Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease
Identifieur interne : 001225 ( Istex/Corpus ); précédent : 001224; suivant : 001226Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease
Auteurs : Janne Gierthmühlen ; Philipp Arning ; Andreas Binder ; Jan Herzog ; Günther Deuschl ; Gunnar Wasner ; Ralf BaronSource :
- Movement Disorders [ 0885-3185 ] ; 2010-07-15.
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Abstract
To examine the effects of levodopa (L‐dopa) and deep brain stimulation of the subthalamic nucleus (STN‐DBS) on sensory symptoms and signs in Parkinson's disease (PD). Seventeen patients with PD were included. (1) Presence of sensory symptoms and (2) effects of L‐dopa and STN‐DBS on sensory symptoms and signs [assessed by quantitative sensory testing (QST)] were examined 6 months after starting STN‐DBS. In addition, in 12 of these patients, presence of sensory symptoms prior and post STN‐DBS was compared. Pain was most frequently nociceptive. In about 30–40%, pain and sensory symptoms were associated with PD motor symptoms. In most of these cases, pain responded to L‐dopa. Intensity of pain was reduced post STN‐DBS compared to pre STN‐DBS. L‐Dopa had no influence on detection thresholds, whereas STN‐DBS improved thermal detection thresholds. However, thermal and mechanical pain thresholds were uninfluenced by L‐dopa or STN‐DBS. Although some patients reported an improvement of pain with STN‐DBS or L‐dopa, objectively pain sensitivity as assessed by QST was not altered by STN‐DBS or L‐dopa suggesting that there is no evidence for a direct modulation of central pain processing by L‐dopa or STN‐DBS. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23128
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Seventeen patients with PD were included. (1) Presence of sensory symptoms and (2) effects of L‐dopa and STN‐DBS on sensory symptoms and signs [assessed by quantitative sensory testing (QST)] were examined 6 months after starting STN‐DBS. In addition, in 12 of these patients, presence of sensory symptoms prior and post STN‐DBS was compared. Pain was most frequently nociceptive. In about 30–40%, pain and sensory symptoms were associated with PD motor symptoms. In most of these cases, pain responded to L‐dopa. Intensity of pain was reduced post STN‐DBS compared to pre STN‐DBS. L‐Dopa had no influence on detection thresholds, whereas STN‐DBS improved thermal detection thresholds. However, thermal and mechanical pain thresholds were uninfluenced by L‐dopa or STN‐DBS. Although some patients reported an improvement of pain with STN‐DBS or L‐dopa, objectively pain sensitivity as assessed by QST was not altered by STN‐DBS or L‐dopa suggesting that there is no evidence for a direct modulation of central pain processing by L‐dopa or STN‐DBS. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Janne Gierthmühlen MD</name><affiliations><json:string>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Philipp Arning</name><affiliations><json:string>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Andreas Binder MD</name><affiliations><json:string>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Jan Herzog MD</name><affiliations><json:string>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Günther Deuschl MD</name><affiliations><json:string>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Gunnar Wasner MD</name><affiliations><json:string>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Ralf Baron MD</name><affiliations><json:string>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</json:string></affiliations></json:item></author><subject><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>somatosensory processing</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>quantitative sensory testing</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>levodopa</value></json:item></subject><language><json:string>eng</json:string></language><abstract>To examine the effects of levodopa (L‐dopa) and deep brain stimulation of the subthalamic nucleus (STN‐DBS) on sensory symptoms and signs in Parkinson's disease (PD). Seventeen patients with PD were included. (1) Presence of sensory symptoms and (2) effects of L‐dopa and STN‐DBS on sensory symptoms and signs [assessed by quantitative sensory testing (QST)] were examined 6 months after starting STN‐DBS. In addition, in 12 of these patients, presence of sensory symptoms prior and post STN‐DBS was compared. Pain was most frequently nociceptive. In about 30–40%, pain and sensory symptoms were associated with PD motor symptoms. In most of these cases, pain responded to L‐dopa. Intensity of pain was reduced post STN‐DBS compared to pre STN‐DBS. L‐Dopa had no influence on detection thresholds, whereas STN‐DBS improved thermal detection thresholds. However, thermal and mechanical pain thresholds were uninfluenced by L‐dopa or STN‐DBS. Although some patients reported an improvement of pain with STN‐DBS or L‐dopa, objectively pain sensitivity as assessed by QST was not altered by STN‐DBS or L‐dopa suggesting that there is no evidence for a direct modulation of central pain processing by L‐dopa or STN‐DBS. