Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease
Identifieur interne : 002260 ( Main/Corpus ); précédent : 002259; suivant : 002261Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease
Auteurs : Tobias B Umer ; Ute Hidding ; Wolfgang Hamel ; Carsten Buhmann ; Christian K. E. Moll ; Christian Gerloff ; Michael Orth ; Hartwig Roman Siebner ; Alexander MünchauSource :
- Movement Disorders [ 0885-3185 ] ; 2009-04-15.
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Abstract
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a widely used and highly effective treatment for patients with advanced Parkinson's disease (PD). Repetitive TMS (rTMS) applied to motor cortical areas has also been shown to improve symptoms in PD and modulate motor cortical excitability. Here, we compared clinical and neurophysiological effects of STN stimulation with those of 1 Hz rTMS given to the dorsal premotor cortex (PMd) and those following intake of levodopa in a group of PD patients with advanced disease. Ten PD patients were studied on 2 consecutive days before and after surgery. Clinical effects were determined using the UPDRS motor score. Motor thresholds, motor‐evoked potential (MEP) amplitudes during slight voluntary contraction, and the cortical silent periods (SP) were measured using TMS. Before surgery effects of levodopa and 1 Hz PMd rTMS and after surgery those of STN stimulation with or without additional levodopa were determined. Levodopa significantly improved clinical symptoms and increased the SP duration. STN stimulation improved clinical symptoms without changing the SP duration. In contrast, 1 Hz PMd rTMS was not effective clinically but normalized the SP duration. Whereas levodopa had widespread effects at different levels of an abnormally active motor network in PD, STN stimulation and PMd rTMS led to either clinical improvement or SP normalization, i.e., only partially reversed abnormal motor network activity. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22417
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In contrast, 1 Hz PMd rTMS was not effective clinically but normalized the SP duration. Whereas levodopa had widespread effects at different levels of an abnormally active motor network in PD, STN stimulation and PMd rTMS led to either clinical improvement or SP normalization, i.e., only partially reversed abnormal motor network activity. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Tobias Bäumer MD</name><affiliations><json:string>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Ute Hidding MD</name><affiliations><json:string>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Wolfgang Hamel MD</name><affiliations><json:string>Department of Neurosurgery, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Carsten Buhmann MD</name><affiliations><json:string>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Christian K.E. Moll MD</name><affiliations><json:string>Institute of Neurophysiology and Pathophysiology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Christian Gerloff MD</name><affiliations><json:string>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Michael Orth MD, PhD</name><affiliations><json:string>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Hartwig Roman Siebner MD</name><affiliations><json:string>NeuroImage Nord, Hamburg‐Kiel‐Lübeck, Germany</json:string><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Alexander Münchau MD</name><affiliations><json:string>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>deep brain stimulation</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>premotor cortex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>L‐dopa</value></json:item></subject><articleId><json:string>MDS22417</json:string></articleId><language><json:string>eng</json:string></language><abstract>Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a widely used and highly effective treatment for patients with advanced Parkinson's disease (PD). Repetitive TMS (rTMS) applied to motor cortical areas has also been shown to improve symptoms in PD and modulate motor cortical excitability. Here, we compared clinical and neurophysiological effects of STN stimulation with those of 1 Hz rTMS given to the dorsal premotor cortex (PMd) and those following intake of levodopa in a group of PD patients with advanced disease. Ten PD patients were studied on 2 consecutive days before and after surgery. Clinical effects were determined using the UPDRS motor score. Motor thresholds, motor‐evoked potential (MEP) amplitudes during slight voluntary contraction, and the cortical silent periods (SP) were measured using TMS. Before surgery effects of levodopa and 1 Hz PMd rTMS and after surgery those of STN stimulation with or without additional levodopa were determined. Levodopa significantly improved clinical symptoms and increased the SP duration. STN stimulation improved clinical symptoms without changing the SP duration. In contrast, 1 Hz PMd rTMS was not effective clinically but normalized the SP duration. Whereas levodopa had widespread effects at different levels of an abnormally active motor network in PD, STN stimulation and PMd rTMS led to either clinical improvement or SP normalization, i.e., only partially reversed abnormal motor network activity. © 2009 Movement Disorder Society</abstract><qualityIndicators><score>6.1</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1512</abstractCharCount><pdfWordCount>3376</pdfWordCount><pdfCharCount>20799</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>227</abstractWordCount></qualityIndicators><title>Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>24</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>5</total><last>676</last><first>672</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1002/mds.22417</json:string></doi><id>3FB88501C5AC0C93DBA9F77FE9F42BDF269AA851</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/3FB88501C5AC0C93DBA9F77FE9F42BDF269AA851/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/3FB88501C5AC0C93DBA9F77FE9F42BDF269AA851/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3FB88501C5AC0C93DBA9F77FE9F42BDF269AA851/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2009</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: Nothing to Report.