Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder
Identifieur interne : 000238 ( Istex/Corpus ); précédent : 000237; suivant : 000239Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder
Auteurs : Valerie Voon ; Christina Brezing ; Cecile Gallea ; Mark HallettSource :
- Movement Disorders [ 0885-3185 ] ; 2011-11.
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- KwdEn :
Abstract
Conversion disorder (CD) is characterized by unexplained neurological symptoms presumed related to psychological issues. The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self‐monitoring, limbic processing or top‐down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2‐button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age‐ and gender‐matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top‐down regulation. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23890
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The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self‐monitoring, limbic processing or top‐down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2‐button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age‐ and gender‐matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top‐down regulation. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Valerie Voon MD PhD</name><affiliations><json:string>Behavioral and Clinical Neurosciences Institute, University of Cambridge, Cambridge, UK</json:string></affiliations></json:item><json:item><name>Christina Brezing MD</name><affiliations><json:string>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Cecile Gallea PhD</name><affiliations><json:string>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Mark Hallett MD</name><affiliations><json:string>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>conversion disorder</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>action selection</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor initiation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>supplementary motor area</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>psychogenic movement disorder</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Conversion disorder (CD) is characterized by unexplained neurological symptoms presumed related to psychological issues. The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self‐monitoring, limbic processing or top‐down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2‐button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age‐ and gender‐matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top‐down regulation. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.885</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1858</abstractCharCount><pdfWordCount>4897</pdfWordCount><pdfCharCount>31998</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>249</abstractWordCount></qualityIndicators><title>Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder</title><genre><json:string>Serial article</json:string></genre><host><volume>26</volume><pages><total>8</total><last>2403</last><first>2396</first></pages><issn><json:string>0885-3185</json:string></issn><issue>13</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>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23890</json:string></doi><id>4B3FD3C9C2A1A0F9A94199948BE9CE3D59204854</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/4B3FD3C9C2A1A0F9A94199948BE9CE3D59204854/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/4B3FD3C9C2A1A0F9A94199948BE9CE3D59204854/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/4B3FD3C9C2A1A0F9A94199948BE9CE3D59204854/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder</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>2011</date></publicationStmt><notesStmt><note type="content">*Funding agencies: Intramural National Institutes of Health.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Dr. Voon has not had any activities to disclose for the last 2 years. Dr. Brezing has not had any activities to disclose for the last 2 years. Dr. Gallea has not had any activities to disclose for the last 2 years. Dr. Hallett serves as Chair of the Medical Advisory Board for and receives honoraria and funding for travel from the Neurotoxin Institute. He may accrue revenue on US Patent #6,780,413 B2 (Issued: August 24, 2004): Immunotoxin (MAB‐Ricin) for the treatment of focal movement disorders, and US Patent #7,407,478 (Issued: August 5, 2008): Coil for Magnetic Stimulation and methods for using the same (H‐coil); in relation to the latter, he has received license fee payments from the NIH (from Brainsway) for licensing of this patent. Dr. Hallett's research at the NIH is largely supported by the NIH Intramural Program. Supplemental research funds came from the US Army via the Henry Jackson Foundation, Ariston Pharmaceutical Company via a Cooperative Research and Development Agreement (CRADA) with NIH, and the Kinetics Foundation via a Clinical Trials Agreement (CTA) with NIH. Dr. Hallett serves as Chair of the Medical Advisory Board of the Benign Essential Blepharospasm Foundation and Chair of the Medical Advisory Board of the International Essential Tremor Foundation. He serves on editorial advisory boards for Clinical Neurophysiology, Brain, Acta Neurologica Scandinavica, Journal of Clinical Neurophysiology, Italian Journal of Neurological Sciences, Medical Problems of Performing Artists, Annals of Neurology, Neurology and Clinical Neurophysiology, The Cerebellum, NeuroRx, Current Trends in Neurology, Faculty of 1000 Medicine, Brain Stimulation, Journal of Movement Disorders (Korea), and is Editor‐in‐Chief of World Neurology. He receives publishing royalties from Blackwell Publisher, Cambridge University Press, Springer Verlag, Taylor & Francis Group, Oxford University Press, John Wiley & Sons, Massachusetts Medical Society, Wolters Kluwer, and Elsevier. He has received honoraria for lecturing from Columbia University, the Parkinson and Aging Research Foundation, University of Maryland, University of Wisconsin, State of New York, and University of Navara.