Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia
Identifieur interne : 000D78 ( Main/Corpus ); précédent : 000D77; suivant : 000D79Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia
Auteurs : Kazutaka Kobayashi ; Anthony E. Lang ; Mark Hallett ; Frederick A. LenzSource :
- Movement Disorders [ 0885-3185 ] ; 2011-06.
English descriptors
- KwdEn :
Abstract
Background:: This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made. Results:: The signal‐to‐noise ratio in the lowest frequency band (dystonia frequency < 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal‐to‐noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia. Conclusions:: These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal‐to‐noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23565
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Lang</name><affiliation><mods:affiliation>Division of Neurology, University Health Network and University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Hallett, Mark" sort="Hallett, Mark" uniqKey="Hallett M" first="Mark" last="Hallett">Mark Hallett</name><affiliation><mods:affiliation>Human Motor Control Section, NINDS, NIH, Bethesda, Maryland, USA</mods:affiliation></affiliation></author><author><name sortKey="Lenz, Frederick A" sort="Lenz, Frederick A" uniqKey="Lenz F" first="Frederick A." last="Lenz">Frederick A. Lenz</name><affiliation><mods:affiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23565</idno><idno type="url">https://api.istex.fr/document/B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000D78</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia</title><author><name sortKey="Kobayashi, Kazutaka" sort="Kobayashi, Kazutaka" uniqKey="Kobayashi K" first="Kazutaka" last="Kobayashi">Kazutaka Kobayashi</name><affiliation><mods:affiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Applied Systems Neuroscience, Department of Advanced Medical Science, Nihon University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E." last="Lang">Anthony E. Lang</name><affiliation><mods:affiliation>Division of Neurology, University Health Network and University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Hallett, Mark" sort="Hallett, Mark" uniqKey="Hallett M" first="Mark" last="Hallett">Mark Hallett</name><affiliation><mods:affiliation>Human Motor Control Section, NINDS, NIH, Bethesda, Maryland, USA</mods:affiliation></affiliation></author><author><name sortKey="Lenz, Frederick A" sort="Lenz, Frederick A" uniqKey="Lenz F" first="Frederick A." last="Lenz">Frederick A. Lenz</name><affiliation><mods:affiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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="2011-06">2011-06</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1348">1348</biblScope><biblScope unit="page" to="1352">1352</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD</idno><idno type="DOI">10.1002/mds.23565</idno><idno type="ArticleID">MDS23565</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>dystonia‐related activity</term><term>human thalamus</term><term>neuronal activity</term><term>organic dystonia</term><term>plasticity</term><term>psychogenic dystonia</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background:: This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made. Results:: The signal‐to‐noise ratio in the lowest frequency band (dystonia frequency < 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal‐to‐noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia. Conclusions:: These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal‐to‐noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Kazutaka Kobayashi MD PhD</name><affiliations><json:string>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</json:string><json:string>Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan</json:string><json:string>Division of Applied Systems Neuroscience, Department of Advanced Medical Science, Nihon University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Anthony E. Lang MD, FRCPC</name><affiliations><json:string>Division of Neurology, University Health Network and University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Mark Hallett MD</name><affiliations><json:string>Human Motor Control Section, NINDS, NIH, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Frederick A. Lenz MD, PhD, FRCSC</name><affiliations><json:string>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>psychogenic dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>organic dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>human thalamus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuronal activity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>plasticity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dystonia‐related activity</value></json:item></subject><articleId><json:string>MDS23565</json:string></articleId><language><json:string>eng</json:string></language><abstract>Background:: This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made. Results:: The signal‐to‐noise ratio in the lowest frequency band (dystonia frequency > 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal‐to‐noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia. Conclusions:: These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal‐to‐noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.784</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1683</abstractCharCount><pdfWordCount>9473</pdfWordCount><pdfCharCount>61784</pdfCharCount><pdfPageCount>16</pdfPageCount><abstractWordCount>232</abstractWordCount></qualityIndicators><title>Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>5</total><last>1352</last><first>1348</first></pages><issn><json:string>0885-3185</json:string></issn><issue>7</issue><subject><json:item><value>Brief Report</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>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23565</json:string></doi><id>B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Relevant conflict of interest/financial disclosures: Nothing to report. This work was supported by the National Institutes of Health—National Institute of Neurological Disorders and Stroke Intramural and Extramural Programs (RO1 NS38493 and ROL NS40059 to F.A.L.). Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia</title><author><persName><forename type="first">Kazutaka</forename><surname>Kobayashi</surname></persName><roleName type="degree">MD PhD</roleName><affiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</affiliation><affiliation>Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan</affiliation><affiliation>Division of Applied Systems Neuroscience, Department of Advanced Medical Science, Nihon University School of Medicine, Tokyo, Japan</affiliation></author><author><persName><forename type="first">Anthony E.</forename><surname>Lang</surname></persName><roleName type="degree">MD, FRCPC</roleName><affiliation>Division of Neurology, University Health Network and University of Toronto, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Mark</forename><surname>Hallett</surname></persName><roleName type="degree">MD</roleName><affiliation>Human Motor Control Section, NINDS, NIH, Bethesda, Maryland, USA</affiliation></author><author><persName><forename type="first">Frederick A.