Restoration of motor inhibition through an abnormal premotor‐motor connection in dystonia
Identifieur interne : 000975 ( Istex/Corpus ); précédent : 000974; suivant : 000976Restoration of motor inhibition through an abnormal premotor‐motor connection in dystonia
Auteurs : Ying-Zu Huang ; John C. Rothwell ; Chin-Song Lu ; Jiunjie Wang ; Rou-Shayn ChenSource :
- Movement Disorders [ 0885-3185 ] ; 2010-04-30.
English descriptors
- KwdEn :
- Premotor, TBS, dystonia, rTMS, theta burst.
Abstract
To clarify the rationale for using rTMS of dorsal premotor cortex (PMd) to treat dystonia, we examined how the motor system reacts to an inhibitory form of rTMS applied to the PMd in healthy subjects and in a group of patients with focal hand dystonia and DYT1 gene carriers. Continuous theta burst transcranial magnetic stimulation (cTBS) with 300 and 600 pulses (cTBS300 and cTBS600) was applied to PMd, and its after‐effects were quantified by measuring the amplitude of MEPs evoked by single pulse transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), short interval intracortical inhibition/facilitation (SICI/ICF) within M1, the third phase of spinal reciprocal inhibition (RI), and writing tests. In addition, in DYT1 gene carriers, the effects of cTBS300 over M1 and PMd on MEPs were studied in separate experiments. In healthy subjects, cTBS300 and cTBS600 over PMd suppressed MEPs for 30 min or more and cTBS600 decreased SICI and RI. In contrast, neither form of cTBS over PMd had any significant effect on MEPs, while cTBS600 increased effectiveness of SICI and RI and improved writing in patients with writer's cramp. NMDYT1 had a normal response to cTBS300 over left PMd. We suggest that the reduced PMd to M1 interaction in dystonic patients is likely to be due to reduced excitability of PMd‐M1 connections. The possible therapeutic effects of premotor rTMS may therefore involve indirect effects of PMd on SICI and RI, which this study has shown can be normalised by cTBS. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22814
Links to Exploration step
ISTEX:64731DEA0D2C1ADA018A1ADBE6B63D904F248232Le document en format XML
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Rothwell</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Lu, Chin Ong" sort="Lu, Chin Ong" uniqKey="Lu C" first="Chin-Song" last="Lu">Chin-Song Lu</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Wang, Jiunjie" sort="Wang, Jiunjie" uniqKey="Wang J" first="Jiunjie" last="Wang">Jiunjie Wang</name><affiliation><mods:affiliation>Department of Medical Imaging and Radiological Sciences, Chang Gung University, Taoyuan, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Magnetic Resonance Imaging Centre, Chang Gung Memorial Hospital, Taoyuan, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chen, Rou Hayn" sort="Chen, Rou Hayn" uniqKey="Chen R" first="Rou-Shayn" last="Chen">Rou-Shayn Chen</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:64731DEA0D2C1ADA018A1ADBE6B63D904F248232</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1002/mds.22814</idno><idno type="url">https://api.istex.fr/document/64731DEA0D2C1ADA018A1ADBE6B63D904F248232/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000975</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Restoration of motor inhibition through an abnormal premotor‐motor connection in dystonia</title><author><name sortKey="Huang, Ying U" sort="Huang, Ying U" uniqKey="Huang Y" first="Ying-Zu" last="Huang">Ying-Zu Huang</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. 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Continuous theta burst transcranial magnetic stimulation (cTBS) with 300 and 600 pulses (cTBS300 and cTBS600) was applied to PMd, and its after‐effects were quantified by measuring the amplitude of MEPs evoked by single pulse transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), short interval intracortical inhibition/facilitation (SICI/ICF) within M1, the third phase of spinal reciprocal inhibition (RI), and writing tests. In addition, in DYT1 gene carriers, the effects of cTBS300 over M1 and PMd on MEPs were studied in separate experiments. In healthy subjects, cTBS300 and cTBS600 over PMd suppressed MEPs for 30 min or more and cTBS600 decreased SICI and RI. In contrast, neither form of cTBS over PMd had any significant effect on MEPs, while cTBS600 increased effectiveness of SICI and RI and improved writing in patients with writer's cramp. NMDYT1 had a normal response to cTBS300 over left PMd. We suggest that the reduced PMd to M1 interaction in dystonic patients is likely to be due to reduced excitability of PMd‐M1 connections. The possible therapeutic effects of premotor rTMS may therefore involve indirect effects of PMd on SICI and RI, which this study has shown can be normalised by cTBS. