Cerebral glucose metabolism in Parkinson's disease with and without dementia
R. F. Peppard, W. R. Martin, G. D. Carr, E. Grochowski, M. Schulzer, M. Guttman, P. L. McGeer, A. G. Phillips, J. K. Tsui and D. B. Calne
Department of Medicine, University of British Columbia, Vancouver, Canada.
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.
