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Cerebral Glucose Metabolism in Parkinson’s Disease

Published online by Cambridge University Press:  18 September 2015

J.H. Beckman
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
D.B. Calne
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
M.J. Adam
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
R. Harrop
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
J.G. Rogers
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
T.J. Ruth
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
C.I. Sayre
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
B.D. Pate
Affiliation:
Division of Neurology, Health Sciences Centre Hospital, and the UBC/TRIUMF Program on Positron Emission Tomography, University of British Columbia, Vancouver, B.C.
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Abstract

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Local cerebral glucose utilization was measured in patients with predominantly unilateral Parkinson’s disease using 18F-2-fluoro-deoxyglucose and positron emission tomography. Preliminary results indicate the presence of asymmetric metabolic rates in the inferior basal ganglia. The structure comprising the largest portion of basal ganglia at this level is globus pallidus. These findings are consistent with metabolic studies on animals with unilateral nigrostriatal lesions in which pallidal hypermetabolism on the lesioned side has been demonstrated. Increased pallidal activity is likely secondary to a loss of inhibitory dopaminergic input to the striatum from substantia nigra.

Type
5. Positron Emission Tomography in Parkinson’s Disease
Copyright
Copyright © Canadian Neurological Sciences Federation 1984

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