremely labile and occasionally inappropriate. She sometimes cries when discussing her father’s death, then stops, thinks a moment, and begins laughing. At this point, we increase lithium to 600 mg tid and quetiapine to 100 mg tid. She is suffering no side effects and infrequently requires haloperidol as a demand dose only.

poll here

The authors’ observations

A patient such as Ms. D who lives in a minimally supportive environment and has paranoid delusions could fabricate an explanation for what she perceives as family members’ incongruent behavior. She could create a reality in which these relatives are impostors.

Although this behavior is not unusual, Ms. D’s extreme reaction toward her siblings suggests Capgras syndrome, a rare misidentification disorder (Box). The syndrome is often missed in clinical practice, and its prevalence has not been quantified.

Capgras syndrome is seen most often in patients with paranoid schizophrenia—the highest functioning and most preserved schizophrenia patients. This association may indicate that both neurologic dysfunction and psychological background are necessary to produce the syndrome.

The belief that family members are impostors could point to a conspiracy theory or paranoid delusion. Ms. D’s suspicion and distrust toward her older brother indicate a paranoid state, and her other delusions—such as her belief that others are stalking her—suggest that her Capgras symptoms are another manifestation of paranoia.

Box

For Ms. D, structural brain deficits probably interacted with her psychosocial milieu to create Capgras delusions, though we did not perform confirmatory brain imaging or functional neurologic testing. Whereas right cortical lesions might impair recognition while preserving familiarity, Capgras syndrome preserves recognition but deadens the emotion that makes faces seem familiar. When focal lesions are found to cause Capgras delusion, however, the right hemisphere—specifically the frontal cortex—usually is affected.^2,3

Table

Proposed causes of Capgras syndrome

The authors’ observations

When interviewing a patient with paranoid delusions, get as much detail as possible about his or her close relationships. Try to interview one or two family members or friends. The information can help determine whether Capgras symptoms underlie paranoia.

Brain imaging might uncover pertinent abnormalities, but the cost could outweigh any benefit. No evidence supports use of CT to diagnose Capgras syndrome. Some evidence supports use of brain MRI, but more research is needed.

No specific treatment exists for Capgras delusions apart from using antipsychotics to treat the psychosis based on clinical suspicion and constellation of symptoms.

Studies have shown no difference in response to atypical antipsychotics between patients with schizophrenia and comcomitant Capgras symptoms and those with schizophrenia alone. In clinical practice, we have found that treating Capgras symptoms does improve schizophrenia’s course.

Adjunctive psychotherapy has not been studied in Capgras syndrome, and directed, insight-guided therapy might not resolve deeply rooted delusions for some patients. With Ms. D, however, “talk therapy” helped us build rapport and gave us insight into her strained familial relationships. Establishing a therapeutic alliance with the patient and encouraging healthy relationships with his or her family and friends can mitigate the effects of Capgras paranoia.

Continued treatment: Gradual change

Day by day Ms. D’s mania subsides gradually, though she still fears that a stranger posing as her brother is stalking her. She talks about her brother less frequently, though she is clearly holding fast to her delusional beliefs.

We discharge Ms. D after 10 days. Although her symptoms have not resolved, she is markedly less manic and less agitated than at admission. We arrange treatment with outpatient psychiatry. She does not follow up with her original psychiatrist and is lost to follow-up.

Related resources

• PsychNet-UK. Disorder information sheet: Capgras (delusion) syndrome. www.psychnet-uk.com/dsm_iv/capgras_syndrome.htm.
  
• Bourget D, Whitehurst L. Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence. Can J Psychiatry 2004;49:719-25. Available at: www.cpa-apc.org/Publications/Archives/CJP/2004/november/bourget.asp.
  
• Barton JJ. Disorders of face perception and recognition. Neurol Clin 2003;21:521-48.
  
• Lewis S. Brain imaging in a case of Capgras’ syndrome. Br J Psychiatry 1987;150:117-21.
  
• Christodoulou GN. The syndrome of Capgras. Br J Psychiatry 1977;130:556-64.
  

• Haloperidol • Haldol
  
• Lithium • Eskalith, others
  
• Quetiapine • Seroquel
  

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

History: ‘They’re making me crazy’

Ms. D, age 22, is brought to the emergency room by her older brother for psychiatric evaluation after a family argument. He tells us that his sister is out most nights, hanging out at nightclubs. When she’s home, he says, she locks herself in her room and avoids him and his younger brother, who also lives with them.

Recently, her brother says, Ms. D signed a contract to appear in pornographic videos. When he found out, he went to the studio’s producer and nullified the contract.

Ms. D, frustrated with her brother’s interference, tells us she dreams of becoming a movie star and going to college, but blames him for “holding me back” and keeping her unemployed.

Worse, she says, he and her two sisters are impostors who are “trying to hurt me” and are “making me go crazy.” She fears her “false brother” will take her house if she leaves, yet she feels unsafe at home because strangers—envious of “my beauty and intelligence”—peek into her windows and stalk her. She tells us her father is near and guards her—even though he died 4 years ago.

Ms. D, who lost her mother at age 2, began having psychotic episodes at age 19, a few months after her father’s death. At that time, she was hospitalized after insisting that her father had faked his death because of a conspiracy against him. A hospital psychiatrist diagnosed bipolar disorder and prescribed a mood stabilizer, but she did not take the medication and her psychosis has worsened.

Ms. D’s Mini-Mental State Examination score of 30 indicates that she is neither grossly confused nor has underlying dementia. However, she is emotionally labile with grossly disorganized thought processes and paranoid and grandiose delusions.

We could not locate other family members, so Ms. D’s family psychiatric history is unknown. She has casual relationships with men but does not have a boyfriend. She acknowledges that she frequents local nightclubs but denies using alcohol.

Blood work and other medical examination results are normal. Negative urine toxicology screen suggests she not abusing substances, and electrolytes and thyroid-stimulating hormone levels are normal. Negative rapid plasma reagin rules out tertiary syphilis. We do not order radiologic studies because her presentation does not suggest focal abnormality, and neurologic exam results are benign.

poll here

The authors’ observations

Patients with both paranoid delusions and manic features are challenging. Prognoses and treatment options for each group of symptoms differ substantially.

Ms. D’s grandiosity, pressured speech, tangential flight of ideas, and hypersexuality strongly suggest bipolar disorder. We could not rule out schizophrenia, however, because of her prominent hallucinations and paranoia.

Pharmacologic intoxication was not likely based on laboratory results and the longstanding, progressive course of Ms. D’s disorder. Organic pathology also was unlikely, given her normal neurologic examination and lack of other medical issues.

Treatment: Talk therapy

We tentatively diagnose Ms. D as having bipolar disorder type I with a manic episode and psychotic features. She does not meet DSM-IV-TR criteria for schizophrenia and lacks affective flattening, poverty of speech, avolition, and other negative symptoms typical of the disorder. We admit her to the inpatient psychiatric unit and prescribe lithium, 300 mg tid, and quetiapine, 50 mg bid.

An internal medicine (IM) resident visits Ms. D for 30 to 45 minutes daily during her hospitalization to check her medical status and to allow her to vent her frustration. A resident in psychiatry also interviews Ms. D for about one half-hour each day. The patient rarely interacts with other patients and speaks only with physicians and nurses.

Ms. D appears to trust the IM resident and confides in her about her brother. During their first meeting, she appears most disturbed that a man who “claims” to be her brother is sabotaging her life. She does not fear that this “impostor” will physically harm her but still distrusts him. She repeatedly reports that her late father is nearby or in the room above hers. She adds that she feels much safer in the hospital, where the “stalkers” cannot reach her.

At times, Ms. D tells the IM resident she has a twin. Other times, she believes her family is much larger than it is, and she sometimes laments that she is losing her identity. She often perseverates on Judgment Day, at which time she says her “fake” relatives will answer for their actions against her.

Ms. D’s delusions of grandiosity, tangentiality, circumferential speech, and flight of ideas persist through 4 days in the hospital. Her affect is extremely labile and occasionally inappropriate. She sometimes cries when discussing her father’s death, then stops, thinks a moment, and begins laughing. At this point, we increase lithium to 600 mg tid and quetiapine to 100 mg tid. She is suffering no side effects and infrequently requires haloperidol as a demand dose only.

poll here

The authors’ observations

A patient such as Ms. D who lives in a minimally supportive environment and has paranoid delusions could fabricate an explanation for what she perceives as family members’ incongruent behavior. She could create a reality in which these relatives are impostors.

Although this behavior is not unusual, Ms. D’s extreme reaction toward her siblings suggests Capgras syndrome, a rare misidentification disorder (Box). The syndrome is often missed in clinical practice, and its prevalence has not been quantified.

Capgras syndrome is seen most often in patients with paranoid schizophrenia—the highest functioning and most preserved schizophrenia patients. This association may indicate that both neurologic dysfunction and psychological background are necessary to produce the syndrome.

The belief that family members are impostors could point to a conspiracy theory or paranoid delusion. Ms. D’s suspicion and distrust toward her older brother indicate a paranoid state, and her other delusions—such as her belief that others are stalking her—suggest that her Capgras symptoms are another manifestation of paranoia.

Box

For Ms. D, structural brain deficits probably interacted with her psychosocial milieu to create Capgras delusions, though we did not perform confirmatory brain imaging or functional neurologic testing. Whereas right cortical lesions might impair recognition while preserving familiarity, Capgras syndrome preserves recognition but deadens the emotion that makes faces seem familiar. When focal lesions are found to cause Capgras delusion, however, the right hemisphere—specifically the frontal cortex—usually is affected.^2,3

Table

Proposed causes of Capgras syndrome

The authors’ observations

When interviewing a patient with paranoid delusions, get as much detail as possible about his or her close relationships. Try to interview one or two family members or friends. The information can help determine whether Capgras symptoms underlie paranoia.

Brain imaging might uncover pertinent abnormalities, but the cost could outweigh any benefit. No evidence supports use of CT to diagnose Capgras syndrome. Some evidence supports use of brain MRI, but more research is needed.

No specific treatment exists for Capgras delusions apart from using antipsychotics to treat the psychosis based on clinical suspicion and constellation of symptoms.

Studies have shown no difference in response to atypical antipsychotics between patients with schizophrenia and comcomitant Capgras symptoms and those with schizophrenia alone. In clinical practice, we have found that treating Capgras symptoms does improve schizophrenia’s course.

Adjunctive psychotherapy has not been studied in Capgras syndrome, and directed, insight-guided therapy might not resolve deeply rooted delusions for some patients. With Ms. D, however, “talk therapy” helped us build rapport and gave us insight into her strained familial relationships. Establishing a therapeutic alliance with the patient and encouraging healthy relationships with his or her family and friends can mitigate the effects of Capgras paranoia.

Continued treatment: Gradual change

Day by day Ms. D’s mania subsides gradually, though she still fears that a stranger posing as her brother is stalking her. She talks about her brother less frequently, though she is clearly holding fast to her delusional beliefs.

We discharge Ms. D after 10 days. Although her symptoms have not resolved, she is markedly less manic and less agitated than at admission. We arrange treatment with outpatient psychiatry. She does not follow up with her original psychiatrist and is lost to follow-up.

