Altered pattern of motor cortical activation–inhibition during voluntary movements in Tourette syndrome
Identifieur interne : 001548 ( Istex/Corpus ); précédent : 001547; suivant : 001549Altered pattern of motor cortical activation–inhibition during voluntary movements in Tourette syndrome
Auteurs : Stephanie Franzkowiak ; Bettina Pollok ; Katja Biermann-Ruben ; Martin Südmeyer ; Jennifer Paszek ; Melanie Jonas ; Götz Thomalla ; Tobias B Umer ; Michael Orth ; Alexander Münchau ; Alfons SchnitzlerSource :
- Movement Disorders [ 0885-3185 ] ; 2010-09-15.
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Abstract
In patients with Gilles de la Tourette syndrome (GTS) alterations of motor cortex (M1) excitability at rest have been evidenced. In contrast, there has so far been little research into changes of motor cortical reactivity during the time course of voluntary movements in GTS patients. The present study investigates neuromagnetic event‐related desynchronization (ERD) and event‐related synchronization (ERS) of bilateral M1 in 11 GTS patients and 11 healthy control subjects. ERD represents motor cortical activation, whereas ERS most likely indicates its inhibition. Subjects performed a self‐paced finger movement task while magnetoencephalography was used to record neuromagnetic activity. In GTS patients, ERD at beta frequency was significantly increased in the contralateral hemisphere before and during movements, whereas ERS following movement termination was increased in M1 ipsilateral. Ipsilateral ERS was inversely correlated with tic severity as determined by the Yale Global Tic Severity Rating Scale. The data of the present study support the hypothesis that during voluntary movements, motor cortical reactivity is pathologically altered in GTS patients. The observed pattern of increased activation (ERD) prior to and during movement execution followed by increased inhibition (ERS) after movement termination at beta frequency suggests abnormally increased motor cortical activation, possibly driving stronger inhibition. The stronger this inhibition is, the better symptoms appear to be controlled. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23186
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Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Biermann Uben, Katja" sort="Biermann Uben, Katja" uniqKey="Biermann Uben K" first="Katja" last="Biermann-Ruben">Katja Biermann-Ruben</name><affiliation><mods:affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Sudmeyer, Martin" sort="Sudmeyer, Martin" uniqKey="Sudmeyer M" first="Martin" last="Südmeyer">Martin Südmeyer</name><affiliation><mods:affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Paszek, Jennifer" sort="Paszek, Jennifer" uniqKey="Paszek J" first="Jennifer" last="Paszek">Jennifer Paszek</name><affiliation><mods:affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Jonas, Melanie" sort="Jonas, Melanie" uniqKey="Jonas M" first="Melanie" last="Jonas">Melanie Jonas</name><affiliation><mods:affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Thomalla, Gotz" sort="Thomalla, Gotz" uniqKey="Thomalla G" first="Götz" last="Thomalla">Götz Thomalla</name><affiliation><mods:affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="B Umer, Tobias" sort="B Umer, Tobias" uniqKey="B Umer T" first="Tobias" last="B Umer">Tobias B Umer</name><affiliation><mods:affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Orth, Michael" sort="Orth, Michael" uniqKey="Orth M" first="Michael" last="Orth">Michael Orth</name><affiliation><mods:affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Ulm, Germany</mods:affiliation></affiliation></author><author><name sortKey="Munchau, Alexander" sort="Munchau, Alexander" uniqKey="Munchau A" first="Alexander" last="Münchau">Alexander Münchau</name><affiliation><mods:affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schnitzler, Alfons" sort="Schnitzler, Alfons" uniqKey="Schnitzler A" first="Alfons" last="Schnitzler">Alfons Schnitzler</name><affiliation><mods:affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-09-15">2010-09-15</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1960">1960</biblScope><biblScope unit="page" to="1966">1966</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E2745540F8CF8A938C861D7F0B4D14E13A85542F</idno><idno type="DOI">10.1002/mds.23186</idno><idno type="ArticleID">MDS23186</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Gilles de la Tourette syndrome</term><term>event‐related desynchronization (ERD)</term><term>magnetoencephalography (MEG)</term><term>motor cortex</term><term>movement</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In patients with Gilles de la Tourette syndrome (GTS) alterations of motor cortex (M1) excitability at rest have been evidenced. In contrast, there has so far been little research into changes of motor cortical reactivity during the time course of voluntary movements in GTS patients. The present study investigates neuromagnetic event‐related desynchronization (ERD) and event‐related synchronization (ERS) of bilateral M1 in 11 GTS patients and 11 healthy control subjects. ERD represents motor cortical activation, whereas ERS most likely indicates its inhibition. Subjects performed a self‐paced finger movement task while magnetoencephalography was used to record neuromagnetic activity. In GTS patients, ERD at beta frequency was significantly increased in the contralateral hemisphere before and during movements, whereas ERS following movement termination was increased in M1 ipsilateral. Ipsilateral ERS was inversely correlated with tic severity as determined by the Yale Global Tic Severity Rating Scale. The data of the present study support the hypothesis that during voluntary movements, motor cortical reactivity is pathologically altered in GTS patients. The observed pattern of increased activation (ERD) prior to and during movement execution followed by increased inhibition (ERS) after movement termination at beta frequency suggests abnormally increased motor cortical activation, possibly driving stronger inhibition. The stronger this inhibition is, the better symptoms appear to be controlled. