A motor cortex excitability and gait analysis on Parkinsonian patients
Identifieur interne : 000317 ( Istex/Corpus ); précédent : 000316; suivant : 000318A motor cortex excitability and gait analysis on Parkinsonian patients
Auteurs : François Vacherot ; Shahram Attarian ; Marianne Vaugoyeau ; Jean-Philippe AzulaySource :
- Movement Disorders [ 0885-3185 ] ; 2010-12-15.
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Abstract
Transcranial magnetic stimulation (TMS) parameters were recorded in a lower limb muscle and correlated with the gait parameters of 25 patients with Parkinson's disease (PD) with and without dopamine substitution treatment (DST) and 10 control subjects. Single and paired‐pulse TMS were recorded in the tibialis anterior muscle (TA). Gait analysis was performed using a 3D motion analysis system. Parkinsonian patients (PP) did not differ from the control subjects (CS) in terms of relaxed motor threshold, active motor threshold (AMT), cortical silent period (CSP), motor‐evoked potential (MEP) amplitude and area, or paired‐pulse TMS with short interstimulus intervals (ISI). At longer ISIs, paired‐pulse TMS showed that the amplitudes of the conditioned MEPs were lower in untreated PP than in CS. DST partially compensated for this difference. Gait analysis showed that the gait of PP undergoing no treatment was slower and the stride length shorter than normal. Both of these parameters improved under DST, however. Analysis of data obtained on all the subjects combined showed that both of the latter parameters were correlated with the paired‐pulse MEP amplitude and area at longer ISIs. In PP, the cortical areas responsible for the lower limb movements seem to undergo intracortical facilitation (ICF) impairments, whereas the intracortical inhibition process is normal. The ICF level was found to be associated to the stride length and the velocity. The fact that only these two gait parameters were found to be dopa responsive indicates that dopaminergic treatment may improve gait disorders by restoring the ICF. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23378
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Single and paired‐pulse TMS were recorded in the tibialis anterior muscle (TA). Gait analysis was performed using a 3D motion analysis system. Parkinsonian patients (PP) did not differ from the control subjects (CS) in terms of relaxed motor threshold, active motor threshold (AMT), cortical silent period (CSP), motor‐evoked potential (MEP) amplitude and area, or paired‐pulse TMS with short interstimulus intervals (ISI). At longer ISIs, paired‐pulse TMS showed that the amplitudes of the conditioned MEPs were lower in untreated PP than in CS. DST partially compensated for this difference. Gait analysis showed that the gait of PP undergoing no treatment was slower and the stride length shorter than normal. Both of these parameters improved under DST, however. Analysis of data obtained on all the subjects combined showed that both of the latter parameters were correlated with the paired‐pulse MEP amplitude and area at longer ISIs. In PP, the cortical areas responsible for the lower limb movements seem to undergo intracortical facilitation (ICF) impairments, whereas the intracortical inhibition process is normal. The ICF level was found to be associated to the stride length and the velocity. The fact that only these two gait parameters were found to be dopa responsive indicates that dopaminergic treatment may improve gait disorders by restoring the ICF. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>François Vacherot PhD</name><affiliations><json:string>CNRS, UMR 6149, Pôle 3C, Equipe “Développement et Pathologie de l'Action” Université de Provence & CNRS, Centre Saint Charles, Marseille, France</json:string><json:string>Department of Clinical Neuroscience, La Timone Hospital, Marseille, France</json:string></affiliations></json:item><json:item><name>Shahram Attarian MD</name><affiliations><json:string>Department of Clinical Neuroscience, La Timone Hospital, Marseille, France</json:string></affiliations></json:item><json:item><name>Marianne Vaugoyeau MD</name><affiliations><json:string>CNRS, UMR 6149, Pôle 3C, Equipe “Développement et Pathologie de l'Action” Université de Provence & CNRS, Centre Saint Charles, Marseille, France</json:string></affiliations></json:item><json:item><name>Jean‐Philippe Azulay PR</name><affiliations><json:string>CNRS, UMR 6149, Pôle 3C, Equipe “Développement et Pathologie de l'Action” Université de Provence & CNRS, Centre Saint Charles, Marseille, France</json:string><json:string>Department of Clinical Neuroscience, La Timone Hospital, Marseille, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>transcranial magnetic stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gait analysis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>stride length</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Transcranial magnetic stimulation (TMS) parameters were recorded in a lower limb muscle and correlated with the gait parameters of 25 patients with Parkinson's disease (PD) with and without dopamine substitution treatment (DST) and 10 control subjects. 