Voxel‐based morphometry detects cortical atrophy in the Parkinson variant of multiple system atrophy
Identifieur interne : 002099 ( Main/Corpus ); précédent : 002098; suivant : 002100Voxel‐based morphometry detects cortical atrophy in the Parkinson variant of multiple system atrophy
Auteurs : Christian Brenneis ; Klaus Seppi ; Michael F. Schocke ; Jörg Müller ; Elisabeth Luginger ; Sylvia Bösch ; Wolfgang N. Löscher ; Christian Büchel ; Werner Poewe ; Gregor K. WenningSource :
- Movement Disorders [ 0885-3185 ] ; 2003-10.
English descriptors
Abstract
To determine magnetic resonance imaging (MRI) patterns of brain atrophy in parkinsonian syndromes, we applied voxel‐based morphometry (VBM) to segmented gray matter, white matter, and cerebrospinal fluid compartments of T1‐weighted brain volumes of 12 patients with probable multiple system atrophy–parkinson variant (MSA‐P) and 12 Parkinson's disease patients, comparing them with 12 normal controls matched for age. In comparison to controls, a cortical atrophy pattern was observed in MSA‐P patients with significant clusters of volume loss in primary sensorimotor cortices bilateral, supplementary motor areas bilateral, right premotor cortex, prefrontal cortex bilateral (middle frontal gyri) and insular cortices bilateral; subcortical atrophy occurred bilaterally in caudate nuclei and putamen as well as in the midbrain. Furthermore, an enlargement of the cerebrospinal fluid compartment was found in the lateral ventricles, third ventricle, perimesencephalic and cerebellomedullar cavities. In PD patients, significant atrophy only occurred in left caudate head with enlargement of left lateral ventricle. Comparing MSA‐P to PD patients, MSA‐P showed a similar cortical pattern of atrophy as compared to controls. We conclude that VBM reveals selective cortical atrophy in patients with MSA‐P affecting primary and higher order motor areas as well as prefrontal and insular cortices. Further studies are required to determine clinical and/or subclinical correlates of cortical atrophy in MSA‐P. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10502
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In comparison to controls, a cortical atrophy pattern was observed in MSA‐P patients with significant clusters of volume loss in primary sensorimotor cortices bilateral, supplementary motor areas bilateral, right premotor cortex, prefrontal cortex bilateral (middle frontal gyri) and insular cortices bilateral; subcortical atrophy occurred bilaterally in caudate nuclei and putamen as well as in the midbrain. Furthermore, an enlargement of the cerebrospinal fluid compartment was found in the lateral ventricles, third ventricle, perimesencephalic and cerebellomedullar cavities. In PD patients, significant atrophy only occurred in left caudate head with enlargement of left lateral ventricle. Comparing MSA‐P to PD patients, MSA‐P showed a similar cortical pattern of atrophy as compared to controls. We conclude that VBM reveals selective cortical atrophy in patients with MSA‐P affecting primary and higher order motor areas as well as prefrontal and insular cortices. Further studies are required to determine clinical and/or subclinical correlates of cortical atrophy in MSA‐P. © 2003 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Christian Brenneis MD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Klaus Seppi MD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Michael F. Schocke MD</name><affiliations><json:string>Department of Radiology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Jörg Müller MD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Elisabeth Luginger MD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Sylvia Bösch MD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Wolfgang N. Löscher PhD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Christian Büchel MD</name><affiliations><json:string>Department of Neurology, University Hospital, Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Werner Poewe MD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Gregor K. Wenning PhD</name><affiliations><json:string>Department of Neurology, University Hospital, Innsbruck, Austria</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>voxel‐based morphometry</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>cortical atrophy</value></json:item></subject><articleId><json:string>MDS10502</json:string></articleId><language><json:string>eng</json:string></language><abstract>To determine magnetic resonance imaging (MRI) patterns of brain atrophy in parkinsonian syndromes, we applied voxel‐based morphometry (VBM) to segmented gray matter, white matter, and cerebrospinal fluid compartments of T1‐weighted brain volumes of 12 patients with probable multiple system atrophy–parkinson variant (MSA‐P) and 12 Parkinson's disease patients, comparing them