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Stephanie Franzkowiak MSc</name><affiliations><json:string>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</json:string><json:string>Department of Neurology, University Hospital Duesseldorf, Germany</json:string></affiliations></json:item><json:item><name>Bettina Pollok PhD</name><affiliations><json:string>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</json:string><json:string>Department of Neurology, University Hospital Duesseldorf, Germany</json:string></affiliations></json:item><json:item><name>Katja Biermann‐Ruben PhD</name><affiliations><json:string>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</json:string><json:string>Department of Neurology, University Hospital Duesseldorf, Germany</json:string></affiliations></json:item><json:item><name>Martin Südmeyer MD</name><affiliations><json:string>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</json:string><json:string>Department of Neurology, University Hospital Duesseldorf, Germany</json:string></affiliations></json:item><json:item><name>Jennifer Paszek MSc</name><affiliations><json:string>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</json:string><json:string>Department of Neurology, University Hospital Duesseldorf, Germany</json:string></affiliations></json:item><json:item><name>Melanie Jonas PhD</name><affiliations><json:string>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Götz Thomalla MD</name><affiliations><json:string>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Tobias Bäumer MD</name><affiliations><json:string>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Michael Orth MD</name><affiliations><json:string>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</json:string><json:string>Department of Neurology, University of Ulm, Germany</json:string></affiliations></json:item><json:item><name>Alexander Münchau MD</name><affiliations><json:string>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Alfons Schnitzler MD</name><affiliations><json:string>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</json:string><json:string>Department of Neurology, University Hospital Duesseldorf, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Gilles de la Tourette syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>event‐related desynchronization (ERD)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>magnetoencephalography (MEG)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor cortex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>movement</value></json:item></subject><language><json:string>eng</json:string></language><abstract>In patients with Gilles de la Tourette syndrome (GTS) alterations of motor cortex (M1) excitability at rest have been evidenced. In contrast, there has so far been little research into changes of motor cortical reactivity during the time course of voluntary movements in GTS patients. The present study investigates neuromagnetic event‐related desynchronization (ERD) and event‐related synchronization (ERS) of bilateral M1 in 11 GTS patients and 11 healthy control subjects. ERD represents motor cortical activation, whereas ERS most likely indicates its inhibition. Subjects performed a self‐paced finger movement task while magnetoencephalography was used to record neuromagnetic activity. In GTS patients, ERD at beta frequency was significantly increased in the contralateral hemisphere before and during movements, whereas ERS following movement termination was increased in M1 ipsilateral. Ipsilateral ERS was inversely correlated with tic severity as determined by the Yale Global Tic Severity Rating Scale. The data of the present study support the hypothesis that during voluntary movements, motor cortical reactivity is pathologically altered in GTS patients. The observed pattern of increased activation (ERD) prior to and during movement execution followed by increased inhibition (ERS) after movement termination at beta frequency suggests abnormally increased motor cortical activation, possibly driving stronger inhibition. The stronger this inhibition is, the better symptoms appear to be controlled. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>6.186</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1550</abstractCharCount><pdfWordCount>3606</pdfWordCount><pdfCharCount>24881</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>215</abstractWordCount></qualityIndicators><title>Altered pattern of motor cortical activation–inhibition during voluntary movements in Tourette syndrome</title><genre><json:string>Serial article</json:string></genre><host><volume>25</volume><pages><total>7</total><last>1966</last><first>1960</first></pages><issn><json:string>0885-3185</json:string></issn><issue>12</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23186</json:string></doi><id>E2745540F8CF8A938C861D7F0B4D14E13A85542F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/E2745540F8CF8A938C861D7F0B4D14E13A85542F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/E2745540F8CF8A938C861D7F0B4D14E13A85542F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/E2745540F8CF8A938C861D7F0B4D14E13A85542F/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Altered pattern of motor cortical activation–inhibition during voluntary movements in Tourette syndrome</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: Nothing to report.Financial disclosure: Deutsche Forschungsgemeinschaft (MU1692/1‐2; MU1692/2‐2).