Pathogenetic basis of vascular dementia

Abstract

Vascular dementia (VAD) was studied with reference to pathogenetic aspects, especially the importance of brain infarcts. A VAD diagnosis was chosen when the patients showed dementia in combination with transitory ischemic attacks (TIA), stroke episodes, or other pronounced vascular diseases judged to be causally related to the dementia. Computed tomography (CT) white matter lesions were shown to occur frequently (85%); a pronounced decrease in myelin lipids was common in subcortical white matter; a fronto-subcortical symptom complex was the prevailing clinical pattern; and an overall increased albumin ratio without relation to TIA/stroke was noted, indicating blood-brain barrier (BBB) dysfunction. When infarcts were present, they appeared to be endpoint manifestations of the vascular pathology rather than the cause of the disease. Today, thromboembolism with multiple cerebral infarcts is considered more or less the only pathogenetic substrate of VAD, with multi-infarct dementia (MID) as its clinical counterpart. Our findings suggest that subcortical white matter changes are another important VAD substrate.