Voxel‐based distribution of metabolic impairment in corticobasal degeneration
Identifieur interne : 000541 ( Istex/Corpus ); précédent : 000540; suivant : 000542Voxel‐based distribution of metabolic impairment in corticobasal degeneration
Auteurs : Gaetan Garraux ; Eric Salmon ; Philippe Peigneux ; Alexandre Kreisler ; Christian Degueldre ; Christian Lemaire ; Alain Destée ; Georges FranckSource :
- Movement Disorders [ 0885-3185 ] ; 2000-09.
English descriptors
Abstract
This report emphasizes the precise topographic distribution of cerebral metabolic impairment in corticobasal degeneration (CBD) and the pathophysiological differences between CBD and progressive supranuclear palsy (PSP). Statistical parametric mapping (SPM96) analysis of 18FDG positron emission tomography (PET) data was performed in 22 patients with CBD compared with 46 healthy subjects (HS) and 21 patients with PSP who were studied at rest. A statistical threshold of p <0.001 was fixed, further corrected for multiple or independent comparisons (p <0.05). In comparison with HS, the metabolic impairment in CBD was asymmetrically distributed in the putamen, thalamus, precentral (Brodmann's area, BA 4), lateral premotor (BA 6/44) and supplementary motor areas (SMA, BA 6), dorsolateral prefrontal (8/9/46) cortex, and the anterior part of the inferior parietal lobe (BA 40) including the intraparietal sulcus (BA 7/40). A similar hypometabolic pattern was observed for most individual analyses. When PSP was compared with CBD, metabolic impairment predominated in the midbrain, anterior cingulate (BA 24/32), and orbitofrontal regions (BA 10). The reverse contrast showed more posterior involvement in CBD (BA 6 and 5/7/40) including SMA. Our data suggest that multiple components of neural networks related to both movement execution and production of skilled movements are functionally disturbed in CBD compared with both HS and PSP.
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DOI: 10.1002/1531-8257(200009)15:5<894::AID-MDS1021>3.0.CO;2-S
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Liège, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Lemaire, Christian" sort="Lemaire, Christian" uniqKey="Lemaire C" first="Christian" last="Lemaire">Christian Lemaire</name><affiliation><mods:affiliation>Cyclotron Research Center, University of Liège, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Destee, Alain" sort="Destee, Alain" uniqKey="Destee A" first="Alain" last="Destée">Alain Destée</name><affiliation><mods:affiliation>Department of Neurology, Regional University Hospital of Lille, France</mods:affiliation></affiliation></author><author><name sortKey="Franck, Georges" sort="Franck, Georges" uniqKey="Franck G" first="Georges" last="Franck">Georges Franck</name><affiliation><mods:affiliation>Department of Neurology, University of Liège, Belgium</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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Statistical parametric mapping (SPM96) analysis of 18FDG positron emission tomography (PET) data was performed in 22 patients with CBD compared with 46 healthy subjects (HS) and 21 patients with PSP who were studied at rest. A statistical threshold of p <0.001 was fixed, further corrected for multiple or independent comparisons (p <0.05). In comparison with HS, the metabolic impairment in CBD was asymmetrically distributed in the putamen, thalamus, precentral (Brodmann's area, BA 4), lateral premotor (BA 6/44) and supplementary motor areas (SMA, BA 6), dorsolateral prefrontal (8/9/46) cortex, and the anterior part of the inferior parietal lobe (BA 40) including the intraparietal sulcus (BA 7/40). A similar hypometabolic pattern was observed for most individual analyses. When PSP was compared with CBD, metabolic impairment predominated in the midbrain, anterior cingulate (BA 24/32), and orbitofrontal regions (BA 10). The reverse contrast showed more posterior involvement in CBD (BA 6 and 5/7/40) including SMA. Our data suggest that multiple components of neural networks related to both movement execution and production of skilled movements are functionally disturbed in CBD compared with both HS and PSP.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Gaetan Garraux MD</name><affiliations><json:string>Cyclotron Research Center, University of Liège, Belgium</json:string><json:string>Department of Neurology, University of Liège, Belgium</json:string></affiliations></json:item><json:item><name>Eric Salmon MD</name><affiliations><json:string>Cyclotron Research Center, University of Liège, Belgium</json:string><json:string>Department of Neurology, University of Liège, Belgium</json:string></affiliations></json:item><json:item><name>Philippe Peigneux DPsy</name><affiliations><json:string>Cyclotron Research Center, University of Liège, Belgium</json:string><json:string>Department of Neurology, University of Liège, Belgium</json:string></affiliations></json:item><json:item><name>Alexandre Kreisler MD</name><affiliations><json:string>Department of Neurology, Regional University Hospital of Lille, France</json:string></affiliations></json:item><json:item><name>Christian Degueldre EE</name><affiliations><json:string>Cyclotron Research Center, University of Liège, Belgium</json:string></affiliations></json:item><json:item><name>Christian Lemaire PhD</name><affiliations><json:string>Cyclotron Research Center, University of Liège, Belgium</json:string></affiliations></json:item><json:item><name>Alain Destée MD</name><affiliations><json:string>Department of Neurology, Regional University Hospital of Lille, France</json:string></affiliations></json:item><json:item><name>Georges Franck MD</name><affiliations><json:string>Department of Neurology, University of Liège, Belgium</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Corticobasal degeneration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Progressive supranuclear palsy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item></subject><language><json:string>eng</json:string></language><abstract>This