Levodopa response in Parkinsonism with multiple mitochondrial DNA deletions
Identifieur interne : 003495 ( Istex/Corpus ); précédent : 003494; suivant : 003496Levodopa response in Parkinsonism with multiple mitochondrial DNA deletions
Auteurs : Robert A. Wilcox ; Andrew Churchyard ; Henrik H. Dahl ; Wendy M. Hutchison ; Denise M. Kirby ; Dominic ThyagarajanSource :
- Movement Disorders [ 0885-3185 ] ; 2007-05-15.
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Abstract
We report a patient with an autosomal dominant chronic progressive external ophthalmoplegia phenotype associated with multiple mtDNA deletions in muscle from a family in which linkage analysis excluded mutations in DNA polymerase γ (POLG), adenine nucleotide translocase (ANT‐1) or C10orf2 (Twinkle). She presented with prominent Parkinsonism characterized by prolonged benefit from levodopa (L‐dopa) and the later development of L‐dopa induced dyskinesias and motor fluctuations. Thus L‐dopa responsiveness, L‐dopa induced dyskinesias and motor fluctuations may also occur in atypical Parkinsonism of mitochondrial disease, just as they may in multiple system atrophy. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21416
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ISTEX:BF7AB87EE5184277560D0A4B539369E92A79EEDDLe document en format XML
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Wilcox</name><affiliation><mods:affiliation>Department of Neurology, Flinders Medical Centre, SA, Australia</mods:affiliation></affiliation></author><author><name sortKey="Churchyard, Andrew" sort="Churchyard, Andrew" uniqKey="Churchyard A" first="Andrew" last="Churchyard">Andrew Churchyard</name><affiliation><mods:affiliation>Cabini Medical Centre, Malvern, Victoria, Australia</mods:affiliation></affiliation></author><author><name sortKey="Dahl, Henrik H" sort="Dahl, Henrik H" uniqKey="Dahl H" first="Henrik H." last="Dahl">Henrik H. Dahl</name><affiliation><mods:affiliation>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</mods:affiliation></affiliation></author><author><name sortKey="Hutchison, Wendy M" sort="Hutchison, Wendy M" uniqKey="Hutchison W" first="Wendy M." last="Hutchison">Wendy M. 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She presented with prominent Parkinsonism characterized by prolonged benefit from levodopa (L‐dopa) and the later development of L‐dopa induced dyskinesias and motor fluctuations. Thus L‐dopa responsiveness, L‐dopa induced dyskinesias and motor fluctuations may also occur in atypical Parkinsonism of mitochondrial disease, just as they may in multiple system atrophy. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Robert A. Wilcox BMBS, BSc(Hons), PhD</name><affiliations><json:string>Department of Neurology, Flinders Medical Centre, SA, Australia</json:string></affiliations></json:item><json:item><name>Andrew Churchyard FRACP, PhD</name><affiliations><json:string>Cabini Medical Centre, Malvern, Victoria, Australia</json:string></affiliations></json:item><json:item><name>Henrik H. Dahl PhD</name><affiliations><json:string>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</json:string></affiliations></json:item><json:item><name>Wendy M. Hutchison BAppSc</name><affiliations><json:string>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</json:string></affiliations></json:item><json:item><name>Denise M. Kirby PhD</name><affiliations><json:string>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</json:string></affiliations></json:item><json:item><name>Dominic Thyagarajan FRACP, MD</name><affiliations><json:string>Department of Neurology, Flinders Medical Centre, SA, Australia</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>mitochondrial disease</value></json:item><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>parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>chronic progressive external ophthalmoplegia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuropathy</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We report a patient with an autosomal dominant chronic progressive external ophthalmoplegia phenotype associated with multiple mtDNA deletions in muscle from a family in which linkage analysis excluded mutations in DNA polymerase γ (POLG), adenine nucleotide translocase (ANT‐1) or C10orf2 (Twinkle). 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She presented with prominent Parkinsonism characterized by prolonged benefit from levodopa (L‐dopa) and the later development of L‐dopa induced dyskinesias and motor fluctuations. 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number="2"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="13"></count><count type="wordTotal" number="1829"></count></countGroup><titleGroup><title type="main" xml:lang="en">Levodopa response in Parkinsonism with multiple mitochondrial DNA deletions</title><title type="short" xml:lang="en">Response of Levodopa in Parkinsonism</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Robert A.</givenNames><familyName>Wilcox</familyName><degrees>BMBS, BSc(Hons), PhD</degrees></personName><contactDetails><email>robert_wilcox@health.qld.gov.au</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Andrew</givenNames><familyName>Churchyard</familyName><degrees>FRACP, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Henrik H.</givenNames><familyName>Dahl</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Wendy M.</givenNames><familyName>Hutchison</familyName><degrees>BAppSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Denise M.