622 Neurocognitive Disorders
presentation is therefore very heterogeneous, stemming from the types of vascular lesions
and their extent and location. The lesions may be focal, multifocal, or diffuse and occur in
various combinations. 
Many individuals with major or mild vascul ar NCD present with multiple infarctions,
with an acute stepwise or fluctuating dec line in cognition, and intervening periods of
stability and even some improvement. Others may have gradual onset with slow pro-
gression, a rapid development of deficits follo wed by relative stabilit y, or another complex
presentation. Major or mild vascular NCD wi th a gradual onset an d slow progression is
generally due to small vessel disease leading to lesions in the white matter, basal ganglia,
and/or thalamus. The gradual progression in these cases is often punctuated by acute
events that leave subtle neurological deficits. The cognitive deficits in these cases can be at-
tributed to disruption of cortical-subcortical  circuits, and complex attention, particularly
speed of information processing, and exec utive ability are likely to be affected.
Assessing for the presence of sufficient cerebrovascular disease relies on history, phys-
ical examination, and neuroimaging (Criterion  C). Etiological certainty requires the dem-
onstration of abnormalities on neuroimaging. The lack of neuroimaging can result in
significant diagnostic inaccuracy by overlooking “silent” brain infarction and white mat-
ter lesions. However, if the neurocognitive im pairment is temporally associated with one
or more well-documented  strokes, a probable diagnosis can be made in the absence of neu-
roimaging. Clinical evidence of cerebrovascular disease includes documented history of
stroke, with cognitive decline temporally assoc iated with the event, or physical signs con-