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ying‐Zu Huang MD, PhD</name><affiliations><json:string>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>John C. Rothwell PhD</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Chin‐Song Lu MD</name><affiliations><json:string>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>JiunJie Wang PhD</name><affiliations><json:string>Department of Medical Imaging and Radiological Sciences, Chang Gung University, Taoyuan, Taiwan</json:string><json:string>Magnetic Resonance Imaging Centre, Chang Gung Memorial Hospital, Taoyuan, Taiwan</json:string></affiliations></json:item><json:item><name>Rou‐Shayn Chen MD</name><affiliations><json:string>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Premotor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>rTMS</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>theta burst</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TBS</value></json:item></subject><language><json:string>eng</json:string></language><abstract>To clarify the rationale for using rTMS of dorsal premotor cortex (PMd) to treat dystonia, we examined how the motor system reacts to an inhibitory form of rTMS applied to the PMd in healthy subjects and in a group of patients with focal hand dystonia and DYT1 gene carriers. Continuous theta burst transcranial magnetic stimulation (cTBS) with 300 and 600 pulses (cTBS300 and cTBS600) was applied to PMd, and its after‐effects were quantified by measuring the amplitude of MEPs evoked by single pulse transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), short interval intracortical inhibition/facilitation (SICI/ICF) within M1, the third phase of spinal reciprocal inhibition (RI), and writing tests. In addition, in DYT1 gene carriers, the effects of cTBS300 over M1 and PMd on MEPs were studied in separate experiments. In healthy subjects, cTBS300 and cTBS600 over PMd suppressed MEPs for 30 min or more and cTBS600 decreased SICI and RI. In contrast, neither form of cTBS over PMd had any significant effect on MEPs, while cTBS600 increased effectiveness of SICI and RI and improved writing in patients with writer's cramp. NMDYT1 had a normal response to cTBS300 over left PMd. We suggest that the reduced PMd to M1 interaction in dystonic patients is likely to be due to reduced excitability of PMd‐M1 connections. 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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="2010-04-30"></date><biblScope unit="vol">25</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="696">696</biblScope><biblScope unit="page" to="703">703</biblScope></imprint></monogr><idno type="istex">64731DEA0D2C1ADA018A1ADBE6B63D904F248232</idno><idno type="DOI">10.1002/mds.22814</idno><idno type="ArticleID">MDS22814</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>To clarify the rationale for using rTMS of dorsal premotor cortex (PMd) to treat dystonia, we examined how the motor system reacts to an inhibitory form of rTMS applied to the PMd in healthy subjects and in a group of patients with focal hand dystonia and DYT1 gene carriers. Continuous theta burst transcranial magnetic stimulation (cTBS) with 300 and 600 pulses (cTBS300 and cTBS600) was applied to PMd, and its after‐effects were quantified by measuring the amplitude of MEPs evoked by single pulse transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), short interval intracortical inhibition/facilitation (SICI/ICF) within M1, the third phase of spinal reciprocal inhibition (RI), and writing tests. In addition, in DYT1 gene carriers, the effects of cTBS300 over M1 and PMd on MEPs were studied in separate experiments. In healthy subjects, cTBS300 and cTBS600 over PMd suppressed MEPs for 30 min or more and cTBS600 decreased SICI and RI. In contrast, neither form of cTBS over PMd had any significant effect on MEPs, while cTBS600 increased effectiveness of SICI and RI and improved writing in patients with writer's cramp. NMDYT1 had a normal response to cTBS300 over left PMd. We suggest that the reduced PMd to M1 interaction in dystonic patients is likely to be due to reduced excitability of PMd‐M1 connections. The possible therapeutic effects of premotor rTMS may therefore involve indirect effects of PMd on SICI and RI, which this study has shown can be normalised by cTBS. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Premotor</term></item><item><term>rTMS</term></item><item><term>dystonia</term></item><item><term>theta burst</term></item><item><term>TBS</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="2009-05-25">Received</change><change when="2009-08-28">Registration</change><change when="2010-04-30">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/64731DEA0D2C1ADA018A1ADBE6B63D904F248232/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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NSC96‐2314‐B‐182A‐003</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Chang Gung Memorial Hospital</fundingAgency><fundingNumber>CMRPG34001</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Royal Society of the UK</fundingAgency></fundingInfo><fundingInfo><fundingAgency>UK‐Taiwan Joint Project Grant</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To clarify the rationale for using rTMS of dorsal premotor cortex (PMd) to treat dystonia, we examined how the motor system reacts to an inhibitory form of rTMS applied to the PMd in healthy subjects and in a group of patients with focal hand dystonia and DYT1 gene carriers. Continuous theta burst transcranial magnetic stimulation (cTBS) with 300 and 600 pulses (cTBS300 and cTBS600) was applied to PMd, and its after‐effects were