Robert Hierholzer, MD

History: bipolar for 30 years

Mr. B, age 66, was diagnosed 30 years ago with type I bipolar disorder and has type 2 diabetes, hypertension, alcohol abuse disorder, and cardiac disease. After repeated suicide attempts and hospitalizations in the past, he has been stable for 20 years on lithium, 600 mg bid, and nortriptyline, 50 mg at bedtime. He has had intermittent mania with little evidence of depression.

Two years ago, Mr. B called a local clinic to report that an intruder had him “holed up.” His speech was pressured and garbled, and his thoughts were tangential, irrational, and markedly paranoid. A clinic psychiatrist called Mr. B’s son, who said his father “built a bomb shelter” because “trolls and little people” were out to kill him. A family member called police, and Mr. B was brought to the ER and admitted for treatment.

A hospital psychiatrist stopped lithium in light of Mr. B’s history of cardiac problems and because the psychiatrist considered the medication ineffective, even though serum lithium was only 0.03 mEq/L. The psychiatrist then started:

• divalproex at 500 mg bid, titrated over 1 week to 500 mg each morning and 1,000 mg at bed-time to reach serum valproate of 80 mEq/L
  
• quetiapine at 200 mg at bedtime, titrated over 1 week to 400 mg at bedtime.
  

Mr. B was still manic, paranoid, and hallucinating 1 week later, yet was discharged after he convinced the county hearing officer that he had recovered.

Two weeks later, Mr. B is brought to another psychiatric hospital, where a psychiatrist restarts unknown dosages of lithium, risperidone, and nortriptyline. From there, he is transferred to our in-patient unit. At presentation, he claims he has been drinking and that members of a drug cartel have recruited him. He says he has been skipping medications because he is “unclear which drugs to take.”

We stop lithium and restart divalproex, 500 mg each morning and 1,500 mg at bedtime, to try to treat his mania without causing cognitive problems.

We stop risperidone because of his hypotension and nortriptyline because it was not working, and restart quetiapine, 600 mg at bedtime, for his paranoia. He remains paranoid 1 week later but his mania improves, so we discharge him on the above regimen. We urge him to take his medications and follow up with his outpatient psychiatrist 1 week later.

Divorced, Mr. B lives alone with no family nearby. His son comes in from out of town to help him resettle after discharge, then leaves the next day.

Several months later, Mr. B’s paranoia returns. He is not taking his medications because “the doctors took away my lithium and these new drugs don’t work.” He tells staff he is a martial arts expert and has purchased 7 cars in recent weeks. We restart lithium at 600 mg bid; serum lithium reaches 1.1 mEq/L, but his mania persists. After 5 days, we add aripiprazole, 15 mg/d.

Nearly 2 weeks after admission, a county hearing officer recommends discharging Mr. B despite his severe mania and paranoia. We release him on the above regimen, arrange appointments with his outpatient psychiatrist and primary care physician, and urge medication adherence. We schedule a blood test 3 days after discharge to check serum lithium, but Mr. B does not keep the appointment.

The authors’ observations

Suspect delirium after rapid onset of mania or paranoia in any patient. Also consider dementia and cognitive deficits in older adults, although Mr. B’s symptoms resembled those of previous manic episodes. Although Mr. B’s psychosis was more severe than before, his case underscores the importance of a thorough patient history.

Late-life bipolar disorder. Little is known about diagnosing and treating bipolar disorder (BPD) in older patients. Gaps in empiric knowledge can confound diagnosis, treatment, and outcome. Also, patients age ≥65 with BPD often have severe medical illness and are difficult to treat.¹

Keys to detecting late-life BPD include:

• recognizing clinical features of BPD unique to older persons
  
• differentiating the disorder from late-life schizophrenia (Table).^1,2
  

Older patients’ symptoms usually match DSM-IV-TR criteria for BPD; their response to treatment mirrors that of younger adults.³

Secondary cause. When an older patient’s mania has atypical features or doesn’t respond to conventional treatment, look for a nonpsychiatric process such as a general medical condition or substance abuse (see possible medical causes with this article at www.currentpsychiatry.com). Order laboratory and other tests as clinical suspicion warrants.

Cognitive deficits secondary to BPD can occur at any age and be persistent or progressive,⁴ although Depp et al¹ found more-severe impairment in older patients. Cognitive impairment can endure after successful BPD treatment, although acute treatment might improve cognition in older patients.⁵

 

Lithium can cause dull affect, cognitive slowing, and depersonalization. Titrating to the lowest effective dosage might minimize these effects.

Dementia. Cognitive deficits that accompany mania in older adults could suggest dementia, which usually develops over years and is preceded by cognitive changes without manic-type symptoms. By contrast, bipolar mania emerges more abruptly and is accompanied by affective symptoms. Agitation and psychosis—both symptoms of late-stage dementia—can be early signs of geriatric BPD.²

Delirium. Restlessness, irritability, aggression, and changes in affect can accompany delirium, especially the hyperactive or hyperalert types. Symptoms of anxiety, depression, fear, and loose or tangential thinking also are common.

Mania shares some of these features but typically presents with an abnormally and persistently elevated or irritable mood lasting ≥1 week, usually without prominent cognitive impairment.⁶ Mania can also include:

• grandiosity
  
• decreased need for sleep
  
• flight of ideas
  
• distractibility
  
• pressured or increased rate of speech
  
• psychomotor agitation
  
• potentially harmful activities
  
• increased goal-directed activities.⁶
  

By contrast, delirium is marked by waxing and waning consciousness and changes in cognition, such as disorientation and confusion.⁶

Frontal lobe lesions. Decreased prefrontal executive control could underlie mania’s cognitive and emotional symptoms. Decreased right rostral and orbital prefrontal cortex activation has been associated with impaired planning, judgment, and insight, as well as inappropriate conduct.⁷

Table

Clinical features of geriatric bipolar disorder (BPD)

Psychotic features (delusions, hallucinations)
Mean prevalence of 64% (range 20% to 85%) is similar to that of mixed-age groups; paranoia might be more prevalent
Family history
High rates of psychiatric disorders (“affective disorder” in most studies) reported in 10 studies
Compared with younger adults with BPD, older patients:
show longer latency from first depression to mania onset might be more likely to relapse into depression after mania might have less-intense mania are hospitalized longer, possibly because of greater medical comorbidity have less comorbid substance abuse and more-prominent age-associated morphologic abnormalities on neuroimaging2
Compared with late-life schizophrenia, late-life BPD patients show:
more depressive symptoms fewer positive and negative symptoms greater community living and relationship skills, with similar activities of daily living
Source: References 1,2

Continued treatment: depression emerges

Several months later, Mr. B presents with severe depression and continued medication nonadherence. He complains of hypersomnia, poor appetite, anhedonia, amotivation, and a leaden-like paresis in his hands and feet.

We readmit Mr. B to the psychiatric unit. He avoids contact with others, has lost 18 lbs over 6 weeks, and suffers hypotension caused by poor hydration before admission. Three weeks later, he complains that ants are crawling around his room and into his mouth.

Noncontrast brain CT shows no abnormalities. Laboratory tests performed at admission show a subtherapeutic lithium level (0.03 mEq/L), unremarkable thyroid panel, and normal B12 and folate, so we begin to rule out a medical cause for his psychiatric symptoms.

The authors’ observations

Check for these and other possible causes of depressive symptoms in older patients with a history of BPD. Mr. B’s depression likely resulted from multiple causes, including medical disease, functional impairment, loss of social and family contacts, and substance abuse—all late-life predictors of depression. BPD also predisposed him to depression.

Bipolar depression. Despite its profound morbidity and mortality, bipolar depression remains a mystery, especially in the elderly. Mr. B’s depression emerged after he was free of depressive symptoms for more than 20 years.

Some researchers believe that compared with other depressions, bipolar depression has a more acute onset, marked psychomotor retardation, and lessened response to antidepressants.^6,8 Kraepelin associated bipolar depression with lethargy, mental slowing, and hypersomnia, whereas agitation and insomnia signal unipolar depression.⁹

To differentiate bipolar from unipolar or secondary depression in older patients, watch for:

• suicide risk, which is heightened during BPD’s depressive phase⁹
  
• secondary manias, for which underlying causes must be determined and treated if possible.
  

Medication-induced depression. Medications can cause depressive symptoms (see Related resources), but identifying an offending agent without an obvious chronologic relationship can be difficult, especially in older patients who are taking numerous medications.⁹

Depression caused by medication might be limited to somatic complaints such as fatigue or tiredness,⁹ and often lacks features seen with mood disorders such as depressed mood, anhedonia, guilt, and diminished interest in activities. Mr. B’s anhedonia and amotivation suggest his depression was not medication-induced.¹⁰

Disease-induced depression. Medical comorbidities are common among older persons with mood disorders and can complicate treatment response and outcome. Physical disease can cause or worsen depression:¹¹

• Endocrine and immunologic diseases might cause depression or mania.
  
• Cardiovascular and cerebrovascular diseases; CNS disorders such as dementia, Parkinson’s disease, and multiple sclerosis; cancer; and connective tissue disease increase risk for comorbid depression.
  

Mr. B’s hypertension, diabetes, or coronary artery disease could have contributed to his depression or complicated the course.

 

¹¹

Vascular depression. Comorbid depressive symptoms and vascular disease—or “vascular depression”—can cause ischemic brain lesions, cognitive impairment, increased apathy and retardation, and impaired fluency and naming.¹²

What defines vascular depression has been debated. Watch for clinical or laboratory evidence of vascular disease, depression, and neuropsychological impairment.¹³

Treatment: searching for evidence

Two days after admission, Mr. B is transferred to the ICU after suffering severe hypoglycemia and showing signs of medically induced delirium. Elevated creatinine (1.7 mg/dL) indicates acute renal failure, which could be related to his elevated serum lithium (1.7 mEq/L). Acting on the internist’s advice, the consulting psychiatrist stops lithium and restarts valproate, 500 mg bid.

