Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity
Identifieur interne : 002695 ( Istex/Corpus ); précédent : 002694; suivant : 002696Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity
Auteurs : Michael Sharman ; Romain Valabregue ; Vincent Perlbarg ; Linda Marrakchi-Kacem ; Marie Vidailhet ; Habib Benali ; Alexis Brice ; Stephane LehéricySource :
- Movement Disorders [ 0885-3185 ] ; 2013-04.
Abstract
Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico–basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion‐weighted magnetic resonance imaging (MRI) and resting‐state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico–basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere. © 2012 Movement Disorder Society
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DOI: 10.1002/mds.25255
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sensorimotor connectivity</title><author><name sortKey="Sharman, Michael" sort="Sharman, Michael" uniqKey="Sharman M" first="Michael" last="Sharman">Michael Sharman</name><affiliation><mods:affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</mods:affiliation></affiliation><affiliation><mods:affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: michael.sharman@etu.upmc.fr</mods:affiliation></affiliation></author><author><name sortKey="Valabregue, Romain" sort="Valabregue, Romain" uniqKey="Valabregue R" first="Romain" last="Valabregue">Romain Valabregue</name><affiliation><mods:affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</mods:affiliation></affiliation><affiliation><mods:affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>UMR 7225, CNRS, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Perlbarg, Vincent" sort="Perlbarg, Vincent" uniqKey="Perlbarg V" first="Vincent" last="Perlbarg">Vincent Perlbarg</name><affiliation><mods:affiliation>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Marrakchi Acem, Linda" sort="Marrakchi Acem, Linda" uniqKey="Marrakchi Acem L" first="Linda" last="Marrakchi-Kacem">Linda Marrakchi-Kacem</name><affiliation><mods:affiliation>Neurospin, CEA, Gif‐Sur‐Yvette, France</mods:affiliation></affiliation><affiliation><mods:affiliation>IFR49, UPMC Paris 6, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Vidailhet, Marie" sort="Vidailhet, Marie" uniqKey="Vidailhet M" first="Marie" last="Vidailhet">Marie Vidailhet</name><affiliation><mods:affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</mods:affiliation></affiliation><affiliation><mods:affiliation>UMR 7225, CNRS, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>IFR49, UPMC Paris 6, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Benali, Habib" sort="Benali, Habib" uniqKey="Benali H" first="Habib" last="Benali">Habib Benali</name><affiliation><mods:affiliation>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>IFR49, UPMC Paris 6, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité de Neuroimagerie Fonctionnelle, CRIUGM, Université de Montréal, Quebec, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name><affiliation><mods:affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</mods:affiliation></affiliation><affiliation><mods:affiliation>UMR 7225, CNRS, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Département de Génétique et Cytogénétique, Hôpital Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Lehericy, Stephane" sort="Lehericy, Stephane" uniqKey="Lehericy S" first="Stephane" last="Lehéricy">Stephane Lehéricy</name><affiliation><mods:affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</mods:affiliation></affiliation><affiliation><mods:affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>UMR 7225, CNRS, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>IFR49, UPMC Paris 6, Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov Disord</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><date type="published" when="2013-04">2013-04</date><biblScope unit="volume">28</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="447">447</biblScope><biblScope unit="page" to="454">454</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3B0AFFE5B35B059096DF9986C6898C347CFBE530</idno><idno type="DOI">10.1002/mds.25255</idno><idno type="ArticleID">MDS25255</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico–basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion‐weighted magnetic resonance imaging (MRI) and resting‐state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico–basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere. © 2012 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Michael Sharman PhD</name><affiliations><json:string>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</json:string><json:string>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</json:string><json:string>E-mail: michael.sharman@etu.upmc.fr</json:string></affiliations></json:item><json:item><name>Romain Valabregue PhD</name><affiliations><json:string>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</json:string><json:string>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</json:string><json:string>UMR 7225, CNRS, Paris, France</json:string></affiliations></json:item><json:item><name>Vincent Perlbarg PhD</name><affiliations><json:string>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</json:string></affiliations></json:item><json:item><name>Linda Marrakchi‐Kacem PhD</name><affiliations><json:string>Neurospin, CEA, Gif‐Sur‐Yvette, France</json:string><json:string>IFR49, UPMC