Mental rotation of body parts and sensory temporal discrimination in fixed dystonia
Identifieur interne : 000670 ( Istex/Corpus ); précédent : 000669; suivant : 000671Mental rotation of body parts and sensory temporal discrimination in fixed dystonia
Auteurs : Petra Katschnig ; Mark J. Edwards ; Petra Schwingenschuh ; Maria Aguirregomozcorta ; Georg K Gi ; John C. Rothwell ; Kailash P. BhatiaSource :
- Movement Disorders [ 0885-3185 ] ; 2010-06-15.
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- KwdEn :
Abstract
Fixed dystonia is an uncommon but severely disabling condition typically affecting young women following a minor peripheral injury. There is no evidence of any structural lesions of the central nervous system nor any clear peripheral nerve or root damage. Electrophysiological techniques such as short intracortical inhibition, cortical silent period and a plasticity inducing protocol have revealed similarities but also differences compared to classical mobile dystonia. To further explore the pathophysiology of fixed dystonia we compared mental rotation of body parts and sensory temporal discrimination in 11 patients with fixed dystonia, 11 patients with classical mobile dystonia and 10 healthy controls. In the mental rotation task subjects were presented with realistic photos of left or right hands, feet and the head of a young women with a black patch covering the left or the right eye in six different orientations. Subjects had to verbally report the laterality of the presented stimuli. To assess sensory temporal discrimination subjects were asked to discriminate whether pairs of visual, tactile (electrical), or visuo‐tactile stimuli were simultaneous or sequential (temporal discrimination threshold) and in the latter case which stimulus preceded the other (temporal order judgement). In accordance with previous studies patients with mobile dystonia were abnormal in mental rotation and temporal discrimination, whereas patients with fixed dystonia were only impaired in mental rotation. Possible explanations for this deficit may include the influence of the abnormal body posture itself, a shared predisposing pathophysiology for mobile and fixed dystonia, or a body image disturbance. These findings add information to the developing pathophysiological picture of fixed dystonia. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23047
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ISTEX:65F3E7E331C9C071195EE30ACEFFACA01F27D8CDLe document en format XML
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There is no evidence of any structural lesions of the central nervous system nor any clear peripheral nerve or root damage. Electrophysiological techniques such as short intracortical inhibition, cortical silent period and a plasticity inducing protocol have revealed similarities but also differences compared to classical mobile dystonia. To further explore the pathophysiology of fixed dystonia we compared mental rotation of body parts and sensory temporal discrimination in 11 patients with fixed dystonia, 11 patients with classical mobile dystonia and 10 healthy controls. In the mental rotation task subjects were presented with realistic photos of left or right hands, feet and the head of a young women with a black patch covering the left or the right eye in six different orientations. Subjects had to verbally report the laterality of the presented stimuli. To assess sensory temporal discrimination subjects were asked to discriminate whether pairs of visual, tactile (electrical), or visuo‐tactile stimuli were simultaneous or sequential (temporal discrimination threshold) and in the latter case which stimulus preceded the other (temporal order judgement). In accordance with previous studies patients with mobile dystonia were abnormal in mental rotation and temporal discrimination, whereas patients with fixed dystonia were only impaired in mental rotation. Possible explanations for this deficit may include the influence of the abnormal body posture itself, a shared predisposing pathophysiology for mobile and fixed dystonia, or a body image disturbance. 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There is no evidence of any structural lesions of the central nervous system nor any clear peripheral nerve or root damage. Electrophysiological techniques such as short intracortical inhibition, cortical silent period and a plasticity inducing protocol have revealed similarities but also differences compared to classical mobile dystonia. To further explore the pathophysiology of fixed dystonia we compared mental rotation of body parts and sensory temporal discrimination in 11 patients with fixed dystonia, 11 patients with classical mobile dystonia and 10 healthy controls. In the mental rotation task subjects were presented with realistic photos of left or right hands, feet and the head of a young women with a black patch covering the left or the right eye in six different orientations. Subjects had to verbally report the laterality of the presented stimuli. To assess sensory temporal discrimination subjects were asked to discriminate whether pairs of visual, tactile (electrical), or visuo‐tactile stimuli were simultaneous or sequential (temporal discrimination threshold) and in the latter case which stimulus preceded the other (temporal order judgement). In accordance with previous studies patients with mobile dystonia were abnormal in mental rotation and temporal discrimination, whereas patients with fixed dystonia were only impaired in mental rotation. Possible explanations for this deficit may include the influence of the abnormal body posture itself, a shared predisposing pathophysiology for mobile and fixed dystonia, or a body image disturbance. 