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Brain energy metabolism and dopaminergic function in Huntington's disease measured in vivo using positron emission tomography
Author(s) -
Leenders K. L.,
Frackowiak R. S. J.,
Quinn N.,
Marsden C. D.
Publication year - 1986
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.870010110
Subject(s) - positron emission tomography , cerebral blood flow , striatum , dopamine , dopaminergic , brain positron emission tomography , frontal lobe , endocrinology , medicine , atrophy , caudate nucleus , nuclear medicine , chemistry , in vivo , neuroscience , psychology , preclinical imaging , biology , microbiology and biotechnology
Abstract A 48‐year‐old man with typical Huntington's disease was investigated with computed tomography (CT) and positron emission tomography. Regional cerebral blood flow, oxygen extraction, oxygen and glucose utilisation, L ‐Dopa uptake, and dopamine (D2) receptor binding were measured using several positron‐labelled tracers. CT showed slight atrophy of the head of caudate but no cortical atrophy, although distinct frontal lobe dysfunction was present on psychometric testing. Oxygen and glucose metabolism and cerebral blood flow were decreased in the striata and to a lesser extent in frontal cortex. Cerebral blood flow was in the low normal range throughout the remainder of the brain. A normal metabolic ration was found in all regions, since the changes in glucose utilisation paralleled those in oxygen consumption. The capacity of the striatum to store dopamine as assessed by L ‐[ 18 F]‐fluorodopa uptake was normal, but dopamine (D2) receptor binding was decreased when compared to normal subjects.