Vascular dementia (VD) was studied with regard to pathogenesis and symptomatology. The material comprised both clinically and postmortem diagnosed cases and patients investigated at a special diagnostic unit in a psychiatric hospital. At postmortem, a small mean volume of infarcted tissue was found together with an obvious reduction of 5-hydroxyindoleacetic acid in subcortical areas and of choline acetyltransferase in cortical areas and the hippocampus. In subcortical white matter a pronounced decrease of myelin lipids and almost intact levels of gangliosides were found. In the clinical studies, a VD diagnosis was chosen when the patients showed dementia in combination with either transitory ischemic attacks (TIA) or stroke episodes, or other pronounced vascular diseases. On computed tomography white matter low attenuation was found to be extensive and to occur frequently (85%). In the cerebrospinal fluid (CSF) studies an increased albumin ratio without relation to TIA/stroke was found, indicating blood-brain barrier dysfunction. Intrathecal immunoglobulin G (IgG) production was found in 9% of the VD patients, and the IgG index was related to severity of disease and to hypertension. A frontosubcortical symptom complex was the dominating clinical pattern, and the more obvious the subcortical symptom complex, the lower was the 5-HIAA concentration in CSF. The combination of decreased myelin lipids, white matter low attenuation, blood-brain barrier dysfunction, immunological and symptomatological findings suggests that VD in this study was a subcortical non-infarct disorder, possibly a small vessel disease and that infarcts, when present, were end point manifestations of the vascular pathology rather than the cause of the disease. Today, multi-infarct dementia is looked upon as the main category of VD. Our findings suggest that subcortical non-infarct VD is another important VD group that ought to be taken into account.
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