Primary care doctors refer patients with dementia to psychiatrists when the diagnosis or disease course is unclear. Psychiatrists thus must often discern non-Alzheimer’s dementias— particularly the vascular and Lewy body types— from Alzheimer’s dementia. This article describes:

• features that distinguish vascular, Lewy body, and Alzheimer’s dementias
• cognitive and medical tests to help determine dementia type and facilitate treatment
• risk factors that promote cognitive and functional decline
• strategies for using medication while minimizing side-effect risks.

CASE REPORT: DISRUPTIVE IN DAY CARE

Ms. Z, age 82, is referred to a psychiatrist after numerous failed attempts by her primary care physician to stop her medical and psychiatric deterioration.

Table 1

Estimated dementia type prevalence among patients with dementia

The patient was functioning well at home until 6 months ago, when her husband’s death triggered a dramatic functional decline. She has Parkinson’s disease and has had dementia symptoms for 3 years, but family members do not recall a dementia diagnosis.

Ms. Z has become increasingly disruptive in day care; she yelled at and slapped a staff member during one episode. Her son is concerned that additional outbursts will prompt her dismissal. Her Mini-Mental State Examination (MMSE) score is 19, indicating moderate dementia.

Donepezil, 10 mg/d across 2 years, has not slowed Ms. Z’s memory decline. Carbidopa/levadopa, 25/250 mg tid over 1 year, has not improved her Parkinson’s symptoms. Risperidone, 0.5 mg bid, caused marked sedation and unsteady gait and was stopped after 4 weeks. She also is taking hydrocodone/acetaminophen, 5/500 mg/d for osteoarthritis, and lisinopril/hydrochlorothiazide, 10/12.5 mg/d for hypertension.

Discussion. As with Ms. Z, a significant other can mask a dementia patient’s cognitive deficits, but these deficits become apparent after the partner dies. Family members then discover that a parent or sibling cannot function independently.

Treatment should target Ms. Z’s aggression to allow her to stay in day care and her son to care for her at home. Determining the dementia type is crucial to planning treatment and preserving function.

WHICH DEMENTIA IS WHICH?

Non-Alzheimer’s dementias account for up to 35% of dementia cases (Table 1).¹ The pathologic correlations separating Alzheimer’s, vascular, and Lewy body dementias are often confusing:

• Beta-amyloid plaques are common in Alzheimer’s and Lewy body dementias, although neurofibrillary tangles are much less common in the Lewy body type.
• Synaptic cholinergic deficiencies are seen in Alzheimer’s and vascular dementias.
• Hypertension and hyperlipidemia—both traditional vascular risk factors—also appear to contribute to Alzheimer’s dementia.

Vascular dementia. Large, single-vessel hemispheric infarcts cause substantial damage, whereas multiple small vascular lesions (such as lacunae or mini-infarcts) can have more-subtle effects when strategically located, such as in the basal ganglia, hippocampus, or thalamus. These smaller lesions can disrupt frontal cortical-subcortical neural pathways and contribute to difficulties with executive functions (judgment, insight), emotional control, and behavior.

Lesions from a cerebrovascular accident, however, do not necessarily cause dementia, and the mechanism by which lesions cause dementia is not fully understood. Post-stroke dementia sometimes is progressive, suggesting a degenerative rather than vascular cause.

Lewy body dementia is associated with Parkinson’s disease, as Lewy body inclusion deposits are common to both disorders. The deposits typically appear in the cerebral cortex in Lewy body dementia but not in Parkinson’s.

Amyloid protein deposits alter the clinical presentation. Patients with these lesions have fewer visual hallucinations and motor problems, making diagnosis more difficult.

Lewy body dementia, like all major dementias, usually surfaces after age 75. Its clinical course generally is considered worse than that of Alzheimer’s dementia, but these two dementia types do not differ substantially in age of onset, age of death, or survival rates.

Table 2

Clinical features that characterize Lewy body dementia

FEATURES OF VASCULAR DEMENTIA

Onset can be gradual but is more often sudden— usually occurring shortly after an ischemic stroke. Disease progression can be gradual or dramatic, depending on the vascular event type. Cognitive and physical decline in vascular dementia usually is stepwise over time, whereas decline in Alzheimer’s dementia is more gradual with progressive severity.

Patients with vascular dementia classically present with memory loss temporally associated with other typical stroke stigmata. Brain imaging often uncovers evidence of stroke that is otherwise not clinically evident.

CNS manifestations of vascular dementia often include memory loss, emotional lability (including depression), and executive-task dysfunction. Patients usually have atrial fibrillation or vascular risk factors, including diabetes mellitus, hypertension, hyperlipidemia, obesity, or tobacco use. Patients with previous stroke, coronary artery disease, or peripheral vascular disease are at increased risk.

Vascular dementia is categorized by stroke type:

Embolic infarct. Emboli, typically cardiac in origin, can occlude small or large cerebral arteries, resulting in correspondingly sized infarcts. Atrial fibrillation can promote areas in the atria with relatively low flow turbulence. Blood clots can form that eventually embolize via the carotid arteries. Multiple emboli can occur, causing progressive dementia.

Cerebral hemorrhage —small or large—can be devastating. Hypertension is the major risk factor for this form of stroke.

Multi-infarct dementia. Multiple cerebral blood vessel infarcts classically lead to stepwise functional decline after each event. Multiple small infarcts can occur in various brain regions, including the cortex and basal ganglia. Binswanger’s disease, a variant of vascular dementia in which incomplete ischemia is limited to the hemispheric white matter, tends to be fairly progressive.²

Small-vessel disease. Reduced blood flow and tissue perfusion can cause small-vessel disease. Often the ischemia is “silent,” detectable only on MRI or CT. The infarcts typically cause lacunar lesions, nerve demyelination, and gliosis.³ These can occur to some extent in nondemented patients but become significant with more-extensive disease.

FEATURES OF LEWY BODY DEMENTIA

As with all dementias, permanent memory loss must be present to diagnose this dementia sub-type. Overall cognitive deficits may be more prominent than memory loss, however. The patient may have trouble performing cognitive tasks that employ visuospatial abilities, executive functions, and attention. Neuropsychiatric symptoms that overlap with Alzheimer’s dementia include apathy, anxiety, agitation, depression, anhedonia, and paranoia.

The presence of visual hallucinations, fluctuating cognition, or extrapyramidal symptoms (EPS) distinguish Lewy body from Alzheimer’s dementia.

Visual hallucinations are prominent in Lewy body dementia and often prompt psychiatric referral (Table 2). They usually surface early in the disease course and tend to persist. Other sensory hallucinations also can occur.

The hallucinations often are detailed and vivid and the patient may be aware they are occurring, especially if the dementia is not advanced. Treatment might not be necessary for mild hallucinations, which can concern the caregiver more than the patient.

Antipsychotics paradoxically worsen hallucinations in Lewy body dementia, and many patients present to psychiatrists after failing an empiric trial. A failed antipsychotic course in a patient diagnosed with Alzheimer’s dementia could indicate that the diagnosis is incorrect.

Fluctuating cognition occurs in 50% to 75% of Lewy body cases. Alertness, attention, and concentration are variable and can cycle within hours to weeks. The patient often is fairly interactive and social for a time, then has periods of diminished function and being “out of it.” Some patients have recurrent delirium and undergo multiple workups in search of a cause.

EPS. As many as 75% of Lewy body patients have parkinsonian motor features.⁴ Because these features are not essential to the diagnosis, their absence is the most common reason Lewy body dementia goes unrecognized.¹

Motor involvement varies and can be worsened by antipsychotics. Overuse of antipsychotics in Alzheimer’s or vascular dementia also can cause motor symptoms that mimic Lewy body features.

EPS orientation tends to be axial, showing less facial expressivity and more postural imbalance. Peripheral signs such as tremor and extremity rigidity tend to be less dominant.

MAKING THE DIAGNOSIS

Vascular and Lewy body dementia diagnoses are primarily based on clinical features and findings. Memory loss is necessary for either diagnosis.

Vascular dementia. Most consensus criteria require presence of dementia, physical or radiologic signs of a stroke, and a temporal relationship between the stroke and the dementia for a vascular dementia diagnosis.

Hachinski’s “ischemia scale” can help differentiate multi-infarct from Alzheimer’s dementia.⁵ Cases are scored on a 0-to-9 scale, with point values for abrupt onset; stepwise course; history of stroke; and presence of somatic complaints, emotional lability, hypertension, and focal neurologic signs. A score ≥4 suggests vascular dementia.

The scale, however, does not account for imaging studies, vascular risk factors other than hypertension, or repeated silent strokes that can cause symptoms. Also, some patients who score below the cutoff have strategic infarct dementias.

Lewy body dementia. Clinical consensus guidelines developed by McKeith et al⁶ can help clinicians recognize and categorize this dementia type (Table 2). Several studies of diagnostic criteria have shown very good specificity but variable sensitivity.⁷ Because no standard imaging modalities or serum markers exist, presence of progressive memory loss, fluctuating cognition, visual hallucinations, and EPS should drive the diagnosis.

Lewy body dementia is commonly misdiagnosed as Parkinson’s dementia. The two types are readily differentiated by onset of memory loss, which emerges late in Parkinson’s dementia but is early and prominent in Lewy body dementia.

CASE CONTINUED: HISTORY LEADS TO DIAGNOSIS

Ms. Z was diagnosed as having Lewy body dementia, as her cognitive decline clearly preceded her motor deficits. Further questioning revealed fluctuating attention levels and a history of visual hallucinations.

TESTING PATIENT FUNCTION

Neuropsychiatric tests. DSM-IV recommends testing memory, orientation, language, praxis, constructional ability, and executive control function in patients with dementia. Numerous tests can aid in diagnosis, but they generally are too lengthy to be practical. The MMSE takes 5 to 10 minutes, but it might miss mild memory loss or executive dysfunction.

Giving a quick clock-drawing test in tandem with the MMSE can help measure basic executive control and constructional ability. Also, patients with Lewy body or vascular dementia often are more proficient than patients with Alzheimer’s dementia on verbal memory tests but less proficient on visuospatial performance. Consider referring clinically challenging patients for more-extensive neuropsychiatric testing.

Lab tests. Blood tests including TSH and B¹²/folate screens are usually performed but rarely positive. Rapid plasma reagin testing for syphilis is no longer recommended unless syphilis is suspected.

Table 3

Potential cognitive side effects associated with psychotropic classes*

Radiologic imaging. Radiologic imaging (MRI or CT) can show infarcts in vascular dementia and can rule out:

• a brain tumor
• a subdural hemorrhage after recent head trauma
• or normal-pressure hydrocephalus in patients with dementia, gait instability, and/or urinary incontinence.

Brain imaging in Lewy body dementia can show hippocampal preservation⁸ but is not specific and does not significantly support the diagnosis. Specialized tests such as single-photon emission computed tomography or positron-emission tomography show occipital hypoperfusion⁹ but are expensive, not sufficiently specific, and do not add substantial value over clinical criteria.

MANAGING SYMPTOMS

Medication may be necessary if the patient is frequently and significantly agitated. Consider prescribing a selective serotonin reuptake inhibitor, an anticonvulsant such as divalproex or carbamazepine as a mood stabilizer, or a short-acting benzodiazepine. Start low and titrate slowly if needed.

