The pathology of ischemic-vascular dementia: An update

Abstract

In Western memory clinic-based series, ischemic-vascular dementia (IVD) is seen in 8–10% of cognitively impaired elderly subjects. Its prevalence in autopsy series ranges from 0.03% to 58% with reasonable values of 4–10%, while in Japan, IVD is seen in 22–35% and mixed-type dementia (MTD) (Alzheimer disease/AD+IVD) in 6–11%. In a large Viennese autopsy series, “pure” IVD was observed in 9.4% of demented elderly and in 2.9% of those clinically diagnosed as possible/probable AD MTD was observed in 3.1% and 1.3% respectively. The major morphological types of IVD are multi-infarct encephalopathy (MIE), small vessel infarct type-strategic infarct dementia (SID), subcortical arteriosclerotic leukoencephalopathy (Binswanger), multilacunar state, mixed cortico-subcortical type, granular cortical atrophy, and post-ischemic encephalopathy. In contrast to previous suggestions that IVD is mainly the result of large hemispheral infarcts or losses of over 100 ml of brain tissue, recent data indicate that cognitive decline is commonly associated with widespread small ischemic or vascular lesions (microinfarcts, lacunes) throughout the brain with predominant involvement of the basal ganglia, white matter, and hippocampus. The lesion pattern of “pure” IVD, which is related to arteriolosclerosis and hypertensive microangiopathy, differs from that in mixed-type dementia, more often showing large infarcts. Although recent studies suggest that concomitant small cerebral infarcts do not significantly influence the overall rate of cognitive decline in AD patients or may be important for mental decline in early AD, both mild AD pathology and microvascular cerebral lesions appear to be common and may interact in “unmasking” or promoting dementia.