Paris 6, Paris, France</json:string></affiliations></json:item><json:item><name>Marie Vidailhet MD, PhD</name><affiliations><json:string>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</json:string><json:string>UMR 7225, CNRS, Paris, France</json:string><json:string>IFR49, UPMC Paris 6, Paris, France</json:string><json:string>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>Habib Benali PhD</name><affiliations><json:string>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</json:string><json:string>IFR49, UPMC Paris 6, Paris, France</json:string><json:string>Unité de Neuroimagerie Fonctionnelle, CRIUGM, Université de Montréal, Quebec, Montréal, Canada</json:string></affiliations></json:item><json:item><name>Alexis Brice MD</name><affiliations><json:string>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</json:string><json:string>UMR 7225, CNRS, Paris, France</json:string><json:string>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</json:string><json:string>Département de Génétique et Cytogénétique, Hôpital Pitié‐Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>Stephane Lehéricy MD, PhD</name><affiliations><json:string>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</json:string><json:string>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</json:string><json:string>UMR 7225, CNRS, Paris, France</json:string><json:string>IFR49, UPMC Paris 6, Paris, 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>fMRI</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>diffusion imaging</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>basal ganglia</value></json:item></subject><articleId><json:string>MDS25255</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico–basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion‐weighted magnetic resonance imaging (MRI) and resting‐state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico–basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere. © 2012 Movement Disorder Society</abstract><qualityIndicators><score>7.366</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 809.972 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1771</abstractCharCount><pdfWordCount>4450</pdfWordCount><pdfCharCount>31684</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>243</abstractWordCount></qualityIndicators><title>Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity</title><genre><json:string>article</json:string></genre><host><title>Movement 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connectivity</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><availability><p>Copyright © 2012 Movement Disorders SocietyCopyright © 2012 Movement Disorders Society</p></availability><date>2013-04-02</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity</title><author xml:id="author-1"><persName><forename type="first">Michael</forename><surname>Sharman</surname></persName><roleName type="degree">PhD</roleName><email>michael.sharman@etu.upmc.fr</email><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Romain</forename><surname>Valabregue</surname></persName><roleName type="degree">PhD</roleName><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">Vincent</forename><surname>Perlbarg</surname></persName><roleName type="degree">PhD</roleName><affiliation>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">Linda</forename><surname>Marrakchi‐Kacem</surname></persName><roleName type="degree">PhD</roleName><affiliation>Neurospin, CEA, Gif‐Sur‐Yvette, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">Marie</forename><surname>Vidailhet</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation><affiliation>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">Habib</forename><surname>Benali</surname></persName><roleName type="degree">PhD</roleName><affiliation>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation><affiliation>Unité de Neuroimagerie Fonctionnelle, CRIUGM, Université de Montréal, Quebec, Montréal, Canada</affiliation></author><author xml:id="author-7"><persName><forename type="first">Alexis</forename><surname>Brice</surname></persName><roleName type="degree">MD</roleName><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation><affiliation>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>Département de Génétique et Cytogénétique, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation></author><author xml:id="author-8"><persName><forename type="first">Stephane</forename><surname>Lehéricy</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov 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>Blackwell Publishing Ltd</publisher><date type="published" when="2013-04"></date><biblScope unit="volume">28</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="447">447</biblScope><biblScope unit="page" to="454">454</biblScope></imprint></monogr><idno type="istex">3B0AFFE5B35B059096DF9986C6898C347CFBE530</idno><idno type="DOI">10.1002/mds.25255</idno><idno type="ArticleID">MDS25255</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2013-04-02</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico–basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion‐weighted magnetic resonance imaging (MRI) and resting‐state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico–basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere. © 2012 Movement Disorder