Abstract
Cerebral blood flow and oxygen metabolism were studied in three normal aged subjects and twelve patients with multi-infarct dementia (MID) by positron emission tomography (PET) using 0-15. Cerebral glucose metabolism was studied in three normal aged subjects and eight patients with MID by PET using C-11-glucose.
The diagnosis of MID was done according to the Loeb's modified ischemic score and X-ray CT findings. The X-ray CT findings of MID patients were the localized low density areas in the suboortical white matter, basal ganglia and thalamus. No occulusion but arteriosclerosis was observed in anterior and/or middle cerebral arteries on a cerebral angiography.
Regional cerebral blood flow (rCBF), oxygen extraction fraction (rOEF) and the cerebral metabolic rate for oxygen (rCMRO2) were measured by the steady state technique, and regional distribution of glycogenic metabolites (RDGM) were measured by the quantitation method described by M.lio et al.
The values of rCBF in MID were significantly low compared with those of the normal aged subjects in frontal, temporal, occipital and parietal cortices and in thalamus. The values of rCMRO2 in MID were significantly low in frontal, temporal and occipital cortices and in thalamus compared with those of the normal aged subjects. The glucose metabolism expressed as RDGM decreased equally with oxygen metabolism.
The OEF was 0.46 in normal aged subjects, and 0.48 in MID. The MID patients in the early stage of dementia showed increased OEF, and this fact suggests that ischemia due to cerebral arteriosclerosis and lacunes is a significant pathogenic mechanism in the production and progression of MID.
The decrease of rCBF and rCMRO2 in MID compared with that of the normal subjects was most remarkable in the frontal cortex. The values of rCBF and rCMRO2 in moderate dementias were significantly low compared with those of mild dementias in the frontal cortex. The impairment of mental functions in MID must have been caused by decreased neuronal activities in the frontal association cortex.
