GLUCOSE-METABOLISM IN THE CORTICAL AND SUBCORTICAL BRAIN STRUCTURES IN MULTIPLE SYSTEM ATROPHY AND PARKINSONS-DISEASE - A POSITRON EMISSIONTOMOGRAPHIC STUDY

The brain glucose metabolism was studied by PET with F-18-FDG in 11 pa tients with multiple system atrophy (MSA) and 12 patients with idiopat hic Parkinson's disease (PD). Seven of the 11 MSA patients were diagno sed as having olivopontocerebellar atrophy, two had striaronigral dege neration, while two demonstrated Shy-Drager syndrome. The glucose meta bolic rates for each region in the PD patients showed no difference fr om the normal controls. The frontal, temporal and parietal cortical gl ucose metabolic rates and the caudate, the putaminal, the cerebellar a nd the brainstem glucose metabolic rates in the MSA patients decreased significantly from the controls. The atrophy of the cerebellum and th e brainstem in the MSA patients were scored by MRI. The cerebellar and brainstem glucose metabolism in the MSA patients decreased as the atr ophy score in such regions advanced in each group; however, some patie nts with no atrophy showed a decreased glucose metabolism. Although th e cerebellar and the brainstem glucose metabolism decreased in all MSA patients, such a decrease was not observed in the SND patients, The d ecrease in the glucose metabolism for the non-cortical regions in the MSA patients seems to be due to a diffuse depletion of the neurons not restricted to the nigrostriatal neurons. Deafferentation to the cereb ral cortices seems to result in a decreased cortical metabolism. The d ifferences in the glucose metabolism between MSA and PD as assessed by PET may be caused by the pathophysiological differences between MSA a nd PD, and such differences therefore appear to be useful when making a differential diagnosis between MSA and PD. The relative sparing of t he brainstem and cerebellar glucose metabolism is considered to be a f eature of patients with SND.