Related resources

• PsychNet-UK. Disorder information sheet: Capgras (delusion) syndrome. www.psychnet-uk.com/dsm_iv/capgras_syndrome.htm.
  
• Bourget D, Whitehurst L. Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence. Can J Psychiatry 2004;49:719-25. Available at: www.cpa-apc.org/Publications/Archives/CJP/2004/november/bourget.asp.
  
• Barton JJ. Disorders of face perception and recognition. Neurol Clin 2003;21:521-48.
  
• Lewis S. Brain imaging in a case of Capgras’ syndrome. Br J Psychiatry 1987;150:117-21.
  
• Christodoulou GN. The syndrome of Capgras. Br J Psychiatry 1977;130:556-64.
  

• Haloperidol • Haldol
  
• Lithium • Eskalith, others
  
• Quetiapine • Seroquel
  

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

Matt, age 17, grew up in a household of gamblers. He learned to play poker from his father at age 8 and bet on sports with his friends in the 5th grade. For 2 years he has been playing poker three to four nights per week and watching a lot of televised poker. His parents worry he might be “addicted” to gambling and bring him for evaluation.

Easy access to gambling through casinos, lotteries, and Internet games has affected many social groups, particularly adolescents.¹ Teens such as Matt are more likely than adults to become pathological gamblers,² and they often have psychiatric disorders and antisocial behavior patterns that interfere with normal development. This article:

• suggests screening tools to identify problem teen gambling
  
• discusses how to use psychotherapy, medications, and other options to help gambling-obsessed adolescents change their high-risk behavior.
  

Why adolescents gamble

Gambling activates the same neural reward pathways affected by cocaine and amphetamines.³ Even so, many adolescents view gambling as less harmful than drugs⁴ and consider it a rite of passage:

• 90% report having gambled for money
  
• 75% have gambled at home for money
  
• 85% of parents do not object to gambling behaviors, teens say.^4,5
  

Adolescent gambling behavior. For approximately 85% of adolescents, gambling becomes no more than a social activity. For others, it can become problematic or even pathological (Table 1).^5,7 Approximately 4 to 8% of adolescents meet criteria for pathological gambling, compared with 1% of adults.

Adolescents’ higher rate might reflect pathological gambling’s natural course—peaking during adolescence, then tapering during adulthood. Some adolescents may adapt their gambling behavior over time. Problem gambling tends to be more transient and episodic than pathological gambling, remitting when adolescents take on new responsibilities (such as with college, marriage, employment, or death of parents).⁸

Table 1

Adolescent gambling: From entertainment to mental illness

Case continued: ‘Up big-time’

Matt says he loves to gamble and believes he is more gifted at poker than his peers. He also recognizes his behavior could be addictive and admits lying to his parents about his gambling. He plays Internet poker 3 to 4 hours per day and claims he wins more often than he loses. “I’m up big time,” he boasts.

Matt denies going to casinos or using bookies. He says he is managing school and home responsibilities without difficulty. He denies mood or anxiety symptoms but admits using methylphenidate while gambling. He obtains the stimulant from friends at school and usually snorts it to get “a bigger rush.”

Matt is clearly at risk for problem gambling. He was exposed to gambling early, is becoming preoccupied with it, lies about how much he gambles, and combines gambling with substance abuse. progress more rapidly and can become problem gamblers within 12 to 14 months.²

Neurobiologic differences between adolescent and adult pathological gamblers are not well-defined. Adults show evidence of dysregulated dopamine, norepinephrine, and serotonin neuro-transmission.⁹ Neuroimaging in adult pathological gamblers shows perturbations in reward processing centers and frontal lobe structures that control inhibition. These factors have been examined little in adolescents.

Identifying problem gambling in teens

Diagnostic “red flags” for problem gambling in adolescents include declining school performance, sleep disturbance, generalized anxiety or irritability, or possibly lack of response to general psychiatric treatment. Three tools can be useful for screening adolescents:

The Lie-Bet Questionnaire¹⁰ is a 2-question screen for problem gambling:

• Have you ever lied to anyone important about how often you gamble?
  
• Have you ever had to increase your bet to get the same excitement from gambling?
  

The South-Oaks Gambling Screen¹¹ is the standard pathological gambling screen for adults. Like the (SOGS-RA) is based and validated using DSM-III criteria (see Related resources). A score of 2 to 5 indicates at-risk gambling behaviors, and ≥6 indicate need for treatment.

The Gamblers Anonymous questionnaire¹² comprises 20 questions that identify negative social, physical, and emotional consequences of gambling behaviors (Box). Seven or more positive responses indicate probable pathological gambling. This screen has shown reliability in adolescents.

Use one or more of these quick screens with every adolescent presenting for treatment—especially in substance abuse treatment settings. When results are positive, probe for gambling behaviors and consequences. Rely on DSM-IV-TR criteria and clinical presentation to differentiate social gambling from pathological gambling.

Box

Behaviors and comorbidities

Negative consequences. Pathological gambling often consumes 10 to 20 hours per week of the adolescent’s time,¹³ hurting school performance and delaying developmental milestones. Teen gamblers may abandon extracurricular school activities, and their few friends often gamble, too. They are at risk for delinquency, criminal activity, and antisocial behaviors (such as selling drugs, engaging in prostitution)¹⁴ unprotected sexual activity, drug use, reckless driving, and carrying weapons.^15,16

Psychiatric comorbidity is the rule and often what brings adolescent gamblers to treatment. Substance abuse, major depression, attention-deficit/hyperactivity disorder, and personality disorders are most common (Table 2) Adolescent substance abuse at least triples the risk of pathological gambling.¹⁸

Adolescent pathological gamblers have increased rates of suicidal ideation and suicide attempts.¹⁷ They are at risk for other impulsive behaviors as well,¹⁹ although they are unlikely to volunteer this information. The Minnesota Impulsive Disorders Interview help identify comorbid pathological gambling, trichotillomania, kleptomania, pyromania, intermittent explosive disorder, compulsive buying, and compulsive sexual behaviors.¹⁹ Screen for these comorbidities during the first sessions or if a patient does not respond to treatment of gambling behavior.

Table 2

Risk factors for pathological adolescent gambling

Treating adolescent gamblers

Matt’s answers to the gambling screening questionnaires (one “yes” to the Lie-Bet Questionnaire, a SOGS-RA score of 4, and a GA-20 Questions score of 5) indicate problem gambling but not pathological gambling. You recommend that he attend Gamblers Anonymous, but he refuses. He also rejects individual therapy or taking medications.

Matt acknowledges misusing methylphenidate, however, and agrees to consider an outpatient substance abuse program. He also agrees to six sessions with a gambling treatment specialist to learn about problem gambling’s signs and symptoms, how to cope with betting loses, and how to reduce his preoccupation with gambling.

No guidelines exist for treating adolescent pathological gamblers, and specialized teen treatment programs are rare. Most services are provided in mental health or substance abuse settings, using adult treatments modified for adolescents.

Cognitive behavioral therapy (CBT) can be successful for highly motivated gamblers, although adolescents might not want to change their pathological behaviors. In case reports, four adolescents achieved remission after 6 months of CBT.^20,21 CBT appears to have long-term benefits for adults, but this has not been evaluated in teens. Even so, individual CBT may be ideal for adolescent gamblers because side effects are minimal.

Gamblers Anonymous (GA) in adults has shown a low retention rate and a 1-year abstinence rate of 22 Its effectiveness for adolescents lacks empiric support, but the 12-step program’s availability, structure, and fellowship may be useful.

Medications. Consider medication as first-line treatment for adolescents with psychiatric comorbidity. Try psychosocial treatment first for those without psychiatric comorbidity; consider medication as second-line therapy if response to psychosocial treatment is inadequate.

No medications are FDA-approved for pathological gambling, and no studies have examined medication use for adolescent gamblers. Controlled trials with adults suggest some medications may reduce urges and cravings or decrease gambling behaviors. These include:

• selective serotonin reuptake inhibitors
  
• opioid antagonists such as naltrexone or its analogue nalmefene
  
• or mood stabilizers such as lithium, divalproex sodium, or possibly topiramate.²³
  

Working with families. Many parents are aware of the destructive potential of substance abuse but not of gambling. They may feel shame that they did not recognize their teen’s gambling problem or “control” their child’s behavior. The adolescent may feel remorse for having bet with the parents’ money.

Even when the family recognizes the teen’s problem, denial or enabling can perpetuate the behavior. For teens such as Matt who learned to gamble at a home, advise the parents to abstain from gambling as well. Consider screening the parents for pathological gambling, given its high rate of heritability.

Address guilt and shame by acknowledging that pathological gambling is a psychiatric disease caused by biological, psychological, and social factors—not dysfunctional family relations. Emphasize that treatment works. Because gambling is easily hidden, educate families about relapse signs, such as preoccupation with money, personality changes, or failing to fulfill family responsibilities.²⁵

Related resources

• Wiebe JM, Cox BJ, Mehmel BG. The South Oaks Gambling Screen Revised for Adolescents (SOGS-RA): further psychometric findings from a community sample. J Gambl Stud 2000;16(2-3):275-88.
  
• Gamblers Anonymous. www.gamblersanonymous.org.
  
• National Council on Problem Gambling. www.ncpgambling.org.
  
• International Centre for Youth Gambling Problems and High-Risk Behaviors. www.youthgambling.com.
  

• Nalmefene • Revex
  
• Naltrexone • ReVia
  
• Lithium • Lithobid, others
  
• Divalproex sodium • Depakote, others
  
• Topiramate • Topamax
  

Dr. Fong receives grant/research support from Ortho McNeil Pharmaceutical and Somaxon Pharmaceuticals and is a speaker for Forest Pharmaceuticals.

Matt, age 17, grew up in a household of gamblers. He learned to play poker from his father at age 8 and bet on sports with his friends in the 5th grade. For 2 years he has been playing poker three to four nights per week and watching a lot of televised poker. His parents worry he might be “addicted” to gambling and bring him for evaluation.

Easy access to gambling through casinos, lotteries, and Internet games has affected many social groups, particularly adolescents.¹ Teens such as Matt are more likely than adults to become pathological gamblers,² and they often have psychiatric disorders and antisocial behavior patterns that interfere with normal development. This article:

• suggests screening tools to identify problem teen gambling
  
• discusses how to use psychotherapy, medications, and other options to help gambling-obsessed adolescents change their high-risk behavior.
  

Why adolescents gamble

Gambling activates the same neural reward pathways affected by cocaine and amphetamines.³ Even so, many adolescents view gambling as less harmful than drugs⁴ and consider it a rite of passage:

• 90% report having gambled for money
  
• 75% have gambled at home for money
  
• 85% of parents do not object to gambling behaviors, teens say.^4,5
  

Adolescent gambling behavior. For approximately 85% of adolescents, gambling becomes no more than a social activity. For others, it can become problematic or even pathological (Table 1).^5,7 Approximately 4 to 8% of adolescents meet criteria for pathological gambling, compared with 1% of adults.

