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dc.contributor.authorHolthoff, Vjera A.en_US
dc.contributor.authorKoeppe, Robert A.en_US
dc.contributor.authorFrey, Kirk A.en_US
dc.contributor.authorPenney, John B.en_US
dc.contributor.authorMarkel, Dorene S.en_US
dc.contributor.authorKuhl, David E.en_US
dc.contributor.authorYoung, Anne B.en_US
dc.date.accessioned2007-04-06T18:54:54Z
dc.date.available2007-04-06T18:54:54Z
dc.date.issued1993-07en_US
dc.identifier.citationHolthoff, Vjera A.; Koeppe, Robert A.; Frey, Kirk A.; Penney, John B.; Markel, Dorene S.; Kuhl, David E.; Young, Anne B. (1993)."Positron emission tomography measures of benzodiazepine receptors in Huntington's disease." Annals of Neurology 34(1): 76-81. <http://hdl.handle.net/2027.42/50353>en_US
dc.identifier.issn0364-5134en_US
dc.identifier.issn1531-8249en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50353
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8390806&dopt=citationen_US
dc.description.abstractWe performed positron emission tomographic (PET) measurements of the regional distribution volume of benzodiazepine receptors and regional glucose metabolism in 6 drug-free patients with early Huntington's disease following injection of [ 11 C] flumazenil, a nonsubtype selective central benzodiazepine receptor antagonist, and 18 F-2-fluoro-2-deoxy- D -glucose, respectively. Flumazenil data were analyzed with a recently developed two-compartment, two-parameter tracer kinetic model. Benzodiazepine receptor density is related to distribution volume for flumazenil. In comparison with a group of healthy volunteers, benzodiazepine receptor density was significantly decreased in the caudate nucleus. Glucose metabolism was significantly reduced not only in the caudate nucleus but also in the putamen and thalamus. The changes in benzodiazepine receptor density observed in the caudate nucleus are commensurate with data obtained in postmortem autoradiographic studies of receptor density. Based on such postmortem studies we also anticipated changes in putamen and thalamic benzodiazepine receptor density. However, relatively little is known on receptor changes in early Huntington's disease, because the autoradiographic data available were obtained mostly in patients with advanced disease. The decreased glucose metabolism in the caudate and putamen agrees well with previously published results of PET studies, whereas metabolic impairment of the thalamus has not yet been described in Huntington's disease. The present study suggests that regional metabolism and Γ-aminobutyric acid (GABA)-benzodiazepine receptor changes in subcortical structures of patients with early Huntington's disease do not occur with the same time course: Caudate benzodiazepine receptor density is already severely impaired when other subcortical structures reveal only minor abnormalities. Impairment of neuronal metabolism seems to predate GABA/benzodiazepine receptor changes since the putamen and thalamus demonstrate metabolic impairment without detectable loss of benzodiazepine receptor density.en_US
dc.format.extent660244 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology, and Psychiatryen_US
dc.titlePositron emission tomography measures of benzodiazepine receptors in Huntington's diseaseen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPsychiatryen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Nuclear Medicine, University of Michigan Medical School, Ann Arbor, MI ; Max-Planck-Institut fÜr Neurologische Forschung, KÖln, Federal Republic of Germany ; Max-Planck-Institut fÜr Neurologische Forschung, Gleuelerstr. 50, 5000 KÖln 41, FRGen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Nuclear Medicine, University of Michigan Medical School, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Nuclear Medicine, University of Michigan Medical School, Ann Arbor, MI ; Department of Neurology, University of Michigan Medical School, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan Medical School, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan Medical School, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Nuclear Medicine, University of Michigan Medical School, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan Medical School, Ann Arbor, MIen_US
dc.identifier.pmid8390806en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50353/1/410340114_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/ana.410340114en_US
dc.identifier.sourceAnnals of Neurologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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