Impact of subcortical ischemic lesions on behavior and cognition.
Both cerebrovascular disease and AD are common in the elderly. There are various types of underlying damage to tissue and vessels in vascular cognitive impairment, and the neural mechanisms producing cognitive impairment and the clinical picture are different among the subtypes. Among them, small subcortical infarcts disrupting cortico-subcortical circuits and white matter lesions are the commonest types, and the combination of these two types of lesions might be more realistic than each pure form. Moreover, cognitive impairment of vascular origin may be superimposed on AD. Both vascular and degenerative mechanisms contribute to the development of cognitive impairment, especially in old age, whether they are two independent parallel processes or interacting pathologies. Subcortical small lesions involving the thalamus, caudate, and globus pallidus disrupt cortico-subcortical circuits, resulting in cognitive dysfunction. Disruption of the frontal-subcortical circuits leads to cognitive impairment with striking frontal lobe features, and disruption of the memory-related circuits leads to amnesia. White matter changes, which are certainly related to chronic cerebral ischemia in some patients, are another issue. Patients with dementia and white matter changes may have either AD with cerebrovascular changes or a form of VaD, or a combination of these two etiologies. However, our series of studies have suggested that white matter changes in AD patients are superimposed phenomena of vascular origin and that white matter changes contribute to specific neurological and neuropsychiatric manifestations, but not to global cognitive impairment, which is more closely associated with the degenerative process.
Mori
Etsuro
E
Institute for Aging Brain and Cognitive Disorders, Hyogo Brain and Heart Center, 520 Saisho-ko, Himeji 670-0981, Japan. mori@hiabcd.go.jp
D002545:Brain Ischemia / Q000145:classification / Q000503:physiopathology* / Q000523:psychology*; D002544:Cerebral Infarction / Q000503:physiopathology / Q000523:psychology; D003071:Cognition / Q000502:physiology*; D006801:Humans; D009928:Organ Specificity