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February 1995

Clinical/Metabolic Correlations in Multiple System Atrophy: A Fludeoxyglucose F 18 Positron Emission Tomographic Study

Author Affiliations

From the Institute of Neuroscience and Bioimaging, National Council of Research, Milan, Italy (Dr Perani); the Scientific Institute, Hospital San Raffaele, Milan, Italy (Drs Bressi and Grassi); the Scientific Institute of Neurology, "Carlo Besta," Milan, Italy (Drs Testa, Gentrini, Savoiardo, and Caraceni); the Department of Neurology, University of Bologna, Italy (Dr Cortelli); and the Department of Nuclear Medicine, University of Milan, Italy (Dr Fazio).

Arch Neurol. 1995;52(2):179-185. doi:10.1001/archneur.1995.00540260085021

Objective:  To evaluate the regional cerebral metabolic involvement; the relationships among regional brain metabolism, clinical features, and quantitative measures of disease severity; and the patterns of brain involvement that can be related to the different types of onset: striatonigral degeneration vs olivopontocerebellar atrophy.

Design:  Fludeoxyglucose F 18 positron emission tomography (PET) studies performed in patients with multiple system atrophy (MSA) were evaluated for their clinical features at the onset of the disease and at the time of the PET study.

Cases:  Seventeen patients diagnosed as having probable MSA and 10 age-matched controls.

Results:  The hypometabolism in the putamenpallidum complex and in the cerebellum was the best discriminant for disease classification. The efficacy of levodopa treatment was positively correlated with the metabolic activity of the putamen-pallidum complex. The patients with olivopontocerebellar atrophy type (N=8) had a prevalent hypometabolism in the cerebellum, while the patients with striatonigral degeneration type (N=9) had a prevalent impairment in the pallidum-putamen complex. We demonstrated a negative correlation between (1) severity of parkinsonism and metabolic values of putamen and caudate; (2) severity of cerebellar signs and metabolism in the cerebellum; and (3) autonomic dysfunction and metabolic activity in the thalamus, frontal, and temporal regions, bilaterally.

Conclusions:  These findings support the selective metabolic reduction in the putamen and cerebellum as a marker of MSA. The clinical/metabolic correlations, demonstrating the expected dependence of extrapyramidal and cerebellar signs by dysfunction of basal ganglia and cerebellum, also support a possible involvement of central nervous system structures in autonomic control.

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