Adolescents’ higher rate might reflect pathological gambling’s natural course—peaking during adolescence, then tapering during adulthood. Some adolescents may adapt their gambling behavior over time. Problem gambling tends to be more transient and episodic than pathological gambling, remitting when adolescents take on new responsibilities (such as with college, marriage, employment, or death of parents).⁸

Table 1

Adolescent gambling: From entertainment to mental illness

Case continued: ‘Up big-time’

Matt says he loves to gamble and believes he is more gifted at poker than his peers. He also recognizes his behavior could be addictive and admits lying to his parents about his gambling. He plays Internet poker 3 to 4 hours per day and claims he wins more often than he loses. “I’m up big time,” he boasts.

Matt denies going to casinos or using bookies. He says he is managing school and home responsibilities without difficulty. He denies mood or anxiety symptoms but admits using methylphenidate while gambling. He obtains the stimulant from friends at school and usually snorts it to get “a bigger rush.”

Matt is clearly at risk for problem gambling. He was exposed to gambling early, is becoming preoccupied with it, lies about how much he gambles, and combines gambling with substance abuse. progress more rapidly and can become problem gamblers within 12 to 14 months.²

Neurobiologic differences between adolescent and adult pathological gamblers are not well-defined. Adults show evidence of dysregulated dopamine, norepinephrine, and serotonin neuro-transmission.⁹ Neuroimaging in adult pathological gamblers shows perturbations in reward processing centers and frontal lobe structures that control inhibition. These factors have been examined little in adolescents.

Identifying problem gambling in teens

Diagnostic “red flags” for problem gambling in adolescents include declining school performance, sleep disturbance, generalized anxiety or irritability, or possibly lack of response to general psychiatric treatment. Three tools can be useful for screening adolescents:

The Lie-Bet Questionnaire¹⁰ is a 2-question screen for problem gambling:

• Have you ever lied to anyone important about how often you gamble?
  
• Have you ever had to increase your bet to get the same excitement from gambling?
  

The South-Oaks Gambling Screen¹¹ is the standard pathological gambling screen for adults. Like the (SOGS-RA) is based and validated using DSM-III criteria (see Related resources). A score of 2 to 5 indicates at-risk gambling behaviors, and ≥6 indicate need for treatment.

The Gamblers Anonymous questionnaire¹² comprises 20 questions that identify negative social, physical, and emotional consequences of gambling behaviors (Box). Seven or more positive responses indicate probable pathological gambling. This screen has shown reliability in adolescents.

Use one or more of these quick screens with every adolescent presenting for treatment—especially in substance abuse treatment settings. When results are positive, probe for gambling behaviors and consequences. Rely on DSM-IV-TR criteria and clinical presentation to differentiate social gambling from pathological gambling.

Box

Behaviors and comorbidities

Negative consequences. Pathological gambling often consumes 10 to 20 hours per week of the adolescent’s time,¹³ hurting school performance and delaying developmental milestones. Teen gamblers may abandon extracurricular school activities, and their few friends often gamble, too. They are at risk for delinquency, criminal activity, and antisocial behaviors (such as selling drugs, engaging in prostitution)¹⁴ unprotected sexual activity, drug use, reckless driving, and carrying weapons.^15,16

Psychiatric comorbidity is the rule and often what brings adolescent gamblers to treatment. Substance abuse, major depression, attention-deficit/hyperactivity disorder, and personality disorders are most common (Table 2) Adolescent substance abuse at least triples the risk of pathological gambling.¹⁸

Adolescent pathological gamblers have increased rates of suicidal ideation and suicide attempts.¹⁷ They are at risk for other impulsive behaviors as well,¹⁹ although they are unlikely to volunteer this information. The Minnesota Impulsive Disorders Interview help identify comorbid pathological gambling, trichotillomania, kleptomania, pyromania, intermittent explosive disorder, compulsive buying, and compulsive sexual behaviors.¹⁹ Screen for these comorbidities during the first sessions or if a patient does not respond to treatment of gambling behavior.

Table 2

Risk factors for pathological adolescent gambling

Treating adolescent gamblers

Matt’s answers to the gambling screening questionnaires (one “yes” to the Lie-Bet Questionnaire, a SOGS-RA score of 4, and a GA-20 Questions score of 5) indicate problem gambling but not pathological gambling. You recommend that he attend Gamblers Anonymous, but he refuses. He also rejects individual therapy or taking medications.

Matt acknowledges misusing methylphenidate, however, and agrees to consider an outpatient substance abuse program. He also agrees to six sessions with a gambling treatment specialist to learn about problem gambling’s signs and symptoms, how to cope with betting loses, and how to reduce his preoccupation with gambling.

No guidelines exist for treating adolescent pathological gamblers, and specialized teen treatment programs are rare. Most services are provided in mental health or substance abuse settings, using adult treatments modified for adolescents.

Cognitive behavioral therapy (CBT) can be successful for highly motivated gamblers, although adolescents might not want to change their pathological behaviors. In case reports, four adolescents achieved remission after 6 months of CBT.^20,21 CBT appears to have long-term benefits for adults, but this has not been evaluated in teens. Even so, individual CBT may be ideal for adolescent gamblers because side effects are minimal.

Gamblers Anonymous (GA) in adults has shown a low retention rate and a 1-year abstinence rate of 22 Its effectiveness for adolescents lacks empiric support, but the 12-step program’s availability, structure, and fellowship may be useful.

Medications. Consider medication as first-line treatment for adolescents with psychiatric comorbidity. Try psychosocial treatment first for those without psychiatric comorbidity; consider medication as second-line therapy if response to psychosocial treatment is inadequate.

No medications are FDA-approved for pathological gambling, and no studies have examined medication use for adolescent gamblers. Controlled trials with adults suggest some medications may reduce urges and cravings or decrease gambling behaviors. These include:

• selective serotonin reuptake inhibitors
  
• opioid antagonists such as naltrexone or its analogue nalmefene
  
• or mood stabilizers such as lithium, divalproex sodium, or possibly topiramate.²³
  

Working with families. Many parents are aware of the destructive potential of substance abuse but not of gambling. They may feel shame that they did not recognize their teen’s gambling problem or “control” their child’s behavior. The adolescent may feel remorse for having bet with the parents’ money.

Even when the family recognizes the teen’s problem, denial or enabling can perpetuate the behavior. For teens such as Matt who learned to gamble at a home, advise the parents to abstain from gambling as well. Consider screening the parents for pathological gambling, given its high rate of heritability.

Address guilt and shame by acknowledging that pathological gambling is a psychiatric disease caused by biological, psychological, and social factors—not dysfunctional family relations. Emphasize that treatment works. Because gambling is easily hidden, educate families about relapse signs, such as preoccupation with money, personality changes, or failing to fulfill family responsibilities.²⁵

Related resources

• Wiebe JM, Cox BJ, Mehmel BG. The South Oaks Gambling Screen Revised for Adolescents (SOGS-RA): further psychometric findings from a community sample. J Gambl Stud 2000;16(2-3):275-88.
  
• Gamblers Anonymous. www.gamblersanonymous.org.
  
• National Council on Problem Gambling. www.ncpgambling.org.
  
• International Centre for Youth Gambling Problems and High-Risk Behaviors. www.youthgambling.com.
  

• Nalmefene • Revex
  
• Naltrexone • ReVia
  
• Lithium • Lithobid, others
  
• Divalproex sodium • Depakote, others
  
• Topiramate • Topamax
  

Dr. Fong receives grant/research support from Ortho McNeil Pharmaceutical and Somaxon Pharmaceuticals and is a speaker for Forest Pharmaceuticals.

Matt, age 17, grew up in a household of gamblers. He learned to play poker from his father at age 8 and bet on sports with his friends in the 5th grade. For 2 years he has been playing poker three to four nights per week and watching a lot of televised poker. His parents worry he might be “addicted” to gambling and bring him for evaluation.

Easy access to gambling through casinos, lotteries, and Internet games has affected many social groups, particularly adolescents.¹ Teens such as Matt are more likely than adults to become pathological gamblers,² and they often have psychiatric disorders and antisocial behavior patterns that interfere with normal development. This article:

• suggests screening tools to identify problem teen gambling
  
• discusses how to use psychotherapy, medications, and other options to help gambling-obsessed adolescents change their high-risk behavior.
  

Why adolescents gamble

Gambling activates the same neural reward pathways affected by cocaine and amphetamines.³ Even so, many adolescents view gambling as less harmful than drugs⁴ and consider it a rite of passage:

• 90% report having gambled for money
  
• 75% have gambled at home for money
  
• 85% of parents do not object to gambling behaviors, teens say.^4,5
  

Adolescent gambling behavior. For approximately 85% of adolescents, gambling becomes no more than a social activity. For others, it can become problematic or even pathological (Table 1).^5,7 Approximately 4 to 8% of adolescents meet criteria for pathological gambling, compared with 1% of adults.

Adolescents’ higher rate might reflect pathological gambling’s natural course—peaking during adolescence, then tapering during adulthood. Some adolescents may adapt their gambling behavior over time. Problem gambling tends to be more transient and episodic than pathological gambling, remitting when adolescents take on new responsibilities (such as with college, marriage, employment, or death of parents).⁸

Table 1

Adolescent gambling: From entertainment to mental illness

Case continued: ‘Up big-time’

Matt says he loves to gamble and believes he is more gifted at poker than his peers. He also recognizes his behavior could be addictive and admits lying to his parents about his gambling. He plays Internet poker 3 to 4 hours per day and claims he wins more often than he loses. “I’m up big time,” he boasts.

Matt denies going to casinos or using bookies. He says he is managing school and home responsibilities without difficulty. He denies mood or anxiety symptoms but admits using methylphenidate while gambling. He obtains the stimulant from friends at school and usually snorts it to get “a bigger rush.”

Matt is clearly at risk for problem gambling. He was exposed to gambling early, is becoming preoccupied with it, lies about how much he gambles, and combines gambling with substance abuse. progress more rapidly and can become problem gamblers within 12 to 14 months.²

Neurobiologic differences between adolescent and adult pathological gamblers are not well-defined. Adults show evidence of dysregulated dopamine, norepinephrine, and serotonin neuro-transmission.⁹ Neuroimaging in adult pathological gamblers shows perturbations in reward processing centers and frontal lobe structures that control inhibition. These factors have been examined little in adolescents.

Identifying problem gambling in teens

Diagnostic “red flags” for problem gambling in adolescents include declining school performance, sleep disturbance, generalized anxiety or irritability, or possibly lack of response to general psychiatric treatment. Three tools can be useful for screening adolescents:

The Lie-Bet Questionnaire¹⁰ is a 2-question screen for problem gambling:

• Have you ever lied to anyone important about how often you gamble?
  
• Have you ever had to increase your bet to get the same excitement from gambling?
  

The South-Oaks Gambling Screen¹¹ is the standard pathological gambling screen for adults. Like the (SOGS-RA) is based and validated using DSM-III criteria (see Related resources). A score of 2 to 5 indicates at-risk gambling behaviors, and ≥6 indicate need for treatment.

The Gamblers Anonymous questionnaire¹² comprises 20 questions that identify negative social, physical, and emotional consequences of gambling behaviors (Box). Seven or more positive responses indicate probable pathological gambling. This screen has shown reliability in adolescents.

