Patterns of local cerebral glucose utilization determined in Parkinson's disease by the [¹⁸F]fluorodeoxyglucose method

Abstract

[18F]Fluorodeoxyglucose scans were performed on 9 patients with Parkinson's disease and 14 normal subjects. Five patients were restudied after an interval of 3 to 4 years. We found no selective metabolic change in striatum, where dopamine deficit is known to be greatest, in affected patients; cerebral glucose metabolism was reduced uniformly throughout the parkinsonian brain (average 18% decrease). With increased severity of bradykinesia and the development of mild to moderate dementia, global brain metabolism in Parkinson's disease decreased further. In one moderately demented patient with Parkinson's disease, severe parietal cortex hypometabolism was found, similar to that seen in Alzheimer's disease. In contrast, mildly to moderately demented patients with Huntington's disease have marked caudate hypometabolism, but cerebral glucose metabolism is normal elsewhere. It appears that in addition to the well-known neurotransmitter loss in the nigrostriatal system, there is an abnormal metabolic process involving neurons throughout the parkinsonian brain.

N-isopropyl-p-123I Iodoamphetamine Single Photon Emission Computed Tomography Study of Parkinson's Disease with Dementia

“…Although frontal lobe dysfunction has been described clinically in Parkinson's disease (17)(18)(19)(20)(21)(22)(23), there has not been any significant frontal hypoperfusion observed either in our population or in other studies (8,11).…”

“…Although there is general agreement that a global reduction in rCBF and metabolism predominantly affecting the parieto-temporal regions is encountered in Alzheimer's disease, the available data in Parkinson's disease are conflicting, and do not demonstrate distinctions in specific patterns of rCBF or metabolism between Parkinson's disease with or without dementia (8)(9)(10)(11). One of the reasons may be that many factors contribute to the pathophysiology of dementia in Parkinson's disease, such as Alzheimer's disease-like mechanism, diffuse Lewy body disease-like factor or frontal dysfunction due to Parkinson's disease itself.…”

Cerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study

“…Cuneus hypometabolism was observed first in parkinsonian dementia by Kuhl et al in 1985 (18). In subsequent studies of severely affected PDD subjects, glucose metabolic and regional cerebral blood flow studies demonstrated reduced activity in the parietal and temporal neocortices, similar to that seen in AD (19,20). Vander Borght et al, for example, compared metabolic differences between AD and PDD subjects matched for severity of dementia (mean MMSE scores of 18 in both groups) and found similar glucose metabolic reductions globally and regionally, involving the posterior cingulate, lateral parietal, lateral frontal, and lateral tempo-FIGURE 1.…”

Cerebral Mitochondrial Metabolism in Early Parkinson's Disease

“…Thus, although defects in mitochondrial ETS may be present in some patients with PD, the absence of such defects in these 12 patients with early PD indicates that they cannot be essential to the pathogenesis of neuronal death in early PD. (Kuhl et al, 1984;Leenders et al, 1985;Eidelberg et al, 1993Eidelberg et al, , 1994Piert et al, 1996). In one of these studies, reductions in global CMRglc were seen only after L-DOPA was administered, suggesting that the reduction in metabolism may be at least, in part, because of medication effects (Piert et al, 1996).…”