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Austria</affiliation></author><author><persName><forename type="first">Mark J.</forename><surname>Edwards</surname><roleName type="degree">PhD</roleName></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Petra</forename><surname>Schwingenschuh</surname><roleName type="degree">MD</roleName></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><affiliation>Department of Neurology, Division of Special Neurology, Medical University Graz, Austria</affiliation></author><author><persName><forename type="first">Maria</forename><surname>Aguirregomozcorta</surname><roleName type="degree">MD</roleName></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Georg</forename><surname>Kägi</surname><roleName type="degree">MD</roleName></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">John C.</forename><surname>Rothwell</surname><roleName type="degree">PhD</roleName></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Kailash P.</forename><surname>Bhatia</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square WC1N 3BG, London</p></note><affiliation>Sobell Department of Motor 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To assess sensory temporal discrimination subjects were asked to discriminate whether pairs of visual, tactile (electrical), or visuo‐tactile stimuli were simultaneous or sequential (temporal discrimination threshold) and in the latter case which stimulus preceded the other (temporal order judgement). In accordance with previous studies patients with mobile dystonia were abnormal in mental rotation and temporal discrimination, whereas patients with fixed dystonia were only impaired in mental rotation. Possible explanations for this deficit may include the influence of the abnormal body posture itself, a shared predisposing pathophysiology for mobile and fixed dystonia, or a body image disturbance. These findings add information to the developing pathophysiological picture of fixed dystonia. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>fixed dystonia</term></item><item><term>mental rotation</term></item><item><term>sensory discrimination</term></item><item><term>body schema</term></item><item><term>psychogenic</term></item><item><term>endophenotype</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="2009-11-24">Received</change><change when="2010-01-18">Registration</change><change when="2010-06-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/65F3E7E331C9C071195EE30ACEFFACA01F27D8CD/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="80"><doi origin="wiley" registered="yes">10.1002/mds.v25:8</doi><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">8</numbering></numberingGroup><coverDate startDate="2010-06-15">15 June 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="140" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23047</doi><idGroup><id type="unit" value="MDS23047"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2009-11-24"></event><event type="manuscriptRevised" date="2010-01-15"></event><event type="manuscriptAccepted" date="2010-01-18"></event><event type="firstOnline" date="2010-03-22"></event><event type="publishedOnlineFinalForm" date="2010-06-09"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-03-22"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:FullText result:FullText" date="2011-02-24"></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:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1061</numbering><numbering type="pageLast">1067</numbering></numberingGroup><correspondenceTo>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square WC1N 3BG, London</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23047.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="44"></count><count type="wordTotal" number="5227"></count></countGroup><titleGroup><title type="main" xml:lang="en">Mental rotation of body parts and sensory temporal discrimination in fixed dystonia<link href="#fn1"></link></title><title type="short" xml:lang="en">Fixed Dystonia</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Petra</givenNames><familyName>Katschnig</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Mark J.</givenNames><familyName>Edwards</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Petra</givenNames><familyName>Schwingenschuh</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Maria</givenNames><familyName>Aguirregomozcorta</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Georg</givenNames><familyName>Kägi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>John C.</givenNames><familyName>Rothwell</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Kailash P.</givenNames><familyName>Bhatia</familyName><degrees>MD</degrees></personName><contactDetails><email>k.bhatia@ion.ucl.ac.uk</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="AT" type="organization"><unparsedAffiliation>Department of Neurology, Division of Special Neurology, Medical University Graz, Austria</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">fixed dystonia</keyword><keyword xml:id="kwd2">mental rotation</keyword><keyword xml:id="kwd3">sensory discrimination</keyword><keyword xml:id="kwd4">body schema</keyword><keyword xml:id="kwd5">psychogenic</keyword><keyword xml:id="kwd6">endophenotype</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Fixed dystonia is an uncommon but severely disabling condition typically affecting young women following a minor peripheral injury. There is no evidence of any structural lesions of the central nervous system nor any clear peripheral nerve or root