Sensory disinhibition on passive movement in cervical dystonia
Identifieur interne : 001348 ( Istex/Corpus ); précédent : 001347; suivant : 001349Sensory disinhibition on passive movement in cervical dystonia
Auteurs : Mark Obermann ; Clemens Vollrath ; Armin De Greiff ; Elke R. Gizewski ; Hans-Christoph Diener ; Mark Hallett ; Matthias MaschkeSource :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
English descriptors
Abstract
The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23321
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ISTEX:47AD29344CA431C77320B05B89F3312534E4BEFELe document en format XML
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Gizewski</name><affiliation><mods:affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Diener, Hans Hristoph" sort="Diener, Hans Hristoph" uniqKey="Diener H" first="Hans-Christoph" last="Diener">Hans-Christoph Diener</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hallett, Mark" sort="Hallett, Mark" uniqKey="Hallett M" first="Mark" last="Hallett">Mark Hallett</name><affiliation><mods:affiliation>Human Motor Control Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA</mods:affiliation></affiliation></author><author><name sortKey="Maschke, Matthias" sort="Maschke, Matthias" uniqKey="Maschke M" first="Matthias" last="Maschke">Matthias Maschke</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, 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="2010-11-15">2010-11-15</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2627">2627</biblScope><biblScope unit="page" to="2633">2633</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">47AD29344CA431C77320B05B89F3312534E4BEFE</idno><idno type="DOI">10.1002/mds.23321</idno><idno type="ArticleID">MDS23321</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>cervical dystonia</term><term>cortical disinhibition</term><term>fMRI</term><term>focal dystonia</term><term>somatosensory system</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Mark Obermann MD</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Germany</json:string></affiliations></json:item><json:item><name>Clemens Vollrath MD</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Germany</json:string></affiliations></json:item><json:item><name>Armin de Greiff MD</name><affiliations><json:string>Department of Neuroradiology, University of Duisburg‐Essen, Germany</json:string></affiliations></json:item><json:item><name>Elke R. Gizewski MD</name><affiliations><json:string>Department of Neuroradiology, University of Duisburg‐Essen, Germany</json:string></affiliations></json:item><json:item><name>Hans‐Christoph Diener MD</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Germany</json:string></affiliations></json:item><json:item><name>Mark Hallett MD</name><affiliations><json:string>Human Motor Control Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Matthias Maschke MD</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Germany</json:string><json:string>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>focal dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cervical dystonia</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>cortical disinhibition</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>somatosensory system</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>6.356</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1301</abstractCharCount><pdfWordCount>4016</pdfWordCount><pdfCharCount>26693</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>195</abstractWordCount></qualityIndicators><title>Sensory disinhibition on passive movement in cervical dystonia</title><genre><json:string>Serial article</json:string></genre><host><volume>25</volume><pages><total>7</total><last>2633</last><first>2627</first></pages><issn><json:string>0885-3185</json:string></issn><issue>15</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.23321</json:string></doi><id>47AD29344CA431C77320B05B89F3312534E4BEFE</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/47AD29344CA431C77320B05B89F3312534E4BEFE/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/47AD29344CA431C77320B05B89F3312534E4BEFE/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/47AD29344CA431C77320B05B89F3312534E4BEFE/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Sensory disinhibition on passive movement in cervical dystonia</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.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Sensory disinhibition on passive movement in cervical dystonia</title><author><persName><forename type="first">Mark</forename><surname>Obermann</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, University of Duisburg‐Essen, Hufelandstr. 55, 45122 Essen, Germany</p></note><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation></author><author><persName><forename type="first">Clemens</forename><surname>Vollrath</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation></author><author><persName><forename type="first">Armin</forename><surname>de Greiff</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Germany</affiliation></author><author><persName><forename type="first">Elke R.</forename><surname>Gizewski</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Germany</affiliation></author><author><persName><forename type="first">Hans‐Christoph</forename><surname>Diener</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation></author><author><persName><forename type="first">Mark</forename><surname>Hallett</surname><roleName type="degree">MD</roleName></persName><affiliation>Human Motor Control Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA</affiliation></author><author><persName><forename type="first">Matthias</forename><surname>Maschke</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation><affiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, 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="2010-11-15"></date><biblScope unit="vol">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2627">2627</biblScope><biblScope unit="page" to="2633">2633</biblScope></imprint></monogr><idno type="istex">47AD29344CA431C77320B05B89F3312534E4BEFE</idno><idno type="DOI">10.1002/mds.23321</idno><idno type="ArticleID">MDS23321</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>focal dystonia</term></item><item><term>cervical dystonia</term></item><item><term>fMRI</term></item><item><term>cortical disinhibition</term></item><item><term>somatosensory system</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="2010-01-04">Received</change><change when="2010-06-02">Registration</change><change when="2010-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/47AD29344CA431C77320B05B89F3312534E4BEFE/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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href="file:MDS.MDS23321.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="4898"></count></countGroup><titleGroup><title type="main" xml:lang="en">Sensory disinhibition on passive movement in cervical dystonia<link href="#fn1"></link></title><title type="short" xml:lang="en">Sensory Disinhibition on Passive Movement</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Mark</givenNames><familyName>Obermann</familyName><degrees>MD</degrees></personName><contactDetails><email normalForm="mark.obermann@uni-due.de">mark.obermann@uni‐due.de</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Clemens</givenNames><familyName>Vollrath</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Armin</givenNames><familyName>de Greiff</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Elke R.</givenNames><familyName>Gizewski</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hans‐Christoph</givenNames><familyName>Diener</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Mark</givenNames><familyName>Hallett</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af4"><personName><givenNames>Matthias</givenNames><familyName>Maschke</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University of Duisburg‐Essen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neuroradiology, University of Duisburg‐Essen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Human Motor Control Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">focal dystonia</keyword><keyword xml:id="kwd2">cervical dystonia</keyword><keyword xml:id="kwd3">fMRI</keyword><keyword xml:id="kwd4">cortical disinhibition</keyword><keyword xml:id="kwd5">somatosensory system</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Sensory disinhibition on passive movement in cervical dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Sensory Disinhibition on Passive Movement</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Sensory disinhibition on passive movement in cervical dystonia</title></titleInfo><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Obermann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation><description>Correspondence: Department of Neurology, University of Duisburg‐Essen, Hufelandstr. 55, 45122 Essen, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Clemens</namePart><namePart type="family">Vollrath</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Armin</namePart><namePart type="family">de Greiff</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elke R.</namePart><namePart type="family">Gizewski</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hans‐Christoph</namePart><namePart type="family">Diener</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Hallett</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Human Motor Control Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matthias</namePart><namePart type="family">Maschke</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation><affiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, 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">2010-11-15</dateIssued><dateCaptured encoding="w3cdtf">2010-01-04</dateCaptured><dateValid encoding="w3cdtf">2010-06-02</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">3</extent><extent unit="tables">3</extent><extent unit="references">33</extent><extent unit="words">4898</extent></physicalDescription><abstract lang="en">The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><subject lang="en"><genre>Keywords</genre><topic>focal dystonia</topic><topic>cervical dystonia</topic><topic>fMRI</topic><topic>cortical disinhibition</topic><topic>somatosensory system</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><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>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2627</start><end>2633</end><total>7</total></extent></part></relatedItem><identifier type="istex">47AD29344CA431C77320B05B89F3312534E4BEFE</identifier><identifier type="DOI">10.1002/mds.23321</identifier><identifier type="ArticleID">MDS23321</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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