Motor‐related circuit dysfunction in MSA‐P: Usefulness of combined whole‐brain imaging analysis
Identifieur interne : 000747 ( Main/Corpus ); précédent : 000746; suivant : 000748Motor‐related circuit dysfunction in MSA‐P: Usefulness of combined whole‐brain imaging analysis
Auteurs : Mélissa Tir ; Christine Delmaire ; Vianney Le Thuc ; Alain Duhamel ; Alain Destée ; Jean-Pierre Pruvo ; Luc DefebvreSource :
- Movement Disorders [ 0885-3185 ] ; 2009-04-30.
English descriptors
Abstract
The aim of this study was to evaluate in vivo changes in the brain's macro‐ and microstructure (notably in the motor system) in the parkinsonian variant of multiple system atrophy (MSA‐P) and in Parkinson's disease (PD) and to characterize the cerebral anatomical differences between the two conditions. We used a combination of voxel‐based morphometry (VBM) and whole‐brain, voxel‐based diffusion tensor imaging analysis (VB‐DTI). Forty‐seven right‐handed subjects (14 MSA‐P patients, 19 PD patients, and 14 controls) were evaluated using VBM and VB‐DTI in an analysis of covariance (ANCOVA) with a significance threshold set to P < 0.005. In MSA‐P patients, VBM analysis revealed a lower density of grey matter (GM) in a motor‐related circuit (especially in the left primary motor cortex, PMC), relative to PD patients, and in the left supplementary motor area (SMA), relative to controls). Diffusion tensor imaging analysis revealed lower fractional anisotropy (FA) values in the left PMC and the right cerebellum in MSA‐P patients, compared with controls. Using a volumetric diffusion technique, our study revealed selective tissue degeneration in motor circuits, regardless of the volume loss detected in VBM and in agreement with pathology reports and clinical motor characteristics. Our findings suggest that MSA‐P is characterized by both macro‐ and microstructural changes in the sensorimotor circuit. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22463
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We used a combination of voxel‐based morphometry (VBM) and whole‐brain, voxel‐based diffusion tensor imaging analysis (VB‐DTI). Forty‐seven right‐handed subjects (14 MSA‐P patients, 19 PD patients, and 14 controls) were evaluated using VBM and VB‐DTI in an analysis of covariance (ANCOVA) with a significance threshold set to P < 0.005. In MSA‐P patients, VBM analysis revealed a lower density of grey matter (GM) in a motor‐related circuit (especially in the left primary motor cortex, PMC), relative to PD patients, and in the left supplementary motor area (SMA), relative to controls). Diffusion tensor imaging analysis revealed lower fractional anisotropy (FA) values in the left PMC and the right cerebellum in MSA‐P patients, compared with controls. Using a volumetric diffusion technique, our study revealed selective tissue degeneration in motor circuits, regardless of the volume loss detected in VBM and in agreement with pathology reports and clinical motor characteristics. Our findings suggest that MSA‐P is characterized by both macro‐ and microstructural changes in the sensorimotor circuit. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Mélissa Tir MD</name><affiliations><json:string>Department of Neurology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</json:string><json:string>Department of Neurology, Mignot Versailles Hospital, Versailles, France</json:string></affiliations></json:item><json:item><name>Christine Delmaire MD, PhD</name><affiliations><json:string>Department of Neuroradiology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</json:string></affiliations></json:item><json:item><name>Vianney le Thuc PhD</name><affiliations><json:string>Department of Neuroradiology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</json:string></affiliations></json:item><json:item><name>Alain Duhamel PhD</name><affiliations><json:string>Department of Biostatistics, Salengro Hospital, Lille University Medical Centre, Lille, France</json:string></affiliations></json:item><json:item><name>Alain Destée MD</name><affiliations><json:string>Department of Neurology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</json:string></affiliations></json:item><json:item><name>Jean‐Pierre Pruvo MD</name><affiliations><json:string>Department of Neuroradiology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</json:string></affiliations></json:item><json:item><name>Luc Defebvre MD, PhD</name><affiliations><json:string>Department of Neurology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>MRI</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>diffusion‐weighted imaging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>multiple‐system atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor cortex</value></json:item></subject><articleId><json:string>MDS22463</json:string></articleId><language><json:string>eng</json:string></language><abstract>The aim of this study was to evaluate in vivo changes in the brain's macro‐ and microstructure (notably in the motor system) in the parkinsonian variant of multiple system atrophy (MSA‐P) and in Parkinson's disease (PD) and to characterize the cerebral anatomical differences between the two conditions. We used a combination of voxel‐based morphometry (VBM) and whole‐brain, voxel‐based diffusion tensor imaging analysis (VB‐DTI). Forty‐seven right‐handed subjects (14 MSA‐P patients, 19 PD patients, and 14 controls) were evaluated using VBM and VB‐DTI in an analysis of covariance (ANCOVA) with a significance threshold set to P > 0.005. In MSA‐P patients, VBM analysis revealed a lower density of grey matter (GM) in a motor‐related circuit (especially in the left primary motor cortex, PMC), relative to PD patients, and in the left supplementary motor area (SMA), relative to controls). Diffusion tensor imaging analysis revealed lower fractional anisotropy (FA) values in the left PMC and the right cerebellum in MSA‐P patients, compared with controls. Using a volumetric diffusion technique, our study revealed selective tissue degeneration in motor circuits, regardless of the volume loss detected in VBM and in agreement with pathology reports and clinical motor characteristics. 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We used a combination of voxel‐based morphometry (VBM) and whole‐brain, voxel‐based diffusion tensor imaging analysis (VB‐DTI). Forty‐seven right‐handed subjects (14 MSA‐P patients, 19 PD patients, and 14 controls) were evaluated using VBM and VB‐DTI in an analysis of covariance (ANCOVA) with a significance threshold set to P < 0.005. In MSA‐P patients, VBM analysis revealed a lower density of grey matter (GM) in a motor‐related circuit (especially in the left primary motor cortex, PMC), relative to PD patients, and in the left supplementary motor area (SMA), relative to controls). Diffusion tensor imaging analysis revealed lower fractional anisotropy (FA) values in the left PMC and the right cerebellum in MSA‐P patients, compared with controls. Using a volumetric diffusion technique, our study revealed selective tissue degeneration in motor circuits, regardless of the volume loss detected in VBM and in agreement with pathology reports and clinical motor characteristics. 