damage. Electrophysiological techniques such as short intracortical inhibition, cortical silent period and a plasticity inducing protocol have revealed similarities but also differences compared to classical mobile dystonia. To further explore the pathophysiology of fixed dystonia we compared mental rotation of body parts and sensory temporal discrimination in 11 patients with fixed dystonia, 11 patients with classical mobile dystonia and 10 healthy controls. In the mental rotation task subjects were presented with realistic photos of left or right hands, feet and the head of a young women with a black patch covering the left or the right eye in six different orientations. Subjects had to verbally report the laterality of the presented stimuli. To assess sensory temporal discrimination subjects were asked to discriminate whether pairs of visual, tactile (electrical), or visuo‐tactile stimuli were simultaneous or sequential (temporal discrimination threshold) and in the latter case which stimulus preceded the other (temporal order judgement). In accordance with previous studies patients with mobile dystonia were abnormal in mental rotation and temporal discrimination, whereas patients with fixed dystonia were only impaired in mental rotation. Possible explanations for this deficit may include the influence of the abnormal body posture itself, a shared predisposing pathophysiology for mobile and fixed dystonia, or a body image disturbance. These findings add information to the developing pathophysiological picture of fixed dystonia. © 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>Mental rotation of body parts and sensory temporal discrimination in fixed dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Fixed Dystonia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mental rotation of body parts and sensory temporal discrimination in fixed dystonia</title></titleInfo><name type="personal"><namePart type="given">Petra</namePart><namePart type="family">Katschnig</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><affiliation>Department of Neurology, Division of Special Neurology, Medical University Graz, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark J.</namePart><namePart type="family">Edwards</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Petra</namePart><namePart type="family">Schwingenschuh</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><affiliation>Department of Neurology, Division of Special Neurology, Medical University Graz, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maria</namePart><namePart type="family">Aguirregomozcorta</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Georg</namePart><namePart type="family">Kägi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John C.</namePart><namePart type="family">Rothwell</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kailash P.</namePart><namePart type="family">Bhatia</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square, London, United Kingdom</affiliation><description>Correspondence: Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square WC1N 3BG, London</description><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">2010-06-15</dateIssued><dateCaptured encoding="w3cdtf">2009-11-24</dateCaptured><dateValid encoding="w3cdtf">2010-01-18</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">2</extent><extent unit="tables">2</extent><extent unit="references">44</extent><extent unit="words">5227</extent></physicalDescription><abstract lang="en">Fixed dystonia is an uncommon but severely disabling condition typically affecting young women following a minor peripheral injury. There is no evidence of any structural lesions of the central nervous system nor any clear peripheral nerve or root damage. Electrophysiological techniques such as short intracortical inhibition, cortical silent period and a plasticity inducing protocol have revealed similarities but also differences compared to classical mobile dystonia. To further explore the pathophysiology of fixed dystonia we compared mental rotation of body parts and sensory temporal discrimination in 11 patients with fixed dystonia, 11 patients with classical mobile dystonia and 10 healthy controls. In the mental rotation task subjects were presented with realistic photos of left or right hands, feet and the head of a young women with a black patch covering the left or the right eye in six different orientations. Subjects had to verbally report the laterality of the presented stimuli. To assess sensory temporal discrimination subjects were asked to discriminate whether pairs of visual, tactile (electrical), or visuo‐tactile stimuli were simultaneous or sequential (temporal discrimination threshold) and in the latter case which stimulus preceded the other (temporal order judgement). In accordance with previous studies patients with mobile dystonia were abnormal in mental rotation and temporal discrimination, whereas patients with fixed dystonia were only impaired in mental rotation. Possible explanations for this deficit may include the influence of the abnormal body posture itself, a shared predisposing pathophysiology for mobile and fixed dystonia, or a body image disturbance. These findings add information to the developing pathophysiological picture of fixed dystonia. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><subject lang="en"><genre>Keywords</genre><topic>fixed dystonia</topic><topic>mental rotation</topic><topic>sensory discrimination</topic><topic>body schema</topic><topic>psychogenic</topic><topic>endophenotype</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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