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Cerebral Glucose and Dopa Metabolism in Movement Disorders

Published online by Cambridge University Press:  05 January 2016

W.R. Wayne Martin  and
Michael R. Hayden
W.R. Wayne Martin*
Affiliation:
Departments of Medicine (Neurology), and Medical Genetics, University of British Columbia, Vancouver
Michael R. Hayden
Affiliation:
Departments of Medicine (Neurology), and Medical Genetics, University of British Columbia, Vancouver
*
U.B.C. Health Sciences Centre Hospital,2211 Wesbrook Mall, Vancouver, B.C., Canada V6T 1W5
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Abstract:

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The development of positron emission tomography (PET) has enabled us to perform in vivo measurements of certain aspects of regional cerebral function. Regional cerebral glucose metabolism may be readily quantified with [18F] fluoro-2-deoxyglucose (FDG) and presynaptic dopaminergic function may be studied with the labelled dopa analog 6-[18F] fluoro-L-dopa. We have applied a model to the analysis of 6-FD/PET data with which in vivo age-related changes in dopaminergic function may be demonstrated in normal subjects. With this technique, we have studied a series of asymptomatic MPTP-exposed subjects and have shown evidence of subclinical nigrostriatal pathway damage. Studies of regional cerebral glucose metabolism with FDG in early Huntington's disease have shown a characteristic impairment in caudate function which precedes the development of caudate atrophy. In addition, some asymptomatic individuals who are at risk for HD have caudate hypometabolism. We feel that, at the present time, PET provides information which is complementary to the clinical examination in establishing a diagnosis of HD. In the future these studies may also help in the investigation of at risk individuals

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 14 , Issue S3 , August 1987 , pp. 448 - 451
Copyright
Copyright © Canadian Neurological Sciences Federation 1987

References

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