Late‐onset asymmetric myoclonus: An emerging syndrome
Identifieur interne : 000213 ( Istex/Corpus ); précédent : 000212; suivant : 000214Late‐onset asymmetric myoclonus: An emerging syndrome
Auteurs : Petra Katschnig ; João Massano ; Mark J. Edwards ; Petra Schwingenschuh ; Carla Cordivari ; Kailash P. BhatiaSource :
- Movement Disorders [ 0885-3185 ] ; 2011-08-01.
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- KwdEn :
Abstract
Asymmetric cortical myoclonus is typically thought to be associated with either contralateral cortical structural lesions or degenerative disorders such as corticobasal degeneration when onset is in middle‐aged or aged adults. This view has been challenged after a recent case series brought to light a syndrome of senile‐onset, asymmetric cortical myoclonus not associated with any such identifiable disorders, thus, named “primary progressive myoclonus of aging.” This is rare and no other reports have been published; hence, further such cases need to be highlighted.
Here, we describe 3 patients with some similarities, namely, adult‐onset, asymmetric myoclonus that is most likely to be cortical, with an unremarkable thorough diagnostic workup, but with younger age at onset and longer follow‐up time.
This report expands on previous phenotypical descriptions attempting to further develop and refine this possible diagnostic entity. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23676
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ISTEX:3B12ACD04830F34DF13F308658304538F752C4CBLe document en format XML
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This research was supported by National Institutes of Health Grants R01 NS39422, P30 ES09089, P42 ES10349, and R01 CA102484. 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Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="90"><doi origin="wiley" registered="yes">10.1002/mds.v26.9</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2011-08-01">1 August 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="280" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23676</doi><idGroup><id type="unit" value="MDS23676"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-03-20"></event><event type="manuscriptRevised" date="2010-12-31"></event><event type="manuscriptAccepted" date="2011-01-13"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2011-12-16"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-05-26"></event><event type="publishedOnlineFinalForm" date="2011-08-09"></event><event type="firstOnline" date="2011-05-26"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1744</numbering><numbering type="pageLast">1747</numbering></numberingGroup><correspondenceTo>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, WC1N 3BG UK, Box 13</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23676.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="16"></count><count type="wordTotal" number="3201"></count></countGroup><titleGroup><title type="main" xml:lang="en">Late‐onset asymmetric myoclonus: An emerging syndrome<link href="#fn1"></link></title><title type="short" xml:lang="en">Brief Report</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Petra</givenNames><familyName>Katschnig</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>João</givenNames><familyName>Massano</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Mark J.</givenNames><familyName>Edwards</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Petra</givenNames><familyName>Schwingenschuh</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Carla</givenNames><familyName>Cordivari</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Kailash P.</givenNames><familyName>Bhatia</familyName><degrees>MD</degrees></personName><contactDetails><email>k.bhatia@ion.ucl.ac.uk</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="AT" type="organization"><unparsedAffiliation>Department of Neurology, Division of Special Neurology, Medical University Graz, Graz, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="PT" type="organization"><unparsedAffiliation>Department of Neurology, Hospital de S. João, and Faculdade de Medicina da Universidade do Porto, Porto, Portugal</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="GB" type="organization"><unparsedAffiliation>Department of Clinical Neurophysiology, National Hospital for Neurology and Neurosurgery, University College London, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">myoclonus</keyword><keyword xml:id="kwd2">cortex</keyword><keyword xml:id="kwd3">primary</keyword><keyword xml:id="kwd4">asymmetric</keyword><keyword xml:id="kwd5">aging</keyword></keywordGroup><supportingInformation><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23676:Katschnig_1"></mediaResource><caption>Supplemental video</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23676:Katschnig_2"></mediaResource><caption>Supplemental video</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23676:Katschnig_3"></mediaResource><caption>Supplemental video</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Background:</title><p>Asymmetric cortical myoclonus is typically thought to be associated with either contralateral cortical structural lesions or degenerative disorders such as corticobasal degeneration when onset is in middle‐aged or aged adults. This view has been challenged after a recent case series brought to light a syndrome of senile‐onset, asymmetric cortical myoclonus not associated with any such identifiable disorders, thus, named “primary progressive myoclonus of aging.” This is rare and no other reports have been published; hence, further such cases need to be highlighted.