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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="2010-12-15"></date><biblScope unit="vol">25</biblScope><biblScope unit="issue">16</biblScope><biblScope unit="page" from="2747">2747</biblScope><biblScope unit="page" to="2755">2755</biblScope></imprint></monogr><idno type="istex">59A049396C41983AA1CFD7EEC754810480B9CE6C</idno><idno type="DOI">10.1002/mds.23378</idno><idno type="ArticleID">MDS23378</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Transcranial magnetic stimulation (TMS) parameters were recorded in a lower limb muscle and correlated with the gait parameters of 25 patients with Parkinson's disease (PD) with and without dopamine substitution treatment (DST) and 10 control subjects. Single and paired‐pulse TMS were recorded in the tibialis anterior muscle (TA). Gait analysis was performed using a 3D motion analysis system. Parkinsonian patients (PP) did not differ from the control subjects (CS) in terms of relaxed motor threshold, active motor threshold (AMT), cortical silent period (CSP), motor‐evoked potential (MEP) amplitude and area, or paired‐pulse TMS with short interstimulus intervals (ISI). At longer ISIs, paired‐pulse TMS showed that the amplitudes of the conditioned MEPs were lower in untreated PP than in CS. DST partially compensated for this difference. Gait analysis showed that the gait of PP undergoing no treatment was slower and the stride length shorter than normal. Both of these parameters improved under DST, however. Analysis of data obtained on all the subjects combined showed that both of the latter parameters were correlated with the paired‐pulse MEP amplitude and area at longer ISIs. In PP, the cortical areas responsible for the lower limb movements seem to undergo intracortical facilitation (ICF) impairments, whereas the intracortical inhibition process is normal. The ICF level was found to be associated to the stride length and the velocity. The fact that only these two gait parameters were found to be dopa responsive indicates that dopaminergic treatment may improve gait disorders by restoring the ICF. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>transcranial magnetic stimulation</term></item><item><term>Parkinson's disease</term></item><item><term>gait analysis</term></item><item><term>stride length</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="2010-03-25">Received</change><change when="2010-07-04">Registration</change><change when="2010-12-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/59A049396C41983AA1CFD7EEC754810480B9CE6C/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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Single and paired‐pulse TMS were recorded in the tibialis anterior muscle (TA). Gait analysis was performed using a 3D motion analysis system. Parkinsonian patients (PP) did not differ from the control subjects (CS) in terms of relaxed motor threshold, active motor threshold (AMT), cortical silent period (CSP), motor‐evoked potential (MEP) amplitude and area, or paired‐pulse TMS with short interstimulus intervals (ISI). At longer ISIs, paired‐pulse TMS showed that the amplitudes of the conditioned MEPs were lower in untreated PP than in CS. DST partially compensated for this difference. Gait analysis showed that the gait of PP undergoing no treatment was slower and the stride length shorter than normal. Both of these parameters improved under DST, however. Analysis of data obtained on all the subjects combined showed that both of the latter parameters were correlated with the paired‐pulse MEP amplitude and area at longer ISIs. In PP, the cortical areas responsible for the lower limb movements seem to undergo intracortical facilitation (ICF) impairments, whereas the intracortical inhibition process is normal. The ICF level was found to be associated to the stride length and the velocity. The fact that only these two gait parameters were found to be dopa responsive indicates that dopaminergic treatment may improve gait disorders by restoring the ICF. © 