Find out if the patient is taking medications that may be causing bothersome side effects. Avoid agents with potential cognitive or anticholinergic effects (Table 3); the latter can cause confusion, sedation, and falls in the elderly.

Cholinesterase inhibitors, FDA-approved for use in Alzheimer’s dementia, have been shown to reduce cognitive and global functioning decline in vascular dementia.¹⁰ A cholinergic deficit present in vascular dementia may explain the drugs’ effectiveness. Donepezil, galantamine, and rivastigmine have all shown positive effects on cognition.

Because patients with Lewy body hallucinations have greater synaptic acetylcholine deficits, cholinesterase inhibitors tend to be more effective in Lewy body dementia than in other dementia subtypes. In small open-label studies, patients taking cholinesterase inhibitors for Lewy body dementia have shown sustained improvements (up to 96 months) in cognition and behavior. Wild et al,¹¹ however, concluded that the evidence supporting use of these agents—specifically rivastigmine—is weak.

Also, cholinesterase inhibitors offer fairly modest effectiveness, do not work for all patients, and do not prevent cognitive decline even when taken regularly. Because cholinesterase inhibitors are costly and most Medicare patients lack prescription medication coverage, an initial short (6-month) trial is recommended. Re-evaluate the patient periodically by using caregiver reports, caregiver assessment scales, and basic cognitive testing.

Cholinesterase inhibitor dosing is the same for vascular and Lewy body dementia as it is for Alzheimer’s disease. Tell patients to take the agents with food to minimize potential intestinal side effects.

Memantine. In European studies, memantine has shown positive effects on cognition and function in vascular dementia. Memantine, a N-methyl-D-aspartate receptor antagonist, is FDA-approved for moderate to severe Alzheimer’s dementia.¹²

DELAYING DECLINE

Controlling risk factors. Controlling vascular risk factors—especially high blood pressure—is the most effective way to prevent or treat vascular dementia. In primary prevention studies, patients with good hypertension and hyperlipidemia control developed dementia more slowly than did nontreated cohorts.

In patients with coronary artery disease, statins have been shown to lower cholesterol and stabilize pre-existing plaques in the arterial wall, reducing the risk of plaque rupture. Low-density lipoproteincholesterol goals vary according to vascular risk factors but should be <100 mg/dL for patients with vascular dementia, who are at highest risk. Blood pressure goals are ≤140 mm Hg (systolic) and ≤90 mm Hg (diastolic).

Glycemic control (fasting blood glucose <110 mg/dL) and smoking cessation can also reduce the risk of further vascular events. Most patients should be taking an antiplatelet medication, preferably aspirin, to reduce clotting risk.

Although Lewy body dementia has no known risk factors other than age, research will determine whether vascular or other factors contribute to its development.

CASE CONTINUED: TARGETING AGGRESSION

Ms. Z was given divalproex, 250 mg bid, to reduce her frequent aggression. Her visual hallucinations were considered mild and not problematic and therefore were not treated. She responded well to the medication, allowing her to remain in day care and avoid nursing home placement.

Related resources

• Alzheimer’s Association. http://www.alz.org
• American Geriatrics Society. http://www.americangeriatrics.org

Drug brand names

• Carbamazepine • Tegretol, others
• Carbidopa/Levodopa • Various
• Divalproex • Depakote
• Donepezil • Aricept
• Galantamine • Reminyl
• Hydrocodone/acetaminophen • Vicodin, others
• Lisinopril/hydrochlorothiazide • Prinzide, Zestoretic
• Memantine • Namenda
• Risperdone • Risperdal
• Rivastigmine • Exelon

Disclosure

Dr. Bartz is a speaker for Forest Pharmaceuticals and Novartis Pharmaceuticals Corp.

Primary care doctors refer patients with dementia to psychiatrists when the diagnosis or disease course is unclear. Psychiatrists thus must often discern non-Alzheimer’s dementias— particularly the vascular and Lewy body types— from Alzheimer’s dementia. This article describes:

• features that distinguish vascular, Lewy body, and Alzheimer’s dementias
• cognitive and medical tests to help determine dementia type and facilitate treatment
• risk factors that promote cognitive and functional decline
• strategies for using medication while minimizing side-effect risks.

CASE REPORT: DISRUPTIVE IN DAY CARE

Ms. Z, age 82, is referred to a psychiatrist after numerous failed attempts by her primary care physician to stop her medical and psychiatric deterioration.

Table 1

Estimated dementia type prevalence among patients with dementia

The patient was functioning well at home until 6 months ago, when her husband’s death triggered a dramatic functional decline. She has Parkinson’s disease and has had dementia symptoms for 3 years, but family members do not recall a dementia diagnosis.

Ms. Z has become increasingly disruptive in day care; she yelled at and slapped a staff member during one episode. Her son is concerned that additional outbursts will prompt her dismissal. Her Mini-Mental State Examination (MMSE) score is 19, indicating moderate dementia.

Donepezil, 10 mg/d across 2 years, has not slowed Ms. Z’s memory decline. Carbidopa/levadopa, 25/250 mg tid over 1 year, has not improved her Parkinson’s symptoms. Risperidone, 0.5 mg bid, caused marked sedation and unsteady gait and was stopped after 4 weeks. She also is taking hydrocodone/acetaminophen, 5/500 mg/d for osteoarthritis, and lisinopril/hydrochlorothiazide, 10/12.5 mg/d for hypertension.

Discussion. As with Ms. Z, a significant other can mask a dementia patient’s cognitive deficits, but these deficits become apparent after the partner dies. Family members then discover that a parent or sibling cannot function independently.

Treatment should target Ms. Z’s aggression to allow her to stay in day care and her son to care for her at home. Determining the dementia type is crucial to planning treatment and preserving function.

WHICH DEMENTIA IS WHICH?

Non-Alzheimer’s dementias account for up to 35% of dementia cases (Table 1).¹ The pathologic correlations separating Alzheimer’s, vascular, and Lewy body dementias are often confusing:

• Beta-amyloid plaques are common in Alzheimer’s and Lewy body dementias, although neurofibrillary tangles are much less common in the Lewy body type.
• Synaptic cholinergic deficiencies are seen in Alzheimer’s and vascular dementias.
• Hypertension and hyperlipidemia—both traditional vascular risk factors—also appear to contribute to Alzheimer’s dementia.

Vascular dementia. Large, single-vessel hemispheric infarcts cause substantial damage, whereas multiple small vascular lesions (such as lacunae or mini-infarcts) can have more-subtle effects when strategically located, such as in the basal ganglia, hippocampus, or thalamus. These smaller lesions can disrupt frontal cortical-subcortical neural pathways and contribute to difficulties with executive functions (judgment, insight), emotional control, and behavior.

Lesions from a cerebrovascular accident, however, do not necessarily cause dementia, and the mechanism by which lesions cause dementia is not fully understood. Post-stroke dementia sometimes is progressive, suggesting a degenerative rather than vascular cause.

Lewy body dementia is associated with Parkinson’s disease, as Lewy body inclusion deposits are common to both disorders. The deposits typically appear in the cerebral cortex in Lewy body dementia but not in Parkinson’s.

Amyloid protein deposits alter the clinical presentation. Patients with these lesions have fewer visual hallucinations and motor problems, making diagnosis more difficult.

Lewy body dementia, like all major dementias, usually surfaces after age 75. Its clinical course generally is considered worse than that of Alzheimer’s dementia, but these two dementia types do not differ substantially in age of onset, age of death, or survival rates.

Table 2

Clinical features that characterize Lewy body dementia

FEATURES OF VASCULAR DEMENTIA

Onset can be gradual but is more often sudden— usually occurring shortly after an ischemic stroke. Disease progression can be gradual or dramatic, depending on the vascular event type. Cognitive and physical decline in vascular dementia usually is stepwise over time, whereas decline in Alzheimer’s dementia is more gradual with progressive severity.

Patients with vascular dementia classically present with memory loss temporally associated with other typical stroke stigmata. Brain imaging often uncovers evidence of stroke that is otherwise not clinically evident.

CNS manifestations of vascular dementia often include memory loss, emotional lability (including depression), and executive-task dysfunction. Patients usually have atrial fibrillation or vascular risk factors, including diabetes mellitus, hypertension, hyperlipidemia, obesity, or tobacco use. Patients with previous stroke, coronary artery disease, or peripheral vascular disease are at increased risk.

Vascular dementia is categorized by stroke type:

Embolic infarct. Emboli, typically cardiac in origin, can occlude small or large cerebral arteries, resulting in correspondingly sized infarcts. Atrial fibrillation can promote areas in the atria with relatively low flow turbulence. Blood clots can form that eventually embolize via the carotid arteries. Multiple emboli can occur, causing progressive dementia.

Cerebral hemorrhage —small or large—can be devastating. Hypertension is the major risk factor for this form of stroke.

Multi-infarct dementia. Multiple cerebral blood vessel infarcts classically lead to stepwise functional decline after each event. Multiple small infarcts can occur in various brain regions, including the cortex and basal ganglia. Binswanger’s disease, a variant of vascular dementia in which incomplete ischemia is limited to the hemispheric white matter, tends to be fairly progressive.²

Small-vessel disease. Reduced blood flow and tissue perfusion can cause small-vessel disease. Often the ischemia is “silent,” detectable only on MRI or CT. The infarcts typically cause lacunar lesions, nerve demyelination, and gliosis.³ These can occur to some extent in nondemented patients but become significant with more-extensive disease.

FEATURES OF LEWY BODY DEMENTIA

As with all dementias, permanent memory loss must be present to diagnose this dementia sub-type. Overall cognitive deficits may be more prominent than memory loss, however. The patient may have trouble performing cognitive tasks that employ visuospatial abilities, executive functions, and attention. Neuropsychiatric symptoms that overlap with Alzheimer’s dementia include apathy, anxiety, agitation, depression, anhedonia, and paranoia.

The presence of visual hallucinations, fluctuating cognition, or extrapyramidal symptoms (EPS) distinguish Lewy body from Alzheimer’s dementia.

Visual hallucinations are prominent in Lewy body dementia and often prompt psychiatric referral (Table 2). They usually surface early in the disease course and tend to persist. Other sensory hallucinations also can occur.

The hallucinations often are detailed and vivid and the patient may be aware they are occurring, especially if the dementia is not advanced. Treatment might not be necessary for mild hallucinations, which can concern the caregiver more than the patient.

Antipsychotics paradoxically worsen hallucinations in Lewy body dementia, and many patients present to psychiatrists after failing an empiric trial. A failed antipsychotic course in a patient diagnosed with Alzheimer’s dementia could indicate that the diagnosis is incorrect.

Fluctuating cognition occurs in 50% to 75% of Lewy body cases. Alertness, attention, and concentration are variable and can cycle within hours to weeks. The patient often is fairly interactive and social for a time, then has periods of diminished function and being “out of it.” Some patients have recurrent delirium and undergo multiple workups in search of a cause.

EPS. As many as 75% of Lewy body patients have parkinsonian motor features.⁴ Because these features are not essential to the diagnosis, their absence is the most common reason Lewy body dementia goes unrecognized.¹

Motor involvement varies and can be worsened by antipsychotics. Overuse of antipsychotics in Alzheimer’s or vascular dementia also can cause motor symptoms that mimic Lewy body features.

EPS orientation tends to be axial, showing less facial expressivity and more postural imbalance. Peripheral signs such as tremor and extremity rigidity tend to be less dominant.

