Cerebral metabolism of glucose in benign hereditary chorea.
Identifieur interne : 005127 ( PubMed/Corpus ); précédent : 005126; suivant : 005128Cerebral metabolism of glucose in benign hereditary chorea.
Auteurs : O. Suchowersky ; M R Hayden ; W R Martin ; A J Stoessl ; A M Hildebrand ; B D PateSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1986.
English descriptors
- KwdEn :
- Adult, Brain (metabolism), Caudate Nucleus (metabolism), Deoxyglucose (analogs & derivatives), Deoxyglucose (diagnostic use), Female, Fluorine Radioisotopes (diagnostic use), Fluorodeoxyglucose F18, Glucose (metabolism), Humans, Huntington Disease (genetics), Huntington Disease (metabolism), Pedigree, 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.
DOI: 10.1002/mds.870010105
PubMed: 2973557
Links to Exploration step
pubmed:2973557Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cerebral metabolism of glucose in benign hereditary chorea.</title><author><name sortKey="Suchowersky, O" sort="Suchowersky, O" uniqKey="Suchowersky O" first="O" last="Suchowersky">O. Suchowersky</name><affiliation><nlm:affiliation>Department of Medical Genetics, University of British Columbia, Vancouver, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hayden, M R" sort="Hayden, M R" uniqKey="Hayden M" first="M R" last="Hayden">M R Hayden</name></author><author><name sortKey="Martin, W R" sort="Martin, W R" uniqKey="Martin W" first="W R" last="Martin">W R Martin</name></author><author><name sortKey="Stoessl, A J" sort="Stoessl, A J" uniqKey="Stoessl A" first="A J" last="Stoessl">A J Stoessl</name></author><author><name sortKey="Hildebrand, A M" sort="Hildebrand, A M" uniqKey="Hildebrand A" first="A M" last="Hildebrand">A M Hildebrand</name></author><author><name sortKey="Pate, B D" sort="Pate, B D" uniqKey="Pate B" first="B D" last="Pate">B D Pate</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1986">1986</date><idno type="RBID">pubmed:2973557</idno><idno type="pmid">2973557</idno><idno type="doi">10.1002/mds.870010105</idno><idno type="wicri:Area/PubMed/Corpus">005127</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cerebral metabolism of glucose in benign hereditary chorea.</title><author><name sortKey="Suchowersky, O" sort="Suchowersky, O" uniqKey="Suchowersky O" first="O" last="Suchowersky">O. Suchowersky</name><affiliation><nlm:affiliation>Department of Medical Genetics, University of British Columbia, Vancouver, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hayden, M R" sort="Hayden, M R" uniqKey="Hayden M" first="M R" last="Hayden">M R Hayden</name></author><author><name sortKey="Martin, W R" sort="Martin, W R" uniqKey="Martin W" first="W R" last="Martin">W R Martin</name></author><author><name sortKey="Stoessl, A J" sort="Stoessl, A J" uniqKey="Stoessl A" first="A J" last="Stoessl">A J Stoessl</name></author><author><name sortKey="Hildebrand, A M" sort="Hildebrand, A M" uniqKey="Hildebrand A" first="A M" last="Hildebrand">A M Hildebrand</name></author><author><name sortKey="Pate, B D" sort="Pate, B D" uniqKey="Pate B" first="B D" last="Pate">B D Pate</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1986" type="published">1986</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Brain (metabolism)</term><term>Caudate Nucleus (metabolism)</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>Humans</term><term>Huntington Disease (genetics)</term><term>Huntington Disease (metabolism)</term><term>Pedigree</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></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><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">2973557</PMID><DateCreated><Year>1989</Year><Month>01</Month><Day>10</Day></DateCreated><DateCompleted><Year>1989</Year><Month>01</Month><Day>10</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>1</Volume><Issue>1</Issue><PubDate><Year>1986</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Cerebral metabolism of glucose in benign hereditary chorea.</ArticleTitle><Pagination><MedlinePgn>33-44</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Suchowersky</LastName><ForeName>O</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics, University of British Columbia, Vancouver, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hayden</LastName><ForeName>M R</ForeName><Initials>MR</Initials></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>W R</ForeName><Initials>WR</Initials></Author><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Hildebrand</LastName><ForeName>A M</ForeName><Initials>AM</Initials></Author><Author ValidYN="Y"><LastName>Pate</LastName><ForeName>B D</ForeName><Initials>BD</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005462">Fluorine Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0Z5B2CJX4D</RegistryNumber><NameOfSubstance UI="D019788">Fluorodeoxyglucose F18</NameOfSubstance></Chemical><Chemical><RegistryNumber>9G2MP84A8W</RegistryNumber><NameOfSubstance UI="D003847">Deoxyglucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002421">Caudate Nucleus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003847">Deoxyglucose</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000031">analogs & derivatives</QualifierName><QualifierName MajorTopicYN="N" UI="Q000176">diagnostic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005462">Fluorine Radioisotopes</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000176">diagnostic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019788">Fluorodeoxyglucose F18</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005947">Glucose</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006816">Huntington Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010375">Pedigree</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013788">Thalamus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014055">Tomography, Emission-Computed</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1986</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1986</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1986</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2973557</ArticleId><ArticleId IdType="doi">10.1002/mds.870010105</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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