Use one or more of these quick screens with every adolescent presenting for treatment—especially in substance abuse treatment settings. When results are positive, probe for gambling behaviors and consequences. Rely on DSM-IV-TR criteria and clinical presentation to differentiate social gambling from pathological gambling.

Box

Behaviors and comorbidities

Negative consequences. Pathological gambling often consumes 10 to 20 hours per week of the adolescent’s time,¹³ hurting school performance and delaying developmental milestones. Teen gamblers may abandon extracurricular school activities, and their few friends often gamble, too. They are at risk for delinquency, criminal activity, and antisocial behaviors (such as selling drugs, engaging in prostitution)¹⁴ unprotected sexual activity, drug use, reckless driving, and carrying weapons.^15,16

Psychiatric comorbidity is the rule and often what brings adolescent gamblers to treatment. Substance abuse, major depression, attention-deficit/hyperactivity disorder, and personality disorders are most common (Table 2) Adolescent substance abuse at least triples the risk of pathological gambling.¹⁸

Adolescent pathological gamblers have increased rates of suicidal ideation and suicide attempts.¹⁷ They are at risk for other impulsive behaviors as well,¹⁹ although they are unlikely to volunteer this information. The Minnesota Impulsive Disorders Interview help identify comorbid pathological gambling, trichotillomania, kleptomania, pyromania, intermittent explosive disorder, compulsive buying, and compulsive sexual behaviors.¹⁹ Screen for these comorbidities during the first sessions or if a patient does not respond to treatment of gambling behavior.

Table 2

Risk factors for pathological adolescent gambling

Treating adolescent gamblers

Matt’s answers to the gambling screening questionnaires (one “yes” to the Lie-Bet Questionnaire, a SOGS-RA score of 4, and a GA-20 Questions score of 5) indicate problem gambling but not pathological gambling. You recommend that he attend Gamblers Anonymous, but he refuses. He also rejects individual therapy or taking medications.

Matt acknowledges misusing methylphenidate, however, and agrees to consider an outpatient substance abuse program. He also agrees to six sessions with a gambling treatment specialist to learn about problem gambling’s signs and symptoms, how to cope with betting loses, and how to reduce his preoccupation with gambling.

No guidelines exist for treating adolescent pathological gamblers, and specialized teen treatment programs are rare. Most services are provided in mental health or substance abuse settings, using adult treatments modified for adolescents.

Cognitive behavioral therapy (CBT) can be successful for highly motivated gamblers, although adolescents might not want to change their pathological behaviors. In case reports, four adolescents achieved remission after 6 months of CBT.^20,21 CBT appears to have long-term benefits for adults, but this has not been evaluated in teens. Even so, individual CBT may be ideal for adolescent gamblers because side effects are minimal.

Gamblers Anonymous (GA) in adults has shown a low retention rate and a 1-year abstinence rate of 22 Its effectiveness for adolescents lacks empiric support, but the 12-step program’s availability, structure, and fellowship may be useful.

Medications. Consider medication as first-line treatment for adolescents with psychiatric comorbidity. Try psychosocial treatment first for those without psychiatric comorbidity; consider medication as second-line therapy if response to psychosocial treatment is inadequate.

No medications are FDA-approved for pathological gambling, and no studies have examined medication use for adolescent gamblers. Controlled trials with adults suggest some medications may reduce urges and cravings or decrease gambling behaviors. These include:

• selective serotonin reuptake inhibitors
  
• opioid antagonists such as naltrexone or its analogue nalmefene
  
• or mood stabilizers such as lithium, divalproex sodium, or possibly topiramate.²³
  

Working with families. Many parents are aware of the destructive potential of substance abuse but not of gambling. They may feel shame that they did not recognize their teen’s gambling problem or “control” their child’s behavior. The adolescent may feel remorse for having bet with the parents’ money.

Even when the family recognizes the teen’s problem, denial or enabling can perpetuate the behavior. For teens such as Matt who learned to gamble at a home, advise the parents to abstain from gambling as well. Consider screening the parents for pathological gambling, given its high rate of heritability.

Address guilt and shame by acknowledging that pathological gambling is a psychiatric disease caused by biological, psychological, and social factors—not dysfunctional family relations. Emphasize that treatment works. Because gambling is easily hidden, educate families about relapse signs, such as preoccupation with money, personality changes, or failing to fulfill family responsibilities.²⁵

Related resources

• Wiebe JM, Cox BJ, Mehmel BG. The South Oaks Gambling Screen Revised for Adolescents (SOGS-RA): further psychometric findings from a community sample. J Gambl Stud 2000;16(2-3):275-88.
  
• Gamblers Anonymous. www.gamblersanonymous.org.
  
• National Council on Problem Gambling. www.ncpgambling.org.
  
• International Centre for Youth Gambling Problems and High-Risk Behaviors. www.youthgambling.com.
  

• Nalmefene • Revex
  
• Naltrexone • ReVia
  
• Lithium • Lithobid, others
  
• Divalproex sodium • Depakote, others
  
• Topiramate • Topamax
  

Dr. Fong receives grant/research support from Ortho McNeil Pharmaceutical and Somaxon Pharmaceuticals and is a speaker for Forest Pharmaceuticals.

Can corticosteroids “unlock” hidden potential for mania, or are steroid-induced mood symptoms a temporary reaction? And when these mood symptoms occur, what is the best way to treat them?

Psychiatric symptoms develop in 5% to 18% of patients treated with corticosteroids. These effects—most often mania or depression—emerge within days to weeks of starting steroids. To help you head off manic and mixed mood symptoms, this paper examines how to:

• treat steroid-induced mania or mixed bipolar symptoms
• reduce the risk of a mood episode in patients who require sustained corticosteroid therapy.

‘Steroid psychosis’

Jane Pauley, NBC’s Today Show broadcaster, described in her autobiography how hypomania developed within weeks after she started corticosteroids for idiopathic urticaria edema: “I was so energized that I didn’t just walk down the hall, I felt like I was motoring down the hall. I was suddenly the equal of my high-energy friends who move fast and talk fast and loud. I told everyone that I could understand why men felt like they could run the world, because I felt like that. This was a new me, and I liked her!”¹

Pauley’s hypomania led to a manic episode and eventually to depression. She was started on antidepressants, which triggered another manic episode. Pauley—who had no history of bipolar disorder—spent 3 weeks in a New York psychiatric hospital.¹

Diagnostic symptoms. Corticosteroids’ psychiatric effects—cognitive, mood, anxiety, and psychotic symptoms—were first described as “steroid psychosis.” Psychosis can occur, but mood symptoms are more common:

• Among 122 patients, 40% experienced depression, followed by mania (28%), psychosis (14%), delirium (10%), and mixed mood episodes (8%).²
• Among 130 patients, mania was most prevalent (35%), followed by depression (28%), mixed mood episodes (12%), delirium (13%), and psychosis (11%).³
• Corticosteroids caused 54% of organic mania cases on a hospital psychiatric consult service.⁴
• In a prospective study of 50 patients treated with corticosteroids, 13 developed hypomania and 5 developed depression.⁵

Steroid-induced symptoms emerge from 3 to 4 days to a median of 11 days after a patient starts corticosteroid therapy. After steroids are discontinued, depressive symptoms persist approximately 4 weeks, mania 3 weeks, and delirium a few days. Approximately one-half of patients with steroid psychosis improve in 4 days and one-half within 2 weeks.^2,6

Continue to: Who is at risk?

Who is at risk?

Corticosteroids include the steroids produced in the adrenal gland (such as corticosterone) and their synthetic—and often more potent—analogues (such as prednisone).⁷ Because of their glucocorticoid, immunosuppressant, mineralocorticoid, and anti-inflammatory properties, steroids are used as replacement therapy and to treat a wide variety of illnesses (Table 1).

Table 1

Medical conditions for which corticosteroids are commonly used

Age and gender. Patient age appears unrelated to development of psychiatric symptoms after corticosteroid use.² One study suggested women are twice as likely as men to develop psychiatric symptoms (77 versus 38 cases in 115 patients),³ but many illnesses that require corticosteroid treatment occur more frequently in women. Other researchers found a slight female predominance (58% versus 42% of cases) when they excluded patients with systemic lupus erythematosus and rheumatoid arthritis, which are more common in women than in men.²

Dosage. Higher corticosteroid dosages increase the risk of psychiatric symptoms. In patients taking prednisone, the Boston Collaborative Drug Surveillance Project⁸ found the incidence of psychiatric side effects to be:

• 1.3% in patients taking
• 4.6% in those taking 41 to 80 mg
• 18.4% in those taking >80 mg.

Psychiatric history. Past psychiatric illness does not seem to be a risk factor for psychiatric side effects of corticosteroids,⁹ although patients with a history of posttraumatic stress disorder are more likely to suffer depression while taking corticosteroids.¹⁰

Corticosteroid exposure. Patients who did not experience psychiatric side effects with corticosteroids in the past appear not to be protected if corticosteroids are used again. One report examined 17 cases of steroid-induced psychiatric illness in patients with previous exposure to corticosteroid therapy. Six patients had previous psychiatric side effects while taking corticosteroids, and 11 did not.²

Bipolar trigger?

Do corticosteroids’ acute psychiatric side effects have long-term sequelae? Longitudinal evidence is scarce, but a few reports suggest corticosteroids could play a role in the onset of primary bipolar I disorder:

• A 28-year-old woman with no known mood symptoms before a short course of prednisone experienced six episodes of mania and depression when not taking corticosteroids during the subsequent 18 months.¹¹
• Among 16 patients with first-onset mood symptoms after corticosteroid use, a retrospective chart review found 7 had recurrent manic and depressive symptoms unrelated to additional corticosteroid use.¹²

Continue to: ... case reports are inconclusive...

Although intriguing, these case reports are inconclusive. Because bipolar type I incidence in the general population is 1.5%,¹³ many persons with bipolar disorder undergo corticosteroid treatment. Nevertheless, these results—especially from the retrospective review¹²—suggest that corticosteroid use may contribute to the onset of bipolar I illness.

Symptomatic treatment

Corticosteroid-induced side effects are usually managed by tapering off the steroids and treating the psychiatric symptoms.^2,3 Simply tapering off the steroids—without additional treatments—led to recovery in 33 of 36 patients.² Stopping corticosteroids is not always possible or desirable, however, especially in many medically complicated cases seen by psychiatric consult services.

In a recent case, I was asked to see a man, age 69, on the oncology service who was receiving corticosteroids every 2 weeks as part of his chemotherapy. The patient was admitted to the hospital for acute mental status changes 2 days after his last corticosteroid dose. He had pressured speech, grandiosity, and had not slept in 2 days. We started risperidone, 1 mg bid, and most of his manic symptoms resolved within 2 days. His chemotherapy was continued without corticosteroids. If this had not been not possible, I would have recommended continuing risperidone prophylactically.

No double-blind, placebo-controlled studies have examined prevention or treatment of steroid-induced mania or other psychiatric symptoms. Uncontrolled trials and case reports suggest benefit from some symptomatic and preventive treatments (Table 2).

