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December 1992

Cerebral Glucose Metabolism in Parkinson's Disease With and Without Dementia

Author Affiliations

From the Departments of Medicine (Drs Peppard, Martin, Schulzer, Guttman, Tsui, and Calne), Psychology (Drs Carr and Phillips), Psychiatry (Dr McGeer), and Statistics (Dr Schulzer) and the Unversity of British Columbia/TRIUMF Positron Emission Tomography Program (Mr Grochowski), University of British Columbia, Vancouver. Dr Martin is now with the Movement Disorder Clinic, Edmonton (Alberta) General Hospital.

Arch Neurol. 1992;49(12):1262-1268. doi:10.1001/archneur.1992.00530360060019

• Although cognitive impairment is commonly associated with Parkinson's disease, the relative importance of cortical and subcortical pathologic changes to the development of dementia is controversial. Characteristic abnormalities in cortical glucose metabolism have been reported previously in Alzheimer's disease, a disease in which cortical changes predominate. We measured cerebral glucose metabolism with positron emission tomography in 20 control subjects and in 14 patients with PD with mental status ranging from normal to severely demented to determine whether changes in cortical glucose metabolism occur in early PD and whether the degree and pattern of metabolic change relate to the severity of dementia. The patients were divided into demented and nondemented groups according to the results of neuropsychological assessment. Age-adjusted covariance analyses were performed, since the age distribution varied between groups. The nondemented patients with PD showed widespread cortical glucose hypometabolism without any selective temporoparietal defects. The pattern of glucose hypometabolism seen in the demented patients with PD resembled that described in patients with Alzheimer's disease; ie, there was a global decrease in glucose metabolism, with more severe abnormalities observed in the temporoparietal regions.

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