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Vascular dementia is acute or chronic cognitive deterioration due to diffuse or focal cerebral infarction that is most often related to cerebrovascular disease.
Dementia is chronic, global, usually irreversible deterioration of cognition. 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.
Dementia should not be confused with delirium although cognition is disordered in both. The following helps distinguish them:
Other specific characteristics also help distinguish the 2 disorders (see Table: Differences Between Delirium and Dementia*).
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:
Multiple lacunar infarction: Small blood vessels are affected. Multiple lacunar infarcts occur deep within hemispheric white and gray matter.
Multi-infarct dementia: Medium-sized blood vessels are affected.
Strategic single-infarct dementia: A single infarct occurs in a crucial area of the brain (eg, angular gyrus, thalamus).
Binswanger dementia (subcortical arteriosclerotic encephalopathy): This uncommon variant of small-vessel dementia is associated with severe, poorly controlled hypertension and systemic vascular disease. It causes diffuse and irregular loss of axons and myelin with widespread gliosis, tissue death due to an infarction, or loss of blood supply to the white matter of the brain.
Symptoms and signs of vascular dementia are similar to those of other dementias (eg, memory loss, impaired executive function, difficulty initiating actions or tasks, slowed thinking, personality and mood changes, language deficits). However, compared with Alzheimer disease, vascular dementia tends to cause memory loss later and to affect executive function earlier. Also, symptoms can vary depending on where the infarcts occur.
Unlike other dementias, 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. Because loss may be focal, patients may retain more aspects of mental function. Thus, they may be more aware of their deficits, and depression may be more common than in other dementias.
Evaluation of cognitive function involves taking a history from the patient and from someone who knows the patient plus doing a bedside mental status examination or , if bedside testing is inconclusive, formal neuropsychologic testing (see Assessment of cognitive function).
Differentiation of vascular dementia from other dementia is based on clinical judgment. Factors that suggest vascular dementia (or Alzheimer disease with cerebrovascular disease) include the following:
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.
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: Modified Hachinski Ischemic Score).
Modified Hachinski Ischemic Score
Safety and supportive measures are similar to those of other dementias. For example, the environment should be bright, cheerful, and familiar, and it should be designed to reinforce orientation (eg, placement of large clocks and calendars in the room). Measures to ensure patient safety (eg, signal monitoring systems for patients who wander) should be implemented.
Troublesome symptoms can be treated.
Managing vascular risk factors (eg, hypertension, diabetes, hyperlipidemia) may slow the progression of vascular dementia and help prevent future strokes, which could cause more cognitive impairment. Management includes the following:
Drugs, such as cholinesterase inhibitors and memantine, may be helpful in some dementias. Cholinesterase inhibitors may improve cognitive function. Memantine, an NMDA ( N -methyl-d-aspartate) antagonist, may help slow the loss of cognitive function in patients with moderate to severe dementia and may be synergistic when used with a cholinesterase inhibitor.
However, efficacy of cholinesterase inhibitors and memantine is uncertain in vascular dementia. Nonetheless, a trial of these drugs is reasonable because elderly patients with vascular dementia may also have Alzheimer disease.
Adjunctive drugs for depression, psychosis, and sleep disorders are useful.
Vascular dementia can occur as a series of discrete episodes (which may seem like a gradual decline) or in a single episode.
Focal neurologic signs may help differentiate vascular dementia from other dementias.
Confirm that dementia is vascular based on a history of stroke or neuroimaging findings that suggest a vascular cause.
Control vascular risk factors, and if Alzheimer disease could also be present, treat with cholinesterase inhibitors and memantine.
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* This is the Professional Version. *