</note><note>Deutsche Forschungsgesellschaft DFG - No. SCH592/1‐2; No. MU1692/2‐1;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Altered pattern of motor cortical activation–inhibition during voluntary movements in Tourette syndrome</title><author><persName><forename type="first">Stephanie</forename><surname>Franzkowiak</surname><roleName type="degree">MSc</roleName></persName><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation></author><author><persName><forename type="first">Bettina</forename><surname>Pollok</surname><roleName type="degree">PhD</roleName></persName><note type="correspondence"><p>Correspondence: Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</p></note><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation></author><author><persName><forename type="first">Katja</forename><surname>Biermann‐Ruben</surname><roleName type="degree">PhD</roleName></persName><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation></author><author><persName><forename type="first">Martin</forename><surname>Südmeyer</surname><roleName type="degree">MD</roleName></persName><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation></author><author><persName><forename type="first">Jennifer</forename><surname>Paszek</surname><roleName type="degree">MSc</roleName></persName><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation></author><author><persName><forename type="first">Melanie</forename><surname>Jonas</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Götz</forename><surname>Thomalla</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Tobias</forename><surname>Bäumer</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Michael</forename><surname>Orth</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation><affiliation>Department of Neurology, University of Ulm, Germany</affiliation></author><author><persName><forename type="first">Alexander</forename><surname>Münchau</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Alfons</forename><surname>Schnitzler</surname><roleName type="degree">MD</roleName></persName><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-09-15"></date><biblScope unit="vol">25</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1960">1960</biblScope><biblScope unit="page" to="1966">1966</biblScope></imprint></monogr><idno type="istex">E2745540F8CF8A938C861D7F0B4D14E13A85542F</idno><idno type="DOI">10.1002/mds.23186</idno><idno type="ArticleID">MDS23186</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In patients with Gilles de la Tourette syndrome (GTS) alterations of motor cortex (M1) excitability at rest have been evidenced. In contrast, there has so far been little research into changes of motor cortical reactivity during the time course of voluntary movements in GTS patients. The present study investigates neuromagnetic event‐related desynchronization (ERD) and event‐related synchronization (ERS) of bilateral M1 in 11 GTS patients and 11 healthy control subjects. ERD represents motor cortical activation, whereas ERS most likely indicates its inhibition. Subjects performed a self‐paced finger movement task while magnetoencephalography was used to record neuromagnetic activity. In GTS patients, ERD at beta frequency was significantly increased in the contralateral hemisphere before and during movements, whereas ERS following movement termination was increased in M1 ipsilateral. Ipsilateral ERS was inversely correlated with tic severity as determined by the Yale Global Tic Severity Rating Scale. The data of the present study support the hypothesis that during voluntary movements, motor cortical reactivity is pathologically altered in GTS patients. The observed pattern of increased activation (ERD) prior to and during movement execution followed by increased inhibition (ERS) after movement termination at beta frequency suggests abnormally increased motor cortical activation, possibly driving stronger inhibition. The stronger this inhibition is, the better symptoms appear to be controlled. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Gilles de la Tourette syndrome</term></item><item><term>event‐related desynchronization (ERD)</term></item><item><term>magnetoencephalography (MEG)</term></item><item><term>motor cortex</term></item><item><term>movement</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="2009-12-03">Received</change><change when="2010-03-22">Registration</change><change when="2010-09-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E2745540F8CF8A938C861D7F0B4D14E13A85542F/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. 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normalForm="bettina.pollok@uni-duesseldorf.de">bettina.pollok@uni‐duesseldorf.de</email></contactDetails></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Katja</givenNames><familyName>Biermann‐Ruben</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Martin</givenNames><familyName>Südmeyer</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Jennifer</givenNames><familyName>Paszek</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Melanie</givenNames><familyName>Jonas</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Götz</givenNames><familyName>Thomalla</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Tobias</givenNames><familyName>Bäumer</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af3 #af4"><personName><givenNames>Michael</givenNames><familyName>Orth</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Alexander</givenNames><familyName>Münchau</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Alfons</givenNames><familyName>Schnitzler</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital Duesseldorf, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University of Ulm, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Gilles de la Tourette syndrome</keyword><keyword xml:id="kwd2">event‐related desynchronization (ERD)</keyword><keyword xml:id="kwd3">magnetoencephalography (MEG)</keyword><keyword xml:id="kwd4">motor cortex</keyword><keyword xml:id="kwd5">movement</keyword></keywordGroup><fundingInfo><fundingAgency>Deutsche Forschungsgesellschaft DFG</fundingAgency><fundingNumber>SCH592/1‐2</fundingNumber><fundingNumber>MU1692/2‐1</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In patients with Gilles de la Tourette syndrome (GTS) alterations of motor cortex (M1) excitability at rest have been evidenced. In