MAKING THE DIAGNOSIS

Vascular and Lewy body dementia diagnoses are primarily based on clinical features and findings. Memory loss is necessary for either diagnosis.

Vascular dementia. Most consensus criteria require presence of dementia, physical or radiologic signs of a stroke, and a temporal relationship between the stroke and the dementia for a vascular dementia diagnosis.

Hachinski’s “ischemia scale” can help differentiate multi-infarct from Alzheimer’s dementia.⁵ Cases are scored on a 0-to-9 scale, with point values for abrupt onset; stepwise course; history of stroke; and presence of somatic complaints, emotional lability, hypertension, and focal neurologic signs. A score ≥4 suggests vascular dementia.

The scale, however, does not account for imaging studies, vascular risk factors other than hypertension, or repeated silent strokes that can cause symptoms. Also, some patients who score below the cutoff have strategic infarct dementias.

Lewy body dementia. Clinical consensus guidelines developed by McKeith et al⁶ can help clinicians recognize and categorize this dementia type (Table 2). Several studies of diagnostic criteria have shown very good specificity but variable sensitivity.⁷ Because no standard imaging modalities or serum markers exist, presence of progressive memory loss, fluctuating cognition, visual hallucinations, and EPS should drive the diagnosis.

Lewy body dementia is commonly misdiagnosed as Parkinson’s dementia. The two types are readily differentiated by onset of memory loss, which emerges late in Parkinson’s dementia but is early and prominent in Lewy body dementia.

CASE CONTINUED: HISTORY LEADS TO DIAGNOSIS

Ms. Z was diagnosed as having Lewy body dementia, as her cognitive decline clearly preceded her motor deficits. Further questioning revealed fluctuating attention levels and a history of visual hallucinations.

TESTING PATIENT FUNCTION

Neuropsychiatric tests. DSM-IV recommends testing memory, orientation, language, praxis, constructional ability, and executive control function in patients with dementia. Numerous tests can aid in diagnosis, but they generally are too lengthy to be practical. The MMSE takes 5 to 10 minutes, but it might miss mild memory loss or executive dysfunction.

Giving a quick clock-drawing test in tandem with the MMSE can help measure basic executive control and constructional ability. Also, patients with Lewy body or vascular dementia often are more proficient than patients with Alzheimer’s dementia on verbal memory tests but less proficient on visuospatial performance. Consider referring clinically challenging patients for more-extensive neuropsychiatric testing.

Lab tests. Blood tests including TSH and B¹²/folate screens are usually performed but rarely positive. Rapid plasma reagin testing for syphilis is no longer recommended unless syphilis is suspected.

Table 3

Potential cognitive side effects associated with psychotropic classes*

Radiologic imaging. Radiologic imaging (MRI or CT) can show infarcts in vascular dementia and can rule out:

• a brain tumor
• a subdural hemorrhage after recent head trauma
• or normal-pressure hydrocephalus in patients with dementia, gait instability, and/or urinary incontinence.

Brain imaging in Lewy body dementia can show hippocampal preservation⁸ but is not specific and does not significantly support the diagnosis. Specialized tests such as single-photon emission computed tomography or positron-emission tomography show occipital hypoperfusion⁹ but are expensive, not sufficiently specific, and do not add substantial value over clinical criteria.

MANAGING SYMPTOMS

Medication may be necessary if the patient is frequently and significantly agitated. Consider prescribing a selective serotonin reuptake inhibitor, an anticonvulsant such as divalproex or carbamazepine as a mood stabilizer, or a short-acting benzodiazepine. Start low and titrate slowly if needed.

Find out if the patient is taking medications that may be causing bothersome side effects. Avoid agents with potential cognitive or anticholinergic effects (Table 3); the latter can cause confusion, sedation, and falls in the elderly.

Cholinesterase inhibitors, FDA-approved for use in Alzheimer’s dementia, have been shown to reduce cognitive and global functioning decline in vascular dementia.¹⁰ A cholinergic deficit present in vascular dementia may explain the drugs’ effectiveness. Donepezil, galantamine, and rivastigmine have all shown positive effects on cognition.

Because patients with Lewy body hallucinations have greater synaptic acetylcholine deficits, cholinesterase inhibitors tend to be more effective in Lewy body dementia than in other dementia subtypes. In small open-label studies, patients taking cholinesterase inhibitors for Lewy body dementia have shown sustained improvements (up to 96 months) in cognition and behavior. Wild et al,¹¹ however, concluded that the evidence supporting use of these agents—specifically rivastigmine—is weak.

Also, cholinesterase inhibitors offer fairly modest effectiveness, do not work for all patients, and do not prevent cognitive decline even when taken regularly. Because cholinesterase inhibitors are costly and most Medicare patients lack prescription medication coverage, an initial short (6-month) trial is recommended. Re-evaluate the patient periodically by using caregiver reports, caregiver assessment scales, and basic cognitive testing.

Cholinesterase inhibitor dosing is the same for vascular and Lewy body dementia as it is for Alzheimer’s disease. Tell patients to take the agents with food to minimize potential intestinal side effects.

Memantine. In European studies, memantine has shown positive effects on cognition and function in vascular dementia. Memantine, a N-methyl-D-aspartate receptor antagonist, is FDA-approved for moderate to severe Alzheimer’s dementia.¹²

DELAYING DECLINE

Controlling risk factors. Controlling vascular risk factors—especially high blood pressure—is the most effective way to prevent or treat vascular dementia. In primary prevention studies, patients with good hypertension and hyperlipidemia control developed dementia more slowly than did nontreated cohorts.

In patients with coronary artery disease, statins have been shown to lower cholesterol and stabilize pre-existing plaques in the arterial wall, reducing the risk of plaque rupture. Low-density lipoproteincholesterol goals vary according to vascular risk factors but should be <100 mg/dL for patients with vascular dementia, who are at highest risk. Blood pressure goals are ≤140 mm Hg (systolic) and ≤90 mm Hg (diastolic).

Glycemic control (fasting blood glucose <110 mg/dL) and smoking cessation can also reduce the risk of further vascular events. Most patients should be taking an antiplatelet medication, preferably aspirin, to reduce clotting risk.

Although Lewy body dementia has no known risk factors other than age, research will determine whether vascular or other factors contribute to its development.

CASE CONTINUED: TARGETING AGGRESSION

Ms. Z was given divalproex, 250 mg bid, to reduce her frequent aggression. Her visual hallucinations were considered mild and not problematic and therefore were not treated. She responded well to the medication, allowing her to remain in day care and avoid nursing home placement.

Related resources

• Alzheimer’s Association. http://www.alz.org
• American Geriatrics Society. http://www.americangeriatrics.org

Drug brand names

• Carbamazepine • Tegretol, others
• Carbidopa/Levodopa • Various
• Divalproex • Depakote
• Donepezil • Aricept
• Galantamine • Reminyl
• Hydrocodone/acetaminophen • Vicodin, others
• Lisinopril/hydrochlorothiazide • Prinzide, Zestoretic
• Memantine • Namenda
• Risperdone • Risperdal
• Rivastigmine • Exelon

Disclosure

Dr. Bartz is a speaker for Forest Pharmaceuticals and Novartis Pharmaceuticals Corp.

Primary care doctors refer patients with dementia to psychiatrists when the diagnosis or disease course is unclear. Psychiatrists thus must often discern non-Alzheimer’s dementias— particularly the vascular and Lewy body types— from Alzheimer’s dementia. This article describes:

• features that distinguish vascular, Lewy body, and Alzheimer’s dementias
• cognitive and medical tests to help determine dementia type and facilitate treatment
• risk factors that promote cognitive and functional decline
• strategies for using medication while minimizing side-effect risks.

CASE REPORT: DISRUPTIVE IN DAY CARE

Ms. Z, age 82, is referred to a psychiatrist after numerous failed attempts by her primary care physician to stop her medical and psychiatric deterioration.

Table 1

Estimated dementia type prevalence among patients with dementia

The patient was functioning well at home until 6 months ago, when her husband’s death triggered a dramatic functional decline. She has Parkinson’s disease and has had dementia symptoms for 3 years, but family members do not recall a dementia diagnosis.

Ms. Z has become increasingly disruptive in day care; she yelled at and slapped a staff member during one episode. Her son is concerned that additional outbursts will prompt her dismissal. Her Mini-Mental State Examination (MMSE) score is 19, indicating moderate dementia.

Donepezil, 10 mg/d across 2 years, has not slowed Ms. Z’s memory decline. Carbidopa/levadopa, 25/250 mg tid over 1 year, has not improved her Parkinson’s symptoms. Risperidone, 0.5 mg bid, caused marked sedation and unsteady gait and was stopped after 4 weeks. She also is taking hydrocodone/acetaminophen, 5/500 mg/d for osteoarthritis, and lisinopril/hydrochlorothiazide, 10/12.5 mg/d for hypertension.

Discussion. As with Ms. Z, a significant other can mask a dementia patient’s cognitive deficits, but these deficits become apparent after the partner dies. Family members then discover that a parent or sibling cannot function independently.

Treatment should target Ms. Z’s aggression to allow her to stay in day care and her son to care for her at home. Determining the dementia type is crucial to planning treatment and preserving function.

WHICH DEMENTIA IS WHICH?

Non-Alzheimer’s dementias account for up to 35% of dementia cases (Table 1).¹ The pathologic correlations separating Alzheimer’s, vascular, and Lewy body dementias are often confusing:

• Beta-amyloid plaques are common in Alzheimer’s and Lewy body dementias, although neurofibrillary tangles are much less common in the Lewy body type.
• Synaptic cholinergic deficiencies are seen in Alzheimer’s and vascular dementias.
• Hypertension and hyperlipidemia—both traditional vascular risk factors—also appear to contribute to Alzheimer’s dementia.

Vascular dementia. Large, single-vessel hemispheric infarcts cause substantial damage, whereas multiple small vascular lesions (such as lacunae or mini-infarcts) can have more-subtle effects when strategically located, such as in the basal ganglia, hippocampus, or thalamus. These smaller lesions can disrupt frontal cortical-subcortical neural pathways and contribute to difficulties with executive functions (judgment, insight), emotional control, and behavior.

Lesions from a cerebrovascular accident, however, do not necessarily cause dementia, and the mechanism by which lesions cause dementia is not fully understood. Post-stroke dementia sometimes is progressive, suggesting a degenerative rather than vascular cause.

Lewy body dementia is associated with Parkinson’s disease, as Lewy body inclusion deposits are common to both disorders. The deposits typically appear in the cerebral cortex in Lewy body dementia but not in Parkinson’s.

Amyloid protein deposits alter the clinical presentation. Patients with these lesions have fewer visual hallucinations and motor problems, making diagnosis more difficult.

Lewy body dementia, like all major dementias, usually surfaces after age 75. Its clinical course generally is considered worse than that of Alzheimer’s dementia, but these two dementia types do not differ substantially in age of onset, age of death, or survival rates.

Table 2

Clinical features that characterize Lewy body dementia

FEATURES OF VASCULAR DEMENTIA

Onset can be gradual but is more often sudden— usually occurring shortly after an ischemic stroke. Disease progression can be gradual or dramatic, depending on the vascular event type. Cognitive and physical decline in vascular dementia usually is stepwise over time, whereas decline in Alzheimer’s dementia is more gradual with progressive severity.