report emphasizes the precise topographic distribution of cerebral metabolic impairment in corticobasal degeneration (CBD) and the pathophysiological differences between CBD and progressive supranuclear palsy (PSP). Statistical parametric mapping (SPM96) analysis of 18FDG positron emission tomography (PET) data was performed in 22 patients with CBD compared with 46 healthy subjects (HS) and 21 patients with PSP who were studied at rest. A statistical threshold of p >0.001 was fixed, further corrected for multiple or independent comparisons (p >0.05). In comparison with HS, the metabolic impairment in CBD was asymmetrically distributed in the putamen, thalamus, precentral (Brodmann's area, BA 4), lateral premotor (BA 6/44) and supplementary motor areas (SMA, BA 6), dorsolateral prefrontal (8/9/46) cortex, and the anterior part of the inferior parietal lobe (BA 40) including the intraparietal sulcus (BA 7/40). A similar hypometabolic pattern was observed for most individual analyses. When PSP was compared with CBD, metabolic impairment predominated in the midbrain, anterior cingulate (BA 24/32), and orbitofrontal regions (BA 10). The reverse contrast showed more posterior involvement in CBD (BA 6 and 5/7/40) including SMA. Our data suggest that multiple components of neural networks related to both movement execution and production of skilled movements are functionally disturbed in CBD compared with both HS and PSP.</abstract><qualityIndicators><score>7.484</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1442</abstractCharCount><pdfWordCount>5682</pdfWordCount><pdfCharCount>38519</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>207</abstractWordCount></qualityIndicators><title>Voxel‐based distribution of metabolic impairment in corticobasal degeneration</title><genre><json:string>Serial 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Statistical parametric mapping (SPM96) analysis of 18FDG positron emission tomography (PET) data was performed in 22 patients with CBD compared with 46 healthy subjects (HS) and 21 patients with PSP who were studied at rest. A statistical threshold of p <0.001 was fixed, further corrected for multiple or independent comparisons (p <0.05). In comparison with HS, the metabolic impairment in CBD was asymmetrically distributed in the putamen, thalamus, precentral (Brodmann's area, BA 4), lateral premotor (BA 6/44) and supplementary motor areas (SMA, BA 6), dorsolateral prefrontal (8/9/46) cortex, and the anterior part of the inferior parietal lobe (BA 40) including the intraparietal sulcus (BA 7/40). A similar hypometabolic pattern was observed for most individual analyses. When PSP was compared with CBD, metabolic impairment predominated in the midbrain, anterior cingulate (BA 24/32), and orbitofrontal regions (BA 10). The reverse contrast showed more posterior involvement in CBD (BA 6 and 5/7/40) including SMA. Our data suggest that multiple components of neural networks related to both movement execution and production of skilled movements are functionally disturbed in CBD compared with both HS and PSP.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Corticobasal degeneration</term></item><item><term>Progressive supranuclear palsy</term></item><item><term>PET</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1999-05-13">Received</change><change when="2000-03-23">Registration</change><change when="2000-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3A0AAFEC2DE2E4E7C7388AD4ADA17B8FDF8B80A8/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>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</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="short">Mov. 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creatorRole="author" affiliationRef="#af3"><personName><givenNames>Alexandre</givenNames><familyName>Kreisler</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Christian</givenNames><familyName>Degueldre</familyName><degrees>EE</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Christian</givenNames><familyName>Lemaire</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Alain</givenNames><familyName>Destée</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Georges</givenNames><familyName>Franck</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="BE" type="organization"><unparsedAffiliation>Cyclotron Research Center, University of Liège, Belgium</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="BE" type="organization"><unparsedAffiliation>Department of Neurology, University of Liège, Belgium</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neurology, Regional University Hospital of Lille, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Corticobasal degeneration</keyword><keyword xml:id="kwd2">Progressive supranuclear palsy</keyword><keyword xml:id="kwd3">PET</keyword></keywordGroup><fundingInfo><fundingAgency>“Fonds National de la Recherche Scientifique de Belgique” (FNRS)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>the “Fondation Médicale Reine Elisabeth,”</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Interuniversity Pole of Attraction P4/22, Belgian State, Prime Minister's Office, Federal Office for Scientific, Technical and Cultural Affairs</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>This report emphasizes the precise topographic distribution of cerebral metabolic impairment in corticobasal degeneration (CBD) and the pathophysiological differences between CBD and progressive supranuclear palsy (PSP). Statistical parametric mapping (SPM96) analysis of <sup>18</sup>FDG positron emission tomography (PET) data was performed in 22 patients with CBD compared with 46 healthy subjects (HS) and 21 patients with PSP who were studied at rest. A statistical threshold of p <0.001 was fixed, further corrected for multiple or independent comparisons (p <0.05). In comparison with HS, the metabolic impairment in CBD was asymmetrically distributed