Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation
Identifieur interne : 000908 ( Istex/Corpus ); précédent : 000907; suivant : 000909Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation
Auteurs : Ikeda ; Hiroshi Shibasaki ; Ryuji Kaji ; Kiyohito Terada ; Takashi Nagamine ; Manabu Honda ; Toshiaki Hamano ; Jun KimuraSource :
- Movement Disorders [ 0885-3185 ] ; 1996-11.
English descriptors
Abstract
To investigate the pathophysiology of idiopathic focal dystonia, we recorded contingent negative variation (CNV) as a physiological index of sensorimotor intergration in 14 right‐handed patients with writer's cramp and compared it with normative data. CNV was recorded in the S2 choice reaction time paradigm: Two kinds of auditory S2 (Go or No‐Go) were given 2 s after the auditory S1, and the subject reacted only to the Go signal by extending the wrist. In normal subjects, the late CNV amplitude had no difference at Cz between left‐and right‐hand tasks and was symmetric without significant amplitude laterality irrespective of the side of hand movement. In patients with writer's cramp, the late CNV amplitude at Cz was relatively larger for the left‐hand task than the right‐hand task (p<0.03), and a significant amplitude laterality of the late CNV (larger on the right) was present especially at the central area for the right‐hand task (p<0.03). Since the late CNV is known to be generated, at least inpart, from primary and supplementary motor cortices, the significant laterality of the late CNV seen with the right‐hand task in patients with writer's cramp might represent functional abnormality of motor cortices possibly as the result of basal ganglia function.
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DOI: 10.1002/mds.870110614
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ISTEX:194DC9392AF41D54ACBAEAFC20E1C436282C4949Le document en format XML
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Japan</mods:affiliation></affiliation></author><author><name sortKey="Terada, Kiyohito" sort="Terada, Kiyohito" uniqKey="Terada K" first="Kiyohito" last="Terada">Kiyohito Terada</name><affiliation><mods:affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nagamine, Takashi" sort="Nagamine, Takashi" uniqKey="Nagamine T" first="Takashi" last="Nagamine">Takashi Nagamine</name><affiliation><mods:affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Honda, Manabu" sort="Honda, Manabu" uniqKey="Honda M" first="Manabu" last="Honda">Manabu Honda</name><affiliation><mods:affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hamano, Toshiaki" sort="Hamano, Toshiaki" 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Terada</name><affiliation><mods:affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nagamine, Takashi" sort="Nagamine, Takashi" uniqKey="Nagamine T" first="Takashi" last="Nagamine">Takashi Nagamine</name><affiliation><mods:affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Honda, Manabu" sort="Honda, Manabu" uniqKey="Honda M" first="Manabu" last="Honda">Manabu Honda</name><affiliation><mods:affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hamano, Toshiaki" sort="Hamano, Toshiaki" uniqKey="Hamano T" first="Toshiaki" last="Hamano">Toshiaki Hamano</name><affiliation><mods:affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kimura, Jun" sort="Kimura, Jun" uniqKey="Kimura J" first="Jun" last="Kimura">Jun Kimura</name><affiliation><mods:affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="1996-11">1996-11</date><biblScope unit="vol">11</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="683">683</biblScope><biblScope unit="page" to="690">690</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">194DC9392AF41D54ACBAEAFC20E1C436282C4949</idno><idno type="DOI">10.1002/mds.870110614</idno><idno type="ArticleID">MDS870110614</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Contingent negative variation</term><term>Idiopathic focal dystonia</term><term>Writer's cramp</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To investigate the pathophysiology of idiopathic focal dystonia, we recorded contingent negative variation (CNV) as a physiological index of sensorimotor intergration in 14 right‐handed patients with writer's cramp and compared it with normative data. CNV was recorded in the S2 choice reaction time paradigm: Two kinds of auditory S2 (Go or No‐Go) were given 2 s after the auditory S1, and the subject reacted only to the Go signal by extending the wrist. In normal subjects, the late CNV amplitude had no difference at Cz between left‐and right‐hand tasks and was symmetric without significant amplitude laterality irrespective of the side of hand movement. In patients with writer's cramp, the late CNV amplitude at Cz was relatively larger for the left‐hand task than the right‐hand task (p<0.03), and a significant amplitude laterality of the late CNV (larger on the right) was present especially at the central area for the right‐hand task (p<0.03). Since the late CNV is known to be generated, at least inpart, from primary and supplementary motor cortices, the significant laterality of the late CNV seen with the right‐hand task in patients with writer's cramp might represent functional abnormality of motor cortices possibly as the result of basal ganglia function.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Ikeda</name><affiliations><json:string>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Hiroshi Shibasaki</name><affiliations><json:string>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Ryuji Kaji</name><affiliations><json:string>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Kiyohito Terada</name><affiliations><json:string>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Takashi Nagamine</name><affiliations><json:string>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Manabu Honda</name><affiliations><json:string>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Toshiaki Hamano</name><affiliations><json:string>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Jun Kimura</name><affiliations><json:string>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Writer's cramp</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Idiopathic focal dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Contingent negative variation</value></json:item></subject><language><json:string>eng</json:string></language><abstract>To investigate the pathophysiology of idiopathic focal dystonia, we recorded contingent negative