Mr. B becomes medically stable after 3 days, mostly through acute IV hydration and by withholding oral diabetes medications, which normalizes his blood sugar. He is transferred back to the psychiatry unit. We try lithium again at 300 mg bid, but creatinine and serum lithium quickly rise.

Mr. B remains hospitalized for 3 months with severe, treatment-resistant depression. Trials of nearly every second-generation antipsychotic (SGA) cause symptomatic orthostatic hypotension, leading to several falls. He does not respond to divalproex, up to 2,000 mg/d; citalopram, 60 mg/d; mirtazapine, 30 mg at bedtime; venlafaxine, 100 mg tid; or bupropion, 100 mg tid.

We suggest electroconvulsive therapy (ECT) but Mr. B declines, saying this treatment caused his mother to decompensate. We try lamotrigine, 25 mg/d, and titrate it over 6 weeks to 200 mg bid. After we add haloperidol, 5 mg at bedtime, and bupropion, 300 mg/d, Mr. B becomes mentally stable.

The authors’ observations

Numerous clinical challenges—such as managing complicated/refractory BPD, medical comorbidity, and medication adherence (Box)^14,15—complicate treatment of late-life BPD.¹⁶ Regular communication with providers and integrating health care services can minimize complication risk.¹⁶

Pharmacotherapy, a core element of BPD treatment, is challenging in older patients because of their:

• heightened threat of complications and sensitivity to side effects because of age-related pharmacokinetic changes
  
• increased risk of drug-drug interactions
  
• increased potential for age-related psychosocial problems (increased social isolation, financial difficulties, demoralization, increased stress, inability to work).
  

Box

Initial clinical and laboratory evaluations can rule out aggravating or causative factors and identify conditions that can cause drug intolerability.⁵ Check orthostatic vital signs and perform a detailed medical and psychosocial history, neurologic examination, ECG, and cognitive evaluation.

Consider side effects, medical and neurologic comorbidities, and treatment history before prescribing a mood stabilizer, antipsychotic, or antidepressant to an older patient. Avoid unwarranted discontinuation of a previously effective agent, such as when drug concentrations are elevated or inadequate—as happened with Mr. B.⁵ Also investigate the patient’s side-effect history before stopping a medication.⁵

Medications. Mr. B’s inability to tolerate lithium posed a treatment challenge. Adjusting lithium dosages to compensate for age-related pharmacokinetic, pharmacodynamic, and renal clearance changes can prevent toxicity.⁵ Avoid stopping lithium abruptly, as this can trigger recurrence of manic or depressive episodes.¹⁷

Lamotrigine, indicated for BPD maintenance therapy, appears to prevent depressive/mood relapse. Compared with other anticonvulsants, lamotrigine might cause fewer negative effects on cognition and less induction of hepatic enzymes. It is well tolerated by older patients but has not been studied adequately in this age group.¹⁶

Antipsychotics are widely used in BPD,¹⁶ especially when psychosis is present with mania or depression or the patient is agitated. Most studies of antipsychotics in BPD have followed younger adults, however, and most studies in older patients have followed those with dementia or schizophrenia.

Use of first-generation antipsychotics such as haloperidol is especially challenging in the elderly because these drugs increase risk of cardiovascular effects, extrapyramidal symptoms, and tardive dyskinesia and can cause depression in BPD.¹⁶ By comparison, SGAs carry a lower risk of involuntary motion¹⁸ but can increase risk of obesity, diabetes, and dyslipidemia. However:

• The need to manage psychosis usually overrides concerns about metabolic sequelae.
  
• Older patients might be less susceptible to metabolic effects,¹⁶ though this has not been confirmed.
  

 

SGAs can be used safely in patients with a history of diabetes. Start at lower-than-normal dosages and titrate slowly. Perform baseline and regular checks—including weight, blood glucose, lipid levels, and blood pressure—following American Psychiatric Association and American Diabetes Association consensus guidelines.¹⁹ Also check glycosylated hemoglobin every 3 to 6 months in patients with diabetes, and follow up with other providers to ensure proper diabetes management.

As with most aspects of late-life BPD, scant evidence guides SGA use. Avoid low-potency neuroleptics such as chlorpromazine, which can cause severe sedation and orthostatic hypotension. For Mr. B, a more-tolerable SGA such as aripiprazole or ziprasidone might be prudent, given his propensity for orthostatic hypotension and history of diabetes. Olanzapine or clozapine can cause anticholinergic effects and—in Mr. B’s case—lead to weight gain and worsen diabetes.

Antidepressant use in BPD usually is reserved for depressive symptoms that impair occupational or social functioning and exceed DSM-IV-TR diagnostic criteria.^8,9 Consider later-generation antidepressants such as selective serotonin reuptake inhibitors (SSRIs), because tricyclics pose a greater risk of triggering a switch into hypomania or mania and can cause sedation and orthostatic, cardiac, anticholinergic, and anti-alpha 1 effects.

Among SSRIs, consider citalopram, escitalopram, or sertraline for older patients taking one or more other medications, as these antidepressants have less potential for drug-drug interactions than fluoxetine and paroxetine.¹¹ In a recent comparison of newer antidepressants,²⁰ venlafaxine showed the highest relative risk of mood polarity switching and bupropion the lowest.

Consider ECT for older patients with refractory mania or depression or who show evidence of suicidality or inadequate nutrition.⁵

Follow-up: ongoing issues

Three months after his admission, we discharge Mr. B to a board-and-care facility because family members will not take him in. Several weeks later, he again ignores his prescriptions and decompensates with worsening depression.

Family members have Mr. B admitted to an inpatient psychiatric facility closer to their home. He remains depressed, stays at the facility on and off for almost 1 year, and is eventually conserved by the county. Adverse side effects—mostly constipation and orthostatic hypotension—continue to complicate treatment.

Before Mr. B’s most recent discharge, another psychiatrist restarts lithium, 300 mg bid, and nortriptyline, 100 mg at bedtime—the combination that kept Mr. B relatively stable for more than 2 decades.

Related resources

• National Institute of Mental Health—depression information. www.nimh.nih.gov/healthinformation/depressionmenu.cfm.
  
• Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). www.stepbd.org.
  
• Medicinenet.com. Medicines that cause depression. www.medicinenet.com/depression/index.htm. Click on “Medicines that cause depression.”
  

Drug brand name

• Aripiprazole • Abilify
  
• Bupropion • Wellbutrin
  
• Chlorpromazine • Thorazine
  
• Citalopram • Celexa
  
• Clozapine • Clozaril
  
• Divalproex • Depakote
  
• Escitalopram • Lexapro
  
• Fluoxetine • Prozac
  
• Haloperidol • Haldol
  
• Lamotrigine • Lamictal
  
• Lithium • Various
  
• Mirtazapine • Remeron
  
• Nortriptyline • Pamelor
  
• Olanzapine • Zyprexa
  
• Paroxetine • Paxil
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  
• Ziprasidone • Geodon
  

Disclosures

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

History: bipolar for 30 years

Mr. B, age 66, was diagnosed 30 years ago with type I bipolar disorder and has type 2 diabetes, hypertension, alcohol abuse disorder, and cardiac disease. After repeated suicide attempts and hospitalizations in the past, he has been stable for 20 years on lithium, 600 mg bid, and nortriptyline, 50 mg at bedtime. He has had intermittent mania with little evidence of depression.

Two years ago, Mr. B called a local clinic to report that an intruder had him “holed up.” His speech was pressured and garbled, and his thoughts were tangential, irrational, and markedly paranoid. A clinic psychiatrist called Mr. B’s son, who said his father “built a bomb shelter” because “trolls and little people” were out to kill him. A family member called police, and Mr. B was brought to the ER and admitted for treatment.

A hospital psychiatrist stopped lithium in light of Mr. B’s history of cardiac problems and because the psychiatrist considered the medication ineffective, even though serum lithium was only 0.03 mEq/L. The psychiatrist then started:

• divalproex at 500 mg bid, titrated over 1 week to 500 mg each morning and 1,000 mg at bed-time to reach serum valproate of 80 mEq/L
  
• quetiapine at 200 mg at bedtime, titrated over 1 week to 400 mg at bedtime.
  

Mr. B was still manic, paranoid, and hallucinating 1 week later, yet was discharged after he convinced the county hearing officer that he had recovered.

Two weeks later, Mr. B is brought to another psychiatric hospital, where a psychiatrist restarts unknown dosages of lithium, risperidone, and nortriptyline. From there, he is transferred to our in-patient unit. At presentation, he claims he has been drinking and that members of a drug cartel have recruited him. He says he has been skipping medications because he is “unclear which drugs to take.”

We stop lithium and restart divalproex, 500 mg each morning and 1,500 mg at bedtime, to try to treat his mania without causing cognitive problems.

We stop risperidone because of his hypotension and nortriptyline because it was not working, and restart quetiapine, 600 mg at bedtime, for his paranoia. He remains paranoid 1 week later but his mania improves, so we discharge him on the above regimen. We urge him to take his medications and follow up with his outpatient psychiatrist 1 week later.

Divorced, Mr. B lives alone with no family nearby. His son comes in from out of town to help him resettle after discharge, then leaves the next day.

Several months later, Mr. B’s paranoia returns. He is not taking his medications because “the doctors took away my lithium and these new drugs don’t work.” He tells staff he is a martial arts expert and has purchased 7 cars in recent weeks. We restart lithium at 600 mg bid; serum lithium reaches 1.1 mEq/L, but his mania persists. After 5 days, we add aripiprazole, 15 mg/d.

Nearly 2 weeks after admission, a county hearing officer recommends discharging Mr. B despite his severe mania and paranoia. We release him on the above regimen, arrange appointments with his outpatient psychiatrist and primary care physician, and urge medication adherence. We schedule a blood test 3 days after discharge to check serum lithium, but Mr. B does not keep the appointment.

