Cerebral metabolism of glucose in benign hereditary chorea
Identifieur interne : 006691 ( Main/Exploration ); précédent : 006690; suivant : 006692Cerebral metabolism of glucose in benign hereditary chorea
Auteurs : Oksana Suchowersky [Canada] ; Hayden [Canada] ; W. R. Wayne Martin [Canada] ; A. Jon Stoessl [Canada] ; Anne M. Hildebrand [Canada] ; Brian D. Pate [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 1986.
English descriptors
- KwdEn :
- Adult, Benign hereditary chorea, Brain (metabolism), Caudate Nucleus (metabolism), Computed tomography, Deoxyglucose (analogs & derivatives), Deoxyglucose (diagnostic use), Female, Fluorine Radioisotopes (diagnostic use), Fluorodeoxyglucose F18, Glucose (metabolism), Glucose metabolism, Humans, Huntington Disease (genetics), Huntington Disease (metabolism), Huntington's disease, Pedigree, Positron emission tomography, Thalamus (metabolism), Tomography, Emission-Computed.
- MESH :
- chemical , analogs & derivatives : Deoxyglucose.
- chemical , diagnostic use : Deoxyglucose, Fluorine Radioisotopes.
- genetics : Huntington Disease.
- metabolism : Brain, Caudate Nucleus, Glucose, Huntington Disease, Thalamus.
- Adult, Female, Fluorodeoxyglucose F18, Humans, Pedigree, Tomography, Emission-Computed.
Abstract
Benign hereditary chorea (BHC) is an autosomal dominant disorder characterized by chorea of early onset with little or no progression. There is marked clinical variability in this disease with some subjects having onset in infancy and others with onset in early adulthood. In contrast to Huntington's disease (HD), there is no dementia. Computed tomography is normal in all subjects with no evidence of caudate nucleus atrophy. We present the results of positron emission tomography using 18F‐2‐fluorodeoxyglucose on three patients with this disorder from two families. Cerebral glucose metabolism in one patient was decreased in the caudate nucleus, as previously reported in HD. The other two persons from a second family showed a relative decrease in metabolic rates of glucose in the caudate when compared with the thalamus. It appears that caudate hypometabolism is not specific for HD. These findings suggest that the caudate nucleus may play a significant role in the pathophysiology of some persons with BHC.
Url:
DOI: 10.1002/mds.870010105
Affiliations:
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Hildebrand</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="Pate, Brian D" sort="Pate, Brian D" uniqKey="Pate B" first="Brian D." last="Pate">Brian D. Pate</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmaceutical Sciences, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1986">1986</date><biblScope unit="vol">1</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="33">33</biblScope><biblScope unit="page" to="44">44</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">CAB7007EF8134AB7C40DC30D7B59116E871F2AB8</idno><idno type="DOI">10.1002/mds.870010105</idno><idno type="ArticleID">MDS870010105</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Benign hereditary chorea</term><term>Brain (metabolism)</term><term>Caudate Nucleus (metabolism)</term><term>Computed tomography</term><term>Deoxyglucose (analogs & derivatives)</term><term>Deoxyglucose (diagnostic use)</term><term>Female</term><term>Fluorine Radioisotopes (diagnostic use)</term><term>Fluorodeoxyglucose F18</term><term>Glucose (metabolism)</term><term>Glucose metabolism</term><term>Humans</term><term>Huntington Disease (genetics)</term><term>Huntington Disease (metabolism)</term><term>Huntington's disease</term><term>Pedigree</term><term>Positron emission tomography</term><term>Thalamus (metabolism)</term><term>Tomography, Emission-Computed</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Deoxyglucose</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Deoxyglucose</term><term>Fluorine Radioisotopes</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Caudate Nucleus</term><term>Glucose</term><term>Huntington Disease</term><term>Thalamus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Fluorodeoxyglucose F18</term><term>Humans</term><term>Pedigree</term><term>Tomography, Emission-Computed</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Benign hereditary chorea (BHC) is an autosomal dominant disorder characterized by chorea of early onset with little or no progression. There is marked clinical variability in this disease with some subjects having onset in infancy and others with onset in early adulthood. In contrast to Huntington's disease (HD), there is no dementia. Computed tomography is normal in all subjects with no evidence of caudate nucleus atrophy. We present the results of positron emission tomography using 18F‐2‐fluorodeoxyglucose on three patients with this disorder from two families. Cerebral glucose metabolism in one patient was decreased in the caudate nucleus, as previously reported in HD. The other two persons from a second family showed a relative decrease in metabolic rates of glucose in the caudate when compared with the thalamus. It appears that caudate hypometabolism is not specific for HD. These findings suggest that the caudate nucleus may play a significant role in the pathophysiology of some persons with BHC.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name></noRegion><name sortKey="Hayden" sort="Hayden" uniqKey="Hayden" last="Hayden">Hayden</name><name sortKey="Hayden" sort="Hayden" uniqKey="Hayden" last="Hayden">Hayden</name><name sortKey="Hildebrand, Anne M" sort="Hildebrand, Anne M" uniqKey="Hildebrand A" first="Anne M." last="Hildebrand">Anne M. Hildebrand</name><name sortKey="Martin, W R Wayne" sort="Martin, W R Wayne" uniqKey="Martin W" first="W. R. Wayne" last="Martin">W. R. Wayne Martin</name><name sortKey="Pate, Brian D" sort="Pate, Brian D" uniqKey="Pate B" first="Brian D." last="Pate">Brian D. Pate</name><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A. Jon" last="Stoessl">A. Jon Stoessl</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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