variation (CNV) as a physiological index of sensorimotor intergration in 14 right‐handed patients with writer's cramp and compared it with normative data. CNV was recorded in the S2 choice reaction time paradigm: Two kinds of auditory S2 (Go or No‐Go) were given 2 s after the auditory S1, and the subject reacted only to the Go signal by extending the wrist. In normal subjects, the late CNV amplitude had no difference at Cz between left‐and right‐hand tasks and was symmetric without significant amplitude laterality irrespective of the side of hand movement. In patients with writer's cramp, the late CNV amplitude at Cz was relatively larger for the left‐hand task than the right‐hand task (p>0.03), and a significant amplitude laterality of the late CNV (larger on the right) was present especially at the central area for the right‐hand task (p>0.03). Since the late CNV is known to be generated, at least inpart, from primary and supplementary motor cortices, the significant laterality of the late CNV seen with the right‐hand task in patients with writer's cramp might represent functional abnormality of motor cortices possibly as the result of basal ganglia function.</abstract><qualityIndicators><score>7.125</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1276</abstractCharCount><pdfWordCount>4713</pdfWordCount><pdfCharCount>28773</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>201</abstractWordCount></qualityIndicators><title>Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation</title><genre><json:string>Serial article</json:string></genre><host><volume>11</volume><pages><total>8</total><last>690</last><first>683</first></pages><issn><json:string>0885-3185</json:string></issn><issue>6</issue><subject><json:item><value>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>1996</publicationDate><copyrightDate>1996</copyrightDate><doi><json:string>10.1002/mds.870110614</json:string></doi><id>194DC9392AF41D54ACBAEAFC20E1C436282C4949</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/194DC9392AF41D54ACBAEAFC20E1C436282C4949/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/194DC9392AF41D54ACBAEAFC20E1C436282C4949/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/194DC9392AF41D54ACBAEAFC20E1C436282C4949/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation</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>1996</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation</title><author><persName><surname>Ikeda</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Brain Pathophysiology, Kyoto University School of Medicine, Shogoin, Sakyo‐ku, Kyoto, 606, Japan</p></note><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Hiroshi</forename><surname>Shibasaki</surname></persName><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Ryuji</forename><surname>Kaji</surname></persName><affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Kiyohito</forename><surname>Terada</surname></persName><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Takashi</forename><surname>Nagamine</surname></persName><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Manabu</forename><surname>Honda</surname></persName><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Toshiaki</forename><surname>Hamano</surname></persName><affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Jun</forename><surname>Kimura</surname></persName><affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="1996-11"></date><biblScope unit="vol">11</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="683">683</biblScope><biblScope unit="page" to="690">690</biblScope></imprint></monogr><idno type="istex">194DC9392AF41D54ACBAEAFC20E1C436282C4949</idno><idno type="DOI">10.1002/mds.870110614</idno><idno type="ArticleID">MDS870110614</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>To investigate the pathophysiology of idiopathic focal dystonia, we recorded contingent negative variation (CNV) as a physiological index of sensorimotor intergration in 14 right‐handed patients with writer's cramp and compared it with normative data. CNV was recorded in the S2 choice reaction time paradigm: Two kinds of auditory S2 (Go or No‐Go) were given 2 s after the auditory S1, and the subject reacted only to the Go signal by extending the wrist. In normal subjects, the late CNV amplitude had no difference at Cz between left‐and right‐hand tasks and was symmetric without significant amplitude laterality irrespective of the side of hand movement. In patients with writer's cramp, the late CNV amplitude at Cz was relatively larger for the left‐hand task than the right‐hand task (p<0.03), and a significant amplitude laterality of the late CNV (larger on the right) was present especially at the central area for the right‐hand task (p<0.03). Since the late CNV is known to be generated, at least inpart, from primary and supplementary motor cortices, the significant laterality of the late CNV seen with the right‐hand task in patients with writer's cramp might represent functional abnormality of motor cortices possibly as the result of basal ganglia function.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Writer's cramp</term></item><item><term>Idiopathic focal dystonia</term></item><item><term>Contingent negative variation</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-06-20">Received</change><change when="1996-02-19">Registration</change><change when="1996-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/194DC9392AF41D54ACBAEAFC20E1C436282C4949/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="60"><doi origin="wiley" registered="yes">10.1002/mds.v11:6</doi><numberingGroup><numbering type="journalVolume" number="11">11</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="1996-11">November 1996</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="14" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870110614</doi><idGroup><id type="unit" value="MDS870110614"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1996 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1995-06-20"></event><event type="manuscriptRevised" date="1996-01-22"></event><event type="manuscriptAccepted" date="1996-02-19"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></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:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">683</numbering><numbering type="pageLast">690</numbering></numberingGroup><correspondenceTo>Department of Brain Pathophysiology, Kyoto University School of Medicine, Shogoin, Sakyo‐ku, Kyoto, 606, Japan</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870110614.