Abnormal metabolic networks in atypical parkinsonism
Identifieur interne : 001A36 ( Main/Corpus ); précédent : 001A35; suivant : 001A37Abnormal metabolic networks in atypical parkinsonism
Auteurs : Thomas Eckert ; Chengke Tang ; Yilong Ma ; Nathaniel Brown ; Tanya Lin ; Steven Frucht ; Andrew Feigin ; David EidelbergSource :
- Movement Disorders [ 0885-3185 ] ; 2008-04-15.
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Abstract
Spatial covariance analysis has been used with 18F‐fluorodeoxyglucose (FDG) PET to detect and quantify specific metabolic patterns associated with Parkinson's disease (PD). However, PD‐related patterns cannot necessarily serve as biomarkers of the processes that underlie the atypical parkinsonian syndromes. In this FDG PET study, we used strictly defined statistical criteria to identify disease‐related metabolic patterns in the imaging data from patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the two most common of these atypical conditions. We found that MSA and PSP were each associated with a specific, highly stable metabolic brain network (P < 0.0001, bootstrap estimation). The MSA‐related pattern was characterized by decreased metabolism in the putamen and cerebellum. The PSP‐related pattern was characterized by metabolic decreases in the brainstem and medial frontal cortex. For both conditions, pattern expression was significantly elevated in patients relative to age‐matched healthy control subjects (P < 0.001). For each condition, we validated the associated disease‐related metabolic pattern by computing its expression on an individual scan basis in two independent patient cohorts, and in one subsequent healthy volunteer cohort. We found that for both MSA and PSP, prospective assessments of pattern expression accurately discriminated patients from controls (P < 0.001). These findings suggest that the major atypical parkinsonian syndromes are associated with distinct patterns of abnormal regional metabolic activity. These disease‐related networks can potentially be used in conjunction with functional brain imaging as quantifiable biomarkers for the assessment of these pathological conditions. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.21933
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However, PD‐related patterns cannot necessarily serve as biomarkers of the processes that underlie the atypical parkinsonian syndromes. In this FDG PET study, we used strictly defined statistical criteria to identify disease‐related metabolic patterns in the imaging data from patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the two most common of these atypical conditions. We found that MSA and PSP were each associated with a specific, highly stable metabolic brain network (P < 0.0001, bootstrap estimation). The MSA‐related pattern was characterized by decreased metabolism in the putamen and cerebellum. The PSP‐related pattern was characterized by metabolic decreases in the brainstem and medial frontal cortex. For both conditions, pattern expression was significantly elevated in patients relative to age‐matched healthy control subjects (P < 0.001). For each condition, we validated the associated disease‐related metabolic pattern by computing its expression on an individual scan basis in two independent patient cohorts, and in one subsequent healthy volunteer cohort. We found that for both MSA and PSP, prospective assessments of pattern expression accurately discriminated patients from controls (P < 0.001). These findings suggest that the major atypical parkinsonian syndromes are associated with distinct patterns of abnormal regional metabolic activity. These disease‐related networks can potentially be used in conjunction with functional brain imaging as quantifiable biomarkers for the assessment of these pathological conditions. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Thomas Eckert MD</name><affiliations><json:string>Department of Neurology II, University of Magdeburg, Germany</json:string><json:string>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</json:string></affiliations></json:item><json:item><name>Chengke Tang MD</name><affiliations><json:string>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</json:string></affiliations></json:item><json:item><name>Yilong Ma PhD</name><affiliations><json:string>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</json:string><json:string>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</json:string></affiliations></json:item><json:item><name>Nathaniel Brown BA</name><affiliations><json:string>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</json:string></affiliations></json:item><json:item><name>Tanya Lin MS</name><affiliations><json:string>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</json:string><json:string>Albert Einstein College of Medicine, Bronx, New York, USA</json:string></affiliations></json:item><json:item><name>Steven Frucht MD</name><affiliations><json:string>Movement Disorders Center, Neurologic Institute, Columbia University, New York, New York, USA</json:string></affiliations></json:item><json:item><name>Andrew Feigin MD</name><affiliations><json:string>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</json:string><json:string>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</json:string></affiliations></json:item><json:item><name>David Eidelberg MD</name><affiliations><json:string>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</json:string><json:string>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>atypical parkinsonism</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>progressive supranuclear palsy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>metabolic networks</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FDG PET</value></json:item></subject><articleId><json:string>MDS21933</json:string></articleId><language><json:string>eng</json:string></language><abstract>Spatial covariance analysis has been used with 18F‐fluorodeoxyglucose (FDG) PET to detect and quantify specific metabolic patterns associated with Parkinson's disease (PD). However, PD‐related patterns cannot necessarily serve as biomarkers of the processes that underlie the atypical parkinsonian syndromes. In this FDG PET study, we used strictly defined statistical criteria to identify disease‐related metabolic patterns in the imaging data from patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the two most common of these atypical conditions. We found that MSA and PSP were each associated with a specific, highly stable metabolic brain network (P > 0.0001, bootstrap estimation). The MSA‐related pattern was characterized by decreased metabolism in the putamen and cerebellum. The PSP‐related pattern was characterized by metabolic decreases in the brainstem and medial frontal cortex. For both conditions, pattern expression was significantly elevated in patients relative to age‐matched healthy control subjects (P > 0.001). For each condition, we validated the associated disease‐related metabolic pattern by computing its expression on an individual scan basis in two independent patient cohorts, and in one subsequent healthy volunteer cohort. We found that for both MSA and PSP, prospective assessments of pattern expression accurately discriminated patients from controls (P > 0.001). These findings suggest that the major atypical parkinsonian syndromes are associated with distinct patterns of abnormal regional metabolic activity. 