Patients with vascular dementia classically present with memory loss temporally associated with other typical stroke stigmata. Brain imaging often uncovers evidence of stroke that is otherwise not clinically evident.

CNS manifestations of vascular dementia often include memory loss, emotional lability (including depression), and executive-task dysfunction. Patients usually have atrial fibrillation or vascular risk factors, including diabetes mellitus, hypertension, hyperlipidemia, obesity, or tobacco use. Patients with previous stroke, coronary artery disease, or peripheral vascular disease are at increased risk.

Vascular dementia is categorized by stroke type:

Embolic infarct. Emboli, typically cardiac in origin, can occlude small or large cerebral arteries, resulting in correspondingly sized infarcts. Atrial fibrillation can promote areas in the atria with relatively low flow turbulence. Blood clots can form that eventually embolize via the carotid arteries. Multiple emboli can occur, causing progressive dementia.

Cerebral hemorrhage —small or large—can be devastating. Hypertension is the major risk factor for this form of stroke.

Multi-infarct dementia. Multiple cerebral blood vessel infarcts classically lead to stepwise functional decline after each event. Multiple small infarcts can occur in various brain regions, including the cortex and basal ganglia. Binswanger’s disease, a variant of vascular dementia in which incomplete ischemia is limited to the hemispheric white matter, tends to be fairly progressive.²

Small-vessel disease. Reduced blood flow and tissue perfusion can cause small-vessel disease. Often the ischemia is “silent,” detectable only on MRI or CT. The infarcts typically cause lacunar lesions, nerve demyelination, and gliosis.³ These can occur to some extent in nondemented patients but become significant with more-extensive disease.

FEATURES OF LEWY BODY DEMENTIA

As with all dementias, permanent memory loss must be present to diagnose this dementia sub-type. Overall cognitive deficits may be more prominent than memory loss, however. The patient may have trouble performing cognitive tasks that employ visuospatial abilities, executive functions, and attention. Neuropsychiatric symptoms that overlap with Alzheimer’s dementia include apathy, anxiety, agitation, depression, anhedonia, and paranoia.

The presence of visual hallucinations, fluctuating cognition, or extrapyramidal symptoms (EPS) distinguish Lewy body from Alzheimer’s dementia.

Visual hallucinations are prominent in Lewy body dementia and often prompt psychiatric referral (Table 2). They usually surface early in the disease course and tend to persist. Other sensory hallucinations also can occur.

The hallucinations often are detailed and vivid and the patient may be aware they are occurring, especially if the dementia is not advanced. Treatment might not be necessary for mild hallucinations, which can concern the caregiver more than the patient.

Antipsychotics paradoxically worsen hallucinations in Lewy body dementia, and many patients present to psychiatrists after failing an empiric trial. A failed antipsychotic course in a patient diagnosed with Alzheimer’s dementia could indicate that the diagnosis is incorrect.

Fluctuating cognition occurs in 50% to 75% of Lewy body cases. Alertness, attention, and concentration are variable and can cycle within hours to weeks. The patient often is fairly interactive and social for a time, then has periods of diminished function and being “out of it.” Some patients have recurrent delirium and undergo multiple workups in search of a cause.

EPS. As many as 75% of Lewy body patients have parkinsonian motor features.⁴ Because these features are not essential to the diagnosis, their absence is the most common reason Lewy body dementia goes unrecognized.¹

Motor involvement varies and can be worsened by antipsychotics. Overuse of antipsychotics in Alzheimer’s or vascular dementia also can cause motor symptoms that mimic Lewy body features.

EPS orientation tends to be axial, showing less facial expressivity and more postural imbalance. Peripheral signs such as tremor and extremity rigidity tend to be less dominant.

MAKING THE DIAGNOSIS

Vascular and Lewy body dementia diagnoses are primarily based on clinical features and findings. Memory loss is necessary for either diagnosis.

Vascular dementia. Most consensus criteria require presence of dementia, physical or radiologic signs of a stroke, and a temporal relationship between the stroke and the dementia for a vascular dementia diagnosis.

Hachinski’s “ischemia scale” can help differentiate multi-infarct from Alzheimer’s dementia.⁵ Cases are scored on a 0-to-9 scale, with point values for abrupt onset; stepwise course; history of stroke; and presence of somatic complaints, emotional lability, hypertension, and focal neurologic signs. A score ≥4 suggests vascular dementia.

The scale, however, does not account for imaging studies, vascular risk factors other than hypertension, or repeated silent strokes that can cause symptoms. Also, some patients who score below the cutoff have strategic infarct dementias.

Lewy body dementia. Clinical consensus guidelines developed by McKeith et al⁶ can help clinicians recognize and categorize this dementia type (Table 2). Several studies of diagnostic criteria have shown very good specificity but variable sensitivity.⁷ Because no standard imaging modalities or serum markers exist, presence of progressive memory loss, fluctuating cognition, visual hallucinations, and EPS should drive the diagnosis.

Lewy body dementia is commonly misdiagnosed as Parkinson’s dementia. The two types are readily differentiated by onset of memory loss, which emerges late in Parkinson’s dementia but is early and prominent in Lewy body dementia.

CASE CONTINUED: HISTORY LEADS TO DIAGNOSIS

Ms. Z was diagnosed as having Lewy body dementia, as her cognitive decline clearly preceded her motor deficits. Further questioning revealed fluctuating attention levels and a history of visual hallucinations.

TESTING PATIENT FUNCTION

Neuropsychiatric tests. DSM-IV recommends testing memory, orientation, language, praxis, constructional ability, and executive control function in patients with dementia. Numerous tests can aid in diagnosis, but they generally are too lengthy to be practical. The MMSE takes 5 to 10 minutes, but it might miss mild memory loss or executive dysfunction.

Giving a quick clock-drawing test in tandem with the MMSE can help measure basic executive control and constructional ability. Also, patients with Lewy body or vascular dementia often are more proficient than patients with Alzheimer’s dementia on verbal memory tests but less proficient on visuospatial performance. Consider referring clinically challenging patients for more-extensive neuropsychiatric testing.

Lab tests. Blood tests including TSH and B¹²/folate screens are usually performed but rarely positive. Rapid plasma reagin testing for syphilis is no longer recommended unless syphilis is suspected.

Table 3

Potential cognitive side effects associated with psychotropic classes*

Radiologic imaging. Radiologic imaging (MRI or CT) can show infarcts in vascular dementia and can rule out:

• a brain tumor
• a subdural hemorrhage after recent head trauma
• or normal-pressure hydrocephalus in patients with dementia, gait instability, and/or urinary incontinence.

Brain imaging in Lewy body dementia can show hippocampal preservation⁸ but is not specific and does not significantly support the diagnosis. Specialized tests such as single-photon emission computed tomography or positron-emission tomography show occipital hypoperfusion⁹ but are expensive, not sufficiently specific, and do not add substantial value over clinical criteria.

MANAGING SYMPTOMS

Medication may be necessary if the patient is frequently and significantly agitated. Consider prescribing a selective serotonin reuptake inhibitor, an anticonvulsant such as divalproex or carbamazepine as a mood stabilizer, or a short-acting benzodiazepine. Start low and titrate slowly if needed.

Find out if the patient is taking medications that may be causing bothersome side effects. Avoid agents with potential cognitive or anticholinergic effects (Table 3); the latter can cause confusion, sedation, and falls in the elderly.

Cholinesterase inhibitors, FDA-approved for use in Alzheimer’s dementia, have been shown to reduce cognitive and global functioning decline in vascular dementia.¹⁰ A cholinergic deficit present in vascular dementia may explain the drugs’ effectiveness. Donepezil, galantamine, and rivastigmine have all shown positive effects on cognition.

Because patients with Lewy body hallucinations have greater synaptic acetylcholine deficits, cholinesterase inhibitors tend to be more effective in Lewy body dementia than in other dementia subtypes. In small open-label studies, patients taking cholinesterase inhibitors for Lewy body dementia have shown sustained improvements (up to 96 months) in cognition and behavior. Wild et al,¹¹ however, concluded that the evidence supporting use of these agents—specifically rivastigmine—is weak.

Also, cholinesterase inhibitors offer fairly modest effectiveness, do not work for all patients, and do not prevent cognitive decline even when taken regularly. Because cholinesterase inhibitors are costly and most Medicare patients lack prescription medication coverage, an initial short (6-month) trial is recommended. Re-evaluate the patient periodically by using caregiver reports, caregiver assessment scales, and basic cognitive testing.

Cholinesterase inhibitor dosing is the same for vascular and Lewy body dementia as it is for Alzheimer’s disease. Tell patients to take the agents with food to minimize potential intestinal side effects.

Memantine. In European studies, memantine has shown positive effects on cognition and function in vascular dementia. Memantine, a N-methyl-D-aspartate receptor antagonist, is FDA-approved for moderate to severe Alzheimer’s dementia.¹²

DELAYING DECLINE

Controlling risk factors. Controlling vascular risk factors—especially high blood pressure—is the most effective way to prevent or treat vascular dementia. In primary prevention studies, patients with good hypertension and hyperlipidemia control developed dementia more slowly than did nontreated cohorts.

In patients with coronary artery disease, statins have been shown to lower cholesterol and stabilize pre-existing plaques in the arterial wall, reducing the risk of plaque rupture. Low-density lipoproteincholesterol goals vary according to vascular risk factors but should be <100 mg/dL for patients with vascular dementia, who are at highest risk. Blood pressure goals are ≤140 mm Hg (systolic) and ≤90 mm Hg (diastolic).

Glycemic control (fasting blood glucose <110 mg/dL) and smoking cessation can also reduce the risk of further vascular events. Most patients should be taking an antiplatelet medication, preferably aspirin, to reduce clotting risk.

Although Lewy body dementia has no known risk factors other than age, research will determine whether vascular or other factors contribute to its development.

CASE CONTINUED: TARGETING AGGRESSION

Ms. Z was given divalproex, 250 mg bid, to reduce her frequent aggression. Her visual hallucinations were considered mild and not problematic and therefore were not treated. She responded well to the medication, allowing her to remain in day care and avoid nursing home placement.

Related resources

• Alzheimer’s Association. http://www.alz.org
• American Geriatrics Society. http://www.americangeriatrics.org

Drug brand names

• Carbamazepine • Tegretol, others
• Carbidopa/Levodopa • Various
• Divalproex • Depakote
• Donepezil • Aricept
• Galantamine • Reminyl
• Hydrocodone/acetaminophen • Vicodin, others
• Lisinopril/hydrochlorothiazide • Prinzide, Zestoretic
• Memantine • Namenda
• Risperdone • Risperdal
• Rivastigmine • Exelon

Disclosure

Dr. Bartz is a speaker for Forest Pharmaceuticals and Novartis Pharmaceuticals Corp.

Obstructive sleep apnea is underdiagnosed.¹ These recommendations (from the Institute for Clinical Systems Improvement’s Respiratory Steering Committee) can help providers more accurately identify adults who have OSA through a sleep study evaluation, prescribe appropriate treatment, document cases for appropriate follow-up, and increase patient understanding of related health risks. The target audience is physicians, nurses, advanced practice nurses, and physician assistants. The target population is adults.