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>A motor cortex excitability and gait analysis on Parkinsonian patients</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Motor Cortex Excitability and Gait Analysis</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>A motor cortex excitability and gait analysis on Parkinsonian patients</title></titleInfo><name type="personal"><namePart type="given">François</namePart><namePart type="family">Vacherot</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>CNRS, UMR 6149, Pôle 3C, Equipe “Développement et Pathologie de l'Action” Université de Provence & CNRS, Centre Saint Charles, Marseille, France</affiliation><affiliation>Department of Clinical Neuroscience, La Timone Hospital, Marseille, France</affiliation><description>Correspondence: François Vacherot, CNRS, UMR 6149, Pôle 3C, Equipe “Développement et Pathologie de l'Action” Université de Provence & CNRS, Centre Saint Charles, Case B 3, Place Victor Hugo 13331, Marseille cedex 03, France</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shahram</namePart><namePart type="family">Attarian</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neuroscience, La Timone Hospital, Marseille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marianne</namePart><namePart type="family">Vaugoyeau</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>CNRS, UMR 6149, Pôle 3C, Equipe “Développement et Pathologie de l'Action” Université de Provence & CNRS, Centre Saint Charles, Marseille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Philippe</namePart><namePart type="family">Azulay</namePart><namePart type="termsOfAddress">PR</namePart><affiliation>CNRS, UMR 6149, Pôle 3C, Equipe “Développement et Pathologie de l'Action” Université de Provence & CNRS, Centre Saint Charles, Marseille, France</affiliation><affiliation>Department of Clinical Neuroscience, La Timone Hospital, Marseille, France</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">2010-12-15</dateIssued><dateCaptured encoding="w3cdtf">2010-03-25</dateCaptured><dateValid encoding="w3cdtf">2010-07-04</dateValid><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="tables">1</extent><extent unit="references">62</extent><extent unit="words">6036</extent></physicalDescription><abstract lang="en">Transcranial magnetic stimulation (TMS) parameters were recorded in a lower limb muscle and correlated with the gait parameters of 25 patients with Parkinson's disease (PD) with and without dopamine substitution treatment (DST) and 10 control subjects. Single and paired‐pulse TMS were recorded in the tibialis anterior muscle (TA). Gait analysis was performed using a 3D motion analysis system. Parkinsonian patients (PP) did not differ from the control subjects (CS) in terms of relaxed motor threshold, active motor threshold (AMT), cortical silent period (CSP), motor‐evoked potential (MEP) amplitude and area, or paired‐pulse TMS with short interstimulus intervals (ISI). At longer ISIs, paired‐pulse TMS showed that the amplitudes of the conditioned MEPs were lower in untreated PP than in CS. DST partially compensated for this difference. Gait analysis showed that the gait of PP undergoing no treatment was slower and the stride length shorter than normal. Both of these parameters improved under DST, however. Analysis of data obtained on all the subjects combined showed that both of the latter parameters were correlated with the paired‐pulse MEP amplitude and area at longer ISIs. In PP, the cortical areas responsible for the lower limb movements seem to undergo intracortical facilitation (ICF) impairments, whereas the intracortical inhibition process is normal. The ICF level was found to be associated to the stride length and the velocity. The fact that only these two gait parameters were found to be dopa responsive indicates that dopaminergic treatment may improve gait disorders by restoring the ICF. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><note type="funding">France Parkinson</note><subject lang="en"><genre>Keywords</genre><topic>transcranial magnetic stimulation</topic><topic>Parkinson's disease</topic><topic>gait analysis</topic><topic>stride length</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>16</number></detail><extent unit="pages"><start>2747</start><end>2755</end><total>9</total></extent></part></relatedItem><identifier type="istex">59A049396C41983AA1CFD7EEC754810480B9CE6C</identifier><identifier type="DOI">10.1002/mds.23378</identifier><identifier type="ArticleID">MDS23378</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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