The authors’ observations

Suspect delirium after rapid onset of mania or paranoia in any patient. Also consider dementia and cognitive deficits in older adults, although Mr. B’s symptoms resembled those of previous manic episodes. Although Mr. B’s psychosis was more severe than before, his case underscores the importance of a thorough patient history.

Late-life bipolar disorder. Little is known about diagnosing and treating bipolar disorder (BPD) in older patients. Gaps in empiric knowledge can confound diagnosis, treatment, and outcome. Also, patients age ≥65 with BPD often have severe medical illness and are difficult to treat.¹

Keys to detecting late-life BPD include:

• recognizing clinical features of BPD unique to older persons
  
• differentiating the disorder from late-life schizophrenia (Table).^1,2
  

Older patients’ symptoms usually match DSM-IV-TR criteria for BPD; their response to treatment mirrors that of younger adults.³

Secondary cause. When an older patient’s mania has atypical features or doesn’t respond to conventional treatment, look for a nonpsychiatric process such as a general medical condition or substance abuse (see possible medical causes with this article at www.currentpsychiatry.com). Order laboratory and other tests as clinical suspicion warrants.

Cognitive deficits secondary to BPD can occur at any age and be persistent or progressive,⁴ although Depp et al¹ found more-severe impairment in older patients. Cognitive impairment can endure after successful BPD treatment, although acute treatment might improve cognition in older patients.⁵

 

Lithium can cause dull affect, cognitive slowing, and depersonalization. Titrating to the lowest effective dosage might minimize these effects.

Dementia. Cognitive deficits that accompany mania in older adults could suggest dementia, which usually develops over years and is preceded by cognitive changes without manic-type symptoms. By contrast, bipolar mania emerges more abruptly and is accompanied by affective symptoms. Agitation and psychosis—both symptoms of late-stage dementia—can be early signs of geriatric BPD.²

Delirium. Restlessness, irritability, aggression, and changes in affect can accompany delirium, especially the hyperactive or hyperalert types. Symptoms of anxiety, depression, fear, and loose or tangential thinking also are common.

Mania shares some of these features but typically presents with an abnormally and persistently elevated or irritable mood lasting ≥1 week, usually without prominent cognitive impairment.⁶ Mania can also include:

• grandiosity
  
• decreased need for sleep
  
• flight of ideas
  
• distractibility
  
• pressured or increased rate of speech
  
• psychomotor agitation
  
• potentially harmful activities
  
• increased goal-directed activities.⁶
  

By contrast, delirium is marked by waxing and waning consciousness and changes in cognition, such as disorientation and confusion.⁶

Frontal lobe lesions. Decreased prefrontal executive control could underlie mania’s cognitive and emotional symptoms. Decreased right rostral and orbital prefrontal cortex activation has been associated with impaired planning, judgment, and insight, as well as inappropriate conduct.⁷

Table

Clinical features of geriatric bipolar disorder (BPD)

Psychotic features (delusions, hallucinations)
Mean prevalence of 64% (range 20% to 85%) is similar to that of mixed-age groups; paranoia might be more prevalent
Family history
High rates of psychiatric disorders (“affective disorder” in most studies) reported in 10 studies
Compared with younger adults with BPD, older patients:
show longer latency from first depression to mania onset might be more likely to relapse into depression after mania might have less-intense mania are hospitalized longer, possibly because of greater medical comorbidity have less comorbid substance abuse and more-prominent age-associated morphologic abnormalities on neuroimaging2
Compared with late-life schizophrenia, late-life BPD patients show:
more depressive symptoms fewer positive and negative symptoms greater community living and relationship skills, with similar activities of daily living
Source: References 1,2

Continued treatment: depression emerges

Several months later, Mr. B presents with severe depression and continued medication nonadherence. He complains of hypersomnia, poor appetite, anhedonia, amotivation, and a leaden-like paresis in his hands and feet.

We readmit Mr. B to the psychiatric unit. He avoids contact with others, has lost 18 lbs over 6 weeks, and suffers hypotension caused by poor hydration before admission. Three weeks later, he complains that ants are crawling around his room and into his mouth.

Noncontrast brain CT shows no abnormalities. Laboratory tests performed at admission show a subtherapeutic lithium level (0.03 mEq/L), unremarkable thyroid panel, and normal B12 and folate, so we begin to rule out a medical cause for his psychiatric symptoms.

The authors’ observations

Check for these and other possible causes of depressive symptoms in older patients with a history of BPD. Mr. B’s depression likely resulted from multiple causes, including medical disease, functional impairment, loss of social and family contacts, and substance abuse—all late-life predictors of depression. BPD also predisposed him to depression.

Bipolar depression. Despite its profound morbidity and mortality, bipolar depression remains a mystery, especially in the elderly. Mr. B’s depression emerged after he was free of depressive symptoms for more than 20 years.

Some researchers believe that compared with other depressions, bipolar depression has a more acute onset, marked psychomotor retardation, and lessened response to antidepressants.^6,8 Kraepelin associated bipolar depression with lethargy, mental slowing, and hypersomnia, whereas agitation and insomnia signal unipolar depression.⁹

To differentiate bipolar from unipolar or secondary depression in older patients, watch for:

• suicide risk, which is heightened during BPD’s depressive phase⁹
  
• secondary manias, for which underlying causes must be determined and treated if possible.
  

Medication-induced depression. Medications can cause depressive symptoms (see Related resources), but identifying an offending agent without an obvious chronologic relationship can be difficult, especially in older patients who are taking numerous medications.⁹

Depression caused by medication might be limited to somatic complaints such as fatigue or tiredness,⁹ and often lacks features seen with mood disorders such as depressed mood, anhedonia, guilt, and diminished interest in activities. Mr. B’s anhedonia and amotivation suggest his depression was not medication-induced.¹⁰

Disease-induced depression. Medical comorbidities are common among older persons with mood disorders and can complicate treatment response and outcome. Physical disease can cause or worsen depression:¹¹

• Endocrine and immunologic diseases might cause depression or mania.
  
• Cardiovascular and cerebrovascular diseases; CNS disorders such as dementia, Parkinson’s disease, and multiple sclerosis; cancer; and connective tissue disease increase risk for comorbid depression.
  

Mr. B’s hypertension, diabetes, or coronary artery disease could have contributed to his depression or complicated the course.

 

¹¹

Vascular depression. Comorbid depressive symptoms and vascular disease—or “vascular depression”—can cause ischemic brain lesions, cognitive impairment, increased apathy and retardation, and impaired fluency and naming.¹²

What defines vascular depression has been debated. Watch for clinical or laboratory evidence of vascular disease, depression, and neuropsychological impairment.¹³

Treatment: searching for evidence

Two days after admission, Mr. B is transferred to the ICU after suffering severe hypoglycemia and showing signs of medically induced delirium. Elevated creatinine (1.7 mg/dL) indicates acute renal failure, which could be related to his elevated serum lithium (1.7 mEq/L). Acting on the internist’s advice, the consulting psychiatrist stops lithium and restarts valproate, 500 mg bid.

Mr. B becomes medically stable after 3 days, mostly through acute IV hydration and by withholding oral diabetes medications, which normalizes his blood sugar. He is transferred back to the psychiatry unit. We try lithium again at 300 mg bid, but creatinine and serum lithium quickly rise.

Mr. B remains hospitalized for 3 months with severe, treatment-resistant depression. Trials of nearly every second-generation antipsychotic (SGA) cause symptomatic orthostatic hypotension, leading to several falls. He does not respond to divalproex, up to 2,000 mg/d; citalopram, 60 mg/d; mirtazapine, 30 mg at bedtime; venlafaxine, 100 mg tid; or bupropion, 100 mg tid.

We suggest electroconvulsive therapy (ECT) but Mr. B declines, saying this treatment caused his mother to decompensate. We try lamotrigine, 25 mg/d, and titrate it over 6 weeks to 200 mg bid. After we add haloperidol, 5 mg at bedtime, and bupropion, 300 mg/d, Mr. B becomes mentally stable.

The authors’ observations

Numerous clinical challenges—such as managing complicated/refractory BPD, medical comorbidity, and medication adherence (Box)^14,15—complicate treatment of late-life BPD.¹⁶ Regular communication with providers and integrating health care services can minimize complication risk.¹⁶

Pharmacotherapy, a core element of BPD treatment, is challenging in older patients because of their:

• heightened threat of complications and sensitivity to side effects because of age-related pharmacokinetic changes
  
• increased risk of drug-drug interactions
  
• increased potential for age-related psychosocial problems (increased social isolation, financial difficulties, demoralization, increased stress, inability to work).
  

Box

Initial clinical and laboratory evaluations can rule out aggravating or causative factors and identify conditions that can cause drug intolerability.⁵ Check orthostatic vital signs and perform a detailed medical and psychosocial history, neurologic examination, ECG, and cognitive evaluation.

Consider side effects, medical and neurologic comorbidities, and treatment history before prescribing a mood stabilizer, antipsychotic, or antidepressant to an older patient. Avoid unwarranted discontinuation of a previously effective agent, such as when drug concentrations are elevated or inadequate—as happened with Mr. B.⁵ Also investigate the patient’s side-effect history before stopping a medication.⁵

Medications. Mr. B’s inability to tolerate lithium posed a treatment challenge. Adjusting lithium dosages to compensate for age-related pharmacokinetic, pharmacodynamic, and renal clearance changes can prevent toxicity.⁵ Avoid stopping lithium abruptly, as this can trigger recurrence of manic or depressive episodes.¹⁷

Lamotrigine, indicated for BPD maintenance therapy, appears to prevent depressive/mood relapse. Compared with other anticonvulsants, lamotrigine might cause fewer negative effects on cognition and less induction of hepatic enzymes. It is well tolerated by older patients but has not been studied adequately in this age group.¹⁶

Antipsychotics are widely used in BPD,¹⁶ especially when psychosis is present with mania or depression or the patient is agitated. Most studies of antipsychotics in BPD have followed younger adults, however, and most studies in older patients have followed those with dementia or schizophrenia.

