Subthalamic nucleus stimulation restores corticospinal facilitation in Parkinson's disease
Identifieur interne : 000F95 ( Istex/Corpus ); précédent : 000F94; suivant : 000F96Subthalamic nucleus stimulation restores corticospinal facilitation in Parkinson's disease
Auteurs : Monika Pötter-Nerger ; Tihomir V. Ilic ; Hartwiq R. Siebner ; Günther Deuschl ; Jens VolkmannSource :
- Movement Disorders [ 0885-3185 ] ; 2008-11-15.
English descriptors
- KwdEn :
Abstract
We have previously shown that in patients with Parkinson's disease (PD), high‐frequency stimulation (HFS) of the subthalamic nucleus (STN) modifies spinal excitability via subcortical reticulospinal routes. To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; P = 0.005), ISI (F = 6.1; P = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; P = 0.01). STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. In addition to subcortical routes, STN‐DBS also alters spinal excitability via transcortical pathways. © 2008 Movement Disorder Society.
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DOI: 10.1002/mds.22284
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Ilic</name><affiliation><mods:affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Outpatients Neurological Department, Military Medical Academy, Belgrade, Serbia</mods:affiliation></affiliation></author><author><name sortKey="Siebner, Hartwiq R" sort="Siebner, Hartwiq R" uniqKey="Siebner H" first="Hartwiq R." last="Siebner">Hartwiq R. 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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="2008-11-15">2008-11-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2210">2210</biblScope><biblScope unit="page" to="2215">2215</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">97533EC88496F672DF0E15F076F010011DC1EFCF</idno><idno type="DOI">10.1002/mds.22284</idno><idno type="ArticleID">MDS22284</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>H‐reflex</term><term>Parkinson disease</term><term>STN DBS</term><term>motor cortex</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We have previously shown that in patients with Parkinson's disease (PD), high‐frequency stimulation (HFS) of the subthalamic nucleus (STN) modifies spinal excitability via subcortical reticulospinal routes. To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; P = 0.005), ISI (F = 6.1; P = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; P = 0.01). STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. In addition to subcortical routes, STN‐DBS also alters spinal excitability via transcortical pathways. © 2008 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Monika Pötter‐Nerger MD</name><affiliations><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Tihomir V. Ilic PhD</name><affiliations><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string><json:string>Outpatients Neurological Department, Military Medical Academy, Belgrade, Serbia</json:string></affiliations></json:item><json:item><name>Hartwiq R. Siebner PhD</name><affiliations><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Günther Deuschl PhD</name><affiliations><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Jens Volkmann PhD</name><affiliations><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor cortex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STN DBS</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>H‐reflex</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We have previously shown that in patients with Parkinson's disease (PD), high‐frequency stimulation (HFS) of the subthalamic nucleus (STN) modifies spinal excitability via subcortical reticulospinal routes. To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; P = 0.005), ISI (F = 6.1; P = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; P = 0.01). STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. 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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="2008-11-15"></date><biblScope unit="vol">23</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2210">2210</biblScope><biblScope unit="page" to="2215">2215</biblScope></imprint></monogr><idno type="istex">97533EC88496F672DF0E15F076F010011DC1EFCF</idno><idno type="DOI">10.1002/mds.22284</idno><idno type="ArticleID">MDS22284</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We have previously shown that in patients with Parkinson's disease (PD), high‐frequency stimulation (HFS) of the subthalamic nucleus (STN) modifies spinal excitability via subcortical reticulospinal routes. To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; P = 0.005), ISI (F = 6.1; P = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; P = 0.01). STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. In addition to subcortical routes, STN‐DBS also alters spinal excitability via transcortical pathways. © 2008 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson disease</term></item><item><term>motor cortex</term></item><item><term>STN DBS</term></item><item><term>H‐reflex</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="2008-04-18">Received</change><change when="2008-07-23">Registration</change><change when="2008-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/97533EC88496F672DF0E15F076F010011DC1EFCF/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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To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; <i>P</i> = 0.005), ISI (F = 6.1; <i>P</i> = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; <i>P</i> = 0.01)<i>.</i> STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. In addition to subcortical routes, STN‐DBS also alters spinal excitability via transcortical pathways. © 2008 Movement Disorder Society.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</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>Subthalamic nucleus stimulation restores corticospinal facilitation in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>STN‐DBS and Corticospinal Drive in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Subthalamic nucleus stimulation restores corticospinal facilitation in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Monika</namePart><namePart type="family">Pötter‐Nerger</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tihomir V.</namePart><namePart type="family">Ilic</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><affiliation>Outpatients Neurological Department, Military Medical Academy, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hartwiq R.</namePart><namePart type="family">Siebner</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Günther</namePart><namePart type="family">Deuschl</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jens</namePart><namePart type="family">Volkmann</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><description>Correspondence: Department of Neurology, Christian‐Albrechts‐University, Arnold‐Hellerstr. 3, Haus 41, D‐24105 Kiel, Germany</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">2008-11-15</dateIssued><dateCaptured encoding="w3cdtf">2008-04-18</dateCaptured><dateValid encoding="w3cdtf">2008-07-23</dateValid><copyrightDate encoding="w3cdtf">2008</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">35</extent><extent unit="words">3869</extent></physicalDescription><abstract lang="en">We have previously shown that in patients with Parkinson's disease (PD), high‐frequency stimulation (HFS) of the subthalamic nucleus (STN) modifies spinal excitability via subcortical reticulospinal routes. To investigate whether STN‐HFS also modifies spinal excitability via transcortical routes in PD, 10 patients with PD (9 men, 1 woman; 58.3 ± 8.3 years) were investigated in the medical OFF‐state with or without STN‐HFS. The H‐reflex of the right soleus muscle was recorded during slight plantar flexion at 20% of maximum force. A conditioning transcranial stimulus was applied at 95% of active motor threshold to the contralateral primary motor leg area (M1) 0–5 ms after eliciting the H‐reflex. The same paradigm was applied to 8 healthy individuals (5 men, 3 women; 50.8 ± 3.0 years). Transcranial magnetic stimulation (TMS) facilitated the H‐reflex amplitude in healthy controls. A facilitatory effect of the corticospinal input on the H‐reflex was also found in patients with PD, but only with STN‐HFS switched on. When STN‐HFS was discontinued, the H‐reflex was no longer facilitated by the TMS pulse. Accordingly, analysis of variance showed a main effect of stimulation (F = 11.15; P = 0.005), ISI (F = 6.1; P = 0.003), and an interaction between stimulation and group (PD vs. control) (F = 8.9; P = 0.01). STN‐HFS restores the normal facilitatory drive of a transcranially evoked motor cortical response to the spinal motoneuron pool. In addition to subcortical routes, STN‐DBS also alters spinal excitability via transcortical pathways. © 2008 Movement Disorder Society.</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">Deutsche Forschungsgemeinschaft - No. SFB 654 (project A7); </note><note type="funding">German Ministry of Research and Technology - No. FK: 01GI0201; </note><note type="funding">Christian‐Albrechts‐University</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson disease</topic><topic>motor cortex</topic><topic>STN DBS</topic><topic>H‐reflex</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>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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2210</start><end>2215</end><total>6</total></extent></part></relatedItem><identifier type="istex">97533EC88496F672DF0E15F076F010011DC1EFCF</identifier><identifier type="DOI">10.1002/mds.22284</identifier><identifier type="ArticleID">MDS22284</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 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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