Table 2

Mood stabilizers with evidence of benefit in treating corticosteroid-induced mania

Treating manic and mixed mood symptoms. Twelve outpatients with manic or mixed symptoms from corticosteroid use received olanzapine in a 5-week, open-label trial. Flexible dosing started at 2.5 mg/d and was increased as needed (maximum 20 mg/d). One patient dropped out for lack of efficacy. For the others, manic and mixed symptoms improved significantly, as indicated by scores on the Young Mania Rating Scale, Hamilton Rating Scale for Depression, and Brief Psychotic Rating Scale.¹⁴ Patient weight, blood glucose, and involuntary movements did not change significantly.

Evidence from case reports indicates that lithium,¹⁵ carbamazepine,^12,16 haloperidol,^12,16 or quetiapine¹⁷ also can successfully treat steroid-induced manic symptoms.

Continue to: Treating other psychiatric symptoms

Treating other psychiatric symptoms. Case reports support electroconvulsive therapy,^2,15 fluoxetine,¹⁸ amitriptyline,¹² lamotrigine,¹⁹ or lithium^20,21 for steroid-induced depression, and haloperidol²² or risperidone²³ for steroid-induced psychosis.

In four cases,⁶ tricyclic antidepressants appeared to worsen corticosteroids’ psychiatric side effects. These case patients might have had steroid-induced delirium instead of mood disorders or psychosis, however, and the tricyclics’ anticholinergic effects could have worsened the delirium.⁹

Preventing steroid-induced symptoms

Although clear guidelines on when to start preventive treatments do not exist, potential candidates for pretreatment with lithium or other agents include patients who:

• have developed psychiatric symptoms multiple times after repeated corticosteroid use
• are at high risk if psychiatric side effects occur.

Lithium. Prophylactic lithium was given to 27 patients with multiple sclerosis and taking corticosteroids for acute exacerbations. None developed psychiatric symptoms.²⁴ At the same clinic, 6 of 44 patients with multiple sclerosis or retrobulbar neuritis developed psychiatric side effects after using corticosteroids without lithium.

Be cautious when using prophylactic lithium because some conditions treated with corticosteroids—such as systemic lupus erythematosus—can impair renal function.²⁰ Corticosteroids also can affect sodium balance and increase the risk of lithium intoxication.²⁵

Check renal function before and during lithium titration, and initiate corticosteroid therapy when lithium is at effective blood levels (0.8 to 1.2 mEq/L). Monitor lithium levels and renal function frequently during steroid treatment.

Other mood stabilizers. Two case reports describe patients who repeatedly developed manic symptoms after multiple corticosteroid doses. Carbamazepine, 600 mg qd,¹⁶ and gabapentin, 300 mg tid,²⁶ prevented manic symptoms after additional corticosteroid pulses.

Related resources

• Brown ES, Chandler PA. Mood and cognitive changes during systemic corticosteroid therapy. Prim Care Companion J Clin Psychiatry 2001;3(1):17-21. www.psychiatrist.com/pcc/abstracts/pcc030103.htm.
• Merrill W. Case 35-1998: use of lithium to prevent corticosteroid-induced mania. N Engl J Med 1999;340:1123.

Drug brand names

• Amitriptyline • Elavil
• Carbamazepine • Tegretol
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Haloperidol • Haldol
• Lamotrigine • Lamictal
• Lithium • Eskalith, others
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal

Can corticosteroids “unlock” hidden potential for mania, or are steroid-induced mood symptoms a temporary reaction? And when these mood symptoms occur, what is the best way to treat them?

Psychiatric symptoms develop in 5% to 18% of patients treated with corticosteroids. These effects—most often mania or depression—emerge within days to weeks of starting steroids. To help you head off manic and mixed mood symptoms, this paper examines how to:

• treat steroid-induced mania or mixed bipolar symptoms
• reduce the risk of a mood episode in patients who require sustained corticosteroid therapy.

‘Steroid psychosis’

Jane Pauley, NBC’s Today Show broadcaster, described in her autobiography how hypomania developed within weeks after she started corticosteroids for idiopathic urticaria edema: “I was so energized that I didn’t just walk down the hall, I felt like I was motoring down the hall. I was suddenly the equal of my high-energy friends who move fast and talk fast and loud. I told everyone that I could understand why men felt like they could run the world, because I felt like that. This was a new me, and I liked her!”¹

Pauley’s hypomania led to a manic episode and eventually to depression. She was started on antidepressants, which triggered another manic episode. Pauley—who had no history of bipolar disorder—spent 3 weeks in a New York psychiatric hospital.¹

Diagnostic symptoms. Corticosteroids’ psychiatric effects—cognitive, mood, anxiety, and psychotic symptoms—were first described as “steroid psychosis.” Psychosis can occur, but mood symptoms are more common:

• Among 122 patients, 40% experienced depression, followed by mania (28%), psychosis (14%), delirium (10%), and mixed mood episodes (8%).²
• Among 130 patients, mania was most prevalent (35%), followed by depression (28%), mixed mood episodes (12%), delirium (13%), and psychosis (11%).³
• Corticosteroids caused 54% of organic mania cases on a hospital psychiatric consult service.⁴
• In a prospective study of 50 patients treated with corticosteroids, 13 developed hypomania and 5 developed depression.⁵

Steroid-induced symptoms emerge from 3 to 4 days to a median of 11 days after a patient starts corticosteroid therapy. After steroids are discontinued, depressive symptoms persist approximately 4 weeks, mania 3 weeks, and delirium a few days. Approximately one-half of patients with steroid psychosis improve in 4 days and one-half within 2 weeks.^2,6

Continue to: Who is at risk?

Who is at risk?

Corticosteroids include the steroids produced in the adrenal gland (such as corticosterone) and their synthetic—and often more potent—analogues (such as prednisone).⁷ Because of their glucocorticoid, immunosuppressant, mineralocorticoid, and anti-inflammatory properties, steroids are used as replacement therapy and to treat a wide variety of illnesses (Table 1).

Table 1

Medical conditions for which corticosteroids are commonly used

Age and gender. Patient age appears unrelated to development of psychiatric symptoms after corticosteroid use.² One study suggested women are twice as likely as men to develop psychiatric symptoms (77 versus 38 cases in 115 patients),³ but many illnesses that require corticosteroid treatment occur more frequently in women. Other researchers found a slight female predominance (58% versus 42% of cases) when they excluded patients with systemic lupus erythematosus and rheumatoid arthritis, which are more common in women than in men.²

Dosage. Higher corticosteroid dosages increase the risk of psychiatric symptoms. In patients taking prednisone, the Boston Collaborative Drug Surveillance Project⁸ found the incidence of psychiatric side effects to be:

• 1.3% in patients taking
• 4.6% in those taking 41 to 80 mg
• 18.4% in those taking >80 mg.

Psychiatric history. Past psychiatric illness does not seem to be a risk factor for psychiatric side effects of corticosteroids,⁹ although patients with a history of posttraumatic stress disorder are more likely to suffer depression while taking corticosteroids.¹⁰

Corticosteroid exposure. Patients who did not experience psychiatric side effects with corticosteroids in the past appear not to be protected if corticosteroids are used again. One report examined 17 cases of steroid-induced psychiatric illness in patients with previous exposure to corticosteroid therapy. Six patients had previous psychiatric side effects while taking corticosteroids, and 11 did not.²

Bipolar trigger?

Do corticosteroids’ acute psychiatric side effects have long-term sequelae? Longitudinal evidence is scarce, but a few reports suggest corticosteroids could play a role in the onset of primary bipolar I disorder:

• A 28-year-old woman with no known mood symptoms before a short course of prednisone experienced six episodes of mania and depression when not taking corticosteroids during the subsequent 18 months.¹¹
• Among 16 patients with first-onset mood symptoms after corticosteroid use, a retrospective chart review found 7 had recurrent manic and depressive symptoms unrelated to additional corticosteroid use.¹²

Continue to: ... case reports are inconclusive...

Although intriguing, these case reports are inconclusive. Because bipolar type I incidence in the general population is 1.5%,¹³ many persons with bipolar disorder undergo corticosteroid treatment. Nevertheless, these results—especially from the retrospective review¹²—suggest that corticosteroid use may contribute to the onset of bipolar I illness.

Symptomatic treatment

Corticosteroid-induced side effects are usually managed by tapering off the steroids and treating the psychiatric symptoms.^2,3 Simply tapering off the steroids—without additional treatments—led to recovery in 33 of 36 patients.² Stopping corticosteroids is not always possible or desirable, however, especially in many medically complicated cases seen by psychiatric consult services.

In a recent case, I was asked to see a man, age 69, on the oncology service who was receiving corticosteroids every 2 weeks as part of his chemotherapy. The patient was admitted to the hospital for acute mental status changes 2 days after his last corticosteroid dose. He had pressured speech, grandiosity, and had not slept in 2 days. We started risperidone, 1 mg bid, and most of his manic symptoms resolved within 2 days. His chemotherapy was continued without corticosteroids. If this had not been not possible, I would have recommended continuing risperidone prophylactically.

No double-blind, placebo-controlled studies have examined prevention or treatment of steroid-induced mania or other psychiatric symptoms. Uncontrolled trials and case reports suggest benefit from some symptomatic and preventive treatments (Table 2).

Table 2

Mood stabilizers with evidence of benefit in treating corticosteroid-induced mania

Treating manic and mixed mood symptoms. Twelve outpatients with manic or mixed symptoms from corticosteroid use received olanzapine in a 5-week, open-label trial. Flexible dosing started at 2.5 mg/d and was increased as needed (maximum 20 mg/d). One patient dropped out for lack of efficacy. For the others, manic and mixed symptoms improved significantly, as indicated by scores on the Young Mania Rating Scale, Hamilton Rating Scale for Depression, and Brief Psychotic Rating Scale.¹⁴ Patient weight, blood glucose, and involuntary movements did not change significantly.

Evidence from case reports indicates that lithium,¹⁵ carbamazepine,^12,16 haloperidol,^12,16 or quetiapine¹⁷ also can successfully treat steroid-induced manic symptoms.

Continue to: Treating other psychiatric symptoms

Treating other psychiatric symptoms. Case reports support electroconvulsive therapy,^2,15 fluoxetine,¹⁸ amitriptyline,¹² lamotrigine,¹⁹ or lithium^20,21 for steroid-induced depression, and haloperidol²² or risperidone²³ for steroid-induced psychosis.

In four cases,⁶ tricyclic antidepressants appeared to worsen corticosteroids’ psychiatric side effects. These case patients might have had steroid-induced delirium instead of mood disorders or psychosis, however, and the tricyclics’ anticholinergic effects could have worsened the delirium.⁹

Preventing steroid-induced symptoms

Although clear guidelines on when to start preventive treatments do not exist, potential candidates for pretreatment with lithium or other agents include patients who:

• have developed psychiatric symptoms multiple times after repeated corticosteroid use
• are at high risk if psychiatric side effects occur.

Lithium. Prophylactic lithium was given to 27 patients with multiple sclerosis and taking corticosteroids for acute exacerbations. None developed psychiatric symptoms.²⁴ At the same clinic, 6 of 44 patients with multiple sclerosis or retrobulbar neuritis developed psychiatric side effects after using corticosteroids without lithium.