</p></section><section xml:id="abs1-2"><title type="main">Case reports:</title><p>Here, we describe 3 patients with some similarities, namely, adult‐onset, asymmetric myoclonus that is most likely to be cortical, with an unremarkable thorough diagnostic workup, but with younger age at onset and longer follow‐up time.</p></section><section xml:id="abs1-3"><title type="main">Conclusions:</title><p>This report expands on previous phenotypical descriptions attempting to further develop and refine this possible diagnostic entity. © 2011 Movement Disorder Society</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Relevant conflicts of interest/financial disclosures: Nothing to report.</p><p>This research was supported by National Institutes of Health Grants R01 NS39422, P30 ES09089, P42 ES10349, and R01 CA102484.</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>Late‐onset asymmetric myoclonus: An emerging syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Brief Report</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Late‐onset asymmetric myoclonus: An emerging syndrome</title></titleInfo><name type="personal"><namePart type="given">Petra</namePart><namePart type="family">Katschnig</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</affiliation><affiliation>Department of Neurology, Division of Special Neurology, Medical University Graz, Graz, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">João</namePart><namePart type="family">Massano</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</affiliation><affiliation>Department of Neurology, Hospital de S. João, and Faculdade de Medicina da Universidade do Porto, Porto, Portugal</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark J.</namePart><namePart type="family">Edwards</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Petra</namePart><namePart type="family">Schwingenschuh</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</affiliation><affiliation>Department of Neurology, Division of Special Neurology, Medical University Graz, Graz, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carla</namePart><namePart type="family">Cordivari</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurophysiology, National Hospital for Neurology and Neurosurgery, University College London, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kailash P.</namePart><namePart type="family">Bhatia</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom</affiliation><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, WC1N 3BG UK, Box 13</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-08-01</dateIssued><dateCaptured encoding="w3cdtf">2010-03-20</dateCaptured><dateValid encoding="w3cdtf">2011-01-13</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">2</extent><extent unit="references">16</extent><extent unit="words">3201</extent></physicalDescription><abstract>Asymmetric cortical myoclonus is typically thought to be associated with either contralateral cortical structural lesions or degenerative disorders such as corticobasal degeneration when onset is in middle‐aged or aged adults. This view has been challenged after a recent case series brought to light a syndrome of senile‐onset, asymmetric cortical myoclonus not associated with any such identifiable disorders, thus, named “primary progressive myoclonus of aging.” This is rare and no other reports have been published; hence, further such cases need to be highlighted.</abstract><abstract>Here, we describe 3 patients with some similarities, namely, adult‐onset, asymmetric myoclonus that is most likely to be cortical, with an unremarkable thorough diagnostic workup, but with younger age at onset and longer follow‐up time.</abstract><abstract>This report expands on previous phenotypical descriptions attempting to further develop and refine this possible diagnostic entity. © 2011 Movement Disorder Society</abstract><note type="additional physical form">Supplemental videoSupplemental videoSupplemental video</note><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report. This research was supported by National Institutes of Health Grants R01 NS39422, P30 ES09089, P42 ES10349, and R01 CA102484. Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>keywords</genre><topic>myoclonus</topic><topic>cortex</topic><topic>primary</topic><topic>asymmetric</topic><topic>aging</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>9</number></detail><extent unit="pages"><start>1744</start><end>1747</end><total>4</total></extent></part></relatedItem><identifier type="istex">3B12ACD04830F34DF13F308658304538F752C4CB</identifier><identifier type="DOI">10.1002/mds.23676</identifier><identifier type="ArticleID">MDS23676</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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