Use of first-generation antipsychotics such as haloperidol is especially challenging in the elderly because these drugs increase risk of cardiovascular effects, extrapyramidal symptoms, and tardive dyskinesia and can cause depression in BPD.¹⁶ By comparison, SGAs carry a lower risk of involuntary motion¹⁸ but can increase risk of obesity, diabetes, and dyslipidemia. However:

• The need to manage psychosis usually overrides concerns about metabolic sequelae.
  
• Older patients might be less susceptible to metabolic effects,¹⁶ though this has not been confirmed.
  

 

SGAs can be used safely in patients with a history of diabetes. Start at lower-than-normal dosages and titrate slowly. Perform baseline and regular checks—including weight, blood glucose, lipid levels, and blood pressure—following American Psychiatric Association and American Diabetes Association consensus guidelines.¹⁹ Also check glycosylated hemoglobin every 3 to 6 months in patients with diabetes, and follow up with other providers to ensure proper diabetes management.

As with most aspects of late-life BPD, scant evidence guides SGA use. Avoid low-potency neuroleptics such as chlorpromazine, which can cause severe sedation and orthostatic hypotension. For Mr. B, a more-tolerable SGA such as aripiprazole or ziprasidone might be prudent, given his propensity for orthostatic hypotension and history of diabetes. Olanzapine or clozapine can cause anticholinergic effects and—in Mr. B’s case—lead to weight gain and worsen diabetes.

Antidepressant use in BPD usually is reserved for depressive symptoms that impair occupational or social functioning and exceed DSM-IV-TR diagnostic criteria.^8,9 Consider later-generation antidepressants such as selective serotonin reuptake inhibitors (SSRIs), because tricyclics pose a greater risk of triggering a switch into hypomania or mania and can cause sedation and orthostatic, cardiac, anticholinergic, and anti-alpha 1 effects.

Among SSRIs, consider citalopram, escitalopram, or sertraline for older patients taking one or more other medications, as these antidepressants have less potential for drug-drug interactions than fluoxetine and paroxetine.¹¹ In a recent comparison of newer antidepressants,²⁰ venlafaxine showed the highest relative risk of mood polarity switching and bupropion the lowest.

Consider ECT for older patients with refractory mania or depression or who show evidence of suicidality or inadequate nutrition.⁵

Follow-up: ongoing issues

Three months after his admission, we discharge Mr. B to a board-and-care facility because family members will not take him in. Several weeks later, he again ignores his prescriptions and decompensates with worsening depression.

Family members have Mr. B admitted to an inpatient psychiatric facility closer to their home. He remains depressed, stays at the facility on and off for almost 1 year, and is eventually conserved by the county. Adverse side effects—mostly constipation and orthostatic hypotension—continue to complicate treatment.

Before Mr. B’s most recent discharge, another psychiatrist restarts lithium, 300 mg bid, and nortriptyline, 100 mg at bedtime—the combination that kept Mr. B relatively stable for more than 2 decades.

Related resources

• National Institute of Mental Health—depression information. www.nimh.nih.gov/healthinformation/depressionmenu.cfm.
  
• Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). www.stepbd.org.
  
• Medicinenet.com. Medicines that cause depression. www.medicinenet.com/depression/index.htm. Click on “Medicines that cause depression.”
  

Drug brand name

• Aripiprazole • Abilify
  
• Bupropion • Wellbutrin
  
• Chlorpromazine • Thorazine
  
• Citalopram • Celexa
  
• Clozapine • Clozaril
  
• Divalproex • Depakote
  
• Escitalopram • Lexapro
  
• Fluoxetine • Prozac
  
• Haloperidol • Haldol
  
• Lamotrigine • Lamictal
  
• Lithium • Various
  
• Mirtazapine • Remeron
  
• Nortriptyline • Pamelor
  
• Olanzapine • Zyprexa
  
• Paroxetine • Paxil
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  
• Ziprasidone • Geodon
  

Disclosures

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

History: bipolar for 30 years

Mr. B, age 66, was diagnosed 30 years ago with type I bipolar disorder and has type 2 diabetes, hypertension, alcohol abuse disorder, and cardiac disease. After repeated suicide attempts and hospitalizations in the past, he has been stable for 20 years on lithium, 600 mg bid, and nortriptyline, 50 mg at bedtime. He has had intermittent mania with little evidence of depression.

Two years ago, Mr. B called a local clinic to report that an intruder had him “holed up.” His speech was pressured and garbled, and his thoughts were tangential, irrational, and markedly paranoid. A clinic psychiatrist called Mr. B’s son, who said his father “built a bomb shelter” because “trolls and little people” were out to kill him. A family member called police, and Mr. B was brought to the ER and admitted for treatment.

A hospital psychiatrist stopped lithium in light of Mr. B’s history of cardiac problems and because the psychiatrist considered the medication ineffective, even though serum lithium was only 0.03 mEq/L. The psychiatrist then started:

• divalproex at 500 mg bid, titrated over 1 week to 500 mg each morning and 1,000 mg at bed-time to reach serum valproate of 80 mEq/L
  
• quetiapine at 200 mg at bedtime, titrated over 1 week to 400 mg at bedtime.
  

Mr. B was still manic, paranoid, and hallucinating 1 week later, yet was discharged after he convinced the county hearing officer that he had recovered.

Two weeks later, Mr. B is brought to another psychiatric hospital, where a psychiatrist restarts unknown dosages of lithium, risperidone, and nortriptyline. From there, he is transferred to our in-patient unit. At presentation, he claims he has been drinking and that members of a drug cartel have recruited him. He says he has been skipping medications because he is “unclear which drugs to take.”

We stop lithium and restart divalproex, 500 mg each morning and 1,500 mg at bedtime, to try to treat his mania without causing cognitive problems.

We stop risperidone because of his hypotension and nortriptyline because it was not working, and restart quetiapine, 600 mg at bedtime, for his paranoia. He remains paranoid 1 week later but his mania improves, so we discharge him on the above regimen. We urge him to take his medications and follow up with his outpatient psychiatrist 1 week later.

Divorced, Mr. B lives alone with no family nearby. His son comes in from out of town to help him resettle after discharge, then leaves the next day.

Several months later, Mr. B’s paranoia returns. He is not taking his medications because “the doctors took away my lithium and these new drugs don’t work.” He tells staff he is a martial arts expert and has purchased 7 cars in recent weeks. We restart lithium at 600 mg bid; serum lithium reaches 1.1 mEq/L, but his mania persists. After 5 days, we add aripiprazole, 15 mg/d.

Nearly 2 weeks after admission, a county hearing officer recommends discharging Mr. B despite his severe mania and paranoia. We release him on the above regimen, arrange appointments with his outpatient psychiatrist and primary care physician, and urge medication adherence. We schedule a blood test 3 days after discharge to check serum lithium, but Mr. B does not keep the appointment.

The authors’ observations

Suspect delirium after rapid onset of mania or paranoia in any patient. Also consider dementia and cognitive deficits in older adults, although Mr. B’s symptoms resembled those of previous manic episodes. Although Mr. B’s psychosis was more severe than before, his case underscores the importance of a thorough patient history.

Late-life bipolar disorder. Little is known about diagnosing and treating bipolar disorder (BPD) in older patients. Gaps in empiric knowledge can confound diagnosis, treatment, and outcome. Also, patients age ≥65 with BPD often have severe medical illness and are difficult to treat.¹

Keys to detecting late-life BPD include:

• recognizing clinical features of BPD unique to older persons
  
• differentiating the disorder from late-life schizophrenia (Table).^1,2
  

Older patients’ symptoms usually match DSM-IV-TR criteria for BPD; their response to treatment mirrors that of younger adults.³

Secondary cause. When an older patient’s mania has atypical features or doesn’t respond to conventional treatment, look for a nonpsychiatric process such as a general medical condition or substance abuse (see possible medical causes with this article at www.currentpsychiatry.com). Order laboratory and other tests as clinical suspicion warrants.

Cognitive deficits secondary to BPD can occur at any age and be persistent or progressive,⁴ although Depp et al¹ found more-severe impairment in older patients. Cognitive impairment can endure after successful BPD treatment, although acute treatment might improve cognition in older patients.⁵

 

Lithium can cause dull affect, cognitive slowing, and depersonalization. Titrating to the lowest effective dosage might minimize these effects.

Dementia. Cognitive deficits that accompany mania in older adults could suggest dementia, which usually develops over years and is preceded by cognitive changes without manic-type symptoms. By contrast, bipolar mania emerges more abruptly and is accompanied by affective symptoms. Agitation and psychosis—both symptoms of late-stage dementia—can be early signs of geriatric BPD.²

Delirium. Restlessness, irritability, aggression, and changes in affect can accompany delirium, especially the hyperactive or hyperalert types. Symptoms of anxiety, depression, fear, and loose or tangential thinking also are common.

Mania shares some of these features but typically presents with an abnormally and persistently elevated or irritable mood lasting ≥1 week, usually without prominent cognitive impairment.⁶ Mania can also include:

• grandiosity
  
• decreased need for sleep
  
• flight of ideas
  
• distractibility
  
• pressured or increased rate of speech
  
• psychomotor agitation
  
• potentially harmful activities
  
• increased goal-directed activities.⁶
  

By contrast, delirium is marked by waxing and waning consciousness and changes in cognition, such as disorientation and confusion.⁶

Frontal lobe lesions. Decreased prefrontal executive control could underlie mania’s cognitive and emotional symptoms. Decreased right rostral and orbital prefrontal cortex activation has been associated with impaired planning, judgment, and insight, as well as inappropriate conduct.⁷

Table

Clinical features of geriatric bipolar disorder (BPD)

Psychotic features (delusions, hallucinations)
Mean prevalence of 64% (range 20% to 85%) is similar to that of mixed-age groups; paranoia might be more prevalent
Family history
High rates of psychiatric disorders (“affective disorder” in most studies) reported in 10 studies
Compared with younger adults with BPD, older patients:
show longer latency from first depression to mania onset might be more likely to relapse into depression after mania might have less-intense mania are hospitalized longer, possibly because of greater medical comorbidity have less comorbid substance abuse and more-prominent age-associated morphologic abnormalities on neuroimaging2
Compared with late-life schizophrenia, late-life BPD patients show:
more depressive symptoms fewer positive and negative symptoms greater community living and relationship skills, with similar activities of daily living
Source: References 1,2

Continued treatment: depression emerges

Several months later, Mr. B presents with severe depression and continued medication nonadherence. He complains of hypersomnia, poor appetite, anhedonia, amotivation, and a leaden-like paresis in his hands and feet.

