Vascular dementia is acute or chronic cognitive deterioration due to diffuse or focal cerebral infarction that is most often related to cerebrovascular disease.
Vascular dementia is the 2nd most common cause of dementia among the elderly. It is more common among men and usually begins after age 70. It occurs more often in people who have vascular risk factors (eg, hypertension, diabetes mellitus, hyperlipidemia, smoking) and in those who have had several strokes. Many people have both vascular dementia and Alzheimer disease.
Vascular dementia typically occurs when multiple small cerebral infarcts (or sometimes hemorrhages) cause enough neuronal or axonal loss to impair brain function. Vascular dementias include the following:
Symptoms and Signs
Symptoms and signs are similar to those of other dementias (see Symptoms and Signs). However, multiple-infarct dementia tends to progress in discrete steps; each episode is accompanied by intellectual decline, sometimes followed by modest recovery. Subcortical vascular dementia caused by small-vessel ischemic damage (which includes multiple lacunar infarction and Binswanger dementia) tends to cause small, incremental deficits; thus, the decline appears to be gradual.
As the disease progresses, focal neurologic deficits often develop:
Cognitive loss may be focal. For example, short-term memory may be less affected than in other dementias. Patients with partial aphasia may be more aware of their deficits; thus, depression may be more common than in other dementias.
Diagnosis is similar to that of other dementias (see Diagnosis). As in other dementias, cognitive impairment must be severe enough to interfere with daily activities. In addition, confirmation of vascular dementia requires a history of stroke or evidence of a vascular cause for dementia detected by neuroimaging. If focal neurologic signs or evidence of cerebrovascular disease is present, a thorough evaluation for stroke should be done (see Evaluation).
CT and MRI may show bilateral multiple infarcts in the dominant hemisphere and limbic structures, multiple lacunar strokes, or periventricular white-matter lesions extending into the deep white matter. In Binswanger dementia, imaging shows leukoencephalopathy in the cerebrum semiovale adjacent to the cortex, often with multiple lacunae affecting structures deep in the gray matter (eg, basal ganglia, thalamic nuclei).
The Hachinski Ischemic Score is sometimes used to help differentiate vascular dementia from Alzheimer disease (see Table 4: Modified Hachinski Ischemic Score).
The 5-yr mortality rate is 61%, which is higher than that for most forms of dementia, presumably because other atherosclerotic disorders coexist.
Generally, treatment is the same as that of other dementias (see Treatment). However, vascular dementia may be preventable, and its progression may be slowed by BP control, cholesterol-lowering therapy, regulation of plasma glucose (90 to 150 mg/dL), and smoking cessation.
Efficacy of cholinesterase inhibitors and memantine is uncertain in vascular dementia. However, these drugs are commonly used, partly because elderly patients with vascular dementia may also have Alzheimer disease. Adjunctive drugs for depression, psychosis, and sleep disorders are useful.
Last full review/revision April 2013 by Juebin Huang, MD, PhD
Content last modified May 2013