with 12 normal controls matched for age. In comparison to controls, a cortical atrophy pattern was observed in MSA‐P patients with significant clusters of volume loss in primary sensorimotor cortices bilateral, supplementary motor areas bilateral, right premotor cortex, prefrontal cortex bilateral (middle frontal gyri) and insular cortices bilateral; subcortical atrophy occurred bilaterally in caudate nuclei and putamen as well as in the midbrain. Furthermore, an enlargement of the cerebrospinal fluid compartment was found in the lateral ventricles, third ventricle, perimesencephalic and cerebellomedullar cavities. In PD patients, significant atrophy only occurred in left caudate head with enlargement of left lateral ventricle. Comparing MSA‐P to PD patients, MSA‐P showed a similar cortical pattern of atrophy as compared to controls. We conclude that VBM reveals selective cortical atrophy in patients with MSA‐P affecting primary and higher order motor areas as well as prefrontal and insular cortices. 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In comparison to controls, a cortical atrophy pattern was observed in MSA‐P patients with significant clusters of volume loss in primary sensorimotor cortices bilateral, supplementary motor areas bilateral, right premotor cortex, prefrontal cortex bilateral (middle frontal gyri) and insular cortices bilateral; subcortical atrophy occurred bilaterally in caudate nuclei and putamen as well as in the midbrain. Furthermore, an enlargement of the cerebrospinal fluid compartment was found in the lateral ventricles, third ventricle, perimesencephalic and cerebellomedullar cavities. In PD patients, significant atrophy only occurred in left caudate head with enlargement of left lateral ventricle. Comparing MSA‐P to PD patients, MSA‐P showed a similar cortical pattern of atrophy as compared to controls. We conclude that VBM reveals selective cortical atrophy in patients with MSA‐P affecting primary and higher order motor areas as well as prefrontal and insular cortices. 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href="file:MDS.MDS10502.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="47"></count><count type="wordTotal" number="4316"></count></countGroup><titleGroup><title type="main" xml:lang="en">Voxel‐based morphometry detects cortical atrophy in the Parkinson variant of multiple system atrophy</title><title type="short" xml:lang="en">VBM in Multiple System Atrophy</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Christian</givenNames><familyName>Brenneis</familyName><degrees>MD</degrees></personName><contactDetails><email>christian.brenneis@uibk.ac.at</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Klaus</givenNames><familyName>Seppi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Michael F.</givenNames><familyName>Schocke</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jörg</givenNames><familyName>Müller</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Elisabeth</givenNames><familyName>Luginger</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Sylvia</givenNames><familyName>Bösch</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Wolfgang N.</givenNames><familyName>Löscher</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Christian</givenNames><familyName>Büchel</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Werner</givenNames><familyName>Poewe</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Gregor K.</givenNames><familyName>Wenning</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="AT" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital, Innsbruck, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="AT" type="organization"><unparsedAffiliation>Department of Radiology, University Hospital, Innsbruck, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital, Eppendorf, Hamburg, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">voxel‐based morphometry</keyword><keyword xml:id="kwd2">multiple system atrophy</keyword><keyword xml:id="kwd3">cortical atrophy</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To determine magnetic resonance imaging (MRI) patterns of brain atrophy in parkinsonian syndromes, we applied voxel‐based morphometry (VBM) to segmented gray matter, white matter, and cerebrospinal fluid compartments of T<sub>1</sub>‐weighted brain volumes of 12 patients with probable multiple system atrophy–parkinson variant (MSA‐P) and 12 Parkinson's disease patients, comparing them with 12 normal controls matched for age. In comparison to controls, a cortical atrophy pattern was observed in MSA‐P patients with significant clusters of volume loss in primary sensorimotor cortices bilateral, supplementary motor areas bilateral, right premotor cortex, prefrontal cortex bilateral (middle frontal gyri) and insular cortices bilateral; subcortical atrophy occurred bilaterally