Abstract

Abstract Patterns of local cerebral glucose utilization were measured with positron emission computed tomography using the 18 F‐fluorodeoxyglucose method in 13 patients with Huntington's disease (HD), 15 subjects at risk for HD, and 40 normal control subjects. These data were compared with computed tomographic measures of cerebral atrophy, with age, and with duration and severity of symptoms. The results indicate that in HD there is a characteristic decrease in glucose utilization in the caudate and putamen and that this local hypometabolism appears early and precedes bulk tissue loss. In contrast to patients with senile dementia, in these HD patients glucose utilization typically was normal throughout the rest of the brain, regardless of the severity of symptoms and despite apparent shrinkage of brain tissue. Our results suggest the possibility that the caudate may be hypometabolic in some asymptomatic subjects who are potential carriers of the autosomal dominant gene for HD.

Keywords

PutamenAtrophyCaudate nucleusCerebral atrophyMedicineAsymptomaticPositron emission tomographyHuntington's diseaseDementiaFluorodeoxyglucoseNuclear medicineInternal medicineComputed tomographicDegenerative diseasePathologyRadiologyCentral nervous system diseaseDiseaseComputed tomography

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Publication Info

Year
1982
Type
article
Volume
12
Issue
5
Pages
425-434
Citations
452
Access
Closed

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David E. Kuhl, Michael E. Phelps, Charles H. Markham et al. (1982). Cerebral metabolism and atrophy in huntington's disease determined by <sup>18</sup>FDG and computed tomographic scan. Annals of Neurology , 12 (5) , 425-434. https://doi.org/10.1002/ana.410120504

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DOI
10.1002/ana.410120504