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PET scan investigations of Huntington's disease: Cerebral metabolic correlates of neurological features and functional decline
Journal article   Peer reviewed

PET scan investigations of Huntington's disease: Cerebral metabolic correlates of neurological features and functional decline

Anne B Young, John B Penney, Simon Starosta-Rubinstein, Dorene S Markel, Stanley Berent, Bruno Giordani, Richard Ehrenkaufer, Douglas Jewett and Richard Hichwa
Annals of neurology, Vol.20(3), pp.296-303
09/1986
DOI: 10.1002/ana.410200305
PMID: 2945510
url
https://hdl.handle.net/2027.42/50317View
Open Access

Abstract

Fifteen drug‐free patients with early to midstage Huntington's disease were evaluated with quantitative neurological examinations, scales for functional capacity, computed tomographic (CT) scans, and positron emission tomographic (PET) scans of 18F‐2‐fluoro‐2‐deoxyglucose (18F‐FDG) uptake. All patients had abnormal indices of caudate metabolism on PET scanning, whereas in patients with early disease indices of putamen metabolism and CT measures of caudate atrophy were normal. Indices of caudate metabolism correlated highly with the patients' overall functional capacity (r = 0.906; p < 0.001) and bradykinesia/rigidity (r = −0.692; p < 0.01). Indices of putamen metabolism correlated highly with motor functions: Chorea (r = −0.841; p < 0.01), oculomotor abnormalities (r = −0.849; p < 0.01), and fine motor coordination (r = −0.866; p < 0.01). Indices of thalamic metabolism correlated positively with dystonia (r = 0.559; p < 0.05). The data suggest that PET scanning with 18F‐FDG is a sensitive measure of brain dysfunction in Huntington's disease and that basal ganglia metabolism is highly correlated with the overall functional capacity of individual patients and with the degree of their motor abnormalities. Copyright © 1986 American Neurological Association

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