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>6.498</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1247</abstractCharCount><pdfWordCount>4218</pdfWordCount><pdfCharCount>28072</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>190</abstractWordCount></qualityIndicators><title>Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease</title><genre><json:string>Serial article</json:string></genre><host><volume>25</volume><pages><total>8</total><last>1202</last><first>1195</first></pages><issn><json:string>0885-3185</json:string></issn><issue>9</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23128</json:string></doi><id>AFB71037C3008BDF2D268256EA887E5F58AD8FD8</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/AFB71037C3008BDF2D268256EA887E5F58AD8FD8/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/AFB71037C3008BDF2D268256EA887E5F58AD8FD8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/AFB71037C3008BDF2D268256EA887E5F58AD8FD8/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None of the sponsors was involved in design and conduct of the study, in collection, management, analysis, and interpretation of the data, in preparation, review, or approval of the manuscript. There was no ghost writing by anyone not named on the author list.</note><note>Bundesministerium für Bildung und Forschung - No. BMBF, 01EM05/04;</note><note>Deutsche Forschungsgemeinschaft - No. DFG Ba1921/1–1/3;</note><note>National Health and Medical Research Council of Australia (NHMRC)</note><note>EFIC‐Grünenthal‐Grant (E‐G‐G)</note><note>Pfizer Deutschland</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease</title><author><persName><forename type="first">Janne</forename><surname>Gierthmühlen</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Campus Kiel, Arnold‐Heller‐Strasse 3, Haus 41, Kiel 24105, Germany</p></note><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation></author><author><persName><forename type="first">Philipp</forename><surname>Arning</surname></persName><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation></author><author><persName><forename type="first">Andreas</forename><surname>Binder</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation></author><author><persName><forename type="first">Jan</forename><surname>Herzog</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation></author><author><persName><forename type="first">Günther</forename><surname>Deuschl</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation></author><author><persName><forename type="first">Gunnar</forename><surname>Wasner</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation></author><author><persName><forename type="first">Ralf</forename><surname>Baron</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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Seventeen patients with PD were included. (1) Presence of sensory symptoms and (2) effects of L‐dopa and STN‐DBS on sensory symptoms and signs [assessed by quantitative sensory testing (QST)] were examined 6 months after starting STN‐DBS. In addition, in 12 of these patients, presence of sensory symptoms prior and post STN‐DBS was compared. Pain was most frequently nociceptive. In about 30–40%, pain and sensory symptoms were associated with PD motor symptoms. In most of these cases, pain responded to L‐dopa. Intensity of pain was reduced post STN‐DBS compared to pre STN‐DBS. L‐Dopa had no influence on detection thresholds, whereas STN‐DBS improved thermal detection thresholds. However, thermal and mechanical pain thresholds were uninfluenced by L‐dopa or STN‐DBS. 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affiliationRef="#af1"><personName><givenNames>Philipp</givenNames><familyName>Arning</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Andreas</givenNames><familyName>Binder</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jan</givenNames><familyName>Herzog</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Günther</givenNames><familyName>Deuschl</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Gunnar</givenNames><familyName>Wasner</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ralf</givenNames><familyName>Baron</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">somatosensory processing</keyword><keyword xml:id="kwd3">deep brain stimulation</keyword><keyword xml:id="kwd4">quantitative sensory testing</keyword><keyword xml:id="kwd5">levodopa</keyword></keywordGroup><fundingInfo><fundingAgency>Bundesministerium für Bildung und Forschung</fundingAgency><fundingNumber>BMBF, 01EM05/04</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Deutsche Forschungsgemeinschaft</fundingAgency><fundingNumber>DFG Ba1921/1–1/3</fundingNumber></fundingInfo><fundingInfo><fundingAgency>National Health and Medical Research Council of Australia (NHMRC)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>EFIC‐Grünenthal‐Grant (E‐G‐G)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Pfizer Deutschland</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To examine the effects of levodopa (<sc>L</sc>‐dopa) and deep brain stimulation of the subthalamic nucleus (STN‐DBS) on sensory symptoms and signs in Parkinson's disease (PD). Seventeen patients with PD were included. (1) Presence of sensory symptoms and (2) effects of <sc>L</sc>‐dopa and STN‐DBS on sensory symptoms and signs [assessed by quantitative sensory testing (QST)] were examined 6 months after starting STN‐DBS. In addition, in 