The evidence categories for this guideline are diagnosis, evaluation, management, risk assessment, and treatment. Outcomes considered are signs and symptoms of OSA; patient risk factors, including comorbidities; accuracy of diagnostic tests; effects of treatment on apneahypopnea index and other measures; patient compliance and satisfaction with treatment; and complications of treatment. Their rating scheme has been updated to comply with the SORT taxonomy.²

Relevance and limitations

OSA affects more than 12 million people in the US, 2% of women and 4% of men aged >35 years. The patient with OSA commonly consults a physician after a sleep partner reports loud snoring and irregular breathing. The methods used to collect and select evidence is not stated.

Development and review

This guideline was accessed through the National Guideline Clearinghouse (www.ngc.gov). The Institute for Clinical Systems Improvement is an independent, nonprofit organization sponsored by 6 Minnesota health plans.

The authors completed an electronic search of databases. Data were analyzed by systematic review with evidence table and were validated by clinical validation-pilot testing and internal peer review. The methods used to make the recommendations were not discussed. Quality and strength of evidence were weighted according to a rating scheme furnished in the guideline. Two excellent algorithms are attached to this guideline: diagnosis and treatment. There are 92 references.

Guideline source

Institute for Clinical Systems Improvement. Diagnosis and Treatment of Obstructive Sleep Apnea. Bloomington, Minn: Institute for Clinical Systems Improvement; 2003. 53 pages.

Other guidelines on osa

• Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. Standards of Practice Committee. Sleep 2002; 25:143–147 [29 references]. Web access at: www.aasmnet.org/PDF/autotitratingreview.pdf.
• Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Chesson AL Jr, Berry RB, Pack A. Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Sleep2003; 26:907–913 [11 references]. Web access at: www.aasmnet.org/PDF/260719.pdf.
• Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002; 109:704–712 [63 references]. Web access at: www.aappolicy. aappublications.org/cgi/content/full/pediatrics; 109/4/704.

Obstructive sleep apnea is underdiagnosed.¹ These recommendations (from the Institute for Clinical Systems Improvement’s Respiratory Steering Committee) can help providers more accurately identify adults who have OSA through a sleep study evaluation, prescribe appropriate treatment, document cases for appropriate follow-up, and increase patient understanding of related health risks. The target audience is physicians, nurses, advanced practice nurses, and physician assistants. The target population is adults.

The evidence categories for this guideline are diagnosis, evaluation, management, risk assessment, and treatment. Outcomes considered are signs and symptoms of OSA; patient risk factors, including comorbidities; accuracy of diagnostic tests; effects of treatment on apneahypopnea index and other measures; patient compliance and satisfaction with treatment; and complications of treatment. Their rating scheme has been updated to comply with the SORT taxonomy.²

Relevance and limitations

OSA affects more than 12 million people in the US, 2% of women and 4% of men aged >35 years. The patient with OSA commonly consults a physician after a sleep partner reports loud snoring and irregular breathing. The methods used to collect and select evidence is not stated.

Development and review

This guideline was accessed through the National Guideline Clearinghouse (www.ngc.gov). The Institute for Clinical Systems Improvement is an independent, nonprofit organization sponsored by 6 Minnesota health plans.

The authors completed an electronic search of databases. Data were analyzed by systematic review with evidence table and were validated by clinical validation-pilot testing and internal peer review. The methods used to make the recommendations were not discussed. Quality and strength of evidence were weighted according to a rating scheme furnished in the guideline. Two excellent algorithms are attached to this guideline: diagnosis and treatment. There are 92 references.

Guideline source

Institute for Clinical Systems Improvement. Diagnosis and Treatment of Obstructive Sleep Apnea. Bloomington, Minn: Institute for Clinical Systems Improvement; 2003. 53 pages.

Other guidelines on osa

• Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. Standards of Practice Committee. Sleep 2002; 25:143–147 [29 references]. Web access at: www.aasmnet.org/PDF/autotitratingreview.pdf.
• Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Chesson AL Jr, Berry RB, Pack A. Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Sleep2003; 26:907–913 [11 references]. Web access at: www.aasmnet.org/PDF/260719.pdf.
• Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002; 109:704–712 [63 references]. Web access at: www.aappolicy. aappublications.org/cgi/content/full/pediatrics; 109/4/704.

Obstructive sleep apnea is underdiagnosed.¹ These recommendations (from the Institute for Clinical Systems Improvement’s Respiratory Steering Committee) can help providers more accurately identify adults who have OSA through a sleep study evaluation, prescribe appropriate treatment, document cases for appropriate follow-up, and increase patient understanding of related health risks. The target audience is physicians, nurses, advanced practice nurses, and physician assistants. The target population is adults.

The evidence categories for this guideline are diagnosis, evaluation, management, risk assessment, and treatment. Outcomes considered are signs and symptoms of OSA; patient risk factors, including comorbidities; accuracy of diagnostic tests; effects of treatment on apneahypopnea index and other measures; patient compliance and satisfaction with treatment; and complications of treatment. Their rating scheme has been updated to comply with the SORT taxonomy.²

Relevance and limitations

OSA affects more than 12 million people in the US, 2% of women and 4% of men aged >35 years. The patient with OSA commonly consults a physician after a sleep partner reports loud snoring and irregular breathing. The methods used to collect and select evidence is not stated.

Development and review

This guideline was accessed through the National Guideline Clearinghouse (www.ngc.gov). The Institute for Clinical Systems Improvement is an independent, nonprofit organization sponsored by 6 Minnesota health plans.

The authors completed an electronic search of databases. Data were analyzed by systematic review with evidence table and were validated by clinical validation-pilot testing and internal peer review. The methods used to make the recommendations were not discussed. Quality and strength of evidence were weighted according to a rating scheme furnished in the guideline. Two excellent algorithms are attached to this guideline: diagnosis and treatment. There are 92 references.

Guideline source

Institute for Clinical Systems Improvement. Diagnosis and Treatment of Obstructive Sleep Apnea. Bloomington, Minn: Institute for Clinical Systems Improvement; 2003. 53 pages.

Other guidelines on osa

• Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. Standards of Practice Committee. Sleep 2002; 25:143–147 [29 references]. Web access at: www.aasmnet.org/PDF/autotitratingreview.pdf.
• Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Chesson AL Jr, Berry RB, Pack A. Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Sleep2003; 26:907–913 [11 references]. Web access at: www.aasmnet.org/PDF/260719.pdf.
• Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002; 109:704–712 [63 references]. Web access at: www.aappolicy. aappublications.org/cgi/content/full/pediatrics; 109/4/704.

Evidence summary

A systematic review encompassing 127 trial centers and 4723 patients concluded that inhaled nedocromil was effective for a variety of patients with asthma. Significant improvements were noted in FEV₁, PEFR, use of bronchodilators, symptom scores, and quality of life scores. The reviewers found nedocromil to be most effective for patients with moderate disease already taking bronchodilators,² corresponding to the “mild persistent asthma” category ( Table ).

A contemporaneous European RCT, not included in the review, compared 4 mg of inhaled nedocromil 4 times daily with inhaled placebo among 209 asthmatic children for 12 weeks.3 After 8 weeks, they found a statistically significant reduction in total daily asthma symptom scores (50% nedocromil vs 9% placebo; P<.01). The proportion of parents and children rating treatment as moderately or very effective was 78% in the treatment group and 59% in the placebo group (number needed to treat [NNT]=5.2; P<.01); clinicians’ ratings were 73% for nedocromil and 50% for placebo (NNT=4.3; P<.01). The frequency of side effects—including nausea, headache, and sleepiness—did not reach statistical significance; however, the nedocromil group reported up to a 20% incidence of sore throat. Most of the studies reported no dropouts due to side effects.

When patients are already using inhaled steroids, the evidence is less clear whether nedocromil confers additional benefits, such as fewer exacerbations or lower inhaled steroid doses. Two small studies of patients either already on inhaled steroids⁴ or considered to be steroid-resistant⁵ found nonsignificant trends towards reductions in bronchodilator use, increased PEFR, increased FEV₁, and improved quality of life. Although both studies were underpowered, the study on steroid-resistant asthma did find a statistically significant 20% improvement in PEFR and decreased bronchodilator use for 50% of patients at 8 and 12 weeks.

The inherent waxing and waning nature of asthma makes demonstrating benefits difficult. Furthermore, nedocromil tends to have an all-ornothing effect rather than a dose-response gradient. Unfortunately, none of these trials found useful predictors to help clinicians determine which patients respond.^1,5

In a Cochrane Review, 20 RCTs involving 280 participants showed that 4 mg (2 puffs) of nedocromil inhaled 15 to 60 minutes prior to exercise significantly reduced the severity and duration of exercise-induced asthma for both adults and children. The maximum percentage fall in FEV₁ improved significantly compared with placebo, with a weighted mean difference of 15.5% (95% confidence interval, 13.2–18.1). In addition, the time to complete recovery was shortened from 30 minutes with placebo to 10 minutes with nedocromil.⁶

TABLE
Classification of asthma

Recommendations from others

The Global Initiative for Asthma and the National Heart, Lung and Blood Institute Expert Panel Report list nedocromil as an option for the treatment of exercise-induced asthma and mild persistent asthma for adults and children. However, it is listed as a second choice to the use of inhaled steroids in the case of mild persistent asthma. It is not recommended for moderate or severe persistent asthma, or for mild intermittent asthma.⁷

Evidence summary

A systematic review encompassing 127 trial centers and 4723 patients concluded that inhaled nedocromil was effective for a variety of patients with asthma. Significant improvements were noted in FEV₁, PEFR, use of bronchodilators, symptom scores, and quality of life scores. The reviewers found nedocromil to be most effective for patients with moderate disease already taking bronchodilators,² corresponding to the “mild persistent asthma” category ( Table ).

A contemporaneous European RCT, not included in the review, compared 4 mg of inhaled nedocromil 4 times daily with inhaled placebo among 209 asthmatic children for 12 weeks.3 After 8 weeks, they found a statistically significant reduction in total daily asthma symptom scores (50% nedocromil vs 9% placebo; P<.01). The proportion of parents and children rating treatment as moderately or very effective was 78% in the treatment group and 59% in the placebo group (number needed to treat [NNT]=5.2; P<.01); clinicians’ ratings were 73% for nedocromil and 50% for placebo (NNT=4.3; P<.01). The frequency of side effects—including nausea, headache, and sleepiness—did not reach statistical significance; however, the nedocromil group reported up to a 20% incidence of sore throat. Most of the studies reported no dropouts due to side effects.

When patients are already using inhaled steroids, the evidence is less clear whether nedocromil confers additional benefits, such as fewer exacerbations or lower inhaled steroid doses. Two small studies of patients either already on inhaled steroids⁴ or considered to be steroid-resistant⁵ found nonsignificant trends towards reductions in bronchodilator use, increased PEFR, increased FEV₁, and improved quality of life. Although both studies were underpowered, the study on steroid-resistant asthma did find a statistically significant 20% improvement in PEFR and decreased bronchodilator use for 50% of patients at 8 and 12 weeks.

