Cerebral metabolism of glucose in benign hereditary chorea
Identifieur interne : 001D92 ( Istex/Corpus ); précédent : 001D91; suivant : 001D93Cerebral metabolism of glucose in benign hereditary chorea
Auteurs : Oksana Suchowersky ; Hayden ; W. R. Wayne Martin ; A. Jon Stoessl ; Anne M. Hildebrand ; Brian D. PateSource :
- Movement Disorders [ 0885-3185 ] ; 1986.
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- KwdEn :
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.
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DOI: 10.1002/mds.870010105
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ISTEX:CAB7007EF8134AB7C40DC30D7B59116E871F2AB8Le document en format XML
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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><istex><corpusName>wiley</corpusName><author><json:item><name>Oksana Suchowersky</name><affiliations><json:string>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Dr. Hayden</name><affiliations><json:string>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</json:string><json:string>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>W. R. Wayne Martin</name><affiliations><json:string>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>A. Jon Stoessl</name><affiliations><json:string>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Anne M. Hildebrand</name><affiliations><json:string>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Brian D. Pate</name><affiliations><json:string>Faculty of Pharmaceutical Sciences, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Benign hereditary chorea</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Huntington's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Positron emission tomography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Computed tomography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glucose metabolism</value></json:item></subject><language><json:string>eng</json:string></language><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. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="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></monogr><idno type="istex">CAB7007EF8134AB7C40DC30D7B59116E871F2AB8</idno><idno type="DOI">10.1002/mds.870010105</idno><idno type="ArticleID">MDS870010105</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1986</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Benign hereditary chorea (BHC) is an autosomal dominant disorder characterized by chorea of early onset with little or no progression. 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These findings suggest that the caudate nucleus may play a significant role in the pathophysiology of some persons with BHC.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Benign hereditary chorea</term></item><item><term>Huntington's disease</term></item><item><term>Positron emission tomography</term></item><item><term>Computed tomography</term></item><item><term>Glucose metabolism</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1986">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CAB7007EF8134AB7C40DC30D7B59116E871F2AB8/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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R. Wayne</givenNames><familyName>Martin</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>A. Jon</givenNames><familyName>Stoessl</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Anne M.</givenNames><familyName>Hildebrand</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Brian D.</givenNames><familyName>Pate</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Faculty of Pharmaceutical Sciences, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Benign hereditary chorea</keyword><keyword xml:id="kwd2">Huntington's disease</keyword><keyword xml:id="kwd3">Positron emission tomography</keyword><keyword xml:id="kwd4">Computed tomography</keyword><keyword xml:id="kwd5">Glucose metabolism</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>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 <sup>18</sup>F‐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.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>A videotape segment accompanies this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Cerebral metabolism of glucose in benign hereditary chorea</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>GLUCOSE METABOLISM IN BENIGN HEREDITARY CHOREA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cerebral metabolism of glucose in benign hereditary chorea</title></titleInfo><name type="personal"><namePart type="given">Oksana</namePart><namePart type="family">Suchowersky</namePart><affiliation>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Hayden</namePart><affiliation>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><affiliation>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><description>Correspondence: Department of Medical Genetics, Health Sciences Centre Hospital, 2211 Wesbrook Mall, University of British Columbia, Vancouver, British Columbia, Canada V6T 2B5</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W. R. Wayne</namePart><namePart type="family">Martin</namePart><affiliation>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. Jon</namePart><namePart type="family">Stoessl</namePart><affiliation>Department of Medicine, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anne M.</namePart><namePart type="family">Hildebrand</namePart><affiliation>Department of Medical Genetics, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Brian D.</namePart><namePart type="family">Pate</namePart><affiliation>Faculty of Pharmaceutical Sciences, UBC/TRIUMF PET Program, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1986</dateIssued><copyrightDate encoding="w3cdtf">1986</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="tables">3</extent><extent unit="references">25</extent></physicalDescription><abstract 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.</abstract><note type="content">*A videotape segment accompanies this article.</note><subject lang="en"><genre>Keywords</genre><topic>Benign hereditary chorea</topic><topic>Huntington's disease</topic><topic>Positron emission tomography</topic><topic>Computed tomography</topic><topic>Glucose metabolism</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1986</date><detail type="volume"><caption>vol.</caption><number>1</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>33</start><end>44</end><total>12</total></extent></part></relatedItem><identifier type="istex">CAB7007EF8134AB7C40DC30D7B59116E871F2AB8</identifier><identifier type="DOI">10.1002/mds.870010105</identifier><identifier type="ArticleID">MDS870010105</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1986 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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