Vascular dementia revisited: diagnosis, pathogenesis, treatment, and prevention

Abstract

VaD is the second most common cause of dementia in the elderly after AD. VaD is defined as the loss of cognitive function resulting from ischemic, ischemic-hypoxic, or hemorrhagic brain lesions as a result of CVD and cardiovascular pathologic changes. Diagnosis requires (1) cognitive loss (often predominantly subcortical), (2) vascular brain lesions demonstrated by imaging, and (3) exclusion of other causes of dementia, such as AD. VaD is excluded by brain imaging showing no evidence of vascular lesions. VaD may be caused by multiple strokes (MID or poststroke dementia) but also by single strategic strokes, multiple lacunes, and hypoperfusive lesions such as border zone infarcts and ischemic periventricular leukoencephalopathy (Binswanger's disease). Primary and secondary prevention of stroke and cardiovascular disease decreases the burden of VaD. Genetic advice is needed in patients with familial forms, such as CADASIL. Treatment involves control of risk factors (i.e., hypertension, diabetes, smoking, hyperfibrinogenemia, hyperhomocystinemia, orthostatic hypotension, cardiac arrhythmias). Anticholinergic medications used for AD are also useful in VaD, and atypical antipsychotic agents and antidepressants (e.g., selective serotonin reuptake inhibitors) may be required in some patients.