We readmit Mr. B to the psychiatric unit. He avoids contact with others, has lost 18 lbs over 6 weeks, and suffers hypotension caused by poor hydration before admission. Three weeks later, he complains that ants are crawling around his room and into his mouth.

Noncontrast brain CT shows no abnormalities. Laboratory tests performed at admission show a subtherapeutic lithium level (0.03 mEq/L), unremarkable thyroid panel, and normal B12 and folate, so we begin to rule out a medical cause for his psychiatric symptoms.

The authors’ observations

Check for these and other possible causes of depressive symptoms in older patients with a history of BPD. Mr. B’s depression likely resulted from multiple causes, including medical disease, functional impairment, loss of social and family contacts, and substance abuse—all late-life predictors of depression. BPD also predisposed him to depression.

Bipolar depression. Despite its profound morbidity and mortality, bipolar depression remains a mystery, especially in the elderly. Mr. B’s depression emerged after he was free of depressive symptoms for more than 20 years.

Some researchers believe that compared with other depressions, bipolar depression has a more acute onset, marked psychomotor retardation, and lessened response to antidepressants.^6,8 Kraepelin associated bipolar depression with lethargy, mental slowing, and hypersomnia, whereas agitation and insomnia signal unipolar depression.⁹

To differentiate bipolar from unipolar or secondary depression in older patients, watch for:

• suicide risk, which is heightened during BPD’s depressive phase⁹
  
• secondary manias, for which underlying causes must be determined and treated if possible.
  

Medication-induced depression. Medications can cause depressive symptoms (see Related resources), but identifying an offending agent without an obvious chronologic relationship can be difficult, especially in older patients who are taking numerous medications.⁹

Depression caused by medication might be limited to somatic complaints such as fatigue or tiredness,⁹ and often lacks features seen with mood disorders such as depressed mood, anhedonia, guilt, and diminished interest in activities. Mr. B’s anhedonia and amotivation suggest his depression was not medication-induced.¹⁰

Disease-induced depression. Medical comorbidities are common among older persons with mood disorders and can complicate treatment response and outcome. Physical disease can cause or worsen depression:¹¹

• Endocrine and immunologic diseases might cause depression or mania.
  
• Cardiovascular and cerebrovascular diseases; CNS disorders such as dementia, Parkinson’s disease, and multiple sclerosis; cancer; and connective tissue disease increase risk for comorbid depression.
  

Mr. B’s hypertension, diabetes, or coronary artery disease could have contributed to his depression or complicated the course.

 

¹¹

Vascular depression. Comorbid depressive symptoms and vascular disease—or “vascular depression”—can cause ischemic brain lesions, cognitive impairment, increased apathy and retardation, and impaired fluency and naming.¹²

What defines vascular depression has been debated. Watch for clinical or laboratory evidence of vascular disease, depression, and neuropsychological impairment.¹³

Treatment: searching for evidence

Two days after admission, Mr. B is transferred to the ICU after suffering severe hypoglycemia and showing signs of medically induced delirium. Elevated creatinine (1.7 mg/dL) indicates acute renal failure, which could be related to his elevated serum lithium (1.7 mEq/L). Acting on the internist’s advice, the consulting psychiatrist stops lithium and restarts valproate, 500 mg bid.

Mr. B becomes medically stable after 3 days, mostly through acute IV hydration and by withholding oral diabetes medications, which normalizes his blood sugar. He is transferred back to the psychiatry unit. We try lithium again at 300 mg bid, but creatinine and serum lithium quickly rise.

Mr. B remains hospitalized for 3 months with severe, treatment-resistant depression. Trials of nearly every second-generation antipsychotic (SGA) cause symptomatic orthostatic hypotension, leading to several falls. He does not respond to divalproex, up to 2,000 mg/d; citalopram, 60 mg/d; mirtazapine, 30 mg at bedtime; venlafaxine, 100 mg tid; or bupropion, 100 mg tid.

We suggest electroconvulsive therapy (ECT) but Mr. B declines, saying this treatment caused his mother to decompensate. We try lamotrigine, 25 mg/d, and titrate it over 6 weeks to 200 mg bid. After we add haloperidol, 5 mg at bedtime, and bupropion, 300 mg/d, Mr. B becomes mentally stable.

The authors’ observations

Numerous clinical challenges—such as managing complicated/refractory BPD, medical comorbidity, and medication adherence (Box)^14,15—complicate treatment of late-life BPD.¹⁶ Regular communication with providers and integrating health care services can minimize complication risk.¹⁶

Pharmacotherapy, a core element of BPD treatment, is challenging in older patients because of their:

• heightened threat of complications and sensitivity to side effects because of age-related pharmacokinetic changes
  
• increased risk of drug-drug interactions
  
• increased potential for age-related psychosocial problems (increased social isolation, financial difficulties, demoralization, increased stress, inability to work).
  

Box

Initial clinical and laboratory evaluations can rule out aggravating or causative factors and identify conditions that can cause drug intolerability.⁵ Check orthostatic vital signs and perform a detailed medical and psychosocial history, neurologic examination, ECG, and cognitive evaluation.

Consider side effects, medical and neurologic comorbidities, and treatment history before prescribing a mood stabilizer, antipsychotic, or antidepressant to an older patient. Avoid unwarranted discontinuation of a previously effective agent, such as when drug concentrations are elevated or inadequate—as happened with Mr. B.⁵ Also investigate the patient’s side-effect history before stopping a medication.⁵

Medications. Mr. B’s inability to tolerate lithium posed a treatment challenge. Adjusting lithium dosages to compensate for age-related pharmacokinetic, pharmacodynamic, and renal clearance changes can prevent toxicity.⁵ Avoid stopping lithium abruptly, as this can trigger recurrence of manic or depressive episodes.¹⁷

Lamotrigine, indicated for BPD maintenance therapy, appears to prevent depressive/mood relapse. Compared with other anticonvulsants, lamotrigine might cause fewer negative effects on cognition and less induction of hepatic enzymes. It is well tolerated by older patients but has not been studied adequately in this age group.¹⁶

Antipsychotics are widely used in BPD,¹⁶ especially when psychosis is present with mania or depression or the patient is agitated. Most studies of antipsychotics in BPD have followed younger adults, however, and most studies in older patients have followed those with dementia or schizophrenia.

Use of first-generation antipsychotics such as haloperidol is especially challenging in the elderly because these drugs increase risk of cardiovascular effects, extrapyramidal symptoms, and tardive dyskinesia and can cause depression in BPD.¹⁶ By comparison, SGAs carry a lower risk of involuntary motion¹⁸ but can increase risk of obesity, diabetes, and dyslipidemia. However:

• The need to manage psychosis usually overrides concerns about metabolic sequelae.
  
• Older patients might be less susceptible to metabolic effects,¹⁶ though this has not been confirmed.
  

 

SGAs can be used safely in patients with a history of diabetes. Start at lower-than-normal dosages and titrate slowly. Perform baseline and regular checks—including weight, blood glucose, lipid levels, and blood pressure—following American Psychiatric Association and American Diabetes Association consensus guidelines.¹⁹ Also check glycosylated hemoglobin every 3 to 6 months in patients with diabetes, and follow up with other providers to ensure proper diabetes management.

As with most aspects of late-life BPD, scant evidence guides SGA use. Avoid low-potency neuroleptics such as chlorpromazine, which can cause severe sedation and orthostatic hypotension. For Mr. B, a more-tolerable SGA such as aripiprazole or ziprasidone might be prudent, given his propensity for orthostatic hypotension and history of diabetes. Olanzapine or clozapine can cause anticholinergic effects and—in Mr. B’s case—lead to weight gain and worsen diabetes.

Antidepressant use in BPD usually is reserved for depressive symptoms that impair occupational or social functioning and exceed DSM-IV-TR diagnostic criteria.^8,9 Consider later-generation antidepressants such as selective serotonin reuptake inhibitors (SSRIs), because tricyclics pose a greater risk of triggering a switch into hypomania or mania and can cause sedation and orthostatic, cardiac, anticholinergic, and anti-alpha 1 effects.

Among SSRIs, consider citalopram, escitalopram, or sertraline for older patients taking one or more other medications, as these antidepressants have less potential for drug-drug interactions than fluoxetine and paroxetine.¹¹ In a recent comparison of newer antidepressants,²⁰ venlafaxine showed the highest relative risk of mood polarity switching and bupropion the lowest.

Consider ECT for older patients with refractory mania or depression or who show evidence of suicidality or inadequate nutrition.⁵

Follow-up: ongoing issues

Three months after his admission, we discharge Mr. B to a board-and-care facility because family members will not take him in. Several weeks later, he again ignores his prescriptions and decompensates with worsening depression.

Family members have Mr. B admitted to an inpatient psychiatric facility closer to their home. He remains depressed, stays at the facility on and off for almost 1 year, and is eventually conserved by the county. Adverse side effects—mostly constipation and orthostatic hypotension—continue to complicate treatment.

Before Mr. B’s most recent discharge, another psychiatrist restarts lithium, 300 mg bid, and nortriptyline, 100 mg at bedtime—the combination that kept Mr. B relatively stable for more than 2 decades.

