Vascular Dementia

Introduction & Clinical Features

Vascular Dementia (VaD) also called Dementia due to Cerebrovascular Disease usually results from multiple cerebrovascular accidents (CVAs) or one significant CVA. It is generally considered the second-most-common cause of dementia after Alzheimer’s disease, accounting for about 10% of all cases.

In patients with Vascular Dementia, cognitive impairment is typically abrupt in onset with stepwise deterioration. Cognitive impairment has its onset or dramatic worsening typically in association with a stroke or clear imaging evidence of infarctions. Some stroke-related syndromes include the clinical phenotype of anterograde amnesia Opens in new window that is identical to that of Alzheimer’s disease Opens in new window (AD). Memory function, while impaired in VaD, is not the principal and devastating feature that it is with AD.

Impaired judgment, personality changes, frank aphasia, or visuo-spatial disturbances may predominate either alone or in combination. The mental status changes exhibited by this population of vascular dementia patients is characterized by slowness in mental processes, problems with decision-making, poor organizational ability, difficulty adjusting to change (impaired executive functions of the frontal lobe), difficulty sustaining attention, and the appearance of apathy.

Men are twice as likely as women to be diagnosed with Vascular Dementia. Vascular Dementia is characterized by a stepwise progression of cognitive deterioration with accompanying lateralizing signs. It is always associated with evidence of systemic hypertension and usually involves renal and cardiac abnormalities.

Risk factors for the development of vascular Dementia include those generally associated with obstructive coronary artery disease, including obesity, hypercholesterolemia, smoking, hypertension, stress, and lack of exercise. The actual incidence of Vascular Dementia has decreased somewhat with better standards of care, improved diagnostic techniques, and lifestyle changes.

Vascular Dementia is characterized by the early appearance of lateralizing signs. Spasticity, hemiparesis, ataxia, and pseudobulbar palsy are common. Pseudobulbar palsy is associated with injury to the frontal lobes and results in the impairment of the corticobulbar tracts. It is characterized by extreme emotional lability, abnormal speech cadence, dysphagia, hyperactive jaw jerk, deep tendon reflexes, and Babinski’s reflex.

CT, MRI, and gross specimens show cerebral atrophy and infarctions, with the radiological procedures showing multiple lucencies and the gross specimens revealing distinct white matter lesions. The EEG is abnormal but nonspecific, and positron emission tomography reveals hypometabolic areas.

Vascular Dementia is differentiated from Alzheimer’s disease on the basis of its mode of progression, early appearance of neurological signs, and radiographical evidence of cerebral ischemia.

Vascular Dementia and Alzheimer’s Opens in new window are sometimes difficult to distinguish, however, because of overlaps in symptoms, pathology, and comorbidity patterns. In addition, many patients have concomitant Alzheimer’s and Vascular Dementia share several risk factors and have a shared pathology (e.g. lacunae, white matter lesions). The presence of mixed Vascular Dementia and Alzheimer’s disease in combination has been underestimated in the older population.


Primary prevention and secondary prevention are important in the treatment of cerebrovascular disorders. Lifestyle changes are effective in arresting the progress of the disease; however, no known pharmacological treatment can reverse the effects of a completed stroke.

Such interventions as anticoagulants for frequent transient ischemic attacks after a cerebrovascular event is excluded, aspirin for decreasing platelet aggregation, and surgical removal of obstructing plaques probably do not reverse the mental state.

Depression occurs in 50% to 60% of patients with CVAs and responds to traditional antidepressants. Amitrptyline, in less-than-antidepressant doses, improves both CVA depression and pseudobulbar palsy. SSRIs should be avoided after an acute hemorrhagic stroke because of their tendency to increase bleeding time.

In ischemic stroke Opens in new window patients who are prescribed warfarin, such agents as paroxetine and fluoxetine, which affect warfarin metabolism, should be avoided. Physical rehabilitation is essential and often results in an improvement in mood and outlook.

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