</note><note type="content">*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">Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder</title><author><persName><forename type="first">Valerie</forename><surname>Voon</surname><roleName type="degree">MD PhD</roleName></persName><note type="correspondence"><p>Correspondence: Behavioural and Clinical Neurosciences Institute, Department of Experimental Psychology, University of Cambridge, Downing Site, Cambridge, CB2 3EB, UK</p></note><affiliation>Behavioral and Clinical Neurosciences Institute, University of Cambridge, Cambridge, UK</affiliation></author><author><persName><forename type="first">Christina</forename><surname>Brezing</surname><roleName type="degree">MD</roleName></persName><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</affiliation></author><author><persName><forename type="first">Cecile</forename><surname>Gallea</surname><roleName type="degree">PhD</roleName></persName><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</affiliation></author><author><persName><forename type="first">Mark</forename><surname>Hallett</surname><roleName type="degree">MD</roleName></persName><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, 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="2011-11"></date><biblScope unit="vol">26</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="2396">2396</biblScope><biblScope unit="page" to="2403">2403</biblScope></imprint></monogr><idno type="istex">4B3FD3C9C2A1A0F9A94199948BE9CE3D59204854</idno><idno type="DOI">10.1002/mds.23890</idno><idno type="ArticleID">MDS23890</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Conversion disorder (CD) is characterized by unexplained neurological symptoms presumed related to psychological issues. The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self‐monitoring, limbic processing or top‐down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2‐button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age‐ and gender‐matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top‐down regulation. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>conversion disorder</term></item><item><term>action selection</term></item><item><term>motor initiation</term></item><item><term>supplementary motor area</term></item><item><term>psychogenic movement disorder</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="2011-05-01">Received</change><change when="2011-07-03">Registration</change><change when="2011-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/4B3FD3C9C2A1A0F9A94199948BE9CE3D59204854/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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The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self‐monitoring, limbic processing or top‐down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2‐button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age‐ and gender‐matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top‐down regulation. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Funding agencies:</b> Intramural National Institutes of Health.</p></note><note xml:id="fn2"><p><b>Relevant conflicts of interest/financial disclosures:</b> Dr. Voon has not had any activities to disclose for the last 2 years. Dr. Brezing has not had any activities to disclose for the last 2 years. Dr. Gallea has not had any activities to disclose for the last 2 years. Dr. Hallett serves as Chair of the Medical Advisory Board for and receives honoraria and funding for travel from the Neurotoxin Institute. He may accrue revenue on US Patent #6,780,413 B2 (Issued: August 24, 2004): Immunotoxin (MAB‐Ricin) for the treatment of focal movement disorders, and US Patent #7,407,478 (Issued: August 5, 2008): Coil for Magnetic Stimulation and methods for using the same (H‐coil); in relation to the latter, he has received license fee payments from the NIH (from Brainsway) for licensing of this patent. Dr. Hallett's research at the NIH is largely supported by the NIH Intramural Program. Supplemental research funds came from the US Army via the Henry Jackson Foundation, Ariston Pharmaceutical Company via a Cooperative Research and Development Agreement (CRADA) with NIH, and the Kinetics Foundation via a Clinical Trials Agreement (CTA) with NIH. Dr. Hallett serves as Chair of the Medical Advisory Board of the Benign Essential Blepharospasm Foundation and Chair of the Medical Advisory Board of the International Essential Tremor Foundation. He serves on editorial advisory boards for Clinical Neurophysiology, Brain, Acta Neurologica Scandinavica, Journal of Clinical Neurophysiology, Italian Journal of Neurological Sciences, Medical Problems of Performing Artists, Annals of Neurology, Neurology and Clinical Neurophysiology, The Cerebellum, NeuroRx, Current Trends in Neurology, Faculty of 1000 Medicine, Brain Stimulation, Journal of Movement Disorders (Korea), and is Editor‐in‐Chief of World Neurology. He receives publishing royalties from Blackwell Publisher, Cambridge University Press, Springer Verlag, Taylor & Francis Group, Oxford University Press, John Wiley & Sons, Massachusetts Medical Society, Wolters Kluwer, and Elsevier. He has received honoraria for lecturing from Columbia University, the Parkinson and Aging Research Foundation, University of Maryland, University of Wisconsin, State of New York, and University of Navara.