Related resources

• National Institute of Mental Health—depression information. www.nimh.nih.gov/healthinformation/depressionmenu.cfm.
  
• Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). www.stepbd.org.
  
• Medicinenet.com. Medicines that cause depression. www.medicinenet.com/depression/index.htm. Click on “Medicines that cause depression.”
  

Drug brand name

• Aripiprazole • Abilify
  
• Bupropion • Wellbutrin
  
• Chlorpromazine • Thorazine
  
• Citalopram • Celexa
  
• Clozapine • Clozaril
  
• Divalproex • Depakote
  
• Escitalopram • Lexapro
  
• Fluoxetine • Prozac
  
• Haloperidol • Haldol
  
• Lamotrigine • Lamictal
  
• Lithium • Various
  
• Mirtazapine • Remeron
  
• Nortriptyline • Pamelor
  
• Olanzapine • Zyprexa
  
• Paroxetine • Paxil
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  
• Ziprasidone • Geodon
  

Disclosures

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

HISTORY: REPEAT OFFENDER

Mr. V, age 68, was incarcerated for 13 years for two separate pedophilia convictions. During that time, he passed numerous rehabilitative courses. With several years left on his sentence, he was paroled on condition that he undergo a bilateral orchiectomy.

Eight months later, Mr. V complained to his primary care physician that he could not have sex with his girlfriend, even after taking 50 mg of sildenafil, which he had obtained from a friend. He requested testosterone injections to allow him to have intercourse. After consulting an endocrinologist, the physician ordered Mr. V to undergo a psychiatric assessment before receiving testosterone. He was referred to our outpatient clinic.

During our evaluation, Mr. V described both pedophilia incidents. In the first, he had fondled a 14-year-old girl who was a friend of his family. He pled guilty to a charge of inappropriate sexual contact with a minor and was sentenced to 3 years in a state prison for sex offenders.

Less than 2 years after he was paroled, Mr. V said, he fondled his 12-year-old granddaughter. He said his daughter “should have known better” than to leave him home alone with the child. Again he was convicted of illegal sexual relations with a minor and sentenced to 10 years at the state hospital for the criminally insane.

As Mr. V describes his past offenses, we begin feeling tremendously uneasy. Although forthcoming, he blandly denies responsibility for either incident. He acknowledges that society views his actions as wrong, but he never indicates that he believes them to be wrong. At times he tries to normalize his behavior, saying “What man would have acted differently?”

Mr. V is polite and appropriate and promises to abide by our recommendation, yet he sees no reason for us to deny his request and no connection between his criminal record and the nature of his crimes or the terms of his parole. His denial and lack of insight are typical of convicted pedophiles (Box 1).

Box 1

The authors’ observations

Anyone evaluating Mr. V would be inclined to treat or dismiss him, or to suppress his or her feelings to avoid prejudice.

Treat or dismiss. As physicians, we are trained to “First, do no harm.” In this case, however, we must consider who could be harmed by treatment or dismissal.

“First, do no harm” is usually taken to mean “no harm to the patient” but could also be interpreted as “no harm to society.” Even if testosterone treatment did not physically harm Mr. V, activating his sex drive could endanger society by spurring him on to molest another child (Box 2). The treatment could also harm Mr. V by making it easier for him to violate parole.

Although failure to treat Mr. V’s sexual dysfunction would likely pose no harm to society, not assessing him might endanger society by clearing the path toward this treatment.

Box 2

Avoiding prejudice. When facing an unpleasant task, people often tell themselves consciously or unconsciously that their reaction is wrong and that they must carry on.⁷ Our revulsion toward Mr. V prompted us to be dispassionate and objective, but suppressing our emotions altogether could have obscured potentially serious objections. At the same time, giving ascendancy to negative emotions without questioning them could harm the patient—or at least obscure an opportunity to do good.

 

When treating patients such as Mr. V, we must not dismiss our feelings—however uncomfortable or unprofessional they might seem—so that we can manage them appropriately. Don’t be ashamed of your feelings—or at least be aware of your shame.

In such cases, these important steps can minimize the risk of compromising treatment or assessment:

• Be aware of your feelings. Reflecting on countertransference after the session, either alone or with other therapists, can help you recognize your feelings.
  
• Seek peer supervision when evaluating a patient such as Mr. V to help identify potential “blind spots.”
  
• Be aware of your limitations. Hubris is among a therapist’s most serious potential pitfalls. We all have strengths and weaknesses and should be mindful of them.
  

The authors’ observations

We took a passive-neutral stance. Sitting with Mr. V without deciding a course of action gave us time to assess our own reactions and limitations and how they might influence our actions.

CONSULTATION: OTHER OPINIONS

The examining psychiatrist (a psychiatric resident) sought advice from an experienced geriatric psychiatrist, a neuropsychologist, and other residents. We discussed our countertransference toward Mr. V and provided mutual supervision. We then acknowledged that none of us had expertise in treating pedophiles and that treating an unfamiliar mental condition would be unethical.

The authors’ observations

In requesting other opinions, we also weighed these important questions:

Is Mr. V violating parole by requesting testosterone injections and taking (unprescribed) sildenafil? We felt we could not rightfully answer this question, since our expertise in the standard of care for patients such as Mr. V was insufficient and any recommendation would be ill-informed.

Sildenafil use is fairly common among convicted sex offenders, as evidenced by the recent controversy over Medicaid providing the drug to this group (see Related resources).

Assuming the testosterone injections promote intercourse, would they increase Mr. V’s arousal? Hall found that offenders who can voluntarily and completely inhibit sexual arousal are less deviant when not attempting to inhibit arousal than are those who cannot completely inhibit arousal.⁸

Hall, however, urges clinicians to consider variables that influence sexual response before determining how arousal affects an offender’s behavior. With no objective measure of sexual arousal, it is unclear whether increasing Mr. V’s testosterone would heighten it—and his potential threat to society.

The Abel Assessment of Sexual Interest was devised to determine sexual pathology, but evidence suggests this test is clinically unreliable.

Would enhancing Mr. V’s arousal increase his risk of recidivism? Although some studies have found that castration decreases a sex offender’s sexual activity, evidence suggests that sexual responsiveness after castration varies considerably. Heim found that:

• 31% of castrates could still have intercourse
  
• rapists are more sexually active than pedophiles after castration
  
• men ages 46 to 59 experience a greater reduction in sexual behavior than do men age 9
  

These findings suggest that castration’s effects on male sexuality are unpredictable, making it an unreliable treatment for incarcerated sex offenders.⁹ They also suggest that enhancing Mr. V’s arousal could increase his odds of recidivism. Stone et al,¹⁰ however, recorded recidivism rates of 3% across 30 years among castrated sex offenders, compared with 58% among non-castrates.

What standard of care applies to Mr. V? Treating pedophilia is difficult and poorly understood. Psychotherapy is considered an adjunct to medication or surgery. Surgical interventions are akin to punishment, whereas medications—well-studied and often augmented with psychotherapy—are associated with high recidivism rates.^11,14

Surgery. Orchiectomy is by far the most common surgical intervention. Experimental procedures have targeted stereotaxic ablation of specific parts of the brain, usually the hypothalamus or amygdala, but these techniques have not been adequately studied in humans.¹¹ Even so, testosterone therapy can restore sexual function after castration.¹⁰

Medications. Antiandrogens such as medroxy-progesterone acetate (MPA) inhibit intracellular uptake of androgens (such as testosterone) by blocking their binding to the receptor.¹² MPA is most frequently used in the United States.

Long-acting analogs of gonadotropin-releasing hormone (GnRH), such as leuprolide, nafarelin, goserelin, and triptorelin, have shown efficacy in early studies.¹² These agents down-regulate gonadotroph cells, inducing severe but reversible hypogonadism with few other side effects.

Although decreased libido is a common side effect of selective serotonin reuptake inhibitors (SSRIs), use of these agents to reduce sex drive in convicted pedophiles has not been studied. Because onset of decreased libido with SSRI use is unpredictable, we cannot recommend their use to reduce sex drive in convicted offenders.

Psychotherapy. Power¹⁴ nicely outlines the elements of psychotherapy for pedophilia:

• explanation and education
  
• manipulating the environment
  
• suggestion, including hypnosis and persuasion
  
• superficial analysis
  
• deep-transference analysis
  
• sublimation.
  

If Mr. V commits another sexual offense after receiving testosterone, can the doctors who prescribed, authorized, or gave the injections be held liable?

 

Stone et al¹⁰ draw several germane conclusions:

• Sentencing laws are often unclear or do not take into account scientific research on pedophilia. For example, psychological testing often is not ordered before a treatment is mandated, even though knowing the patient’s psychological profile and the nature of his predilections are crucial to treatment and prognosis.¹²
  
• Many laws do not suggest an instrument of implementation. For example, most laws that mandate a patient evaluation do not specify whether a licensed psychiatrist, psychologist, or other clinician should evaluate the patient.
  
• Many laws directed against pedophilia are punitive in nature. Mandated treatment—or the informed consent that precedes it—is often inadequate,¹⁰ and physicians can be held liable in either case. However, we could not determine the liability that could result from enhancing a convicted pedophile’s libido.
  

REFERRAL: TREATMENT ADVICE

We referred Mr. V back to his primary care physician and advised the doctor to:

• discuss the testosterone treatment request with physicians who treated Mr. V at the state prison
  
• call our hospital’s attorney to investigate the legal implications of treating Mr. V.
  

We also recommended against enhancing Mr. V’s libido, given his poor insight and denial and the primary care physician’s lack of expertise in this treatment. A recent check of Mr. V’s electronic record indicated that he was not given medication to enhance sexual performance.

Related resources

• Sex offenders get Medicaid-paid Viagra. Associated Press May 22, 2005. http://msnbc.msn.com/id/7946129/.
  
• Conte JR, Wolf S, Smith T. What sexual offenders tell us about prevention strategies. Child Abuse Negl 1989;13:293-301.
  