contrast, there has so far been little research into changes of motor cortical reactivity during the time course of voluntary movements in GTS patients. The present study investigates neuromagnetic event‐related desynchronization (ERD) and event‐related synchronization (ERS) of bilateral M1 in 11 GTS patients and 11 healthy control subjects. ERD represents motor cortical activation, whereas ERS most likely indicates its inhibition. Subjects performed a self‐paced finger movement task while magnetoencephalography was used to record neuromagnetic activity. In GTS patients, ERD at beta frequency was significantly increased in the contralateral hemisphere before and during movements, whereas ERS following movement termination was increased in M1 ipsilateral. Ipsilateral ERS was inversely correlated with tic severity as determined by the Yale Global Tic Severity Rating Scale. The data of the present study support the hypothesis that during voluntary movements, motor cortical reactivity is pathologically altered in GTS patients. The observed pattern of increased activation (ERD) prior to and during movement execution followed by increased inhibition (ERS) after movement termination at beta frequency suggests abnormally increased motor cortical activation, possibly driving stronger inhibition. The stronger this inhibition is, the better symptoms appear to be controlled. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn2"><p>Potential conflict of interest: Nothing to report.</p><p>Financial disclosure: Deutsche Forschungsgemeinschaft (MU1692/1‐2; MU1692/2‐2).</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Altered pattern of motor cortical activation–inhibition during voluntary movements in Tourette syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Oscillatory Reactivity in Tourette Syndrome</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Altered pattern of motor cortical activation–inhibition during voluntary movements in Tourette syndrome</title></titleInfo><name type="personal"><namePart type="given">Stephanie</namePart><namePart type="family">Franzkowiak</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bettina</namePart><namePart type="family">Pollok</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation><description>Correspondence: Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katja</namePart><namePart type="family">Biermann‐Ruben</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin</namePart><namePart type="family">Südmeyer</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jennifer</namePart><namePart type="family">Paszek</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Melanie</namePart><namePart type="family">Jonas</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Götz</namePart><namePart type="family">Thomalla</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tobias</namePart><namePart type="family">Bäumer</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Orth</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation><affiliation>Department of Neurology, University of Ulm, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexander</namePart><namePart type="family">Münchau</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Center Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alfons</namePart><namePart type="family">Schnitzler</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Clinical Neuroscience and Medical Psychology, Heinrich‐Heine University, Duesseldorf, Germany</affiliation><affiliation>Department of Neurology, University Hospital Duesseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-09-15</dateIssued><dateCaptured encoding="w3cdtf">2009-12-03</dateCaptured><dateValid encoding="w3cdtf">2010-03-22</dateValid><copyrightDate encoding="w3cdtf">2010</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">31</extent><extent unit="words">4942</extent></physicalDescription><abstract lang="en">In patients with Gilles de la Tourette syndrome (GTS) alterations of motor cortex (M1) excitability at rest have been evidenced. In contrast, there has so far been little research into changes of motor cortical reactivity during the time course of voluntary movements in GTS patients. The present study investigates neuromagnetic event‐related desynchronization (ERD) and event‐related synchronization (ERS) of bilateral M1 in 11 GTS patients and 11 healthy control subjects. ERD represents motor cortical activation, whereas ERS most likely indicates its inhibition. Subjects performed a self‐paced finger movement task while magnetoencephalography was used to record neuromagnetic activity. In GTS patients, ERD at beta frequency was significantly increased in the contralateral hemisphere before and during movements, whereas ERS following movement termination was increased in M1 ipsilateral. Ipsilateral ERS was inversely correlated with tic severity as determined by the Yale Global Tic Severity Rating Scale. The data of the present study support the hypothesis that during voluntary movements, motor cortical reactivity is pathologically altered in GTS patients. The observed pattern of increased activation (ERD) prior to and during movement execution followed by increased inhibition (ERS) after movement termination at beta frequency suggests abnormally increased motor cortical activation, possibly driving stronger inhibition. The stronger this inhibition is, the better symptoms appear to be controlled. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report. Financial disclosure: Deutsche Forschungsgemeinschaft (MU1692/1‐2; MU1692/2‐2).</note><note type="funding">Deutsche Forschungsgesellschaft DFG - No. SCH592/1‐2; No. MU1692/2‐1; </note><subject lang="en"><genre>Keywords</genre><topic>Gilles de la Tourette syndrome</topic><topic>event‐related desynchronization (ERD)</topic><topic>magnetoencephalography (MEG)</topic><topic>motor cortex</topic><topic>movement</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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