It is now clear from autopsy studies of individuals who were carefully studied during life that various types of vascular injury to the brain can result in dementia.
Some individuals with a rapidly progressive cognitive decline have vasculitis (discussed above) and will often show improvement with treatment.
Among the irreversible disorders, several specific entities have been identified, which can be separated in part by their clinical course (typically a stepwise progression rather than a gradual decline) and imaging features.
Various etiologies include small areas of infarction (granular atrophy from cortical microinfarcts, multiple lacunar infarcts, cortical laminar necrosis associated with reduced perfusion/oxygenation) and diffuse white matter injury (Binswanger disease, CADASIL).
Additionally, dementia has been associated with so-called strategic infarcts, which are usually embolic and involve brain regions such as the hippocampus, dorsomedial thalamus, or frontal cortex including cingulate gyrus.
Many individuals, in fact, will demonstrate a combination of pathologic changes. There is also an interaction between vascular injury and other dementing disorders, such as AD.
It has been found that patients with vascular changes above a certain threshold have a lower burden of plaques and tangles for their level of cognitive impairment than do those without vascular-based cerebral pathology.