Vascular Dementia

Vascular dementia results from brain tissue damage due to infarction. Clinical progression typically occurs in steps. Focal neurologic deficits are often present. Diagnosis is by history and physical examination, often supplemented with CT or MRI. Treatment is control of risk factors for stroke, supportive measures, and sometimes a cholinesterase inhibitor with or without memantine.

Geriatric Essentials

• Vascular dementia is more common among patients with hypertension or diabetes.
• Patients with vascular dementia may be depressed more often than patients with Alzheimer's disease.
• Controlling risk factors for stroke is likely to slow progression of the dementia and improve function.

Vascular dementia accounts for about 1/10 to 1/3 of dementia cases and is probably the 2nd most common form of dementia after Alzheimer's disease (AD). Many patients with vascular damage also have concomitant manifestations of AD. Vascular dementia is particularly common among patients who have had transient ischemic attacks or strokes or who have hypertension, diabetes, or other risk factors for stroke (eg, coronary artery disease, peripheral arterial disease, valvular heart disease, atrial fibrillation, hyperlipidemia, cigarette smoking).

Several distinct patterns exist:

• Classic multi-infarct dementia is caused by >= 2 major cerebral infarcts in the anterior, middle, or posterior cerebral artery territories.
• Strategic infarct dementia is caused by a single infarct in a crucial area of the brain (eg, angular gyrus, thalamus).
• Lacunar states are caused by the buildup of multiple small infarcts in the subcortical nuclei (most commonly) and in white matter.

Symptoms and Signs

Symptoms and signs depend somewhat on which pattern is present. The classic presentation (except in strategic infarct dementia) is stepwise cognitive decline; each step is characterized by an ischemic insult and sometimes followed by modest cognitive recovery. However, in dementia caused by a lacunar state or ischemic injury largely limited to white matter, the steps may be so small that they are clinically indistinguishable from gradual decline.

Brain impairment in vascular dementia is patchier than that in AD, and some cognitive areas may be entirely unaffected. Unlike in AD, short-term memory is sometimes relatively preserved. Focal, often asymmetric neurologic deficits (eg, weakness of an extremity, sensory loss, exaggerated deep tendon reflexes, Babinski's sign, visual field defects, gait abnormalities, pseudobulbar palsy, incontinence) occur early; in AD, these deficits are symmetric and occur mainly in late stages. Visuospatial deficits are common. Patients with vascular dementia tend to be more aware of their deficits than patients with AD, and the prevalence of depression may be higher.

Death tends to occur somewhat earlier than in AD because patients often have diffuse vascular disorders that affect other arteries (eg, aorta, coronary arteries, peripheral arteries).

Diagnosis

Diagnosis is based on a typical clinical history, focal neurologic findings, and evidence of strokes (lacunar or larger strokes) detected by brain imaging. CT and MRI findings typical of dementia secondary to a lacunar state include lacunae in subcortical nuclei (eg, basal ganglia, thalamus) accompanied by periventricular and white-matter abnormalities, often without zones of cortical infarction. In the elderly, changes in white matter are common and sometimes nonspecific; unless extensive, these changes should be interpreted with caution when dementia is being considered.

Several assessment tools, such as the Hachinski Ischemic Score (see Table 40-4), may help differentiate vascular dementia from AD, but accuracy is limited. Thus, clinical differentiation has limited reliability. Also, in many patients who present with classic vascular dementia, postmortem examination of the brain detects evidence of AD as well as infarcts compatible with vascular dementia.

Treatment

No treatment has been shown to slow progression. Nonetheless, a logical approach is to try to decrease risk of stroke, eg, by controlling hypertension (including isolated systolic hypertension), treating patients with aspirin or warfarin as indicated, and treating patients who have hyperlipidemia with lipid-lowering drugs. Some patients respond to a cholinesterase inhibitor and memantine. Adjunctive drugs for depression and sleep disorders are sometimes warranted.

This topic was last updated February 2006.