Be cautious when using prophylactic lithium because some conditions treated with corticosteroids—such as systemic lupus erythematosus—can impair renal function.²⁰ Corticosteroids also can affect sodium balance and increase the risk of lithium intoxication.²⁵

Check renal function before and during lithium titration, and initiate corticosteroid therapy when lithium is at effective blood levels (0.8 to 1.2 mEq/L). Monitor lithium levels and renal function frequently during steroid treatment.

Other mood stabilizers. Two case reports describe patients who repeatedly developed manic symptoms after multiple corticosteroid doses. Carbamazepine, 600 mg qd,¹⁶ and gabapentin, 300 mg tid,²⁶ prevented manic symptoms after additional corticosteroid pulses.

Related resources

• Brown ES, Chandler PA. Mood and cognitive changes during systemic corticosteroid therapy. Prim Care Companion J Clin Psychiatry 2001;3(1):17-21. www.psychiatrist.com/pcc/abstracts/pcc030103.htm.
• Merrill W. Case 35-1998: use of lithium to prevent corticosteroid-induced mania. N Engl J Med 1999;340:1123.

Drug brand names

• Amitriptyline • Elavil
• Carbamazepine • Tegretol
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Haloperidol • Haldol
• Lamotrigine • Lamictal
• Lithium • Eskalith, others
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal

Can corticosteroids “unlock” hidden potential for mania, or are steroid-induced mood symptoms a temporary reaction? And when these mood symptoms occur, what is the best way to treat them?

Psychiatric symptoms develop in 5% to 18% of patients treated with corticosteroids. These effects—most often mania or depression—emerge within days to weeks of starting steroids. To help you head off manic and mixed mood symptoms, this paper examines how to:

• treat steroid-induced mania or mixed bipolar symptoms
• reduce the risk of a mood episode in patients who require sustained corticosteroid therapy.

‘Steroid psychosis’

Jane Pauley, NBC’s Today Show broadcaster, described in her autobiography how hypomania developed within weeks after she started corticosteroids for idiopathic urticaria edema: “I was so energized that I didn’t just walk down the hall, I felt like I was motoring down the hall. I was suddenly the equal of my high-energy friends who move fast and talk fast and loud. I told everyone that I could understand why men felt like they could run the world, because I felt like that. This was a new me, and I liked her!”¹

Pauley’s hypomania led to a manic episode and eventually to depression. She was started on antidepressants, which triggered another manic episode. Pauley—who had no history of bipolar disorder—spent 3 weeks in a New York psychiatric hospital.¹

Diagnostic symptoms. Corticosteroids’ psychiatric effects—cognitive, mood, anxiety, and psychotic symptoms—were first described as “steroid psychosis.” Psychosis can occur, but mood symptoms are more common:

• Among 122 patients, 40% experienced depression, followed by mania (28%), psychosis (14%), delirium (10%), and mixed mood episodes (8%).²
• Among 130 patients, mania was most prevalent (35%), followed by depression (28%), mixed mood episodes (12%), delirium (13%), and psychosis (11%).³
• Corticosteroids caused 54% of organic mania cases on a hospital psychiatric consult service.⁴
• In a prospective study of 50 patients treated with corticosteroids, 13 developed hypomania and 5 developed depression.⁵

Steroid-induced symptoms emerge from 3 to 4 days to a median of 11 days after a patient starts corticosteroid therapy. After steroids are discontinued, depressive symptoms persist approximately 4 weeks, mania 3 weeks, and delirium a few days. Approximately one-half of patients with steroid psychosis improve in 4 days and one-half within 2 weeks.^2,6

Continue to: Who is at risk?

Who is at risk?

Corticosteroids include the steroids produced in the adrenal gland (such as corticosterone) and their synthetic—and often more potent—analogues (such as prednisone).⁷ Because of their glucocorticoid, immunosuppressant, mineralocorticoid, and anti-inflammatory properties, steroids are used as replacement therapy and to treat a wide variety of illnesses (Table 1).

Table 1

Medical conditions for which corticosteroids are commonly used

Age and gender. Patient age appears unrelated to development of psychiatric symptoms after corticosteroid use.² One study suggested women are twice as likely as men to develop psychiatric symptoms (77 versus 38 cases in 115 patients),³ but many illnesses that require corticosteroid treatment occur more frequently in women. Other researchers found a slight female predominance (58% versus 42% of cases) when they excluded patients with systemic lupus erythematosus and rheumatoid arthritis, which are more common in women than in men.²

Dosage. Higher corticosteroid dosages increase the risk of psychiatric symptoms. In patients taking prednisone, the Boston Collaborative Drug Surveillance Project⁸ found the incidence of psychiatric side effects to be:

• 1.3% in patients taking
• 4.6% in those taking 41 to 80 mg
• 18.4% in those taking >80 mg.

Psychiatric history. Past psychiatric illness does not seem to be a risk factor for psychiatric side effects of corticosteroids,⁹ although patients with a history of posttraumatic stress disorder are more likely to suffer depression while taking corticosteroids.¹⁰

Corticosteroid exposure. Patients who did not experience psychiatric side effects with corticosteroids in the past appear not to be protected if corticosteroids are used again. One report examined 17 cases of steroid-induced psychiatric illness in patients with previous exposure to corticosteroid therapy. Six patients had previous psychiatric side effects while taking corticosteroids, and 11 did not.²

Bipolar trigger?

Do corticosteroids’ acute psychiatric side effects have long-term sequelae? Longitudinal evidence is scarce, but a few reports suggest corticosteroids could play a role in the onset of primary bipolar I disorder:

• A 28-year-old woman with no known mood symptoms before a short course of prednisone experienced six episodes of mania and depression when not taking corticosteroids during the subsequent 18 months.¹¹
• Among 16 patients with first-onset mood symptoms after corticosteroid use, a retrospective chart review found 7 had recurrent manic and depressive symptoms unrelated to additional corticosteroid use.¹²

Continue to: ... case reports are inconclusive...

Although intriguing, these case reports are inconclusive. Because bipolar type I incidence in the general population is 1.5%,¹³ many persons with bipolar disorder undergo corticosteroid treatment. Nevertheless, these results—especially from the retrospective review¹²—suggest that corticosteroid use may contribute to the onset of bipolar I illness.

Symptomatic treatment

Corticosteroid-induced side effects are usually managed by tapering off the steroids and treating the psychiatric symptoms.^2,3 Simply tapering off the steroids—without additional treatments—led to recovery in 33 of 36 patients.² Stopping corticosteroids is not always possible or desirable, however, especially in many medically complicated cases seen by psychiatric consult services.

In a recent case, I was asked to see a man, age 69, on the oncology service who was receiving corticosteroids every 2 weeks as part of his chemotherapy. The patient was admitted to the hospital for acute mental status changes 2 days after his last corticosteroid dose. He had pressured speech, grandiosity, and had not slept in 2 days. We started risperidone, 1 mg bid, and most of his manic symptoms resolved within 2 days. His chemotherapy was continued without corticosteroids. If this had not been not possible, I would have recommended continuing risperidone prophylactically.

No double-blind, placebo-controlled studies have examined prevention or treatment of steroid-induced mania or other psychiatric symptoms. Uncontrolled trials and case reports suggest benefit from some symptomatic and preventive treatments (Table 2).

Table 2

Mood stabilizers with evidence of benefit in treating corticosteroid-induced mania

Treating manic and mixed mood symptoms. Twelve outpatients with manic or mixed symptoms from corticosteroid use received olanzapine in a 5-week, open-label trial. Flexible dosing started at 2.5 mg/d and was increased as needed (maximum 20 mg/d). One patient dropped out for lack of efficacy. For the others, manic and mixed symptoms improved significantly, as indicated by scores on the Young Mania Rating Scale, Hamilton Rating Scale for Depression, and Brief Psychotic Rating Scale.¹⁴ Patient weight, blood glucose, and involuntary movements did not change significantly.

Evidence from case reports indicates that lithium,¹⁵ carbamazepine,^12,16 haloperidol,^12,16 or quetiapine¹⁷ also can successfully treat steroid-induced manic symptoms.

Continue to: Treating other psychiatric symptoms

Treating other psychiatric symptoms. Case reports support electroconvulsive therapy,^2,15 fluoxetine,¹⁸ amitriptyline,¹² lamotrigine,¹⁹ or lithium^20,21 for steroid-induced depression, and haloperidol²² or risperidone²³ for steroid-induced psychosis.

In four cases,⁶ tricyclic antidepressants appeared to worsen corticosteroids’ psychiatric side effects. These case patients might have had steroid-induced delirium instead of mood disorders or psychosis, however, and the tricyclics’ anticholinergic effects could have worsened the delirium.⁹

Preventing steroid-induced symptoms

Although clear guidelines on when to start preventive treatments do not exist, potential candidates for pretreatment with lithium or other agents include patients who:

• have developed psychiatric symptoms multiple times after repeated corticosteroid use
• are at high risk if psychiatric side effects occur.

Lithium. Prophylactic lithium was given to 27 patients with multiple sclerosis and taking corticosteroids for acute exacerbations. None developed psychiatric symptoms.²⁴ At the same clinic, 6 of 44 patients with multiple sclerosis or retrobulbar neuritis developed psychiatric side effects after using corticosteroids without lithium.

Be cautious when using prophylactic lithium because some conditions treated with corticosteroids—such as systemic lupus erythematosus—can impair renal function.²⁰ Corticosteroids also can affect sodium balance and increase the risk of lithium intoxication.²⁵

Check renal function before and during lithium titration, and initiate corticosteroid therapy when lithium is at effective blood levels (0.8 to 1.2 mEq/L). Monitor lithium levels and renal function frequently during steroid treatment.

Other mood stabilizers. Two case reports describe patients who repeatedly developed manic symptoms after multiple corticosteroid doses. Carbamazepine, 600 mg qd,¹⁶ and gabapentin, 300 mg tid,²⁶ prevented manic symptoms after additional corticosteroid pulses.

Related resources

• Brown ES, Chandler PA. Mood and cognitive changes during systemic corticosteroid therapy. Prim Care Companion J Clin Psychiatry 2001;3(1):17-21. www.psychiatrist.com/pcc/abstracts/pcc030103.htm.
• Merrill W. Case 35-1998: use of lithium to prevent corticosteroid-induced mania. N Engl J Med 1999;340:1123.

Drug brand names

• Amitriptyline • Elavil
• Carbamazepine • Tegretol
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Haloperidol • Haldol
• Lamotrigine • Lamictal
• Lithium • Eskalith, others
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal

Mr. P, age 39, attacks a convenience store clerk with a knife and is charged with aggravated assault. The judge grants the defense attorney’s request that Mr. P’s competency to stand trial be evaluated. Mr. P’s medical records show paranoid schizophrenia diagnosed at age 22, multiple psychiatric hospitalizations, and chronic medication noncompliance.

You may be called on to determine capacity—such as whether a patient can provide informed consent for a medical procedure. Judges or juries make decisions about competency—often based on a psychiatrist’s opinion about a person’s capacity.

This article describes how to prepare a report stating your opinion about whether a defendant such as Mr. P is competent to stand trial.

What is competency?