</forename><surname>Lenz</surname></persName><roleName type="degree">MD, PhD, FRCSC</roleName><note type="correspondence"><p>Correspondence: Department of Neurosurgery, Johns Hopkins Hospital, Meyer Building 8‐181, 600 North Wolfe Street, Baltimore, MD 21287‐7713, USA</p></note><affiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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="2011-06"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1348">1348</biblScope><biblScope unit="page" to="1352">1352</biblScope></imprint></monogr><idno type="istex">B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD</idno><idno type="DOI">10.1002/mds.23565</idno><idno type="ArticleID">MDS23565</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background:: This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made. Results:: The signal‐to‐noise ratio in the lowest frequency band (dystonia frequency < 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal‐to‐noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia. Conclusions:: These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal‐to‐noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>psychogenic dystonia</term></item><item><term>organic dystonia</term></item><item><term>human thalamus</term></item><item><term>neuronal activity</term></item><item><term>plasticity</term></item><item><term>dystonia‐related activity</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-05-27">Received</change><change when="2010-11-11">Registration</change><change when="2011-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD/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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href="file:MDS.MDS23565.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="25"></count><count type="wordTotal" number="3483"></count></countGroup><titleGroup><title type="main" xml:lang="en">Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia<link href="#fn1"></link></title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2 #af3"><personName><givenNames>Kazutaka</givenNames><familyName>Kobayashi</familyName><degrees>MD PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Anthony E.</givenNames><familyName>Lang</familyName><degrees>MD, FRCPC</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Mark</givenNames><familyName>Hallett</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Frederick A.</givenNames><familyName>Lenz</familyName><degrees>MD, PhD, FRCSC</degrees></personName><contactDetails><email>flenz1@jhmi.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="JP" type="organization"><unparsedAffiliation>Division of Applied Systems Neuroscience, Department of Advanced Medical Science, Nihon University School of Medicine, Tokyo, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="CA" type="organization"><unparsedAffiliation>Division of Neurology, University Health Network and University of Toronto, Toronto, Ontario, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Human Motor Control Section, NINDS, NIH, Bethesda, Maryland, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">psychogenic dystonia</keyword><keyword xml:id="kwd2">organic dystonia</keyword><keyword xml:id="kwd3">human thalamus</keyword><keyword xml:id="kwd4">neuronal activity</keyword><keyword xml:id="kwd5">plasticity</keyword><keyword xml:id="kwd6">dystonia‐related activity</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Background:</title><p>This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made.</p></section><section xml:id="abs1-2"><title type="main">Results:</title><p>The signal‐to‐noise ratio in the lowest frequency band (dystonia frequency < 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal‐to‐noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia.</p></section><section xml:id="abs1-3"><title type="main">Conclusions:</title><p>These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal‐to‐noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflict of interest/financial disclosures:</b> Nothing to report. This work was supported by the National Institutes of Health—National Institute of Neurological Disorders and Stroke Intramural and Extramural Programs (RO1 NS38493 and ROL NS40059 to F.A.L.).</p><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia</title></titleInfo><name type="personal"><namePart type="given">Kazutaka</namePart><namePart type="family">Kobayashi</namePart><namePart type="termsOfAddress">MD PhD</namePart><affiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</affiliation><affiliation>Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan</affiliation><affiliation>Division of Applied Systems Neuroscience, Department of Advanced Medical Science, Nihon University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anthony E.</namePart><namePart type="family">Lang</namePart><namePart type="termsOfAddress">MD, FRCPC</namePart><affiliation>Division of Neurology, University Health Network and University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Hallett</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Human Motor Control Section, NINDS, NIH, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Frederick A.</namePart><namePart type="family">Lenz</namePart><namePart type="termsOfAddress">MD, PhD, FRCSC</namePart><affiliation>Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, Maryland, USA</affiliation><description>Correspondence: Department of Neurosurgery, Johns Hopkins Hospital, Meyer Building 8‐181, 600 North Wolfe Street, Baltimore, MD 21287‐7713, USA</description><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">2011-06</dateIssued><dateCaptured encoding="w3cdtf">2010-05-27</dateCaptured><dateValid encoding="w3cdtf">2010-11-11</dateValid><copyrightDate encoding="w3cdtf">2011</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">1</extent><extent unit="references">25</extent><extent unit="words">3483</extent></physicalDescription><abstract lang="en">Background:: This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made. Results:: The signal‐to‐noise ratio in the lowest frequency band (dystonia frequency < 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal‐to‐noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia. Conclusions:: These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal‐to‐noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflict of interest/financial disclosures: Nothing to report. This work was supported by the National Institutes of Health—National Institute of Neurological Disorders and Stroke Intramural and Extramural Programs (RO1 NS38493 and ROL NS40059 to F.A.L.). Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>psychogenic dystonia</topic><topic>organic dystonia</topic><topic>human thalamus</topic><topic>neuronal activity</topic><topic>plasticity</topic><topic>dystonia‐related activity</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Brief Report</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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1348</start><end>1352</end><total>5</total></extent></part></relatedItem><identifier type="istex">B12229A3A7E35E4D6D1A01D86470A3E3A2FF66CD</identifier><identifier type="DOI">10.1002/mds.23565</identifier><identifier type="ArticleID">MDS23565</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 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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