Somatosensory disinhibition in dystonia
Identifieur interne : 000090 ( Istex/Corpus ); précédent : 000089; suivant : 000091Somatosensory disinhibition in dystonia
Auteurs : Emma Frasson ; Alberto Priori ; Laura Bertolasi ; Francois Mauguière ; Antonio Fiaschi ; Michele TinazziSource :
- Movement Disorders [ 0885-3185 ] ; 2001-07.
English descriptors
- KwdEn :
Abstract
Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1142
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ISTEX:E0941C5106E2E0B09507D76E8F291750C93241BELe document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-07">2001-07</date><biblScope unit="vol">16</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="674">674</biblScope><biblScope unit="page" to="682">682</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E0941C5106E2E0B09507D76E8F291750C93241BE</idno><idno type="DOI">10.1002/mds.1142</idno><idno type="ArticleID">MDS1142</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>dystonia</term><term>paired stimulation</term><term>recovery cycle</term><term>somatosensory evoked potentials</term><term>somatosensory system</term><term>upper limb SEPs</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Emma Frasson MD</name><affiliations><json:string>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</json:string></affiliations></json:item><json:item><name>Alberto Priori MD</name><affiliations><json:string>Istituto di Clinica Neurologica, Università di Milano, IRCCS Ospedale Maggiore di Milano, Italy</json:string></affiliations></json:item><json:item><name>Laura Bertolasi MD</name><affiliations><json:string>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</json:string></affiliations></json:item><json:item><name>Francois Mauguière PhD</name><affiliations><json:string>Functional Neurology and Epileptology Department, Hopital Neurologique, Lyon, France</json:string></affiliations></json:item><json:item><name>Antonio Fiaschi MD</name><affiliations><json:string>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</json:string></affiliations></json:item><json:item><name>Michele Tinazzi MD</name><affiliations><json:string>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>upper limb SEPs</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>somatosensory evoked potentials</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>somatosensory system</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>recovery cycle</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>paired stimulation</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. 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The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs.These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>upper limb SEPs</term></item><item><term>somatosensory evoked potentials</term></item><item><term>dystonia</term></item><item><term>somatosensory system</term></item><item><term>recovery cycle</term></item><item><term>paired stimulation</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="2000-05-20">Received</change><change when="2000-09-04">Registration</change><change when="2001-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E0941C5106E2E0B09507D76E8F291750C93241BE/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>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</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="40"><doi origin="wiley" registered="yes">10.1002/mds.v16:4</doi><numberingGroup><numbering type="journalVolume" number="16">16</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="2001-07">July 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="12" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.1142</doi><idGroup><id type="unit" value="MDS1142"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2001 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2000-05-20"></event><event type="manuscriptRevised" date="2000-08-26"></event><event type="manuscriptAccepted" date="2000-09-04"></event><event type="firstOnline" date="2001-07-16"></event><event type="publishedOnlineFinalForm" date="2001-07-26"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" 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">674</numbering><numbering type="pageLast">682</numbering></numberingGroup><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS1142.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="55"></count><count type="wordTotal" number="5280"></count></countGroup><titleGroup><title type="main" xml:lang="en">Somatosensory disinhibition in dystonia</title><title type="short" xml:lang="en">Paired Stimulation SEPS in Dystonia</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Emma</givenNames><familyName>Frasson</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Alberto</givenNames><familyName>Priori</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Laura</givenNames><familyName>Bertolasi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Francois</givenNames><familyName>Mauguière</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Antonio</givenNames><familyName>Fiaschi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michele</givenNames><familyName>Tinazzi</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IT" type="organization"><unparsedAffiliation>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IT" type="organization"><unparsedAffiliation>Istituto di Clinica Neurologica, Università di Milano, IRCCS Ospedale Maggiore di Milano, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Functional Neurology and Epileptology Department, Hopital Neurologique, Lyon, France</unparsedAffiliation></affiliation><affiliation xml:id="corr1" countryCode="IT"><unparsedAffiliation>Dipartimento di Scienze Neurologiche e della Visione, Sez. di Neurologia Riabilitativa, via delle Menegone 6, 37134 Verona, Italy.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">upper limb SEPs</keyword><keyword xml:id="kwd2">somatosensory evoked potentials</keyword><keyword xml:id="kwd3">dystonia</keyword><keyword xml:id="kwd4">somatosensory system</keyword><keyword xml:id="kwd5">recovery cycle</keyword><keyword xml:id="kwd6">paired stimulation</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs.</p><p>These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society.</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>Somatosensory disinhibition in dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Paired Stimulation SEPS in Dystonia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Somatosensory disinhibition in dystonia</title></titleInfo><name type="personal"><namePart type="given">Emma</namePart><namePart type="family">Frasson</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alberto</namePart><namePart type="family">Priori</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Istituto di Clinica Neurologica, Università di Milano, IRCCS Ospedale Maggiore di Milano, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laura</namePart><namePart type="family">Bertolasi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francois</namePart><namePart type="family">Mauguière</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Functional Neurology and Epileptology Department, Hopital Neurologique, Lyon, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Antonio</namePart><namePart type="family">Fiaschi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michele</namePart><namePart type="family">Tinazzi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2001-07</dateIssued><dateCaptured encoding="w3cdtf">2000-05-20</dateCaptured><dateValid encoding="w3cdtf">2000-09-04</dateValid><copyrightDate encoding="w3cdtf">2001</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">2</extent><extent unit="references">55</extent><extent unit="words">5280</extent></physicalDescription><abstract lang="en">Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society.</abstract><subject lang="en"><genre>Keywords</genre><topic>upper limb SEPs</topic><topic>somatosensory evoked potentials</topic><topic>dystonia</topic><topic>somatosensory system</topic><topic>recovery cycle</topic><topic>paired stimulation</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>2001</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>674</start><end>682</end><total>9</total></extent></part></relatedItem><identifier type="istex">E0941C5106E2E0B09507D76E8F291750C93241BE</identifier><identifier type="DOI">10.1002/mds.1142</identifier><identifier type="ArticleID">MDS1142</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>John Wiley & Sons, Inc.</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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