</p></note><note xml:id="fn3"><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><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Motor Preparation in Conversion Disorder</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder</title></titleInfo><name type="personal"><namePart type="given">Valerie</namePart><namePart type="family">Voon</namePart><namePart type="termsOfAddress">MD PhD</namePart><affiliation>Behavioral and Clinical Neurosciences Institute, University of Cambridge, Cambridge, UK</affiliation><description>Correspondence: Behavioural and Clinical Neurosciences Institute, Department of Experimental Psychology, University of Cambridge, Downing Site, Cambridge, CB2 3EB, UK</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christina</namePart><namePart type="family">Brezing</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cecile</namePart><namePart type="family">Gallea</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</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>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</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">2011-11</dateIssued><dateCaptured encoding="w3cdtf">2011-05-01</dateCaptured><dateValid encoding="w3cdtf">2011-07-03</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">4</extent><extent unit="tables">1</extent><extent unit="references">39</extent><extent unit="words">6153</extent></physicalDescription><abstract lang="en">Conversion disorder (CD) is characterized by unexplained neurological symptoms presumed related to psychological issues. The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self‐monitoring, limbic processing or top‐down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2‐button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age‐ and gender‐matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top‐down regulation. © 2011 Movement Disorder Society</abstract><note type="content">*Funding agencies: Intramural National Institutes of Health.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Dr. Voon has not had any activities to disclose for the last 2 years. Dr. Brezing has not had any activities to disclose for the last 2 years. Dr. Gallea has not had any activities to disclose for the last 2 years. Dr. Hallett serves as Chair of the Medical Advisory Board for and receives honoraria and funding for travel from the Neurotoxin Institute. He may accrue revenue on US Patent #6,780,413 B2 (Issued: August 24, 2004): Immunotoxin (MAB‐Ricin) for the treatment of focal movement disorders, and US Patent #7,407,478 (Issued: August 5, 2008): Coil for Magnetic Stimulation and methods for using the same (H‐coil); in relation to the latter, he has received license fee payments from the NIH (from Brainsway) for licensing of this patent. Dr. Hallett's research at the NIH is largely supported by the NIH Intramural Program. Supplemental research funds came from the US Army via the Henry Jackson Foundation, Ariston Pharmaceutical Company via a Cooperative Research and Development Agreement (CRADA) with NIH, and the Kinetics Foundation via a Clinical Trials Agreement (CTA) with NIH. Dr. Hallett serves as Chair of the Medical Advisory Board of the Benign Essential Blepharospasm Foundation and Chair of the Medical Advisory Board of the International Essential Tremor Foundation. He serves on editorial advisory boards for Clinical Neurophysiology, Brain, Acta Neurologica Scandinavica, Journal of Clinical Neurophysiology, Italian Journal of Neurological Sciences, Medical Problems of Performing Artists, Annals of Neurology, Neurology and Clinical Neurophysiology, The Cerebellum, NeuroRx, Current Trends in Neurology, Faculty of 1000 Medicine, Brain Stimulation, Journal of Movement Disorders (Korea), and is Editor‐in‐Chief of World Neurology. He receives publishing royalties from Blackwell Publisher, Cambridge University Press, Springer Verlag, Taylor & Francis Group, Oxford University Press, John Wiley & Sons, Massachusetts Medical Society, Wolters Kluwer, and Elsevier. He has received honoraria for lecturing from Columbia University, the Parkinson and Aging Research Foundation, University of Maryland, University of Wisconsin, State of New York, and University of Navara.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>conversion disorder</topic><topic>action selection</topic><topic>motor initiation</topic><topic>supplementary motor area</topic><topic>psychogenic movement disorder</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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>13</number></detail><extent unit="pages"><start>2396</start><end>2403</end><total>8</total></extent></part></relatedItem><identifier type="istex">4B3FD3C9C2A1A0F9A94199948BE9CE3D59204854</identifier><identifier type="DOI">10.1002/mds.23890</identifier><identifier type="ArticleID">MDS23890</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 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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