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PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neurology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neurology, Mignot Versailles Hospital, Versailles, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neuroradiology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>Department of Biostatistics, Salengro Hospital, Lille University Medical Centre, Lille, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">MRI</keyword><keyword xml:id="kwd2">diffusion‐weighted imaging</keyword><keyword xml:id="kwd3">multiple‐system atrophy</keyword><keyword xml:id="kwd4">Parkinson's disease</keyword><keyword xml:id="kwd5">motor cortex</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The aim of this study was to evaluate <i>in vivo</i> changes in the brain's macro‐ and microstructure (notably in the motor system) in the parkinsonian variant of multiple system atrophy (MSA‐P) and in Parkinson's disease (PD) and to characterize the cerebral anatomical differences between the two conditions. We used a combination of voxel‐based morphometry (VBM) and whole‐brain, voxel‐based diffusion tensor imaging analysis (VB‐DTI). Forty‐seven right‐handed subjects (14 MSA‐P patients, 19 PD patients, and 14 controls) were evaluated using VBM and VB‐DTI in an analysis of covariance (ANCOVA) with a significance threshold set to <i>P</i> < 0.005. In MSA‐P patients, VBM analysis revealed a lower density of grey matter (GM) in a motor‐related circuit (especially in the left primary motor cortex, PMC), relative to PD patients, and in the left supplementary motor area (SMA), relative to controls). Diffusion tensor imaging analysis revealed lower fractional anisotropy (FA) values in the left PMC and the right cerebellum in MSA‐P patients, compared with controls. Using a volumetric diffusion technique, our study revealed selective tissue degeneration in motor circuits, regardless of the volume loss detected in VBM and in agreement with pathology reports and clinical motor characteristics. Our findings suggest that MSA‐P is characterized by both macro‐ and microstructural changes in the sensorimotor circuit. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Motor‐related circuit dysfunction in MSA‐P: Usefulness of combined whole‐brain imaging analysis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Motor‐Related Circuit Dysfunction in MSA‐P</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Motor‐related circuit dysfunction in MSA‐P: Usefulness of combined whole‐brain imaging analysis</title></titleInfo><name type="personal"><namePart type="given">Mélissa</namePart><namePart type="family">Tir</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</affiliation><affiliation>Department of Neurology, Mignot Versailles Hospital, Versailles, France</affiliation><description>Correspondence: Neurology Department, Hôpital Roger Salengro, CHU de Lille, F‐59037 Lille Cedex, France</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Delmaire</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neuroradiology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vianney</namePart><namePart type="family">le Thuc</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neuroradiology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alain</namePart><namePart type="family">Duhamel</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biostatistics, Salengro Hospital, Lille University Medical Centre, Lille, France</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, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Pierre</namePart><namePart type="family">Pruvo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroradiology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luc</namePart><namePart type="family">Defebvre</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, EA2683, Salengro Hospital, Lille University Medical Centre, Lille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-04-30</dateIssued><dateCaptured encoding="w3cdtf">2008-06-18</dateCaptured><dateValid encoding="w3cdtf">2008-12-21</dateValid><copyrightDate encoding="w3cdtf">2009</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">2</extent><extent unit="tables">3</extent><extent unit="references">46</extent><extent unit="words">5381</extent></physicalDescription><abstract lang="en">The aim of this study was to evaluate in vivo changes in the brain's macro‐ and microstructure (notably in the motor system) in the parkinsonian variant of multiple system atrophy (MSA‐P) and in Parkinson's disease (PD) and to characterize the cerebral anatomical differences between the two conditions. We used a combination of voxel‐based morphometry (VBM) and whole‐brain, voxel‐based diffusion tensor imaging analysis (VB‐DTI). Forty‐seven right‐handed subjects (14 MSA‐P patients, 19 PD patients, and 14 controls) were evaluated using VBM and VB‐DTI in an analysis of covariance (ANCOVA) with a significance threshold set to P < 0.005. In MSA‐P patients, VBM analysis revealed a lower density of grey matter (GM) in a motor‐related circuit (especially in the left primary motor cortex, PMC), relative to PD patients, and in the left supplementary motor area (SMA), relative to controls). Diffusion tensor imaging analysis revealed lower fractional anisotropy (FA) values in the left PMC and the right cerebellum in MSA‐P patients, compared with controls. Using a volumetric diffusion technique, our study revealed selective tissue degeneration in motor circuits, regardless of the volume loss detected in VBM and in agreement with pathology reports and clinical motor characteristics. Our findings suggest that MSA‐P is characterized by both macro‐ and microstructural changes in the sensorimotor circuit. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><subject lang="en"><genre>Keywords</genre><topic>MRI</topic><topic>diffusion‐weighted imaging</topic><topic>multiple‐system atrophy</topic><topic>Parkinson's disease</topic><topic>motor cortex</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><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research 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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>863</start><end>870</end><total>8</total></extent></part></relatedItem><identifier type="istex">42E49C9BED3CD62552BDC932F427A78766B77349</identifier><identifier type="DOI">10.1002/mds.22463</identifier><identifier type="ArticleID">MDS22463</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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