quantified by measuring the amplitude of MEPs evoked by single pulse transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), short interval intracortical inhibition/facilitation (SICI/ICF) within M1, the third phase of spinal reciprocal inhibition (RI), and writing tests. In addition, in DYT1 gene carriers, the effects of cTBS300 over M1 and PMd on MEPs were studied in separate experiments. In healthy subjects, cTBS300 and cTBS600 over PMd suppressed MEPs for 30 min or more and cTBS600 decreased SICI and RI. In contrast, neither form of cTBS over PMd had any significant effect on MEPs, while cTBS600 increased effectiveness of SICI and RI and improved writing in patients with writer's cramp. NMDYT1 had a normal response to cTBS300 over left PMd. We suggest that the reduced PMd to M1 interaction in dystonic patients is likely to be due to reduced excitability of PMd‐M1 connections. The possible therapeutic effects of premotor rTMS may therefore involve indirect effects of PMd on SICI and RI, which this study has shown can be normalised by cTBS. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn3"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Restoration of motor inhibition through an abnormal premotor‐motor connection in dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Premotor rTMS and Dystonia Treatment</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Restoration of motor inhibition through an abnormal premotor‐motor connection in dystonia</title></titleInfo><name type="personal"><namePart type="given">Ying‐Zu</namePart><namePart type="family">Huang</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</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, University College London, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chin‐Song</namePart><namePart type="family">Lu</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JiunJie</namePart><namePart type="family">Wang</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Medical Imaging and Radiological Sciences, Chang Gung University, Taoyuan, Taiwan</affiliation><affiliation>Magnetic Resonance Imaging Centre, Chang Gung Memorial Hospital, Taoyuan, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rou‐Shayn</namePart><namePart type="family">Chen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taipei, Taiwan</affiliation><description>Correspondence: Department of Neurology, Chang Gung Memorial Hospital, 199, Dunhwa North Road, Taipei 10507, Taiwan</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">2010-04-30</dateIssued><dateCaptured encoding="w3cdtf">2009-05-25</dateCaptured><dateValid encoding="w3cdtf">2009-08-28</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">27</extent><extent unit="words">4842</extent></physicalDescription><abstract lang="en">To clarify the rationale for using rTMS of dorsal premotor cortex (PMd) to treat dystonia, we examined how the motor system reacts to an inhibitory form of rTMS applied to the PMd in healthy subjects and in a group of patients with focal hand dystonia and DYT1 gene carriers. Continuous theta burst transcranial magnetic stimulation (cTBS) with 300 and 600 pulses (cTBS300 and cTBS600) was applied to PMd, and its after‐effects were quantified by measuring the amplitude of MEPs evoked by single pulse transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), short interval intracortical inhibition/facilitation (SICI/ICF) within M1, the third phase of spinal reciprocal inhibition (RI), and writing tests. In addition, in DYT1 gene carriers, the effects of cTBS300 over M1 and PMd on MEPs were studied in separate experiments. In healthy subjects, cTBS300 and cTBS600 over PMd suppressed MEPs for 30 min or more and cTBS600 decreased SICI and RI. In contrast, neither form of cTBS over PMd had any significant effect on MEPs, while cTBS600 increased effectiveness of SICI and RI and improved writing in patients with writer's cramp. NMDYT1 had a normal response to cTBS300 over left PMd. We suggest that the reduced PMd to M1 interaction in dystonic patients is likely to be due to reduced excitability of PMd‐M1 connections. The possible therapeutic effects of premotor rTMS may therefore involve indirect effects of PMd on SICI and RI, which this study has shown can be normalised by cTBS. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><note type="funding">National Science Council of Taiwan - No. NSC 94‐2314‐B‐182A‐057/ NSC 95‐2314‐B‐182A‐012/ NSC96‐2314‐B‐182A‐003; </note><note type="funding">Chang Gung Memorial Hospital - No. CMRPG34001; </note><note type="funding">Royal Society of the UK</note><note type="funding">UK‐Taiwan Joint Project Grant</note><subject lang="en"><genre>Keywords</genre><topic>Premotor</topic><topic>rTMS</topic><topic>dystonia</topic><topic>theta burst</topic><topic>TBS</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>6</number></detail><extent unit="pages"><start>696</start><end>703</end><total>8</total></extent></part></relatedItem><identifier type="istex">64731DEA0D2C1ADA018A1ADBE6B63D904F248232</identifier><identifier type="DOI">10.1002/mds.22814</identifier><identifier type="ArticleID">MDS22814</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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