in caudate nuclei and putamen as well as in the midbrain. Furthermore, an enlargement of the cerebrospinal fluid compartment was found in the lateral ventricles, third ventricle, perimesencephalic and cerebellomedullar cavities. In PD patients, significant atrophy only occurred in left caudate head with enlargement of left lateral ventricle. Comparing MSA‐P to PD patients, MSA‐P showed a similar cortical pattern of atrophy as compared to controls. We conclude that VBM reveals selective cortical atrophy in patients with MSA‐P affecting primary and higher order motor areas as well as prefrontal and insular cortices. Further studies are required to determine clinical and/or subclinical correlates of cortical atrophy in MSA‐P. © 2003 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Voxel‐based morphometry detects cortical atrophy in the Parkinson variant of multiple system atrophy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>VBM in Multiple System Atrophy</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Voxel‐based morphometry detects cortical atrophy in the Parkinson variant of multiple system atrophy</title></titleInfo><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Brenneis</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><description>Correspondence: Department of Neurology, University Hospital, Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus</namePart><namePart type="family">Seppi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael F.</namePart><namePart type="family">Schocke</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Radiology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jörg</namePart><namePart type="family">Müller</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elisabeth</namePart><namePart type="family">Luginger</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sylvia</namePart><namePart type="family">Bösch</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfgang N.</namePart><namePart type="family">Löscher</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Büchel</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital, Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregor K.</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, University Hospital, Innsbruck, Austria</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">2003-10</dateIssued><dateCaptured encoding="w3cdtf">2002-09-16</dateCaptured><dateValid encoding="w3cdtf">2003-03-14</dateValid><copyrightDate encoding="w3cdtf">2003</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">47</extent><extent unit="words">4316</extent></physicalDescription><abstract lang="en">To determine magnetic resonance imaging (MRI) patterns of brain atrophy in parkinsonian syndromes, we applied voxel‐based morphometry (VBM) to segmented gray matter, white matter, and cerebrospinal fluid compartments of T1‐weighted brain volumes of 12 patients with probable multiple system atrophy–parkinson variant (MSA‐P) and 12 Parkinson's disease patients, comparing them with 12 normal controls matched for age. In comparison to controls, a cortical atrophy pattern was observed in MSA‐P patients with significant clusters of volume loss in primary sensorimotor cortices bilateral, supplementary motor areas bilateral, right premotor cortex, prefrontal cortex bilateral (middle frontal gyri) and insular cortices bilateral; subcortical atrophy occurred bilaterally in caudate nuclei and putamen as well as in the midbrain. Furthermore, an enlargement of the cerebrospinal fluid compartment was found in the lateral ventricles, third ventricle, perimesencephalic and cerebellomedullar cavities. In PD patients, significant atrophy only occurred in left caudate head with enlargement of left lateral ventricle. Comparing MSA‐P to PD patients, MSA‐P showed a similar cortical pattern of atrophy as compared to controls. We conclude that VBM reveals selective cortical atrophy in patients with MSA‐P affecting primary and higher order motor areas as well as prefrontal and insular cortices. Further studies are required to determine clinical and/or subclinical correlates of cortical atrophy in MSA‐P. © 2003 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>voxel‐based morphometry</topic><topic>multiple system atrophy</topic><topic>cortical atrophy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></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>2003</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1132</start><end>1138</end><total>7</total></extent></part></relatedItem><identifier type="istex">A06B06831AA8F4002B33D63B3538801B0E94A7A7</identifier><identifier type="DOI">10.1002/mds.10502</identifier><identifier type="ArticleID">MDS10502</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 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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