The inherent waxing and waning nature of asthma makes demonstrating benefits difficult. Furthermore, nedocromil tends to have an all-ornothing effect rather than a dose-response gradient. Unfortunately, none of these trials found useful predictors to help clinicians determine which patients respond.^1,5

In a Cochrane Review, 20 RCTs involving 280 participants showed that 4 mg (2 puffs) of nedocromil inhaled 15 to 60 minutes prior to exercise significantly reduced the severity and duration of exercise-induced asthma for both adults and children. The maximum percentage fall in FEV₁ improved significantly compared with placebo, with a weighted mean difference of 15.5% (95% confidence interval, 13.2–18.1). In addition, the time to complete recovery was shortened from 30 minutes with placebo to 10 minutes with nedocromil.⁶

TABLE
Classification of asthma

Recommendations from others

The Global Initiative for Asthma and the National Heart, Lung and Blood Institute Expert Panel Report list nedocromil as an option for the treatment of exercise-induced asthma and mild persistent asthma for adults and children. However, it is listed as a second choice to the use of inhaled steroids in the case of mild persistent asthma. It is not recommended for moderate or severe persistent asthma, or for mild intermittent asthma.⁷

Evidence summary

A systematic review encompassing 127 trial centers and 4723 patients concluded that inhaled nedocromil was effective for a variety of patients with asthma. Significant improvements were noted in FEV₁, PEFR, use of bronchodilators, symptom scores, and quality of life scores. The reviewers found nedocromil to be most effective for patients with moderate disease already taking bronchodilators,² corresponding to the “mild persistent asthma” category ( Table ).

A contemporaneous European RCT, not included in the review, compared 4 mg of inhaled nedocromil 4 times daily with inhaled placebo among 209 asthmatic children for 12 weeks.3 After 8 weeks, they found a statistically significant reduction in total daily asthma symptom scores (50% nedocromil vs 9% placebo; P<.01). The proportion of parents and children rating treatment as moderately or very effective was 78% in the treatment group and 59% in the placebo group (number needed to treat [NNT]=5.2; P<.01); clinicians’ ratings were 73% for nedocromil and 50% for placebo (NNT=4.3; P<.01). The frequency of side effects—including nausea, headache, and sleepiness—did not reach statistical significance; however, the nedocromil group reported up to a 20% incidence of sore throat. Most of the studies reported no dropouts due to side effects.

When patients are already using inhaled steroids, the evidence is less clear whether nedocromil confers additional benefits, such as fewer exacerbations or lower inhaled steroid doses. Two small studies of patients either already on inhaled steroids⁴ or considered to be steroid-resistant⁵ found nonsignificant trends towards reductions in bronchodilator use, increased PEFR, increased FEV₁, and improved quality of life. Although both studies were underpowered, the study on steroid-resistant asthma did find a statistically significant 20% improvement in PEFR and decreased bronchodilator use for 50% of patients at 8 and 12 weeks.

The inherent waxing and waning nature of asthma makes demonstrating benefits difficult. Furthermore, nedocromil tends to have an all-ornothing effect rather than a dose-response gradient. Unfortunately, none of these trials found useful predictors to help clinicians determine which patients respond.^1,5

In a Cochrane Review, 20 RCTs involving 280 participants showed that 4 mg (2 puffs) of nedocromil inhaled 15 to 60 minutes prior to exercise significantly reduced the severity and duration of exercise-induced asthma for both adults and children. The maximum percentage fall in FEV₁ improved significantly compared with placebo, with a weighted mean difference of 15.5% (95% confidence interval, 13.2–18.1). In addition, the time to complete recovery was shortened from 30 minutes with placebo to 10 minutes with nedocromil.⁶

TABLE
Classification of asthma

Recommendations from others

The Global Initiative for Asthma and the National Heart, Lung and Blood Institute Expert Panel Report list nedocromil as an option for the treatment of exercise-induced asthma and mild persistent asthma for adults and children. However, it is listed as a second choice to the use of inhaled steroids in the case of mild persistent asthma. It is not recommended for moderate or severe persistent asthma, or for mild intermittent asthma.⁷

Marijuana has long been known to stimulate appetite, particularly for sweet foods.¹ The naughty boys in my fraternity called it “the munchies;” the professionals call it hyperphagia. Cannabinoid receptor (CB₁) stimulation by marijuana’s main active component—9-THC—is believed to induce this behavior. Clinicians have successfully used this effect to treat AIDS-related wasting syndrome and other anorexic conditions.²

CB₁ is widely expressed throughout the brain and seems to inhibit release of various neurotransmitters.³ How this effect leads to increased appetite is unclear, but it may result from a decrease in the appetite-suppressing effects of hormones such as leptin. In other words, tweaking the CB₁ receptor may take the “brakes” off appetite.

Some researchers have speculated that if stimulating CB₁ triggers appetite, blocking the receptor might inhibit it (Figure 1).

THE ‘MUNCHIES’ IN MICE

Rimonabant (SR141716), an experimental agent, is a potent and selective CB₁ antagonist.

Ravinet Trillou et al fed mice a high-fat diet known to induce obesity.⁴ The mice were randomized to receive rimonabant or placebo while maintained on the highly palatable diet. The authors asked: Would rimonabant help the mice lose weight even when they could eat as much delicious fatty food as they wanted?

Figure 1 Blocking CB₁ may prevent weight gain

Δ9-THC activates the cannabinoid receptor (CB₁), stimulating appetite and leading to weight gain in mice (left). When the same receptor is blocked, appetite is controlled (right).

Source: Illustration for CURRENT PSYCHIATRY by Marcia HartsockRimonabant induced a sustained body weight reduction of approximately 20% in the treatment group compared with the placebo group across 5 weeks (Figure 2). Estimated fat stores among the treatment group were depleted by slightly more than 50%.

The authors noted that the mice in the treatment group had decreased their food intake, but the decrease was not sufficient to explain the weight loss. They speculate that rimonabant could activate metabolic processes and decrease intake.

RIMONABANT’S ROLE IN PSYCHIATRY

Phase III human trials of rimonabant are under way for obesity as well as smoking cessation.⁵ In uncontrolled studies, rimonabant has been shown to help people avoid weight gain while quitting smoking.⁵

If rimonabant shows effectiveness in controlled trials and is safe in humans, it could be most valuable. Obesity in industrial countries is epidemic and causes serious secondary morbidity, including diabetes, arthritis, and hypertension. Rimonabant, if approved by the FDA, could reach the market by early 2006.⁶

It is unknown whether rimonabant’s metabolic effects could offset those of many psychotropics. As psychiatrists, we often must stop an effective antipsychotic or antidepressant because it is causing significant weight gain. A treatment that would prevent medication-induced weight gain could improve patient compliance and, ultimately, outcomes.

MANAGING SCHIZOPHRENIA

Some evidence also suggests that rimonabant may offer additional benefits for patients with schizophrenia beyond weight reduction or smoking cessation.

Figure 2 Rimonabant’s effects on weight in mice on a high-fat diet

Source: Adapted from reference 4.Leweke et al found increased endogenous cannabinoids in the CSF of patients with schizophrenia, suggesting that a cannabinoid signaling imbalance may contribute to the disorder’s pathogenesis.⁷ However, 72 patients with schizophrenia or schizoaffective disorder who took rimonabant for 6 weeks showed no improvement compared with a placebo group.⁸

Marijuana has long been known to stimulate appetite, particularly for sweet foods.¹ The naughty boys in my fraternity called it “the munchies;” the professionals call it hyperphagia. Cannabinoid receptor (CB₁) stimulation by marijuana’s main active component—9-THC—is believed to induce this behavior. Clinicians have successfully used this effect to treat AIDS-related wasting syndrome and other anorexic conditions.²

CB₁ is widely expressed throughout the brain and seems to inhibit release of various neurotransmitters.³ How this effect leads to increased appetite is unclear, but it may result from a decrease in the appetite-suppressing effects of hormones such as leptin. In other words, tweaking the CB₁ receptor may take the “brakes” off appetite.

Some researchers have speculated that if stimulating CB₁ triggers appetite, blocking the receptor might inhibit it (Figure 1).

THE ‘MUNCHIES’ IN MICE

Rimonabant (SR141716), an experimental agent, is a potent and selective CB₁ antagonist.

Ravinet Trillou et al fed mice a high-fat diet known to induce obesity.⁴ The mice were randomized to receive rimonabant or placebo while maintained on the highly palatable diet. The authors asked: Would rimonabant help the mice lose weight even when they could eat as much delicious fatty food as they wanted?

Figure 1 Blocking CB₁ may prevent weight gain

Δ9-THC activates the cannabinoid receptor (CB₁), stimulating appetite and leading to weight gain in mice (left). When the same receptor is blocked, appetite is controlled (right).

Source: Illustration for CURRENT PSYCHIATRY by Marcia HartsockRimonabant induced a sustained body weight reduction of approximately 20% in the treatment group compared with the placebo group across 5 weeks (Figure 2). Estimated fat stores among the treatment group were depleted by slightly more than 50%.

The authors noted that the mice in the treatment group had decreased their food intake, but the decrease was not sufficient to explain the weight loss. They speculate that rimonabant could activate metabolic processes and decrease intake.

RIMONABANT’S ROLE IN PSYCHIATRY

Phase III human trials of rimonabant are under way for obesity as well as smoking cessation.⁵ In uncontrolled studies, rimonabant has been shown to help people avoid weight gain while quitting smoking.⁵

If rimonabant shows effectiveness in controlled trials and is safe in humans, it could be most valuable. Obesity in industrial countries is epidemic and causes serious secondary morbidity, including diabetes, arthritis, and hypertension. Rimonabant, if approved by the FDA, could reach the market by early 2006.⁶

It is unknown whether rimonabant’s metabolic effects could offset those of many psychotropics. As psychiatrists, we often must stop an effective antipsychotic or antidepressant because it is causing significant weight gain. A treatment that would prevent medication-induced weight gain could improve patient compliance and, ultimately, outcomes.

MANAGING SCHIZOPHRENIA

Some evidence also suggests that rimonabant may offer additional benefits for patients with schizophrenia beyond weight reduction or smoking cessation.

Figure 2 Rimonabant’s effects on weight in mice on a high-fat diet

Source: Adapted from reference 4.Leweke et al found increased endogenous cannabinoids in the CSF of patients with schizophrenia, suggesting that a cannabinoid signaling imbalance may contribute to the disorder’s pathogenesis.⁷ However, 72 patients with schizophrenia or schizoaffective disorder who took rimonabant for 6 weeks showed no improvement compared with a placebo group.⁸

Marijuana has long been known to stimulate appetite, particularly for sweet foods.¹ The naughty boys in my fraternity called it “the munchies;” the professionals call it hyperphagia. Cannabinoid receptor (CB₁) stimulation by marijuana’s main active component—9-THC—is believed to induce this behavior. Clinicians have successfully used this effect to treat AIDS-related wasting syndrome and other anorexic conditions.²

CB₁ is widely expressed throughout the brain and seems to inhibit release of various neurotransmitters.³ How this effect leads to increased appetite is unclear, but it may result from a decrease in the appetite-suppressing effects of hormones such as leptin. In other words, tweaking the CB₁ receptor may take the “brakes” off appetite.

Some researchers have speculated that if stimulating CB₁ triggers appetite, blocking the receptor might inhibit it (Figure 1).

THE ‘MUNCHIES’ IN MICE

Rimonabant (SR141716), an experimental agent, is a potent and selective CB₁ antagonist.

Ravinet Trillou et al fed mice a high-fat diet known to induce obesity.⁴ The mice were randomized to receive rimonabant or placebo while maintained on the highly palatable diet. The authors asked: Would rimonabant help the mice lose weight even when they could eat as much delicious fatty food as they wanted?