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Health System, Manhasset, New York, USA</affiliation><affiliation>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</affiliation></author><author><persName><forename type="first">Nathaniel</forename><surname>Brown</surname></persName><roleName type="degree">BA</roleName><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation></author><author><persName><forename type="first">Tanya</forename><surname>Lin</surname></persName><roleName type="degree">MS</roleName><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><affiliation>Albert Einstein College of Medicine, Bronx, New York, USA</affiliation></author><author><persName><forename type="first">Steven</forename><surname>Frucht</surname></persName><roleName 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However, PD‐related patterns cannot necessarily serve as biomarkers of the processes that underlie the atypical parkinsonian syndromes. In this FDG PET study, we used strictly defined statistical criteria to identify disease‐related metabolic patterns in the imaging data from patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the two most common of these atypical conditions. We found that MSA and PSP were each associated with a specific, highly stable metabolic brain network (P < 0.0001, bootstrap estimation). The MSA‐related pattern was characterized by decreased metabolism in the putamen and cerebellum. The PSP‐related pattern was characterized by metabolic decreases in the brainstem and medial frontal cortex. For both conditions, pattern expression was significantly elevated in patients relative to age‐matched healthy control subjects (P < 0.001). For each condition, we validated the associated disease‐related metabolic pattern by computing its expression on an individual scan basis in two independent patient cohorts, and in one subsequent healthy volunteer cohort. We found that for both MSA and PSP, prospective assessments of pattern expression accurately discriminated patients from controls (P < 0.001). These findings suggest that the major atypical parkinsonian syndromes are associated with distinct patterns of abnormal regional metabolic activity. These disease‐related networks can potentially be used in conjunction with functional brain imaging as quantifiable biomarkers for the assessment of these pathological conditions. © 2008 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>atypical parkinsonism</term></item><item><term>multiple system atrophy</term></item><item><term>progressive supranuclear palsy</term></item><item><term>metabolic networks</term></item><item><term>FDG PET</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-07-11">Received</change><change when="2007-11-30">Registration</change><change when="2008-04-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6FCC5CCAD56CA3A34C4864249C184789F93A7D23/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="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley" registered="yes">10.1002/mds.v23:5</doi><numberingGroup><numbering type="journalVolume" number="23">23</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2008-04-15">15 April 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="140" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.21933</doi><idGroup><id type="unit" value="MDS21933"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2008 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2007-07-11"></event><event type="manuscriptRevised" date="2007-10-03"></event><event 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href="file:MDS.MDS21933.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="37"></count><count type="wordTotal" number="4637"></count></countGroup><titleGroup><title type="main" xml:lang="en">Abnormal metabolic networks in atypical parkinsonism</title><title type="short" xml:lang="en">Metabolic Patterns in Atypical Parkinsonism</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" noteRef="#fn1"><personName><givenNames>Thomas</givenNames><familyName>Eckert</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2" noteRef="#fn1"><personName><givenNames>Chengke</givenNames><familyName>Tang</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Yilong</givenNames><familyName>Ma</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Nathaniel</givenNames><familyName>Brown</familyName><degrees>BA</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2 #af4"><personName><givenNames>Tanya</givenNames><familyName>Lin</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Steven</givenNames><familyName>Frucht</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Andrew</givenNames><familyName>Feigin</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2 #af3" corresponding="yes"><personName><givenNames>David</givenNames><familyName>Eidelberg</familyName><degrees>MD</degrees></personName><contactDetails><email>david1@nshs.