Levodopa‐induced dyskinesias
Identifieur interne : 000224 ( Main/Corpus ); précédent : 000223; suivant : 000225Levodopa‐induced dyskinesias
Auteurs : Giovanni Fabbrini ; Jonathan M. Brotchie ; Francisco Grandas ; Masahiro Nomoto ; Christopher G. GoetzSource :
- Movement Disorders [ 0885-3185 ] ; 2007-07-30.
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- KwdEn :
Abstract
Levodopa‐induced dyskinesias (LID) are common and difficult to treat. This review focuses on three issues related to LID: clinical features, classification and rating, pathophysiology and pathogenesis, and management. The three primary clinical syndromes are OFF‐period dystonia, peak‐dose dyskinesia, and diphasic dyskinesia. Several other forms also occur, making the evaluation and choice of treatment complicated. A core component of the pathophysiology of LID is overactivity of the direct striatal output pathway. This pathway provides a direct GABAergic connection by which the striatum inhibits the output regions of the basal ganglia, i.e., the internal globus pallidus and the substantia nigra pars reticulata. Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α2 adrenergic, serotonergic (5HT1A, 5HT2A), opioid, histamine H3, adenosine A2A receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence‐based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. New rating measures to assess severity and disability related to dyskinesia are in the process of development and clinimetric testing. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21475
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This review focuses on three issues related to LID: clinical features, classification and rating, pathophysiology and pathogenesis, and management. The three primary clinical syndromes are OFF‐period dystonia, peak‐dose dyskinesia, and diphasic dyskinesia. Several other forms also occur, making the evaluation and choice of treatment complicated. A core component of the pathophysiology of LID is overactivity of the direct striatal output pathway. This pathway provides a direct GABAergic connection by which the striatum inhibits the output regions of the basal ganglia, i.e., the internal globus pallidus and the substantia nigra pars reticulata. Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α2 adrenergic, serotonergic (5HT1A, 5HT2A), opioid, histamine H3, adenosine A2A receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence‐based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. New rating measures to assess severity and disability related to dyskinesia are in the process of development and clinimetric testing. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Giovanni Fabbrini MD</name><affiliations><json:string>Department of Neurological Sciences University of Rome “La Sapienza”, Rome, Italy</json:string></affiliations></json:item><json:item><name>Jonathan M. Brotchie PhD</name><affiliations><json:string>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</json:string></affiliations></json:item><json:item><name>Francisco Grandas MD, PhD</name><affiliations><json:string>Department of Neurology, Hospital General Universitario “Gregorio Marañón”, Madrid, Spain</json:string></affiliations></json:item><json:item><name>Masahiro Nomoto MD, PhD</name><affiliations><json:string>Department of Therapeutic Medicine, Faculty of Medicine, Ehime University Hospital, Ehime, Japan</json:string></affiliations></json:item><json:item><name>Christopher G. Goetz MD</name><affiliations><json:string>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dyskinesia</value></json:item></subject><articleId><json:string>MDS21475</json:string></articleId><language><json:string>eng</json:string></language><abstract>Levodopa‐induced dyskinesias (LID) are common and difficult to treat. This review focuses on three issues related to LID: clinical features, classification and rating, pathophysiology and pathogenesis, and management. The three primary clinical syndromes are OFF‐period dystonia, peak‐dose dyskinesia, and diphasic dyskinesia. Several other forms also occur, making the evaluation and choice of treatment complicated. A core component of the pathophysiology of LID is overactivity of the direct striatal output pathway. This pathway provides a direct GABAergic connection by which the striatum inhibits the output regions of the basal ganglia, i.e., the internal globus pallidus and the substantia nigra pars reticulata. Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α2 adrenergic, serotonergic (5HT1A, 5HT2A), opioid, histamine H3, adenosine A2A receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence‐based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. 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All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Levodopa‐induced dyskinesias</title><author><persName><forename type="first">Giovanni</forename><surname>Fabbrini</surname></persName><roleName type="degree">MD</roleName><note type="biography">This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</note><affiliation>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</affiliation><note type="correspondence"><p>Correspondence: Department of Neurological Sciences, University “La Sapienza”, Viale dell'Università 30, 00185 Rome, Italy</p></note><affiliation>Department of Neurological Sciences University of Rome “La Sapienza”, Rome, Italy</affiliation></author><author><persName><forename type="first">Jonathan M.