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
| Dementia type | Prevalence |
|---|---|
| Alzheimer's | 65% |
| Lewy body | 0-15% |
| Vascular | 10-15% |
| Mixed | 10-15% |
| Source: reference 1 | |
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
| Central | Progressive cognitive decline that interferes with normal social and occupational function; deficits on tests of attention, frontal-subcortical skills, and visuospatial ability can be especially prominent |
| Core | Two of three needed for probable diagnosis:
|
| Supportive | Repeated falls Syncope Transient loss of consciousness REM sleep behavior disorder Systematized delusions Hallucinations in other modalities Neuroleptic sensitivity Depression |
| Features less likely to be present | History of stroke Another physical illness or brain disorder that interferes with cognitive performance |
| Source: reference 6 | |
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.