in the putamen, thalamus, precentral (Brodmann's area, BA 4), lateral premotor (BA 6/44) and supplementary motor areas (SMA, BA 6), dorsolateral prefrontal (8/9/46) cortex, and the anterior part of the inferior parietal lobe (BA 40) including the intraparietal sulcus (BA 7/40). A similar hypometabolic pattern was observed for most individual analyses. When PSP was compared with CBD, metabolic impairment predominated in the midbrain, anterior cingulate (BA 24/32), and orbitofrontal regions (BA 10). The reverse contrast showed more posterior involvement in CBD (BA 6 and 5/7/40) including SMA. Our data suggest that multiple components of neural networks related to both movement execution and production of skilled movements are functionally disturbed in CBD compared with both HS and PSP. </p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Voxel‐based distribution of metabolic impairment in corticobasal degeneration</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Metabolism in CBD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Voxel‐based distribution of metabolic impairment in corticobasal degeneration</title></titleInfo><name type="personal"><namePart type="given">Gaetan</namePart><namePart type="family">Garraux</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Cyclotron Research Center, University of Liège, Belgium</affiliation><affiliation>Department of Neurology, University of Liège, Belgium</affiliation><description>Correspondence: Department of Neurology, University Hospital, Sart Tilman B35, B‐4000 Liège, Belgium</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eric</namePart><namePart type="family">Salmon</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Cyclotron Research Center, University of Liège, Belgium</affiliation><affiliation>Department of Neurology, University of Liège, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Peigneux</namePart><namePart type="termsOfAddress">DPsy</namePart><affiliation>Cyclotron Research Center, University of Liège, Belgium</affiliation><affiliation>Department of Neurology, University of Liège, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexandre</namePart><namePart type="family">Kreisler</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Regional University Hospital of Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Degueldre</namePart><namePart type="termsOfAddress">EE</namePart><affiliation>Cyclotron Research Center, University of Liège, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Lemaire</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Cyclotron Research Center, University of Liège, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alain</namePart><namePart type="family">Destée</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Regional University Hospital of Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Georges</namePart><namePart type="family">Franck</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Liège, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2000-09</dateIssued><dateCaptured encoding="w3cdtf">1999-05-13</dateCaptured><dateValid encoding="w3cdtf">2000-03-23</dateValid><copyrightDate encoding="w3cdtf">2000</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">3</extent><extent unit="tables">3</extent><extent unit="references">56</extent><extent unit="words">5482</extent></physicalDescription><abstract lang="en">This report emphasizes the precise topographic distribution of cerebral metabolic impairment in corticobasal degeneration (CBD) and the pathophysiological differences between CBD and progressive supranuclear palsy (PSP). Statistical parametric mapping (SPM96) analysis of 18FDG positron emission tomography (PET) data was performed in 22 patients with CBD compared with 46 healthy subjects (HS) and 21 patients with PSP who were studied at rest. A statistical threshold of p <0.001 was fixed, further corrected for multiple or independent comparisons (p <0.05). In comparison with HS, the metabolic impairment in CBD was asymmetrically distributed in the putamen, thalamus, precentral (Brodmann's area, BA 4), lateral premotor (BA 6/44) and supplementary motor areas (SMA, BA 6), dorsolateral prefrontal (8/9/46) cortex, and the anterior part of the inferior parietal lobe (BA 40) including the intraparietal sulcus (BA 7/40). A similar hypometabolic pattern was observed for most individual analyses. When PSP was compared with CBD, metabolic impairment predominated in the midbrain, anterior cingulate (BA 24/32), and orbitofrontal regions (BA 10). The reverse contrast showed more posterior involvement in CBD (BA 6 and 5/7/40) including SMA. Our data suggest that multiple components of neural networks related to both movement execution and production of skilled movements are functionally disturbed in CBD compared with both HS and PSP.</abstract><note type="funding">“Fonds National de la Recherche Scientifique de Belgique” (FNRS)</note><note type="funding">the “Fondation Médicale Reine Elisabeth,”</note><note type="funding">Interuniversity Pole of Attraction P4/22, Belgian State, Prime Minister's Office, Federal Office for Scientific, Technical and Cultural Affairs</note><subject lang="en"><genre>Keywords</genre><topic>Corticobasal degeneration</topic><topic>Progressive supranuclear palsy</topic><topic>PET</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>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>2000</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>894</start><end>904</end><total>11</total></extent></part></relatedItem><identifier type="istex">3A0AAFEC2DE2E4E7C7388AD4ADA17B8FDF8B80A8</identifier><identifier type="DOI">10.1002/1531-8257(200009)15:5<894::AID-MDS1021>3.0.CO;2-S</identifier><identifier type="ArticleID">MDS1021</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2000 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>John Wiley & Sons, Inc.</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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