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="43"></count></countGroup><titleGroup><title type="main" xml:lang="en">Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation</title><title type="short" xml:lang="en">CNV IN WRITER'S CRAMP</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Akio</givenNames><familyName>Ikeda</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hiroshi</givenNames><familyName>Shibasaki</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Ryuji</givenNames><familyName>Kaji</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Kiyohito</givenNames><familyName>Terada</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Takashi</givenNames><familyName>Nagamine</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Manabu</givenNames><familyName>Honda</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Toshiaki</givenNames><familyName>Hamano</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Jun</givenNames><familyName>Kimura</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="JP" type="organization"><unparsedAffiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Writer's cramp</keyword><keyword xml:id="kwd2">Idiopathic focal dystonia</keyword><keyword xml:id="kwd3">Contingent negative variation</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To investigate the pathophysiology of idiopathic focal dystonia, we recorded contingent negative variation (CNV) as a physiological index of sensorimotor intergration in 14 right‐handed patients with writer's cramp and compared it with normative data. CNV was recorded in the S2 choice reaction time paradigm: Two kinds of auditory S2 (Go or No‐Go) were given 2 s after the auditory S1, and the subject reacted only to the Go signal by extending the wrist. In normal subjects, the late CNV amplitude had no difference at Cz between left‐and right‐hand tasks and was symmetric without significant amplitude laterality irrespective of the side of hand movement. In patients with writer's cramp, the late CNV amplitude at Cz was relatively larger for the left‐hand task than the right‐hand task (p<0.03), and a significant amplitude laterality of the late CNV (larger on the right) was present especially at the central area for the right‐hand task (p<0.03). Since the late CNV is known to be generated, at least inpart, from primary and supplementary motor cortices, the significant laterality of the late CNV seen with the right‐hand task in patients with writer's cramp might represent functional abnormality of motor cortices possibly as the result of basal ganglia function.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CNV IN WRITER'S CRAMP</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Abnormal sensorimotor integration in writer's cramp: Study of contingent negative variation</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Ikeda</namePart><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation><description>Correspondence: Department of Brain Pathophysiology, Kyoto University School of Medicine, Shogoin, Sakyo‐ku, Kyoto, 606, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroshi</namePart><namePart type="family">Shibasaki</namePart><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ryuji</namePart><namePart type="family">Kaji</namePart><affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kiyohito</namePart><namePart type="family">Terada</namePart><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Nagamine</namePart><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Manabu</namePart><namePart type="family">Honda</namePart><affiliation>Department of Brain Pathophysiology, Kyoto University School of Medicine, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Toshiaki</namePart><namePart type="family">Hamano</namePart><affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jun</namePart><namePart type="family">Kimura</namePart><affiliation>Department of Neurology, Kyoto University School of Medicine, Kyoto, Japan</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">1996-11</dateIssued><dateCaptured encoding="w3cdtf">1995-06-20</dateCaptured><dateValid encoding="w3cdtf">1996-02-19</dateValid><copyrightDate encoding="w3cdtf">1996</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">43</extent></physicalDescription><abstract lang="en">To investigate the pathophysiology of idiopathic focal dystonia, we recorded contingent negative variation (CNV) as a physiological index of sensorimotor intergration in 14 right‐handed patients with writer's cramp and compared it with normative data. CNV was recorded in the S2 choice reaction time paradigm: Two kinds of auditory S2 (Go or No‐Go) were given 2 s after the auditory S1, and the subject reacted only to the Go signal by extending the wrist. In normal subjects, the late CNV amplitude had no difference at Cz between left‐and right‐hand tasks and was symmetric without significant amplitude laterality irrespective of the side of hand movement. In patients with writer's cramp, the late CNV amplitude at Cz was relatively larger for the left‐hand task than the right‐hand task (p<0.03), and a significant amplitude laterality of the late CNV (larger on the right) was present especially at the central area for the right‐hand task (p<0.03). Since the late CNV is known to be generated, at least inpart, from primary and supplementary motor cortices, the significant laterality of the late CNV seen with the right‐hand task in patients with writer's cramp might represent functional abnormality of motor cortices possibly as the result of basal ganglia function.</abstract><subject lang="en"><genre>Keywords</genre><topic>Writer's cramp</topic><topic>Idiopathic focal dystonia</topic><topic>Contingent negative variation</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>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>1996</date><detail type="volume"><caption>vol.</caption><number>11</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>683</start><end>690</end><total>8</total></extent></part></relatedItem><identifier type="istex">194DC9392AF41D54ACBAEAFC20E1C436282C4949</identifier><identifier type="DOI">10.1002/mds.870110614</identifier><identifier type="ArticleID">MDS870110614</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1996 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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