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*
| Drug class | Potential cognitive side effects |
|---|---|
| Antidepressants Tricyclics, SSRIs, SNRIs | Confusion, sedation, falls |
| Antihistamines | Confusion, sedation, dizziness |
| Antipsychotics | Sedation, fatigue, anxiety |
| Antispasmodics | Confusion, sedation |
| Benzodiazepines | Sedation, confusion, ataxia, depression |
| Opioids | Sedation, confusion, dizziness |
| Sleep-promoting agents | Amnesia, confusion, ataxia |
| * Not all agents in each class are associated with listed side effects | |
| SSRIs: Selective serotonin reuptake inhibitors | |
| SNRIs: Serotonin-norepinephrine reuptake inhibitors | |
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).