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. 1994 May-Jun;15(3):329-35.
doi: 10.1016/0197-4580(94)90028-0.

Cortical glucose metabolism in Parkinson's disease without dementia

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Cortical glucose metabolism in Parkinson's disease without dementia

J L Eberling et al. Neurobiol Aging. 1994 May-Jun.

Abstract

There have been several reports of decreased regional cerebral metabolic rates for glucose (rCMRglc) in Parkinson's disease (PD), although others find no differences between PD patients and controls. Differences in the cognitive status of the PD patients may account for some of these inconsistencies. We report the results of a PET study using 18F-fluorodeoxyglucose (FDG) to measure rCMRglc in eight nondemented PD patients, six of whom were receiving dopaminergic medications, and eight age-matched control subjects. We scanned one tomographic level through the temporal lobes that included both temporal neocortex and mesial temporal cortex, and one tomographic level through the basal ganglia that included frontal and parietal cortex. Previously determined rate constants and an operational equation were used to determine rCMRglc. On average, rCMRglc values were 23% below control values for all regions studied, with the greatest differences in posterior brain regions (visual association cortex, primary visual cortex, and parietal cortex) and thalamus. These results indicate that PD patients may show neocortical hypometabolism, especially in posterior brain regions, in the absence of any demonstrable cognitive deficits.

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