• U.S. Department of Justice, Bureau of Justice Statistics. Statistics on sex offenders and victims. www.ojp.usdoj.gov/bjs/abstract/saycrle.htm.
  

Drug brand names

• Goserelin • Zoladex
  
• Leuprolide • Eligard, others
  
• Medroxyprogesterone acetate • Depo-Provera, others
  
• Nafarelin • Synarel
  
• Sildenafil • Viagra
  
• Triptorelin • Trelstar Depot
  

Acknowledgment

The authors thank Cynthia Meyer, chief librarian, VA Hospital, Fresno, CA, for her help with researching this article.

Disclosure

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

HISTORY: REPEAT OFFENDER

Mr. V, age 68, was incarcerated for 13 years for two separate pedophilia convictions. During that time, he passed numerous rehabilitative courses. With several years left on his sentence, he was paroled on condition that he undergo a bilateral orchiectomy.

Eight months later, Mr. V complained to his primary care physician that he could not have sex with his girlfriend, even after taking 50 mg of sildenafil, which he had obtained from a friend. He requested testosterone injections to allow him to have intercourse. After consulting an endocrinologist, the physician ordered Mr. V to undergo a psychiatric assessment before receiving testosterone. He was referred to our outpatient clinic.

During our evaluation, Mr. V described both pedophilia incidents. In the first, he had fondled a 14-year-old girl who was a friend of his family. He pled guilty to a charge of inappropriate sexual contact with a minor and was sentenced to 3 years in a state prison for sex offenders.

Less than 2 years after he was paroled, Mr. V said, he fondled his 12-year-old granddaughter. He said his daughter “should have known better” than to leave him home alone with the child. Again he was convicted of illegal sexual relations with a minor and sentenced to 10 years at the state hospital for the criminally insane.

As Mr. V describes his past offenses, we begin feeling tremendously uneasy. Although forthcoming, he blandly denies responsibility for either incident. He acknowledges that society views his actions as wrong, but he never indicates that he believes them to be wrong. At times he tries to normalize his behavior, saying “What man would have acted differently?”

Mr. V is polite and appropriate and promises to abide by our recommendation, yet he sees no reason for us to deny his request and no connection between his criminal record and the nature of his crimes or the terms of his parole. His denial and lack of insight are typical of convicted pedophiles (Box 1).

Box 1

The authors’ observations

Anyone evaluating Mr. V would be inclined to treat or dismiss him, or to suppress his or her feelings to avoid prejudice.

Treat or dismiss. As physicians, we are trained to “First, do no harm.” In this case, however, we must consider who could be harmed by treatment or dismissal.

“First, do no harm” is usually taken to mean “no harm to the patient” but could also be interpreted as “no harm to society.” Even if testosterone treatment did not physically harm Mr. V, activating his sex drive could endanger society by spurring him on to molest another child (Box 2). The treatment could also harm Mr. V by making it easier for him to violate parole.

Although failure to treat Mr. V’s sexual dysfunction would likely pose no harm to society, not assessing him might endanger society by clearing the path toward this treatment.

Box 2

Avoiding prejudice. When facing an unpleasant task, people often tell themselves consciously or unconsciously that their reaction is wrong and that they must carry on.⁷ Our revulsion toward Mr. V prompted us to be dispassionate and objective, but suppressing our emotions altogether could have obscured potentially serious objections. At the same time, giving ascendancy to negative emotions without questioning them could harm the patient—or at least obscure an opportunity to do good.

 

When treating patients such as Mr. V, we must not dismiss our feelings—however uncomfortable or unprofessional they might seem—so that we can manage them appropriately. Don’t be ashamed of your feelings—or at least be aware of your shame.

In such cases, these important steps can minimize the risk of compromising treatment or assessment:

• Be aware of your feelings. Reflecting on countertransference after the session, either alone or with other therapists, can help you recognize your feelings.
  
• Seek peer supervision when evaluating a patient such as Mr. V to help identify potential “blind spots.”
  
• Be aware of your limitations. Hubris is among a therapist’s most serious potential pitfalls. We all have strengths and weaknesses and should be mindful of them.
  

The authors’ observations

We took a passive-neutral stance. Sitting with Mr. V without deciding a course of action gave us time to assess our own reactions and limitations and how they might influence our actions.

CONSULTATION: OTHER OPINIONS

The examining psychiatrist (a psychiatric resident) sought advice from an experienced geriatric psychiatrist, a neuropsychologist, and other residents. We discussed our countertransference toward Mr. V and provided mutual supervision. We then acknowledged that none of us had expertise in treating pedophiles and that treating an unfamiliar mental condition would be unethical.

The authors’ observations

In requesting other opinions, we also weighed these important questions:

Is Mr. V violating parole by requesting testosterone injections and taking (unprescribed) sildenafil? We felt we could not rightfully answer this question, since our expertise in the standard of care for patients such as Mr. V was insufficient and any recommendation would be ill-informed.

Sildenafil use is fairly common among convicted sex offenders, as evidenced by the recent controversy over Medicaid providing the drug to this group (see Related resources).

Assuming the testosterone injections promote intercourse, would they increase Mr. V’s arousal? Hall found that offenders who can voluntarily and completely inhibit sexual arousal are less deviant when not attempting to inhibit arousal than are those who cannot completely inhibit arousal.⁸

Hall, however, urges clinicians to consider variables that influence sexual response before determining how arousal affects an offender’s behavior. With no objective measure of sexual arousal, it is unclear whether increasing Mr. V’s testosterone would heighten it—and his potential threat to society.

The Abel Assessment of Sexual Interest was devised to determine sexual pathology, but evidence suggests this test is clinically unreliable.

Would enhancing Mr. V’s arousal increase his risk of recidivism? Although some studies have found that castration decreases a sex offender’s sexual activity, evidence suggests that sexual responsiveness after castration varies considerably. Heim found that:

• 31% of castrates could still have intercourse
  
• rapists are more sexually active than pedophiles after castration
  
• men ages 46 to 59 experience a greater reduction in sexual behavior than do men age 9
  

These findings suggest that castration’s effects on male sexuality are unpredictable, making it an unreliable treatment for incarcerated sex offenders.⁹ They also suggest that enhancing Mr. V’s arousal could increase his odds of recidivism. Stone et al,¹⁰ however, recorded recidivism rates of 3% across 30 years among castrated sex offenders, compared with 58% among non-castrates.

What standard of care applies to Mr. V? Treating pedophilia is difficult and poorly understood. Psychotherapy is considered an adjunct to medication or surgery. Surgical interventions are akin to punishment, whereas medications—well-studied and often augmented with psychotherapy—are associated with high recidivism rates.^11,14

Surgery. Orchiectomy is by far the most common surgical intervention. Experimental procedures have targeted stereotaxic ablation of specific parts of the brain, usually the hypothalamus or amygdala, but these techniques have not been adequately studied in humans.¹¹ Even so, testosterone therapy can restore sexual function after castration.¹⁰

Medications. Antiandrogens such as medroxy-progesterone acetate (MPA) inhibit intracellular uptake of androgens (such as testosterone) by blocking their binding to the receptor.¹² MPA is most frequently used in the United States.

Long-acting analogs of gonadotropin-releasing hormone (GnRH), such as leuprolide, nafarelin, goserelin, and triptorelin, have shown efficacy in early studies.¹² These agents down-regulate gonadotroph cells, inducing severe but reversible hypogonadism with few other side effects.

Although decreased libido is a common side effect of selective serotonin reuptake inhibitors (SSRIs), use of these agents to reduce sex drive in convicted pedophiles has not been studied. Because onset of decreased libido with SSRI use is unpredictable, we cannot recommend their use to reduce sex drive in convicted offenders.

Psychotherapy. Power¹⁴ nicely outlines the elements of psychotherapy for pedophilia:

• explanation and education
  
• manipulating the environment
  
• suggestion, including hypnosis and persuasion
  
• superficial analysis
  
• deep-transference analysis
  
• sublimation.
  

If Mr. V commits another sexual offense after receiving testosterone, can the doctors who prescribed, authorized, or gave the injections be held liable?

 

Stone et al¹⁰ draw several germane conclusions:

• Sentencing laws are often unclear or do not take into account scientific research on pedophilia. For example, psychological testing often is not ordered before a treatment is mandated, even though knowing the patient’s psychological profile and the nature of his predilections are crucial to treatment and prognosis.¹²
  
• Many laws do not suggest an instrument of implementation. For example, most laws that mandate a patient evaluation do not specify whether a licensed psychiatrist, psychologist, or other clinician should evaluate the patient.
  
• Many laws directed against pedophilia are punitive in nature. Mandated treatment—or the informed consent that precedes it—is often inadequate,¹⁰ and physicians can be held liable in either case. However, we could not determine the liability that could result from enhancing a convicted pedophile’s libido.
  

REFERRAL: TREATMENT ADVICE

We referred Mr. V back to his primary care physician and advised the doctor to:

• discuss the testosterone treatment request with physicians who treated Mr. V at the state prison
  
• call our hospital’s attorney to investigate the legal implications of treating Mr. V.
  

We also recommended against enhancing Mr. V’s libido, given his poor insight and denial and the primary care physician’s lack of expertise in this treatment. A recent check of Mr. V’s electronic record indicated that he was not given medication to enhance sexual performance.

Related resources

• Sex offenders get Medicaid-paid Viagra. Associated Press May 22, 2005. http://msnbc.msn.com/id/7946129/.
  
• Conte JR, Wolf S, Smith T. What sexual offenders tell us about prevention strategies. Child Abuse Negl 1989;13:293-301.
  
• U.S. Department of Justice, Bureau of Justice Statistics. Statistics on sex offenders and victims. www.ojp.usdoj.gov/bjs/abstract/saycrle.htm.
  