The defendant’s attorney usually raises the question of whether a defendant is competent to stand trial, but a judge or prosecuting attorney also may suggest an evaluation. Defense attorneys question their clients’ competence to stand trial in approximately 8% to 15% of felony cases, and up to 50,000 defendants are referred for competency evaluations each year.^1-4 Competency may be questioned when the defendant:

• is obviously mentally ill or has a history of mental illness
  
• appears to be making irrational decisions
  
• has difficulty interacting with the court or defense counsel.⁵
  

“Competency” and “sanity” are often used together in discussions of criminal prosecution of mentally-ill defendants. This article describes evaluating competence to stand trial; we will discuss how to evaluate sanity in a future issue of Current Psychiatry.

Competency is dynamic; the law defines many types, each with a legal definition and requisite capacity. A person may be competent in one area but incompetent in another. He may be incompetent to make a decision about psychiatric hospitalization, for example, yet retain competency to give or withhold informed consent for treatment.

Evaluating competency also is dynamic, depending on the patient’s present state:

• She might be incapable of giving informed consent for surgery while delirious but capable to make a competent decision about treatment after sensorium clears.
  
• A psychotic defendant may be incompetent to stand trial initially but may be restored to competency after treatment.
  

The ‘dusky standard’

Courts have long recognized that the mentally ill may be incapable of defending themselves against criminal charges (Box).⁶ The U.S. Supreme Court in 1960 established in Dusky v. United States that the legal standard for competence to stand trial is “whether [the person] has sufficient present ability to consult with his lawyer with a reasonable degree of rational understanding—and whether he has a rational as well as factual understanding of the proceedings against him.” This standard has been adopted in principle by all states and the federal jurisdiction.⁷

The “Dusky standard” indicates that a defendant is incompetent to stand trial if, because of a mental illness or other condition, he is unable to:

• understand the nature and objectives of the court proceedings
  
• or assist in his defense (Table 1).
  

Judges ultimately determine defendants’ competence to stand trial, but psychiatrists’ opinions are adopted in 90% of cases.^8,9

Box

The ‘Dusky standard’ of competence

How to assess competency

If a judge asks you to evaluate a defendant’s competency, you need to know the standard governing competence to stand trial in the judge’s jurisdiction. All courts in the United States use the Dusky standard, but the wording varies.

Review the defendant’s case records, including court papers (with a list of charges), medical records, and psychiatric records. Then interview the defendant to thoroughly evaluate his mental status and collect a detailed psychiatric history.

If the defendant has a mental disorder, it must impair his ability to understand the proceedings or participate in his defense to result in incompetency. Sources who know the defendant (spouse, family, or friends) may provide useful collateral information.

Assessment tools. Some argue that tools designed to help determine competency can assess understanding of facts related to the trial but not ability to reason. The MacArthur Competency Assessment Tool—Criminal Adjudication is thought to assess both decisional competency and factual understanding.¹⁰ Another new tool, the Evaluation of Competency to Stand Trial-revised (ECST-R), is beginning to be used more frequently to evaluate possible malingering and case-specific information.

These tools can be purchased online through vendors such as www3.parinc.com. Though useful, these tools serve as adjuncts to the clinical interview.

In your report to the court, include relevant information from the mental status evaluation, the diagnosis, and—most important—a clear, concise opinion of the defendant’s current competence to stand trial.

Case: does Mr. P meet the standard?

During your interview, Mr. P endorses chronic auditory hallucinations telling him to harm others. He is alert and oriented to location, date, and current events. He can adequately describe courtroom proceedings and each individual’s role, noting that he had been to court before on a drug possession charge, for which he received probation.

When you ask Mr. P about his attorney, he leans in and whispers, “My attorney and my mother have a secret plan to send me to prison for the rest of my life.” He contends his attorney is telling him to claim he is “crazy” to make him “look bad” in court.

In a separate interview, you question the corrections officer who accompanied Mr. P to the evaluation. He says Mr. P refuses to see his mother and his attorney when they come to visit him in jail and takes his medications only sporadically.

Understanding court proceedings. A defendant such as Mr. P must be able to understand the charges against him, that he is on trial for those charges, and the severity of the charges. He must be able to understand the pleas he can offer (guilty, not guilty, not guilty by reason of insanity, or no contest).

The defendant also must be aware of the roles of trial participants, including defense attorney, prosecutor, witnesses, judge, and jury. He must appreciate the trial’s adversarial nature, that his attorney is acting in his best interests and defending him, and that the prosecutor is trying to convict him.

Ability to assist in defense. A defendant must be able to have logical, coherent discussions with his attorney and be free of paranoid beliefs about the attorney. He must recognize his role as the defendant and maintain no delusions that he is somehow immune to prosecution.

In cooperation with his attorney, he must be able to evaluate the evidence against him and predict the trial’s probable outcome. He must help his attorney formulate a plan for his defense and make reasonable decisions about that plan. If relevant, he must be willing to consider using a mental illness defense at trial; therefore, he must possess a reasonable amount of insight into his mental illness. He also must:

• be able to participate with his attorney in plea bargaining and grasp the meaning and outcome of this process
  
• have sufficient memory and concentration to understand the trial proceedings.
  

Finally, a defendant must be motivated to assist in his defense and free of self-defeating behavior. For example, severely depressed patients seeking to punish themselves by causing an unfavorable trial outcome could be considered incompetent.

Mentally ill and incompetent

Mr. P has a clear history of mental illness, the first criterion for a defendant to be considered incompetent to stand trial. He has psychotic symptoms, but these alone are insufficient to consider him incompetent. Also, having competently stood trial in the past does not necessarily mean he is competent now.

Based on the beginning of the interview, Mr. P appears to understand the nature and objectives of court proceedings. His delusions about his attorney, however, clearly would impair his ability to assist in his defense.

Reporting to the court. A forensic evaluator’s report to the court might say: “It is my opinion, with reasonable medical certainty, that although Mr. P understands the nature and objectives of the court proceedings against him, he has a significant thought disorder that currently impairs his ability to assist in his own defense. In particular, Mr. P maintains delusions (a fixed, false belief held despite evidence to the contrary) that his attorney is plotting against him.”

Treatment to restore competency. Approximately 30% of evaluated defendants are adjudicated incompetent for a variety of reasons (Table 2).¹¹ They often are committed to a forensic mental hospital for treatment to restore competency, which occurs in up to 90% of cases.¹²

Mr. P will likely be committed to restore competency, which may be achieved by treating his schizophrenia.

Defendants with disorders such as dementia or mental retardation may be considered unable to be restored to competency, and their charges are dismissed or held in abeyance. They may then be involuntarily hospitalized if committed through civil proceedings.

Table 2

7 common reasons defendants are found incompetent to stand trial

• Grisso T. Evaluating competencies: forensic assessments and instruments, 2nd ed. New York: Springer; 2002.
  
• Melton GB, Petrila J, Poythress G, Slobogin C. Psychological evaluations for the courts: a handbook for mental health professionals and lawyers, 2nd ed. New York: Guilford Press; 1997.
  
• American Academy of Psychiatry and the Law. www.aapl.org.
  

Mr. P, age 39, attacks a convenience store clerk with a knife and is charged with aggravated assault. The judge grants the defense attorney’s request that Mr. P’s competency to stand trial be evaluated. Mr. P’s medical records show paranoid schizophrenia diagnosed at age 22, multiple psychiatric hospitalizations, and chronic medication noncompliance.

You may be called on to determine capacity—such as whether a patient can provide informed consent for a medical procedure. Judges or juries make decisions about competency—often based on a psychiatrist’s opinion about a person’s capacity.

This article describes how to prepare a report stating your opinion about whether a defendant such as Mr. P is competent to stand trial.

What is competency?

The defendant’s attorney usually raises the question of whether a defendant is competent to stand trial, but a judge or prosecuting attorney also may suggest an evaluation. Defense attorneys question their clients’ competence to stand trial in approximately 8% to 15% of felony cases, and up to 50,000 defendants are referred for competency evaluations each year.^1-4 Competency may be questioned when the defendant:

• is obviously mentally ill or has a history of mental illness
  
• appears to be making irrational decisions
  
• has difficulty interacting with the court or defense counsel.⁵
  

“Competency” and “sanity” are often used together in discussions of criminal prosecution of mentally-ill defendants. This article describes evaluating competence to stand trial; we will discuss how to evaluate sanity in a future issue of Current Psychiatry.

Competency is dynamic; the law defines many types, each with a legal definition and requisite capacity. A person may be competent in one area but incompetent in another. He may be incompetent to make a decision about psychiatric hospitalization, for example, yet retain competency to give or withhold informed consent for treatment.

Evaluating competency also is dynamic, depending on the patient’s present state:

• She might be incapable of giving informed consent for surgery while delirious but capable to make a competent decision about treatment after sensorium clears.
  
• A psychotic defendant may be incompetent to stand trial initially but may be restored to competency after treatment.
  

The ‘dusky standard’

Courts have long recognized that the mentally ill may be incapable of defending themselves against criminal charges (Box).⁶ The U.S. Supreme Court in 1960 established in Dusky v. United States that the legal standard for competence to stand trial is “whether [the person] has sufficient present ability to consult with his lawyer with a reasonable degree of rational understanding—and whether he has a rational as well as factual understanding of the proceedings against him.” This standard has been adopted in principle by all states and the federal jurisdiction.⁷

The “Dusky standard” indicates that a defendant is incompetent to stand trial if, because of a mental illness or other condition, he is unable to:

• understand the nature and objectives of the court proceedings
  
• or assist in his defense (Table 1).
  

Judges ultimately determine defendants’ competence to stand trial, but psychiatrists’ opinions are adopted in 90% of cases.^8,9

Box

The ‘Dusky standard’ of competence

How to assess competency

If a judge asks you to evaluate a defendant’s competency, you need to know the standard governing competence to stand trial in the judge’s jurisdiction. All courts in the United States use the Dusky standard, but the wording varies.

Review the defendant’s case records, including court papers (with a list of charges), medical records, and psychiatric records. Then interview the defendant to thoroughly evaluate his mental status and collect a detailed psychiatric history.

If the defendant has a mental disorder, it must impair his ability to understand the proceedings or participate in his defense to result in incompetency. Sources who know the defendant (spouse, family, or friends) may provide useful collateral information.

Assessment tools. Some argue that tools designed to help determine competency can assess understanding of facts related to the trial but not ability to reason. The MacArthur Competency Assessment Tool—Criminal Adjudication is thought to assess both decisional competency and factual understanding.¹⁰ Another new tool, the Evaluation of Competency to Stand Trial-revised (ECST-R), is beginning to be used more frequently to evaluate possible malingering and case-specific information.

These tools can be purchased online through vendors such as www3.parinc.com. Though useful, these tools serve as adjuncts to the clinical interview.

In your report to the court, include relevant information from the mental status evaluation, the diagnosis, and—most important—a clear, concise opinion of the defendant’s current competence to stand trial.

Case: does Mr. P meet the standard?

During your interview, Mr. P endorses chronic auditory hallucinations telling him to harm others. He is alert and oriented to location, date, and current events. He can adequately describe courtroom proceedings and each individual’s role, noting that he had been to court before on a drug possession charge, for which he received probation.