</forename><surname>Brotchie</surname></persName><roleName type="degree">PhD</roleName><note type="biography">This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</note><affiliation>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</affiliation><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation></author><author><persName><forename type="first">Francisco</forename><surname>Grandas</surname></persName><roleName type="degree">MD, PhD</roleName><note type="biography">This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</note><affiliation>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</affiliation><affiliation>Department of Neurology, Hospital General Universitario “Gregorio Marañón”, Madrid, Spain</affiliation></author><author><persName><forename type="first">Masahiro</forename><surname>Nomoto</surname></persName><roleName type="degree">MD, PhD</roleName><note type="biography">This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</note><affiliation>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</affiliation><affiliation>Department of Therapeutic Medicine, Faculty of Medicine, Ehime University Hospital, Ehime, Japan</affiliation></author><author><persName><forename type="first">Christopher G.</forename><surname>Goetz</surname></persName><roleName type="degree">MD</roleName><note type="biography">This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</note><affiliation>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</affiliation><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α2 adrenergic, serotonergic (5HT1A, 5HT2A), opioid, histamine H3, adenosine A2A receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence‐based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. New rating measures to assess severity and disability related to dyskinesia are in the process of development and clinimetric testing. © 2007 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson</term></item><item><term>levodopa</term></item><item><term>dyskinesia</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Review</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-11-27">Received</change><change when="2007-02-21">Registration</change><change when="2007-07-30">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CC3323805F38A8257F0A40F3113E504989102B49/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="100"><doi origin="wiley" registered="yes">10.1002/mds.v22:10</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue">10</numbering></numberingGroup><coverDate startDate="2007-07-30">30 July 2007</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="30" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.21475</doi><idGroup><id type="unit" value="MDS21475"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="articleCategory">Review</title><title type="tocHeading1">Reviews</title></titleGroup><copyright ownership="thirdParty">Copyright © 2007 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2006-11-27"></event><event type="manuscriptRevised" date="2007-01-31"></event><event type="manuscriptAccepted" date="2007-02-21"></event><event type="publishedOnlineEarlyUnpaginated" date="2007-04-11"></event><event type="firstOnline" date="2007-04-11"></event><event type="publishedOnlineFinalForm" date="2007-07-23"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></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">1379</numbering><numbering type="pageLast">1389</numbering></numberingGroup><correspondenceTo>Department of Neurological Sciences, University “La Sapienza”, Viale dell'Università 30, 00185 Rome, Italy</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21475.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="74"></count><count type="wordTotal" number="8024"></count></countGroup><titleGroup><title type="main" xml:lang="en">Levodopa‐induced dyskinesias<link href="#fn1"></link></title><title type="short" xml:lang="en">Levodopa‐Induced Dyskinesias</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes" noteRef="#fn1"><personName><givenNames>Giovanni</givenNames><familyName>Fabbrini</familyName><degrees>MD</degrees></personName><contactDetails><email>giovanni.fabbrini@uniroma1.it</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2" noteRef="#fn1"><personName><givenNames>Jonathan M.</givenNames><familyName>Brotchie</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3" noteRef="#fn1"><personName><givenNames>Francisco</givenNames><familyName>Grandas</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4" noteRef="#fn1"><personName><givenNames>Masahiro</givenNames><familyName>Nomoto</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af5" noteRef="#fn1"><personName><givenNames>Christopher G.</givenNames><familyName>Goetz</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurological Sciences University of Rome “La Sapienza”, Rome, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="ES" type="organization"><unparsedAffiliation>Department of Neurology, Hospital General Universitario “Gregorio Marañón”, Madrid, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="JP" type="organization"><unparsedAffiliation>Department of Therapeutic Medicine, Faculty of Medicine, Ehime University Hospital, Ehime, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson</keyword><keyword xml:id="kwd2">levodopa</keyword><keyword xml:id="kwd3">dyskinesia</keyword></keywordGroup><supportingInformation><p> This article is part of the journal's CME program. The CME form can be found on page 1523 and is available online at <url href="http://www.movementdisorders.org/education/activities.html"> http://www.movementdisorders.org/education/activities.html </url> . </p></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Levodopa‐induced dyskinesias (LID) are common and difficult to treat. This review focuses on three issues related to LID: clinical features, classification and rating, pathophysiology and pathogenesis, and management. The three primary clinical syndromes are OFF‐period dystonia, peak‐dose dyskinesia, and diphasic dyskinesia. Several other forms also occur, making the evaluation and choice of treatment complicated. A core component of the pathophysiology of LID is overactivity of the direct striatal output pathway. This pathway provides a direct GABAergic connection by which the striatum inhibits the output regions of the basal ganglia, i.e., the internal globus pallidus and the substantia nigra pars reticulata. Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α<sub>2</sub> adrenergic, serotonergic (5HT<sub>1A</sub>, 5HT<sub>2A</sub>), opioid, histamine H<sub>3</sub>, adenosine A<sub>2A</sub> receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence‐based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. New rating measures to assess severity and disability related to dyskinesia are in the process of development and clinimetric testing. © 2007 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Levodopa‐induced dyskinesias</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Levodopa‐Induced Dyskinesias</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa‐induced dyskinesias</title></titleInfo><name type="personal"><namePart type="given">Giovanni</namePart><namePart type="family">Fabbrini</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences University of Rome “La Sapienza”, Rome, Italy</affiliation><description>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</description><description>Correspondence: Department of Neurological Sciences, University “La Sapienza”, Viale dell'Università 30, 00185 Rome, Italy</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jonathan M.</namePart><namePart type="family">Brotchie</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation><description>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francisco</namePart><namePart type="family">Grandas</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Hospital General Universitario “Gregorio Marañón”, Madrid, Spain</affiliation><description>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masahiro</namePart><namePart type="family">Nomoto</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Therapeutic Medicine, Faculty of Medicine, Ehime University Hospital, Ehime, Japan</affiliation><description>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher G.</namePart><namePart type="family">Goetz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation><description>This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-07-30</dateIssued><dateCaptured encoding="w3cdtf">2006-11-27</dateCaptured><dateValid encoding="w3cdtf">2007-02-21</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">1</extent><extent unit="tables">3</extent><extent unit="references">74</extent><extent unit="words">8024</extent></physicalDescription><abstract lang="en">Levodopa‐induced dyskinesias (LID) are common and difficult to treat. This review focuses on three issues related to LID: clinical features, classification and rating, pathophysiology and pathogenesis, and management. The three primary clinical syndromes are OFF‐period dystonia, peak‐dose dyskinesia, and diphasic dyskinesia. Several other forms also occur, making the evaluation and choice of treatment complicated. A core component of the pathophysiology of LID is overactivity of the direct striatal output pathway. This pathway provides a direct GABAergic connection by which the striatum inhibits the output regions of the basal ganglia, i.e., the internal globus pallidus and the substantia nigra pars reticulata. Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α2 adrenergic, serotonergic (5HT1A, 5HT2A), opioid, histamine H3, adenosine A2A receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence‐based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. New rating measures to assess severity and disability related to dyskinesia are in the process of development and clinimetric testing. © 2007 Movement Disorder Society</abstract><note type="content">*This manuscript is an adaptation of a syllabus contribution to the Movement Disorder Society's annual congress, 2006. All authors received an honorarium from the MDS for participation in the program related to the syllabus material. Other disclosures include: Dr. Fabbrini: None; Dr. Brotchie: Consultancy fees from Akuta Ltd; Dr. Grandas: Consultancy fees from Schwarz Pharma; Dr. Nomoto: None; Dr. Goetz: Honoraria received from Merck KaGA for serving on the Publication Committee for Sarizotan Programs.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson</topic><topic>levodopa</topic><topic>dyskinesia</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> This article is part of the journal's CME program. The CME form can be found on page 1523 and is available online at http://www.movementdisorders.org/education/activities.html .</note><subject><genre>article category</genre><topic>Review</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>10</number></detail><extent unit="pages"><start>1379</start><end>1389</end><total>11</total></extent></part></relatedItem><identifier type="istex">CC3323805F38A8257F0A40F3113E504989102B49</identifier><identifier type="DOI">10.1002/mds.21475</identifier><identifier type="ArticleID">MDS21475</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 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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