</note><note>Volkswagenstiftung - No. I/79 932;</note><note>Bundesministerium für Bildung und Forschung - No. 01GO 0511;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease</title><author><persName><forename type="first">Tobias</forename><surname>Bäumer</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Martinistraße 52, 20246 Hamburg, Germany</p></note><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Ute</forename><surname>Hidding</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Wolfgang</forename><surname>Hamel</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurosurgery, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Carsten</forename><surname>Buhmann</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Christian K.E.</forename><surname>Moll</surname></persName><roleName type="degree">MD</roleName><affiliation>Institute of Neurophysiology and Pathophysiology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Christian</forename><surname>Gerloff</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Michael</forename><surname>Orth</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Hartwig Roman</forename><surname>Siebner</surname></persName><roleName type="degree">MD</roleName><affiliation>NeuroImage Nord, Hamburg‐Kiel‐Lübeck, Germany</affiliation><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation></author><author><persName><forename type="first">Alexander</forename><surname>Münchau</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</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. 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Repetitive TMS (rTMS) applied to motor cortical areas has also been shown to improve symptoms in PD and modulate motor cortical excitability. Here, we compared clinical and neurophysiological effects of STN stimulation with those of 1 Hz rTMS given to the dorsal premotor cortex (PMd) and those following intake of levodopa in a group of PD patients with advanced disease. Ten PD patients were studied on 2 consecutive days before and after surgery. Clinical effects were determined using the UPDRS motor score. Motor thresholds, motor‐evoked potential (MEP) amplitudes during slight voluntary contraction, and the cortical silent periods (SP) were measured using TMS. Before surgery effects of levodopa and 1 Hz PMd rTMS and after surgery those of STN stimulation with or without additional levodopa were determined. Levodopa significantly improved clinical symptoms and increased the SP duration. STN stimulation improved clinical symptoms without changing the SP duration. In contrast, 1 Hz PMd rTMS was not effective clinically but normalized the SP duration. Whereas levodopa had widespread effects at different levels of an abnormally active motor network in PD, STN stimulation and PMd rTMS led to either clinical improvement or SP normalization, i.e., only partially reversed abnormal motor network activity. © 2009 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson</term></item><item><term>deep brain stimulation</term></item><item><term>rTMS</term></item><item><term>premotor cortex</term></item><item><term>L‐dopa</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="2008-07-10">Received</change><change when="2008-11-13">Registration</change><change when="2009-04-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3FB88501C5AC0C93DBA9F77FE9F42BDF269AA851/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. 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href="file:MDS.MDS22417.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="26"></count><count type="wordTotal" number="3568"></count></countGroup><titleGroup><title type="main" xml:lang="en">Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease<link href="#fn1"></link></title><title type="short" xml:lang="en">Effects of DBS, Premotor rTMS, and Levodopa</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Tobias</givenNames><familyName>Bäumer</familyName><degrees>MD</degrees></personName><contactDetails><email>baeumer@uke.de</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ute</givenNames><familyName>Hidding</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Wolfgang</givenNames><familyName>Hamel</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Carsten</givenNames><familyName>Buhmann</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Christian K.E.</givenNames><familyName>Moll</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Christian</givenNames><familyName>Gerloff</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michael</givenNames><familyName>Orth</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af4 #af5"><personName><givenNames>Hartwig Roman</givenNames><familyName>Siebner</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Alexander</givenNames><familyName>Münchau</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurosurgery, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Neurophysiology and Pathophysiology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>NeuroImage Nord, Hamburg‐Kiel‐Lübeck, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson</keyword><keyword xml:id="kwd2">deep brain stimulation</keyword><keyword xml:id="kwd3">rTMS</keyword><keyword xml:id="kwd4">premotor cortex</keyword><keyword xml:id="kwd5"><sc>L</sc>‐dopa</keyword></keywordGroup><fundingInfo><fundingAgency>Volkswagenstiftung</fundingAgency><fundingNumber>I/79 932</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Bundesministerium für Bildung und Forschung</fundingAgency><fundingNumber>01GO 