 |
 |

Cerebral Glucose Metabolism in Parkinson's Disease With and Without Dementia
Richard F. Peppard, MD;
W. R. Wayne Martin, MD;
Geoff D. Carr, MD;
Edward Grochowski;
Michael Schulzer, MD;
Mark Guttman, MD;
Patrick L. McGeer, MD;
Anthony G. Phillips, PhD;
Joseph K. C. Tsui;
Donald B. Calne, DM
Arch Neurol. 1992;49(12):1262-1268.
Abstract
 |  |
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.
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.
Footnotes
Accepted for publication June 10, 1992.
Reprint requests to Movement Disorder Clinic, Edmonton General Hospital, 11111 Jasper Ave, Edmonton, Alberta, Canada T5K OL4 (Dr Martin).
CiteULike Connotea Del.icio.us Digg Reddit Technorati Twitter
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
 |
Occipital hypoperfusion in Parkinson's disease without dementia: correlation to impaired cortical visual processing
Abe et al.
J. Neurol. Neurosurg. Psychiatry 2003;74:419-422.
ABSTRACT
| FULL TEXT
Neuroimaging in Dementia with Lewy Bodies: Metabolism, Neurochemistry, and Morphology
Minoshima et al.
J Geriatr Psychiatry Neurol 2002;15:200-209.
ABSTRACT
Familial parkinsonism with synuclein pathology: Clinical and PET studies of A30P mutation carriers
Kruger et al.
Neurology 2001;56:1355-1362.
ABSTRACT
| FULL TEXT
Cortical dysfunction in non-demented Parkinson's disease patients: A combined 31P-MRS and 18FDG-PET study
Hu et al.
Brain 2000;123:340-352.
ABSTRACT
| FULL TEXT
Motor correlates of occipital glucose hypometabolism in Parkinson's disease without dementia
Bohnen et al.
Neurology 1999;52:541-541.
ABSTRACT
| FULL TEXT
Cognitive Loss in Dementia With Lewy Bodies and Alzheimer Disease
Shimomura et al.
Arch Neurol 1998;55:1547-1552.
ABSTRACT
| FULL TEXT
Temporal Lobe Perfusion on Single Photon Emission Computed Tomography Predicts the Rate of Cognitive Decline in Alzheimer's Disease
Wolfe et al.
Arch Neurol 1995;52:257-262.
ABSTRACT
|