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Cerebral glucose hypermetabolism in Friedreich's ataxia detected with positron emission tomography
Author(s) -
Gilman Sid,
Junck Larry,
Markel Dorene S.,
Koeppe Robert A.,
Kluin Karen J.
Publication year - 1990
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.410280605
Subject(s) - ataxia , hypermetabolism , positron emission tomography , medicine , ambulatory , endocrinology , nuclear medicine , psychiatry
Local cerebral metabolic rate for glucose was studied with 18 F‐2‐fluoro‐2‐deoxy‐D‐glucose and positron emission tomography (PET) in 22 patients with Friedreich's ataxia and 23 age‐matched normal control subjects. The diagnosis of Friedreich's ataxia was established by the history and physical findings and by excluding other diseases through laboratory investigations. PET studies revealed a statistically significant widespread increase of local cerebral metabolic rate for glucose in the brains of patients with Friedreich's ataxia who were still ambulatory, in comparison with normal control subjects. Nonambulatory patients with Friedrich's ataxia, in comparison with normal control subjects, had significantly increased local cerebral metabolic rates for glucose in the caudate and lenticular nuclei, but not in the other structures studied. The rate was significantly greater in ambulatory patients with Friedreich's ataxia than in nonambulatory patients in all structures studied except the caudate and lenticular nuclei. The data suggest that early in the course of Friedreich's ataxia, the local cerebral metabolic rate for glucose is increased extensively in the central nervous system, and as the disease progresses, it decreases in a regionally specific manner.