0511</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a widely used and highly effective treatment for patients with advanced Parkinson's disease (PD). Repetitive TMS (rTMS) applied to motor cortical areas has also been shown to improve symptoms in PD and modulate motor cortical excitability. Here, we compared clinical and neurophysiological effects of STN stimulation with those of 1 Hz rTMS given to the dorsal premotor cortex (PMd) and those following intake of levodopa in a group of PD patients with advanced disease. Ten PD patients were studied on 2 consecutive days before and after surgery. Clinical effects were determined using the UPDRS motor score. Motor thresholds, motor‐evoked potential (MEP) amplitudes during slight voluntary contraction, and the cortical silent periods (SP) were measured using TMS. Before surgery effects of levodopa and 1 Hz PMd rTMS and after surgery those of STN stimulation with or without additional levodopa were determined. Levodopa significantly improved clinical symptoms and increased the SP duration. STN stimulation improved clinical symptoms without changing the SP duration. In contrast, 1 Hz PMd rTMS was not effective clinically but normalized the SP duration. Whereas levodopa had widespread effects at different levels of an abnormally active motor network in PD, STN stimulation and PMd rTMS led to either clinical improvement or SP normalization, i.e., only partially reversed abnormal motor network activity. © 2009 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><mods version="3.6"><titleInfo lang="en"><title>Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Effects of DBS, Premotor rTMS, and Levodopa</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effects of DBS, premotor rTMS, and levodopa on motor function and silent period in advanced Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Tobias</namePart><namePart type="family">Bäumer</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><description>Correspondence: Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Martinistraße 52, 20246 Hamburg, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ute</namePart><namePart type="family">Hidding</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfgang</namePart><namePart type="family">Hamel</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosurgery, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carsten</namePart><namePart type="family">Buhmann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian K.E.</namePart><namePart type="family">Moll</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neurophysiology and Pathophysiology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Gerloff</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Orth</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hartwig Roman</namePart><namePart type="family">Siebner</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>NeuroImage Nord, Hamburg‐Kiel‐Lübeck, Germany</affiliation><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexander</namePart><namePart type="family">Münchau</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical Centre Hamburg‐Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-04-15</dateIssued><dateCaptured encoding="w3cdtf">2008-07-10</dateCaptured><dateValid encoding="w3cdtf">2008-11-13</dateValid><copyrightDate encoding="w3cdtf">2009</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">1</extent><extent unit="references">26</extent><extent unit="words">3568</extent></physicalDescription><abstract lang="en">Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a widely used and highly effective treatment for patients with advanced Parkinson's disease (PD). Repetitive TMS (rTMS) applied to motor cortical areas has also been shown to improve symptoms in PD and modulate motor cortical excitability. Here, we compared clinical and neurophysiological effects of STN stimulation with those of 1 Hz rTMS given to the dorsal premotor cortex (PMd) and those following intake of levodopa in a group of PD patients with advanced disease. Ten PD patients were studied on 2 consecutive days before and after surgery. Clinical effects were determined using the UPDRS motor score. Motor thresholds, motor‐evoked potential (MEP) amplitudes during slight voluntary contraction, and the cortical silent periods (SP) were measured using TMS. Before surgery effects of levodopa and 1 Hz PMd rTMS and after surgery those of STN stimulation with or without additional levodopa were determined. Levodopa significantly improved clinical symptoms and increased the SP duration. STN stimulation improved clinical symptoms without changing the SP duration. In contrast, 1 Hz PMd rTMS was not effective clinically but normalized the SP duration. Whereas levodopa had widespread effects at different levels of an abnormally active motor network in PD, STN stimulation and PMd rTMS led to either clinical improvement or SP normalization, i.e., only partially reversed abnormal motor network activity. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to Report.</note><note type="funding">Volkswagenstiftung - No. I/79 932; </note><note type="funding">Bundesministerium für Bildung und Forschung - No. 01GO 0511; </note><subject lang="en"><genre>Keywords</genre><topic>Parkinson</topic><topic>deep brain stimulation</topic><topic>rTMS</topic><topic>premotor cortex</topic><topic>L‐dopa</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><genre type="Journal">journal</genre><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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>672</start><end>676</end><total>5</total></extent></part></relatedItem><identifier type="istex">3FB88501C5AC0C93DBA9F77FE9F42BDF269AA851</identifier><identifier type="DOI">10.1002/mds.22417</identifier><identifier type="ArticleID">MDS22417</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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