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Cerebral metabolism and atrophy in huntington's disease determined by 18 FDG and computed tomographic scan
Author(s) -
Kuhl David E.,
Phelps Michael E.,
Markham Charles H.,
Metter E. Jeffrey,
Riege Walter H.,
Winter James
Publication year - 1982
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410120504
Subject(s) - putamen , atrophy , caudate nucleus , cerebral atrophy , medicine , asymptomatic , positron emission tomography , huntington's disease , dementia , fluorodeoxyglucose , nuclear medicine , computed tomographic , degenerative disease , pathology , radiology , central nervous system disease , disease , computed tomography
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.