Society</p></abstract><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>MRI</term></item><item><term>fMRI</term></item><item><term>diffusion imaging</term></item><item><term>Parkinson's disease</term></item><item><term>basal ganglia</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Featured Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2012-04-18">Received</change><change when="2012-09-25">Registration</change><change when="2013-04-02">Created</change><change when="2013-04">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/3B0AFFE5B35B059096DF9986C6898C347CFBE530/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" xml:id="mds25255"><header><publicationMeta level="product"><doi origin="wiley" 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" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov Disord</title></titleGroup></publicationMeta><publicationMeta level="part" position="40"><doi>10.1002/mds.v28.4</doi><copyright ownership="thirdParty">Copyright © 2012 Movement Disorders Society</copyright><numberingGroup><numbering type="journalVolume" number="28">28</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="2013-04">April 2013</coverDate></publicationMeta><publicationMeta level="unit" position="120" type="article" status="forIssue"><doi>10.1002/mds.25255</doi><idGroup><id type="unit" value="MDS25255"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Featured Article</title><title type="tocHeading1">Featured Article</title></titleGroup><copyright ownership="thirdParty">Copyright © 2012 Movement Disorders Society</copyright><eventGroup><event type="manuscriptReceived" date="2012-04-18"></event><event type="manuscriptRevised" date="2012-07-27"></event><event type="manuscriptAccepted" date="2012-09-25"></event><event type="xmlCreated" agent="Cenveo Publisher Services" date="2013-04-02"></event><event type="publishedOnlineEarlyUnpaginated" date="2012-11-09"></event><event type="publishedOnlineFinalForm" date="2013-04-08"></event><event type="firstOnline" date="2012-11-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-02"></event></eventGroup><numberingGroup><numbering type="pageFirst">447</numbering><numbering type="pageLast">454</numbering></numberingGroup><correspondenceTo><b>Correspondence to:</b> Dr. Michael Sharman, CENIR, ICM, Pitié‐Salpêtrière Hospital, 47‐83 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France; <email>michael.sharman@etu.upmc.fr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS25255.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity</title><title type="short">PD Sensorimotor Connectivity</title><title type="shortAuthors">Sharman et al</title></titleGroup><creators><creator affiliationRef="#mds25255-aff-0001 #mds25255-aff-0002" corresponding="yes" creatorRole="author" xml:id="mds25255-cr-0001"><personName><givenNames>Michael</givenNames><familyName>Sharman</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25255-aff-0001 #mds25255-aff-0002 #mds25255-aff-0003" creatorRole="author" xml:id="mds25255-cr-0002"><personName><givenNames>Romain</givenNames><familyName>Valabregue</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25255-aff-0004" creatorRole="author" xml:id="mds25255-cr-0003"><personName><givenNames>Vincent</givenNames><familyName>Perlbarg</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25255-aff-0005 #mds25255-aff-0006" creatorRole="author" xml:id="mds25255-cr-0004"><personName><givenNames>Linda</givenNames><familyName>Marrakchi‐Kacem</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25255-aff-0001 #mds25255-aff-0003 #mds25255-aff-0006 #mds25255-aff-0007" creatorRole="author" xml:id="mds25255-cr-0005"><personName><givenNames>Marie</givenNames><familyName>Vidailhet</familyName><degrees>MD, PhD</degrees></personName></creator><creator affiliationRef="#mds25255-aff-0004 #mds25255-aff-0006 #mds25255-aff-0008" creatorRole="author" xml:id="mds25255-cr-0006"><personName><givenNames>Habib</givenNames><familyName>Benali</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25255-aff-0001 #mds25255-aff-0003 #mds25255-aff-0007 #mds25255-aff-0009" creatorRole="author" xml:id="mds25255-cr-0007"><personName><givenNames>Alexis</givenNames><familyName>Brice</familyName><degrees>MD</degrees></personName></creator><creator affiliationRef="#mds25255-aff-0001 #mds25255-aff-0002 #mds25255-aff-0003 #mds25255-aff-0006" creatorRole="author" xml:id="mds25255-cr-0008"><personName><givenNames>Stephane</givenNames><familyName>Lehéricy</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation type="organization" xml:id="mds25255-aff-0001" countryCode="FR"><orgDiv>UMR‐S975</orgDiv><orgName>CRICM‐INSERM‐UPMC Paris 6, Paris</orgName><address><city>Île‐de‐France</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0002" countryCode="FR"><orgDiv>CENIR</orgDiv><orgDiv>ICM</orgDiv><orgName>Hôpital Pitié‐Salpêtrière</orgName><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0003" countryCode="FR"><orgDiv>UMR 7225</orgDiv><orgName>CNRS</orgName><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0004" countryCode="FR"><orgDiv>UMR‐S678</orgDiv><orgName>INSERM‐UPMC Paris 6, LIF</orgName><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0005" countryCode="FR"><orgDiv>Neurospin</orgDiv><orgName>CEA</orgName><address><city>Gif‐Sur‐Yvette</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0006" countryCode="FR"><orgDiv>IFR49</orgDiv><orgName>UPMC Paris 