12 of these patients, presence of sensory symptoms prior and post STN‐DBS was compared. Pain was most frequently nociceptive. In about 30–40%, pain and sensory symptoms were associated with PD motor symptoms. In most of these cases, pain responded to <sc>L</sc>‐dopa. Intensity of pain was reduced post STN‐DBS compared to pre STN‐DBS. <sc>L</sc>‐Dopa had no influence on detection thresholds, whereas STN‐DBS improved thermal detection thresholds. However, thermal and mechanical pain thresholds were uninfluenced by <sc>L</sc>‐dopa or STN‐DBS. Although some patients reported an improvement of pain with STN‐DBS or <sc>L</sc>‐dopa, objectively pain sensitivity as assessed by QST was not altered by STN‐DBS or <sc>L</sc>‐dopa suggesting that there is no evidence for a direct modulation of central pain processing by <sc>L</sc>‐dopa or STN‐DBS. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn2"><p>Potential conflict of interest: None of the sponsors was involved in design and conduct of the study, in collection, management, analysis, and interpretation of the data, in preparation, review, or approval of the manuscript. There was no ghost writing by anyone not named on the author list.</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>Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Parkinson and Sensory Alterations</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Janne</namePart><namePart type="family">Gierthmühlen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation><description>Correspondence: Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Campus Kiel, Arnold‐Heller‐Strasse 3, Haus 41, Kiel 24105, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philipp</namePart><namePart type="family">Arning</namePart><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andreas</namePart><namePart type="family">Binder</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Herzog</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, 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">MD</namePart><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gunnar</namePart><namePart type="family">Wasner</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ralf</namePart><namePart type="family">Baron</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Division of Neurological Pain Research and Therapy, Universitätsklinikum Schleswig‐Holstein, Kiel, Germany</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">2010-07-15</dateIssued><dateCaptured encoding="w3cdtf">2009-07-25</dateCaptured><dateValid encoding="w3cdtf">2010-03-07</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">1</extent><extent unit="tables">3</extent><extent unit="references">28</extent><extent unit="words">6348</extent></physicalDescription><abstract lang="en">To examine the effects of levodopa (L‐dopa) and deep brain stimulation of the subthalamic nucleus (STN‐DBS) on sensory symptoms and signs in Parkinson's disease (PD). Seventeen patients with PD were included. (1) Presence of sensory symptoms and (2) effects of L‐dopa and STN‐DBS on sensory symptoms and signs [assessed by quantitative sensory testing (QST)] were examined 6 months after starting STN‐DBS. In addition, in 12 of these patients, presence of sensory symptoms prior and post STN‐DBS was compared. Pain was most frequently nociceptive. In about 30–40%, pain and sensory symptoms were associated with PD motor symptoms. In most of these cases, pain responded to L‐dopa. Intensity of pain was reduced post STN‐DBS compared to pre STN‐DBS. L‐Dopa had no influence on detection thresholds, whereas STN‐DBS improved thermal detection thresholds. However, thermal and mechanical pain thresholds were uninfluenced by L‐dopa or STN‐DBS. Although some patients reported an improvement of pain with STN‐DBS or L‐dopa, objectively pain sensitivity as assessed by QST was not altered by STN‐DBS or L‐dopa suggesting that there is no evidence for a direct modulation of central pain processing by L‐dopa or STN‐DBS. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None of the sponsors was involved in design and conduct of the study, in collection, management, analysis, and interpretation of the data, in preparation, review, or approval of the manuscript. There was no ghost writing by anyone not named on the author list.</note><note type="funding">Bundesministerium für Bildung und Forschung - No. BMBF, 01EM05/04; </note><note type="funding">Deutsche Forschungsgemeinschaft - No. DFG Ba1921/1–1/3; </note><note type="funding">National Health and Medical Research Council of Australia (NHMRC)</note><note type="funding">EFIC‐Grünenthal‐Grant (E‐G‐G)</note><note type="funding">Pfizer Deutschland</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>somatosensory processing</topic><topic>deep brain stimulation</topic><topic>quantitative sensory testing</topic><topic>levodopa</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>9</number></detail><extent unit="pages"><start>1195</start><end>1202</end><total>8</total></extent></part></relatedItem><identifier type="istex">AFB71037C3008BDF2D268256EA887E5F58AD8FD8</identifier><identifier type="DOI">10.1002/mds.23128</identifier><identifier type="ArticleID">MDS23128</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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