Although vascular dementia (VaD) is the second most frequent cause of demen
tia after Alzheimer disease (AD): the concept remains controversial in term
s of delineation. The objective of this review is to investigate, from avai
lable literature, the role of cerebral infarcts in the pathogenesis of VaD
and to identify areas of interest that need further evaluation and research
. The incidence of new onset dementia is increased after stroke. Stroke sub
types, total volume of cerebral infarction and functional tissue loss, and
location of the lesions are probably the major determinants of VaD. Any cau
se of stroke can lead to VaD. In some circumstances the causal relation bet
ween stroke and dementia is clear: (1) in young patients who are unlikely t
o have associated Alzheimer pathology; (2) when the cognitive functioning w
as normal before stroke, impaired immediately after, and does not worsen ov
er time; (3) when the lesions are located in strategic areas; and (4) when
a well-defined vasculopathy known to cause dementia is proven. However, sev
eral issues remain unsolved in VaD: lack of specificity of the diagnostic c
riteria; influence of white matter changes and associated Alzheimer patholo
gy; influence of preexisting cognitive status; possibility of having VaD wi
thout stroke and the clinical relevance of silent infarcts to VaD; and best
therapeutic strategy to be used to prevent VaD and to prevent stroke in pa
tients with VaD. These questions form the basis for proposals for future re
search.