When you ask Mr. P about his attorney, he leans in and whispers, “My attorney and my mother have a secret plan to send me to prison for the rest of my life.” He contends his attorney is telling him to claim he is “crazy” to make him “look bad” in court.

In a separate interview, you question the corrections officer who accompanied Mr. P to the evaluation. He says Mr. P refuses to see his mother and his attorney when they come to visit him in jail and takes his medications only sporadically.

Understanding court proceedings. A defendant such as Mr. P must be able to understand the charges against him, that he is on trial for those charges, and the severity of the charges. He must be able to understand the pleas he can offer (guilty, not guilty, not guilty by reason of insanity, or no contest).

The defendant also must be aware of the roles of trial participants, including defense attorney, prosecutor, witnesses, judge, and jury. He must appreciate the trial’s adversarial nature, that his attorney is acting in his best interests and defending him, and that the prosecutor is trying to convict him.

Ability to assist in defense. A defendant must be able to have logical, coherent discussions with his attorney and be free of paranoid beliefs about the attorney. He must recognize his role as the defendant and maintain no delusions that he is somehow immune to prosecution.

In cooperation with his attorney, he must be able to evaluate the evidence against him and predict the trial’s probable outcome. He must help his attorney formulate a plan for his defense and make reasonable decisions about that plan. If relevant, he must be willing to consider using a mental illness defense at trial; therefore, he must possess a reasonable amount of insight into his mental illness. He also must:

• be able to participate with his attorney in plea bargaining and grasp the meaning and outcome of this process
  
• have sufficient memory and concentration to understand the trial proceedings.
  

Finally, a defendant must be motivated to assist in his defense and free of self-defeating behavior. For example, severely depressed patients seeking to punish themselves by causing an unfavorable trial outcome could be considered incompetent.

Mentally ill and incompetent

Mr. P has a clear history of mental illness, the first criterion for a defendant to be considered incompetent to stand trial. He has psychotic symptoms, but these alone are insufficient to consider him incompetent. Also, having competently stood trial in the past does not necessarily mean he is competent now.

Based on the beginning of the interview, Mr. P appears to understand the nature and objectives of court proceedings. His delusions about his attorney, however, clearly would impair his ability to assist in his defense.

Reporting to the court. A forensic evaluator’s report to the court might say: “It is my opinion, with reasonable medical certainty, that although Mr. P understands the nature and objectives of the court proceedings against him, he has a significant thought disorder that currently impairs his ability to assist in his own defense. In particular, Mr. P maintains delusions (a fixed, false belief held despite evidence to the contrary) that his attorney is plotting against him.”

Treatment to restore competency. Approximately 30% of evaluated defendants are adjudicated incompetent for a variety of reasons (Table 2).¹¹ They often are committed to a forensic mental hospital for treatment to restore competency, which occurs in up to 90% of cases.¹²

Mr. P will likely be committed to restore competency, which may be achieved by treating his schizophrenia.

Defendants with disorders such as dementia or mental retardation may be considered unable to be restored to competency, and their charges are dismissed or held in abeyance. They may then be involuntarily hospitalized if committed through civil proceedings.

Table 2

7 common reasons defendants are found incompetent to stand trial

• Grisso T. Evaluating competencies: forensic assessments and instruments, 2nd ed. New York: Springer; 2002.
  
• Melton GB, Petrila J, Poythress G, Slobogin C. Psychological evaluations for the courts: a handbook for mental health professionals and lawyers, 2nd ed. New York: Guilford Press; 1997.
  
• American Academy of Psychiatry and the Law. www.aapl.org.
  

Mr. P, age 39, attacks a convenience store clerk with a knife and is charged with aggravated assault. The judge grants the defense attorney’s request that Mr. P’s competency to stand trial be evaluated. Mr. P’s medical records show paranoid schizophrenia diagnosed at age 22, multiple psychiatric hospitalizations, and chronic medication noncompliance.

You may be called on to determine capacity—such as whether a patient can provide informed consent for a medical procedure. Judges or juries make decisions about competency—often based on a psychiatrist’s opinion about a person’s capacity.

This article describes how to prepare a report stating your opinion about whether a defendant such as Mr. P is competent to stand trial.

What is competency?

The defendant’s attorney usually raises the question of whether a defendant is competent to stand trial, but a judge or prosecuting attorney also may suggest an evaluation. Defense attorneys question their clients’ competence to stand trial in approximately 8% to 15% of felony cases, and up to 50,000 defendants are referred for competency evaluations each year.^1-4 Competency may be questioned when the defendant:

• is obviously mentally ill or has a history of mental illness
  
• appears to be making irrational decisions
  
• has difficulty interacting with the court or defense counsel.⁵
  

“Competency” and “sanity” are often used together in discussions of criminal prosecution of mentally-ill defendants. This article describes evaluating competence to stand trial; we will discuss how to evaluate sanity in a future issue of Current Psychiatry.

Competency is dynamic; the law defines many types, each with a legal definition and requisite capacity. A person may be competent in one area but incompetent in another. He may be incompetent to make a decision about psychiatric hospitalization, for example, yet retain competency to give or withhold informed consent for treatment.

Evaluating competency also is dynamic, depending on the patient’s present state:

• She might be incapable of giving informed consent for surgery while delirious but capable to make a competent decision about treatment after sensorium clears.
  
• A psychotic defendant may be incompetent to stand trial initially but may be restored to competency after treatment.
  

The ‘dusky standard’

Courts have long recognized that the mentally ill may be incapable of defending themselves against criminal charges (Box).⁶ The U.S. Supreme Court in 1960 established in Dusky v. United States that the legal standard for competence to stand trial is “whether [the person] has sufficient present ability to consult with his lawyer with a reasonable degree of rational understanding—and whether he has a rational as well as factual understanding of the proceedings against him.” This standard has been adopted in principle by all states and the federal jurisdiction.⁷

The “Dusky standard” indicates that a defendant is incompetent to stand trial if, because of a mental illness or other condition, he is unable to:

• understand the nature and objectives of the court proceedings
  
• or assist in his defense (Table 1).
  

Judges ultimately determine defendants’ competence to stand trial, but psychiatrists’ opinions are adopted in 90% of cases.^8,9

Box

The ‘Dusky standard’ of competence

How to assess competency

If a judge asks you to evaluate a defendant’s competency, you need to know the standard governing competence to stand trial in the judge’s jurisdiction. All courts in the United States use the Dusky standard, but the wording varies.

Review the defendant’s case records, including court papers (with a list of charges), medical records, and psychiatric records. Then interview the defendant to thoroughly evaluate his mental status and collect a detailed psychiatric history.

If the defendant has a mental disorder, it must impair his ability to understand the proceedings or participate in his defense to result in incompetency. Sources who know the defendant (spouse, family, or friends) may provide useful collateral information.

Assessment tools. Some argue that tools designed to help determine competency can assess understanding of facts related to the trial but not ability to reason. The MacArthur Competency Assessment Tool—Criminal Adjudication is thought to assess both decisional competency and factual understanding.¹⁰ Another new tool, the Evaluation of Competency to Stand Trial-revised (ECST-R), is beginning to be used more frequently to evaluate possible malingering and case-specific information.

These tools can be purchased online through vendors such as www3.parinc.com. Though useful, these tools serve as adjuncts to the clinical interview.

In your report to the court, include relevant information from the mental status evaluation, the diagnosis, and—most important—a clear, concise opinion of the defendant’s current competence to stand trial.

Case: does Mr. P meet the standard?

During your interview, Mr. P endorses chronic auditory hallucinations telling him to harm others. He is alert and oriented to location, date, and current events. He can adequately describe courtroom proceedings and each individual’s role, noting that he had been to court before on a drug possession charge, for which he received probation.

When you ask Mr. P about his attorney, he leans in and whispers, “My attorney and my mother have a secret plan to send me to prison for the rest of my life.” He contends his attorney is telling him to claim he is “crazy” to make him “look bad” in court.

In a separate interview, you question the corrections officer who accompanied Mr. P to the evaluation. He says Mr. P refuses to see his mother and his attorney when they come to visit him in jail and takes his medications only sporadically.

Understanding court proceedings. A defendant such as Mr. P must be able to understand the charges against him, that he is on trial for those charges, and the severity of the charges. He must be able to understand the pleas he can offer (guilty, not guilty, not guilty by reason of insanity, or no contest).

The defendant also must be aware of the roles of trial participants, including defense attorney, prosecutor, witnesses, judge, and jury. He must appreciate the trial’s adversarial nature, that his attorney is acting in his best interests and defending him, and that the prosecutor is trying to convict him.

Ability to assist in defense. A defendant must be able to have logical, coherent discussions with his attorney and be free of paranoid beliefs about the attorney. He must recognize his role as the defendant and maintain no delusions that he is somehow immune to prosecution.

In cooperation with his attorney, he must be able to evaluate the evidence against him and predict the trial’s probable outcome. He must help his attorney formulate a plan for his defense and make reasonable decisions about that plan. If relevant, he must be willing to consider using a mental illness defense at trial; therefore, he must possess a reasonable amount of insight into his mental illness. He also must:

• be able to participate with his attorney in plea bargaining and grasp the meaning and outcome of this process
  
• have sufficient memory and concentration to understand the trial proceedings.
  

Finally, a defendant must be motivated to assist in his defense and free of self-defeating behavior. For example, severely depressed patients seeking to punish themselves by causing an unfavorable trial outcome could be considered incompetent.

Mentally ill and incompetent

Mr. P has a clear history of mental illness, the first criterion for a defendant to be considered incompetent to stand trial. He has psychotic symptoms, but these alone are insufficient to consider him incompetent. Also, having competently stood trial in the past does not necessarily mean he is competent now.

Based on the beginning of the interview, Mr. P appears to understand the nature and objectives of court proceedings. His delusions about his attorney, however, clearly would impair his ability to assist in his defense.

Reporting to the court. A forensic evaluator’s report to the court might say: “It is my opinion, with reasonable medical certainty, that although Mr. P understands the nature and objectives of the court proceedings against him, he has a significant thought disorder that currently impairs his ability to assist in his own defense. In particular, Mr. P maintains delusions (a fixed, false belief held despite evidence to the contrary) that his attorney is plotting against him.”

Treatment to restore competency. Approximately 30% of evaluated defendants are adjudicated incompetent for a variety of reasons (Table 2).¹¹ They often are committed to a forensic mental hospital for treatment to restore competency, which occurs in up to 90% of cases.¹²

Mr. P will likely be committed to restore competency, which may be achieved by treating his schizophrenia.

Defendants with disorders such as dementia or mental retardation may be considered unable to be restored to competency, and their charges are dismissed or held in abeyance. They may then be involuntarily hospitalized if committed through civil proceedings.

Table 2

7 common reasons defendants are found incompetent to stand trial

• Grisso T. Evaluating competencies: forensic assessments and instruments, 2nd ed. New York: Springer; 2002.
  
• Melton GB, Petrila J, Poythress G, Slobogin C. Psychological evaluations for the courts: a handbook for mental health professionals and lawyers, 2nd ed. New York: Guilford Press; 1997.
  
• American Academy of Psychiatry and the Law. www.aapl.org.