6</orgName><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0007" countryCode="FR"><orgDiv>ICM—Institut du Cerveau et de la Moelle epiniere</orgDiv><orgName>Hôpital Pitié‐Salpêtrière</orgName><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0008" countryCode="CA"><orgDiv>Unité de Neuroimagerie Fonctionnelle</orgDiv><orgDiv>CRIUGM</orgDiv><orgName>Université de Montréal</orgName><address><city>Montréal</city><countryPart>Quebec</countryPart><country>Canada</country></address></affiliation><affiliation type="organization" xml:id="mds25255-aff-0009" countryCode="FR"><orgDiv>Département de Génétique et Cytogénétique</orgDiv><orgName>Hôpital Pitié‐Salpêtrière</orgName><address><city>Paris</city><country>France</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="mds25255-kwd-0001">MRI</keyword><keyword xml:id="mds25255-kwd-0002">fMRI</keyword><keyword xml:id="mds25255-kwd-0003">diffusion imaging</keyword><keyword xml:id="mds25255-kwd-0004">Parkinson's disease</keyword><keyword xml:id="mds25255-kwd-0005">basal ganglia</keyword></keywordGroup><abstractGroup><abstract type="main"><p>Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico–basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion‐weighted magnetic resonance imaging (MRI) and resting‐state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico–basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere. © 2012 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="mds25255-note-0001"><p><b>Funding agencies</b>: This study was supported by European Union (EU) Framework Project 6–GENEPARK: Genomic Biomarkers for Parkinson's Disease, Action Line: LIFESCIHEALTH Life sciences, genomics and biotechnology for health, and LSH‐2005‐1.2.2.2—Development of innovative methods for diagnosis of nervous system disorders.</p></note><note xml:id="mds25255-note-0002"><p><b>Relevant conflicts of interest/financial disclosures</b>: Alexis Brice received honoraria from the Wolfson Foundation for reviewing the scientific project, as well as research support from the French Agency for Research and the European Union.</p></note><note xml:id="mds25255-note-0003"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PD Sensorimotor Connectivity</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity</title></titleInfo><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Sharman</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>E-mail: michael.sharman@etu.upmc.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Romain</namePart><namePart type="family">Valabregue</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vincent</namePart><namePart type="family">Perlbarg</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Linda</namePart><namePart type="family">Marrakchi‐Kacem</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurospin, CEA, Gif‐Sur‐Yvette, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marie</namePart><namePart type="family">Vidailhet</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation><affiliation>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Habib</namePart><namePart type="family">Benali</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>UMR‐S678, INSERM‐UPMC Paris 6, LIF, Paris, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation><affiliation>Unité de Neuroimagerie Fonctionnelle, CRIUGM, Université de Montréal, Quebec, Montréal, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexis</namePart><namePart type="family">Brice</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation><affiliation>ICM—Institut du Cerveau et de la Moelle epiniere, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>Département de Génétique et Cytogénétique, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephane</namePart><namePart type="family">Lehéricy</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>UMR‐S975, CRICM‐INSERM‐UPMC Paris 6, Paris, Île‐de‐France, France</affiliation><affiliation>CENIR, ICM, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>UMR 7225, CNRS, Paris, France</affiliation><affiliation>IFR49, UPMC Paris 6, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2013-04</dateIssued><dateCreated encoding="w3cdtf">2013-04-02</dateCreated><dateCaptured encoding="w3cdtf">2012-04-18</dateCaptured><dateValid encoding="w3cdtf">2012-09-25</dateValid><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico–basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion‐weighted magnetic resonance imaging (MRI) and resting‐state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico–basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere. © 2012 Movement Disorder Society</abstract><subject><genre>keywords</genre><topic>MRI</topic><topic>fMRI</topic><topic>diffusion imaging</topic><topic>Parkinson's disease</topic><topic>basal ganglia</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>Featured 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>2013</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>447</start><end>454</end><total>8</total></extent></part></relatedItem><identifier type="istex">3B0AFFE5B35B059096DF9986C6898C347CFBE530</identifier><identifier type="DOI">10.1002/mds.25255</identifier><identifier type="ArticleID">MDS25255</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2012 Movement Disorders SocietyCopyright © 2012 Movement Disorders Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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