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology II, University of Magdeburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Albert Einstein College of Medicine, Bronx, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Movement Disorders Center, Neurologic Institute, Columbia University, New York, New York, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">atypical parkinsonism</keyword><keyword xml:id="kwd2">multiple system atrophy</keyword><keyword xml:id="kwd3">progressive supranuclear palsy</keyword><keyword xml:id="kwd4">metabolic networks</keyword><keyword xml:id="kwd5">FDG PET</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Spatial covariance analysis has been used with <sup>18</sup>F‐fluorodeoxyglucose (FDG) PET to detect and quantify specific metabolic patterns associated with Parkinson's disease (PD). However, PD‐related patterns cannot necessarily serve as biomarkers of the processes that underlie the atypical parkinsonian syndromes. In this FDG PET study, we used strictly defined statistical criteria to identify disease‐related metabolic patterns in the imaging data from patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the two most common of these atypical conditions. We found that MSA and PSP were each associated with a specific, highly stable metabolic brain network (<i>P</i> < 0.0001, bootstrap estimation). The MSA‐related pattern was characterized by decreased metabolism in the putamen and cerebellum. The PSP‐related pattern was characterized by metabolic decreases in the brainstem and medial frontal cortex. For both conditions, pattern expression was significantly elevated in patients relative to age‐matched healthy control subjects (<i>P</i> < 0.001). For each condition, we validated the associated disease‐related metabolic pattern by computing its expression on an individual scan basis in two independent patient cohorts, and in one subsequent healthy volunteer cohort. We found that for both MSA and PSP, prospective assessments of pattern expression accurately discriminated patients from controls (<i>P</i> < 0.001). These findings suggest that the major atypical parkinsonian syndromes are associated with distinct patterns of abnormal regional metabolic activity. These disease‐related networks can potentially be used in conjunction with functional brain imaging as quantifiable biomarkers for the assessment of these pathological conditions. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Thomas Eckert and Chengke Tang contributed equally to this work as first authors.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Abnormal metabolic networks in atypical parkinsonism</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Metabolic Patterns in Atypical Parkinsonism</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Abnormal metabolic networks in atypical parkinsonism</title></titleInfo><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Eckert</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology II, University of Magdeburg, Germany</affiliation><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><description>Thomas Eckert and Chengke Tang contributed equally to this work as first authors.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chengke</namePart><namePart type="family">Tang</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><description>Thomas Eckert and Chengke Tang contributed equally to this work as first authors.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yilong</namePart><namePart type="family">Ma</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><affiliation>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nathaniel</namePart><namePart type="family">Brown</namePart><namePart type="termsOfAddress">BA</namePart><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tanya</namePart><namePart type="family">Lin</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><affiliation>Albert Einstein College of Medicine, Bronx, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Steven</namePart><namePart type="family">Frucht</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Movement Disorders Center, Neurologic Institute, Columbia University, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew</namePart><namePart type="family">Feigin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><affiliation>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Eidelberg</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore‐Long Island Jewish Health System, Manhasset, New York, USA</affiliation><affiliation>Departments of Neurology and Medicine, New York University School of Medicine, New York, New York, USA</affiliation><description>Correspondence: The Feinstein Institute for Medical Research, North Shore‐LIJ Health System, 350 Community Drive, Manhasset, New York 11030, USA</description><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">2008-04-15</dateIssued><dateCaptured encoding="w3cdtf">2007-07-11</dateCaptured><dateValid encoding="w3cdtf">2007-11-30</dateValid><copyrightDate encoding="w3cdtf">2008</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">1</extent><extent unit="references">37</extent><extent unit="words">4637</extent></physicalDescription><abstract lang="en">Spatial covariance analysis has been used with 18F‐fluorodeoxyglucose (FDG) PET to detect and quantify specific metabolic patterns associated with Parkinson's disease (PD). However, PD‐related patterns cannot necessarily serve as biomarkers of the processes that underlie the atypical parkinsonian syndromes. In this FDG PET study, we used strictly defined statistical criteria to identify disease‐related metabolic patterns in the imaging data from patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the two most common of these atypical conditions. We found that MSA and PSP were each associated with a specific, highly stable metabolic brain network (P < 0.0001, bootstrap estimation). The MSA‐related pattern was characterized by decreased metabolism in the putamen and cerebellum. The PSP‐related pattern was characterized by metabolic decreases in the brainstem and medial frontal cortex. For both conditions, pattern expression was significantly elevated in patients relative to age‐matched healthy control subjects (P < 0.001). For each condition, we validated the associated disease‐related metabolic pattern by computing its expression on an individual scan basis in two independent patient cohorts, and in one subsequent healthy volunteer cohort. We found that for both MSA and PSP, prospective assessments of pattern expression accurately discriminated patients from controls (P < 0.001). These findings suggest that the major atypical parkinsonian syndromes are associated with distinct patterns of abnormal regional metabolic activity. These disease‐related networks can potentially be used in conjunction with functional brain imaging as quantifiable biomarkers for the assessment of these pathological conditions. © 2008 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>atypical parkinsonism</topic><topic>multiple system atrophy</topic><topic>progressive supranuclear palsy</topic><topic>metabolic networks</topic><topic>FDG PET</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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>727</start><end>733</end><total>7</total></extent></part></relatedItem><identifier type="istex">6FCC5CCAD56CA3A34C4864249C184789F93A7D23</identifier><identifier type="DOI">10.1002/mds.21933</identifier><identifier type="ArticleID">MDS21933</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 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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