Figure 1 Blocking CB₁ may prevent weight gain

Δ9-THC activates the cannabinoid receptor (CB₁), stimulating appetite and leading to weight gain in mice (left). When the same receptor is blocked, appetite is controlled (right).

Source: Illustration for CURRENT PSYCHIATRY by Marcia HartsockRimonabant induced a sustained body weight reduction of approximately 20% in the treatment group compared with the placebo group across 5 weeks (Figure 2). Estimated fat stores among the treatment group were depleted by slightly more than 50%.

The authors noted that the mice in the treatment group had decreased their food intake, but the decrease was not sufficient to explain the weight loss. They speculate that rimonabant could activate metabolic processes and decrease intake.

RIMONABANT’S ROLE IN PSYCHIATRY

Phase III human trials of rimonabant are under way for obesity as well as smoking cessation.⁵ In uncontrolled studies, rimonabant has been shown to help people avoid weight gain while quitting smoking.⁵

If rimonabant shows effectiveness in controlled trials and is safe in humans, it could be most valuable. Obesity in industrial countries is epidemic and causes serious secondary morbidity, including diabetes, arthritis, and hypertension. Rimonabant, if approved by the FDA, could reach the market by early 2006.⁶

It is unknown whether rimonabant’s metabolic effects could offset those of many psychotropics. As psychiatrists, we often must stop an effective antipsychotic or antidepressant because it is causing significant weight gain. A treatment that would prevent medication-induced weight gain could improve patient compliance and, ultimately, outcomes.

MANAGING SCHIZOPHRENIA

Some evidence also suggests that rimonabant may offer additional benefits for patients with schizophrenia beyond weight reduction or smoking cessation.

Figure 2 Rimonabant’s effects on weight in mice on a high-fat diet

Source: Adapted from reference 4.Leweke et al found increased endogenous cannabinoids in the CSF of patients with schizophrenia, suggesting that a cannabinoid signaling imbalance may contribute to the disorder’s pathogenesis.⁷ However, 72 patients with schizophrenia or schizoaffective disorder who took rimonabant for 6 weeks showed no improvement compared with a placebo group.⁸

Ameliorating emotional trauma is key to avoiding long-term functional impairment. Consider a FRESH approach that involves families/friends, reassurance/retelling, education, addressing substance abuse, sleeplessness, and suicide risk, and taking a careful history.

Family and friends can be valuable to treatment but clinicians often overlook their importance. Overwhelmed or traumatized family members who are not counseled about the patient’s symptoms can undermine treatment by dismissing symptoms and withdrawing support. Involve them by emphasizing their supportive role. Alert them to normal and problematic trauma responses and stress disorder symptoms.

Reassurance/retelling. Explain that emotional pain is normal but usually fades with time. Consider effects of survivor guilt: Encourage the patient to retell the experience, but do not demand this. Help patients identify and correct thought distortions that foster avoidance. Though controversial,¹ critical incident debriefing and cognitive-behavioral therapy can help the patient recount the trauma and ultimately restore a sense of self, enjoyment of life, and expectations of safety, control, and trust.²

Educate patients about normal variable stress responses. Warn traumatized patients against engaging in high-risk behaviors, through which they may try to deny their vulnerability, fear, and loss of control. Explain symptoms and risk factors for depression, posttraumatic stress disorder (PTSD), and other anxiety disorders.

Substance abuse, sleeplessness, and suicide are possible outcomes of trauma. Prescribe a non-narcotic sleep-promoting medication if insomnia is problematic. Alternately, consider a selective serotonin or serotonin-norepinephrine reuptake inhibitor^3,4 at normal or low starting dosages if presenting symptoms suggest an emerging anxiety or mood disorder or PTSD. Watch for signs of survivor guilt—such as an unrealistic sense of responsibility for the trauma—that can lead to depression with suicide risk after a significant loss.

History. Watch for factors that predict PTSD and comorbid disorders (trauma severity and chronicity, involvement of interpersonal violence, fear of death). Previous trauma, PTSD, depression, anxiety, personality disorder, childhood victimization, substance abuse, and poor social support increase the risk. Avoidance, numbing, dissociation, high guilt, and low acknowledged anger correlate with increased PTSD risk. Follow up with patients who exhibit these risk factors every 1 to 2 weeks with medication and/or psychotherapy.

Ameliorating emotional trauma is key to avoiding long-term functional impairment. Consider a FRESH approach that involves families/friends, reassurance/retelling, education, addressing substance abuse, sleeplessness, and suicide risk, and taking a careful history.

Family and friends can be valuable to treatment but clinicians often overlook their importance. Overwhelmed or traumatized family members who are not counseled about the patient’s symptoms can undermine treatment by dismissing symptoms and withdrawing support. Involve them by emphasizing their supportive role. Alert them to normal and problematic trauma responses and stress disorder symptoms.

Reassurance/retelling. Explain that emotional pain is normal but usually fades with time. Consider effects of survivor guilt: Encourage the patient to retell the experience, but do not demand this. Help patients identify and correct thought distortions that foster avoidance. Though controversial,¹ critical incident debriefing and cognitive-behavioral therapy can help the patient recount the trauma and ultimately restore a sense of self, enjoyment of life, and expectations of safety, control, and trust.²

Educate patients about normal variable stress responses. Warn traumatized patients against engaging in high-risk behaviors, through which they may try to deny their vulnerability, fear, and loss of control. Explain symptoms and risk factors for depression, posttraumatic stress disorder (PTSD), and other anxiety disorders.

Substance abuse, sleeplessness, and suicide are possible outcomes of trauma. Prescribe a non-narcotic sleep-promoting medication if insomnia is problematic. Alternately, consider a selective serotonin or serotonin-norepinephrine reuptake inhibitor^3,4 at normal or low starting dosages if presenting symptoms suggest an emerging anxiety or mood disorder or PTSD. Watch for signs of survivor guilt—such as an unrealistic sense of responsibility for the trauma—that can lead to depression with suicide risk after a significant loss.

History. Watch for factors that predict PTSD and comorbid disorders (trauma severity and chronicity, involvement of interpersonal violence, fear of death). Previous trauma, PTSD, depression, anxiety, personality disorder, childhood victimization, substance abuse, and poor social support increase the risk. Avoidance, numbing, dissociation, high guilt, and low acknowledged anger correlate with increased PTSD risk. Follow up with patients who exhibit these risk factors every 1 to 2 weeks with medication and/or psychotherapy.

Ameliorating emotional trauma is key to avoiding long-term functional impairment. Consider a FRESH approach that involves families/friends, reassurance/retelling, education, addressing substance abuse, sleeplessness, and suicide risk, and taking a careful history.

Family and friends can be valuable to treatment but clinicians often overlook their importance. Overwhelmed or traumatized family members who are not counseled about the patient’s symptoms can undermine treatment by dismissing symptoms and withdrawing support. Involve them by emphasizing their supportive role. Alert them to normal and problematic trauma responses and stress disorder symptoms.

Reassurance/retelling. Explain that emotional pain is normal but usually fades with time. Consider effects of survivor guilt: Encourage the patient to retell the experience, but do not demand this. Help patients identify and correct thought distortions that foster avoidance. Though controversial,¹ critical incident debriefing and cognitive-behavioral therapy can help the patient recount the trauma and ultimately restore a sense of self, enjoyment of life, and expectations of safety, control, and trust.²

Educate patients about normal variable stress responses. Warn traumatized patients against engaging in high-risk behaviors, through which they may try to deny their vulnerability, fear, and loss of control. Explain symptoms and risk factors for depression, posttraumatic stress disorder (PTSD), and other anxiety disorders.

Substance abuse, sleeplessness, and suicide are possible outcomes of trauma. Prescribe a non-narcotic sleep-promoting medication if insomnia is problematic. Alternately, consider a selective serotonin or serotonin-norepinephrine reuptake inhibitor^3,4 at normal or low starting dosages if presenting symptoms suggest an emerging anxiety or mood disorder or PTSD. Watch for signs of survivor guilt—such as an unrealistic sense of responsibility for the trauma—that can lead to depression with suicide risk after a significant loss.

History. Watch for factors that predict PTSD and comorbid disorders (trauma severity and chronicity, involvement of interpersonal violence, fear of death). Previous trauma, PTSD, depression, anxiety, personality disorder, childhood victimization, substance abuse, and poor social support increase the risk. Avoidance, numbing, dissociation, high guilt, and low acknowledged anger correlate with increased PTSD risk. Follow up with patients who exhibit these risk factors every 1 to 2 weeks with medication and/or psychotherapy.

Clinical psychiatrists often find it hard to evaluate suicide risk and understand their potential legal liability. Prevalence of suicidality compounds this challenge: Up to one-third of the general population in the United States have suicidal thoughts at some point.¹ Although most people who consider suicide do not act on those thoughts, 51% of psychiatrists report having had a patient who committed suicide.²

Because patient suicide risk is real, psychiatrists often worry about malpractice claims. Although post-suicide lawsuits account for the largest number of malpractice suits against psychiatrists,^3,4 a psychiatrist’s risk of being sued for malpractice is still quite low.³ Even when sued, clinicians win up to 80% of cases.³

Still, with malpractice claims increasing overall, clinicians should understand their potential liability in preventing suicide and the basic principles behind a malpractice claim.

Patient jumps from window after suicide watch is called off

Los Angeles County (CA) superior court

A 24-year-old man was hospitalized after attempting suicide by ingesting prescription pills and alcohol. He was admitted to the general medical floor with a 24-hour sitter to guard against additional suicide attempts. When the psychiatrist tried to evaluate him, he found the patient unresponsive because of the pills’ effects.

The next day, the psychiatrist evaluated the patient and recommended that the patient be transferred to the psychiatric unit and that the sitter be continued. Four hours later, without a further evaluation, the psychiatrist recommended moving the patient to another room and canceling the sitter.

The next day, the patient jumped from his sixth-floor hospital room window. He sustained traumatic brain injury.

The patient’s guardian ad litem argued that discontinuing the sitter was negligent. The defendant argued that discontinuation was within the parameters of proper care.

• The jury found for the defense.

Patient commits suicide hours after ER discharge

Lake County (IL) circuit court

A 36-year-old man was being treated by a psychiatrist for major depressive disorder. The patient owned several guns for hunting and target shooting and had a state-issued firearm owner’s identification card.

In October 2003, the patient presented to the emergency room and was examined by a mental health assessment staff. The psychiatrist recommended voluntary admission to the psychiatric unit for 23 hours.

The patient’s father discouraged the admission and stated that the patient could lose his gun owner’s card as a result. The patient was subsequently discharged. Within 24 hours after discharge, the patient shot himself in the chest and died.

The deceased’s estate argued that the psychiatrist should have admitted the patient involuntarily. The psychiatrist claimed no obligation to involuntary admission and argued that the patient did not meet criteria typically used for such admission.

• The jury found for the defense.

Doctor’s hanging attempt in hospital causes permanent brain damage

Morris County (NJ) district court

A cardiologist was admitted to the hospital’s psychiatric unit after decompensating. While hospitalized, he attempted suicide by hanging in a clinic bathroom. He suffered permanent brain injury as a result of the hanging. Because the injury left him in a childlike state, he required constant care.

The patient’s attorney argued that hospital personnel knew he was suicidal yet did not adequately supervise him. The attorney also argued that the injury cost his client $5 million in lost income.

