Purpose of reviewCerebrovascular lesions may produce cognitive deficits ranging from subtle impairment of language to full-blown dementia. This article reviews recent research into the prevalence, clinical aspects, and mechanism of post-stroke cognitive deficits.Recent findingsAbout half of those individuals with vascular cognitive impairment may develop dementia within the 5-year period after the stroke. Dementia solely due to cerebrovascular lesions is found only in 3-4% of patients with clinical dementia, and most patients meeting clinical criteria for vascular dementia also show the neuropathology of Alzheimer's disease. Microvascular lesions may play an important role in mixed dementia by lowering the threshold at which Alzheimer's disease neuropathology becomes clinically manifest. Whereas cerebral ischemia may increase amyloidogenesis in hypoperfused areas of the brain, the overexpression of amyloid may produce further vascular pathology and ischemia.SummaryThe review highlights the importance of cerebrovascular damage in the mechanism of cognitive impairment and overt dementia, and suggests the adoption of a classification of cerebrovascular cognitive impairment based on the relationship between the site of the brain lesion and the pattern and progression of cognitive deficits.