Heterogeneity of Vascular Dementia: Mechanisms and Subgroups

Abstract

Today, multiple, thromboembolically generated cerebral infarcts are regarded as the main pathogenetic pathway of vascular dementia (VAD), with multi-infarct dementia (MID) as its clinical counterpart. However, taking into account other vascular mechanisms that may influence the brain, such as vessel-wall damage (atherosclerosis, hyalinosis, amyloid angiopathy, or blood-brain barrier dysfunction), cerebrovascular insufficiency (disturbance of systemic circulation, perfusion vulnerability related to the vascular anatomy of the brain, or disturbance of autoregulation), and hyperviscosity, it is evident that MID is not the only VAD category. The diagnosis of MID ought to be reserved for the combination of progressive dementia associated with cerebral ischemic events and evidence of infarction that is mainly associated with the large cerebral arteries. Subcortical white-matter dementia characterized by frontosubcortical symptomatology, white-matter lesions, and small-vessel involvement with or without lacunes/infarcts—a combination of lacunar dementia and Binswanger's disease—appears to be another important VAD disease.