</givenNames><familyName>Kirby</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Dominic</givenNames><familyName>Thyagarajan</familyName><degrees>FRACP, MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="AU" type="organization"><unparsedAffiliation>Department of Neurology, Flinders Medical Centre, SA, Australia</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="AU" type="organization"><unparsedAffiliation>Cabini Medical Centre, Malvern, Victoria, Australia</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="AU" type="organization"><unparsedAffiliation>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">mitochondrial disease</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">parkinsonism</keyword><keyword xml:id="kwd4">chronic progressive external ophthalmoplegia</keyword><keyword xml:id="kwd5">neuropathy</keyword></keywordGroup><supportingInformation><p> This article includes Supplementary Video, available online at <url href="http://www.interscience.wiley.com/jpages/0885-3185/suppmat"> http://www.interscience.wiley.com/jpages/0885‐3185/suppmat </url></p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds21416:jws-mds"></mediaResource><caption>The early view short clip shows Segments 1 and 3 of the full video. Segment 1.Movements before (A) and 60 min after (B) to L‐dopa treatment (A) Facies generally poorly animated with slow opening and closing of mouth slow extraocular movement show bilateral ptosis, external ophthalmoplegia of eye movements in all directions. But no rest tremor was present. (B) Facial animation and coordination of movements increased. Segment 3.(A) Hand opening and closing relatively slow. (B) Hand opening generally more fluent, rapid and increased amplitude. Increased dyskinetic movement of limbs and torso noted following L‐dopa.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We report a patient with an autosomal dominant chronic progressive external ophthalmoplegia phenotype associated with multiple mtDNA deletions in muscle from a family in which linkage analysis excluded mutations in DNA polymerase γ (POLG), adenine nucleotide translocase (ANT‐1) or C10orf2 (Twinkle). She presented with prominent Parkinsonism characterized by prolonged benefit from levodopa (<sc>L</sc>‐dopa) and the later development of <sc>L</sc>‐dopa induced dyskinesias and motor fluctuations. Thus <sc>L</sc>‐dopa responsiveness, <sc>L</sc>‐dopa induced dyskinesias and motor fluctuations may also occur in atypical Parkinsonism of mitochondrial disease, just as they may in multiple system atrophy. © 2007 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Levodopa response in Parkinsonism with multiple mitochondrial DNA deletions</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Response of Levodopa in Parkinsonism</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa response in Parkinsonism with multiple mitochondrial DNA deletions</title></titleInfo><name type="personal"><namePart type="given">Robert A.</namePart><namePart type="family">Wilcox</namePart><namePart type="termsOfAddress">BMBS, BSc(Hons), PhD</namePart><affiliation>Department of Neurology, Flinders Medical Centre, SA, Australia</affiliation><description>Correspondence: Department of Neurology, Royal Brisbane Hospital, Herston, QLD, 4029, Australia</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew</namePart><namePart type="family">Churchyard</namePart><namePart type="termsOfAddress">FRACP, PhD</namePart><affiliation>Cabini Medical Centre, Malvern, Victoria, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Henrik H.</namePart><namePart type="family">Dahl</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wendy M.</namePart><namePart type="family">Hutchison</namePart><namePart type="termsOfAddress">BAppSc</namePart><affiliation>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Denise M.</namePart><namePart type="family">Kirby</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Paediatrics, The Murdoch Childrens Research Institute and University of Melbourne, Royal Children's Hospital, Parkville, Melbourne, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dominic</namePart><namePart type="family">Thyagarajan</namePart><namePart type="termsOfAddress">FRACP, MD</namePart><affiliation>Department of Neurology, Flinders Medical Centre, SA, Australia</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">2007-05-15</dateIssued><dateCaptured encoding="w3cdtf">2006-09-29</dateCaptured><dateValid encoding="w3cdtf">2006-12-29</dateValid><copyrightDate encoding="w3cdtf">2007</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="tables">1</extent><extent unit="references">13</extent><extent unit="words">1829</extent></physicalDescription><abstract lang="en">We report a patient with an autosomal dominant chronic progressive external ophthalmoplegia phenotype associated with multiple mtDNA deletions in muscle from a family in which linkage analysis excluded mutations in DNA polymerase γ (POLG), adenine nucleotide translocase (ANT‐1) or C10orf2 (Twinkle). She presented with prominent Parkinsonism characterized by prolonged benefit from levodopa (L‐dopa) and the later development of L‐dopa induced dyskinesias and motor fluctuations. Thus L‐dopa responsiveness, L‐dopa induced dyskinesias and motor fluctuations may also occur in atypical Parkinsonism of mitochondrial disease, just as they may in multiple system atrophy. © 2007 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>mitochondrial disease</topic><topic>Parkinson's disease</topic><topic>parkinsonism</topic><topic>chronic progressive external ophthalmoplegia</topic><topic>neuropathy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><note type="content"> This article includes Supplementary Video, available online at http://www.interscience.wiley.com/jpages/0885‐3185/suppmatSupporting Info Item: The early view short clip shows Segments 1 and 3 of the full video. Segment 1.Movements before (A) and 60 min after (B) to L‐dopa treatment (A) Facies generally poorly animated with slow opening and closing of mouth slow extraocular movement show bilateral ptosis, external ophthalmoplegia of eye movements in all directions. But no rest tremor was present. (B) Facial animation and coordination of movements increased. Segment 3.(A) Hand opening and closing relatively slow. (B) Hand opening generally more fluent, rapid and increased amplitude. Increased dyskinetic movement of limbs and torso noted following L‐dopa. - </note><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>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1020</start><end>1023</end><total>4</total></extent></part></relatedItem><identifier type="istex">BF7AB87EE5184277560D0A4B539369E92A79EEDD</identifier><identifier type="DOI">10.1002/mds.21416</identifier><identifier type="ArticleID">MDS21416</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 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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