Drug brand names

• Goserelin • Zoladex
  
• Leuprolide • Eligard, others
  
• Medroxyprogesterone acetate • Depo-Provera, others
  
• Nafarelin • Synarel
  
• Sildenafil • Viagra
  
• Triptorelin • Trelstar Depot
  

Acknowledgment

The authors thank Cynthia Meyer, chief librarian, VA Hospital, Fresno, CA, for her help with researching this article.

Disclosure

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

HISTORY: REPEAT OFFENDER

Mr. V, age 68, was incarcerated for 13 years for two separate pedophilia convictions. During that time, he passed numerous rehabilitative courses. With several years left on his sentence, he was paroled on condition that he undergo a bilateral orchiectomy.

Eight months later, Mr. V complained to his primary care physician that he could not have sex with his girlfriend, even after taking 50 mg of sildenafil, which he had obtained from a friend. He requested testosterone injections to allow him to have intercourse. After consulting an endocrinologist, the physician ordered Mr. V to undergo a psychiatric assessment before receiving testosterone. He was referred to our outpatient clinic.

During our evaluation, Mr. V described both pedophilia incidents. In the first, he had fondled a 14-year-old girl who was a friend of his family. He pled guilty to a charge of inappropriate sexual contact with a minor and was sentenced to 3 years in a state prison for sex offenders.

Less than 2 years after he was paroled, Mr. V said, he fondled his 12-year-old granddaughter. He said his daughter “should have known better” than to leave him home alone with the child. Again he was convicted of illegal sexual relations with a minor and sentenced to 10 years at the state hospital for the criminally insane.

As Mr. V describes his past offenses, we begin feeling tremendously uneasy. Although forthcoming, he blandly denies responsibility for either incident. He acknowledges that society views his actions as wrong, but he never indicates that he believes them to be wrong. At times he tries to normalize his behavior, saying “What man would have acted differently?”

Mr. V is polite and appropriate and promises to abide by our recommendation, yet he sees no reason for us to deny his request and no connection between his criminal record and the nature of his crimes or the terms of his parole. His denial and lack of insight are typical of convicted pedophiles (Box 1).

Box 1

The authors’ observations

Anyone evaluating Mr. V would be inclined to treat or dismiss him, or to suppress his or her feelings to avoid prejudice.

Treat or dismiss. As physicians, we are trained to “First, do no harm.” In this case, however, we must consider who could be harmed by treatment or dismissal.

“First, do no harm” is usually taken to mean “no harm to the patient” but could also be interpreted as “no harm to society.” Even if testosterone treatment did not physically harm Mr. V, activating his sex drive could endanger society by spurring him on to molest another child (Box 2). The treatment could also harm Mr. V by making it easier for him to violate parole.

Although failure to treat Mr. V’s sexual dysfunction would likely pose no harm to society, not assessing him might endanger society by clearing the path toward this treatment.

Box 2

Avoiding prejudice. When facing an unpleasant task, people often tell themselves consciously or unconsciously that their reaction is wrong and that they must carry on.⁷ Our revulsion toward Mr. V prompted us to be dispassionate and objective, but suppressing our emotions altogether could have obscured potentially serious objections. At the same time, giving ascendancy to negative emotions without questioning them could harm the patient—or at least obscure an opportunity to do good.

 

When treating patients such as Mr. V, we must not dismiss our feelings—however uncomfortable or unprofessional they might seem—so that we can manage them appropriately. Don’t be ashamed of your feelings—or at least be aware of your shame.

In such cases, these important steps can minimize the risk of compromising treatment or assessment:

• Be aware of your feelings. Reflecting on countertransference after the session, either alone or with other therapists, can help you recognize your feelings.
  
• Seek peer supervision when evaluating a patient such as Mr. V to help identify potential “blind spots.”
  
• Be aware of your limitations. Hubris is among a therapist’s most serious potential pitfalls. We all have strengths and weaknesses and should be mindful of them.
  

The authors’ observations

We took a passive-neutral stance. Sitting with Mr. V without deciding a course of action gave us time to assess our own reactions and limitations and how they might influence our actions.

CONSULTATION: OTHER OPINIONS

The examining psychiatrist (a psychiatric resident) sought advice from an experienced geriatric psychiatrist, a neuropsychologist, and other residents. We discussed our countertransference toward Mr. V and provided mutual supervision. We then acknowledged that none of us had expertise in treating pedophiles and that treating an unfamiliar mental condition would be unethical.

The authors’ observations

In requesting other opinions, we also weighed these important questions:

Is Mr. V violating parole by requesting testosterone injections and taking (unprescribed) sildenafil? We felt we could not rightfully answer this question, since our expertise in the standard of care for patients such as Mr. V was insufficient and any recommendation would be ill-informed.

Sildenafil use is fairly common among convicted sex offenders, as evidenced by the recent controversy over Medicaid providing the drug to this group (see Related resources).

Assuming the testosterone injections promote intercourse, would they increase Mr. V’s arousal? Hall found that offenders who can voluntarily and completely inhibit sexual arousal are less deviant when not attempting to inhibit arousal than are those who cannot completely inhibit arousal.⁸

Hall, however, urges clinicians to consider variables that influence sexual response before determining how arousal affects an offender’s behavior. With no objective measure of sexual arousal, it is unclear whether increasing Mr. V’s testosterone would heighten it—and his potential threat to society.

The Abel Assessment of Sexual Interest was devised to determine sexual pathology, but evidence suggests this test is clinically unreliable.

Would enhancing Mr. V’s arousal increase his risk of recidivism? Although some studies have found that castration decreases a sex offender’s sexual activity, evidence suggests that sexual responsiveness after castration varies considerably. Heim found that:

• 31% of castrates could still have intercourse
  
• rapists are more sexually active than pedophiles after castration
  
• men ages 46 to 59 experience a greater reduction in sexual behavior than do men age 9
  

These findings suggest that castration’s effects on male sexuality are unpredictable, making it an unreliable treatment for incarcerated sex offenders.⁹ They also suggest that enhancing Mr. V’s arousal could increase his odds of recidivism. Stone et al,¹⁰ however, recorded recidivism rates of 3% across 30 years among castrated sex offenders, compared with 58% among non-castrates.

What standard of care applies to Mr. V? Treating pedophilia is difficult and poorly understood. Psychotherapy is considered an adjunct to medication or surgery. Surgical interventions are akin to punishment, whereas medications—well-studied and often augmented with psychotherapy—are associated with high recidivism rates.^11,14

Surgery. Orchiectomy is by far the most common surgical intervention. Experimental procedures have targeted stereotaxic ablation of specific parts of the brain, usually the hypothalamus or amygdala, but these techniques have not been adequately studied in humans.¹¹ Even so, testosterone therapy can restore sexual function after castration.¹⁰

Medications. Antiandrogens such as medroxy-progesterone acetate (MPA) inhibit intracellular uptake of androgens (such as testosterone) by blocking their binding to the receptor.¹² MPA is most frequently used in the United States.

Long-acting analogs of gonadotropin-releasing hormone (GnRH), such as leuprolide, nafarelin, goserelin, and triptorelin, have shown efficacy in early studies.¹² These agents down-regulate gonadotroph cells, inducing severe but reversible hypogonadism with few other side effects.

Although decreased libido is a common side effect of selective serotonin reuptake inhibitors (SSRIs), use of these agents to reduce sex drive in convicted pedophiles has not been studied. Because onset of decreased libido with SSRI use is unpredictable, we cannot recommend their use to reduce sex drive in convicted offenders.

Psychotherapy. Power¹⁴ nicely outlines the elements of psychotherapy for pedophilia:

• explanation and education
  
• manipulating the environment
  
• suggestion, including hypnosis and persuasion
  
• superficial analysis
  
• deep-transference analysis
  
• sublimation.
  

If Mr. V commits another sexual offense after receiving testosterone, can the doctors who prescribed, authorized, or gave the injections be held liable?

 

Stone et al¹⁰ draw several germane conclusions:

• Sentencing laws are often unclear or do not take into account scientific research on pedophilia. For example, psychological testing often is not ordered before a treatment is mandated, even though knowing the patient’s psychological profile and the nature of his predilections are crucial to treatment and prognosis.¹²
  
• Many laws do not suggest an instrument of implementation. For example, most laws that mandate a patient evaluation do not specify whether a licensed psychiatrist, psychologist, or other clinician should evaluate the patient.
  
• Many laws directed against pedophilia are punitive in nature. Mandated treatment—or the informed consent that precedes it—is often inadequate,¹⁰ and physicians can be held liable in either case. However, we could not determine the liability that could result from enhancing a convicted pedophile’s libido.
  

REFERRAL: TREATMENT ADVICE

We referred Mr. V back to his primary care physician and advised the doctor to:

• discuss the testosterone treatment request with physicians who treated Mr. V at the state prison
  
• call our hospital’s attorney to investigate the legal implications of treating Mr. V.
  

We also recommended against enhancing Mr. V’s libido, given his poor insight and denial and the primary care physician’s lack of expertise in this treatment. A recent check of Mr. V’s electronic record indicated that he was not given medication to enhance sexual performance.

Related resources

• Sex offenders get Medicaid-paid Viagra. Associated Press May 22, 2005. http://msnbc.msn.com/id/7946129/.
  
• Conte JR, Wolf S, Smith T. What sexual offenders tell us about prevention strategies. Child Abuse Negl 1989;13:293-301.
  
• U.S. Department of Justice, Bureau of Justice Statistics. Statistics on sex offenders and victims. www.ojp.usdoj.gov/bjs/abstract/saycrle.htm.
  

Drug brand names

• Goserelin • Zoladex
  
• Leuprolide • Eligard, others
  
• Medroxyprogesterone acetate • Depo-Provera, others
  
• Nafarelin • Synarel
  
• Sildenafil • Viagra
  
• Triptorelin • Trelstar Depot
  

Acknowledgment

The authors thank Cynthia Meyer, chief librarian, VA Hospital, Fresno, CA, for her help with researching this article.

Disclosure

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