The defense reported that the hospital had placed the patient on suicide watch and that staff checked him every 5 minutes. The defense also argued that the bathroom where the suicide was attempted was impossible to monitor.

• The jury found for the defense.

Dr. Grant’s observations

To win a malpractice claim, the injured party must show four things:

Duty to care for the patient existed based on the provider’s relationship with the patient. Whether on a hospital floor or in the emergency room, once a doctor-patient relationship has been established, the provider agrees to provide non-negligent care.

Negligence. The physician or hospital personnel acted negligently and violated the duty of care. This concept is based upon a “standard of care” —ie, what other psychiatrists would do in this situation.

Harm. Even if someone has acted negligently, a malpractice case cannot go forward if no harm has been suffered.

Causation. The negligent act caused the harm.

The defendants most likely won the cases cited above because the injured parties could not establish negligence. Clinicians are not negligent for merely failing to predict suicide, as the inability to predict suicide has been demonstrated.^5,6 Clinicians, however, must follow the profession’s standard of care, assess the relative degree of risk, and form a treatment and safety plan consistent with that risk.⁴

Based on relevant case law, the following actions can decrease the risk of patient suicide—and a resultant malpractice claim:

• Conduct a comprehensive evaluation of the patient and his or her suicide risk. Ask about:
• Consider hospitalizing at-risk patients. If you decide against hospitalization, provide a comprehensive safety plan. In the gun owner’s case, such a plan would include arranging with the family to remove firearms. Implement additional anti-suicide precautions, such as more-intensive outpatient therapy or involving family members in treatment.
• Document suicide risk assessment and the reasons for your treatment decisions. Juries may interpret lack of documented information in the patient’s favor.
• Design a treatment plan for hospitalized patients to reduce suicide risk. Consider the patient’s reaction to constant surveillance. For example, checking a paranoid patient every 5 minutes may be more therapeutic than a constant watch while providing adequate safety. Thoroughly document your reasons behind the plan.

Clinical psychiatrists often find it hard to evaluate suicide risk and understand their potential legal liability. Prevalence of suicidality compounds this challenge: Up to one-third of the general population in the United States have suicidal thoughts at some point.¹ Although most people who consider suicide do not act on those thoughts, 51% of psychiatrists report having had a patient who committed suicide.²

Because patient suicide risk is real, psychiatrists often worry about malpractice claims. Although post-suicide lawsuits account for the largest number of malpractice suits against psychiatrists,^3,4 a psychiatrist’s risk of being sued for malpractice is still quite low.³ Even when sued, clinicians win up to 80% of cases.³

Still, with malpractice claims increasing overall, clinicians should understand their potential liability in preventing suicide and the basic principles behind a malpractice claim.

Patient jumps from window after suicide watch is called off

Los Angeles County (CA) superior court

A 24-year-old man was hospitalized after attempting suicide by ingesting prescription pills and alcohol. He was admitted to the general medical floor with a 24-hour sitter to guard against additional suicide attempts. When the psychiatrist tried to evaluate him, he found the patient unresponsive because of the pills’ effects.

The next day, the psychiatrist evaluated the patient and recommended that the patient be transferred to the psychiatric unit and that the sitter be continued. Four hours later, without a further evaluation, the psychiatrist recommended moving the patient to another room and canceling the sitter.

The next day, the patient jumped from his sixth-floor hospital room window. He sustained traumatic brain injury.

The patient’s guardian ad litem argued that discontinuing the sitter was negligent. The defendant argued that discontinuation was within the parameters of proper care.

• The jury found for the defense.

Patient commits suicide hours after ER discharge

Lake County (IL) circuit court

A 36-year-old man was being treated by a psychiatrist for major depressive disorder. The patient owned several guns for hunting and target shooting and had a state-issued firearm owner’s identification card.

In October 2003, the patient presented to the emergency room and was examined by a mental health assessment staff. The psychiatrist recommended voluntary admission to the psychiatric unit for 23 hours.

The patient’s father discouraged the admission and stated that the patient could lose his gun owner’s card as a result. The patient was subsequently discharged. Within 24 hours after discharge, the patient shot himself in the chest and died.

The deceased’s estate argued that the psychiatrist should have admitted the patient involuntarily. The psychiatrist claimed no obligation to involuntary admission and argued that the patient did not meet criteria typically used for such admission.

• The jury found for the defense.

Doctor’s hanging attempt in hospital causes permanent brain damage

Morris County (NJ) district court

A cardiologist was admitted to the hospital’s psychiatric unit after decompensating. While hospitalized, he attempted suicide by hanging in a clinic bathroom. He suffered permanent brain injury as a result of the hanging. Because the injury left him in a childlike state, he required constant care.

The patient’s attorney argued that hospital personnel knew he was suicidal yet did not adequately supervise him. The attorney also argued that the injury cost his client $5 million in lost income.

The defense reported that the hospital had placed the patient on suicide watch and that staff checked him every 5 minutes. The defense also argued that the bathroom where the suicide was attempted was impossible to monitor.

• The jury found for the defense.

Dr. Grant’s observations

To win a malpractice claim, the injured party must show four things:

Duty to care for the patient existed based on the provider’s relationship with the patient. Whether on a hospital floor or in the emergency room, once a doctor-patient relationship has been established, the provider agrees to provide non-negligent care.

Negligence. The physician or hospital personnel acted negligently and violated the duty of care. This concept is based upon a “standard of care” —ie, what other psychiatrists would do in this situation.

Harm. Even if someone has acted negligently, a malpractice case cannot go forward if no harm has been suffered.

Causation. The negligent act caused the harm.

The defendants most likely won the cases cited above because the injured parties could not establish negligence. Clinicians are not negligent for merely failing to predict suicide, as the inability to predict suicide has been demonstrated.^5,6 Clinicians, however, must follow the profession’s standard of care, assess the relative degree of risk, and form a treatment and safety plan consistent with that risk.⁴

Based on relevant case law, the following actions can decrease the risk of patient suicide—and a resultant malpractice claim:

• Conduct a comprehensive evaluation of the patient and his or her suicide risk. Ask about:
• Consider hospitalizing at-risk patients. If you decide against hospitalization, provide a comprehensive safety plan. In the gun owner’s case, such a plan would include arranging with the family to remove firearms. Implement additional anti-suicide precautions, such as more-intensive outpatient therapy or involving family members in treatment.
• Document suicide risk assessment and the reasons for your treatment decisions. Juries may interpret lack of documented information in the patient’s favor.
• Design a treatment plan for hospitalized patients to reduce suicide risk. Consider the patient’s reaction to constant surveillance. For example, checking a paranoid patient every 5 minutes may be more therapeutic than a constant watch while providing adequate safety. Thoroughly document your reasons behind the plan.

Clinical psychiatrists often find it hard to evaluate suicide risk and understand their potential legal liability. Prevalence of suicidality compounds this challenge: Up to one-third of the general population in the United States have suicidal thoughts at some point.¹ Although most people who consider suicide do not act on those thoughts, 51% of psychiatrists report having had a patient who committed suicide.²

Because patient suicide risk is real, psychiatrists often worry about malpractice claims. Although post-suicide lawsuits account for the largest number of malpractice suits against psychiatrists,^3,4 a psychiatrist’s risk of being sued for malpractice is still quite low.³ Even when sued, clinicians win up to 80% of cases.³

Still, with malpractice claims increasing overall, clinicians should understand their potential liability in preventing suicide and the basic principles behind a malpractice claim.

Patient jumps from window after suicide watch is called off

Los Angeles County (CA) superior court

A 24-year-old man was hospitalized after attempting suicide by ingesting prescription pills and alcohol. He was admitted to the general medical floor with a 24-hour sitter to guard against additional suicide attempts. When the psychiatrist tried to evaluate him, he found the patient unresponsive because of the pills’ effects.

The next day, the psychiatrist evaluated the patient and recommended that the patient be transferred to the psychiatric unit and that the sitter be continued. Four hours later, without a further evaluation, the psychiatrist recommended moving the patient to another room and canceling the sitter.

The next day, the patient jumped from his sixth-floor hospital room window. He sustained traumatic brain injury.

The patient’s guardian ad litem argued that discontinuing the sitter was negligent. The defendant argued that discontinuation was within the parameters of proper care.

• The jury found for the defense.

Patient commits suicide hours after ER discharge

Lake County (IL) circuit court

A 36-year-old man was being treated by a psychiatrist for major depressive disorder. The patient owned several guns for hunting and target shooting and had a state-issued firearm owner’s identification card.

In October 2003, the patient presented to the emergency room and was examined by a mental health assessment staff. The psychiatrist recommended voluntary admission to the psychiatric unit for 23 hours.

The patient’s father discouraged the admission and stated that the patient could lose his gun owner’s card as a result. The patient was subsequently discharged. Within 24 hours after discharge, the patient shot himself in the chest and died.

The deceased’s estate argued that the psychiatrist should have admitted the patient involuntarily. The psychiatrist claimed no obligation to involuntary admission and argued that the patient did not meet criteria typically used for such admission.

• The jury found for the defense.

Doctor’s hanging attempt in hospital causes permanent brain damage

Morris County (NJ) district court

A cardiologist was admitted to the hospital’s psychiatric unit after decompensating. While hospitalized, he attempted suicide by hanging in a clinic bathroom. He suffered permanent brain injury as a result of the hanging. Because the injury left him in a childlike state, he required constant care.

The patient’s attorney argued that hospital personnel knew he was suicidal yet did not adequately supervise him. The attorney also argued that the injury cost his client $5 million in lost income.

The defense reported that the hospital had placed the patient on suicide watch and that staff checked him every 5 minutes. The defense also argued that the bathroom where the suicide was attempted was impossible to monitor.

• The jury found for the defense.

Dr. Grant’s observations

To win a malpractice claim, the injured party must show four things:

Duty to care for the patient existed based on the provider’s relationship with the patient. Whether on a hospital floor or in the emergency room, once a doctor-patient relationship has been established, the provider agrees to provide non-negligent care.

Negligence. The physician or hospital personnel acted negligently and violated the duty of care. This concept is based upon a “standard of care” —ie, what other psychiatrists would do in this situation.

Harm. Even if someone has acted negligently, a malpractice case cannot go forward if no harm has been suffered.

Causation. The negligent act caused the harm.

The defendants most likely won the cases cited above because the injured parties could not establish negligence. Clinicians are not negligent for merely failing to predict suicide, as the inability to predict suicide has been demonstrated.^5,6 Clinicians, however, must follow the profession’s standard of care, assess the relative degree of risk, and form a treatment and safety plan consistent with that risk.⁴

Based on relevant case law, the following actions can decrease the risk of patient suicide—and a resultant malpractice claim:

• Conduct a comprehensive evaluation of the patient and his or her suicide risk. Ask about:
• Consider hospitalizing at-risk patients. If you decide against hospitalization, provide a comprehensive safety plan. In the gun owner’s case, such a plan would include arranging with the family to remove firearms. Implement additional anti-suicide precautions, such as more-intensive outpatient therapy or involving family members in treatment.
• Document suicide risk assessment and the reasons for your treatment decisions. Juries may interpret lack of documented information in the patient’s favor.
• Design a treatment plan for hospitalized patients to reduce suicide risk. Consider the patient’s reaction to constant surveillance. For example, checking a paranoid patient every 5 minutes may be more therapeutic than a constant watch while providing adequate safety. Thoroughly document your reasons behind the plan.