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

[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 wellknown neurotransmitter loss in the nigrostriatal system, there is an abnormal metabolic process involving neurons throughout the parkinsonian brain.