Milestones in Parkinson's disease therapeutics
Identifieur interne : 000106 ( Main/Corpus ); précédent : 000105; suivant : 000107Milestones in Parkinson's disease therapeutics
Auteurs : Olivier Rascol ; Andres Lozano ; Matthew Stern ; Werner PoeweSource :
- Movement Disorders [ 0885-3185 ] ; 2011-05.
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- KwdEn :
Abstract
In the mid‐1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23714
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ISTEX:A1E9CDE32413AB1BF3B0752267721A147AA6986DLe document en format XML
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A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Olivier Rascol MD, PhD</name><affiliations><json:string>Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III, Toulouse, France</json:string></affiliations></json:item><json:item><name>Andres Lozano MD</name><affiliations><json:string>Department of Neurosurgery, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Matthew Stern MD</name><affiliations><json:string>Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA</json:string></affiliations></json:item><json:item><name>Werner Poewe MD</name><affiliations><json:string>Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item></author><subject><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>treatment</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>dopamine agonists</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>catecholmethyltransferase inhibitors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>monoamine oxidase B inhibitors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>deep brain stimulation</value></json:item></subject><articleId><json:string>MDS23714</json:string></articleId><language><json:string>eng</json:string></language><abstract>In the mid‐1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1947</abstractCharCount><pdfWordCount>7818</pdfWordCount><pdfCharCount>53354</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>261</abstractWordCount></qualityIndicators><title>Milestones in Parkinson's disease therapeutics</title><genre><json:string>review-article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>11</total><last>1082</last><first>1072</first></pages><issn><json:string>0885-3185</json:string></issn><issue>6</issue><subject><json:item><value>Review</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23714</json:string></doi><id>A1E9CDE32413AB1BF3B0752267721A147AA6986D</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/A1E9CDE32413AB1BF3B0752267721A147AA6986D/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/A1E9CDE32413AB1BF3B0752267721A147AA6986D/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/A1E9CDE32413AB1BF3B0752267721A147AA6986D/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Milestones in Parkinson's disease therapeutics</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Relevant conflicts of interest/financial disclosures: Olivier Rascol has received honoraria for consultancy and lecture fees from Abbott, Addex, Boehringer Ingelheim, Eisai, GlaxosmithKline, Impax Pharmaceuticals, Lundbeck, Merck Serono, Movement Disorders Society, Novartis, Oxford Biomedica, Schering‐Plough, Servier, Teva Neuroscience, UCB and XenoPort. Andres Lozano is a consultant for Medtronic and Boston Scientific. Matthew Stern is a consultant for Adamas, Ipsen, Teva, Medtronic, and Schering‐Plough. Werner Poewe has received honoraria for consultancy and lecture fees from Astra Zeneca, Teva, Novartis, GSK, Boehringer‐Ingelheim, UCB, Orion Pharma, and Merck Serono in relation to clinical drug development programs for Parkinson's disease.</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">Milestones in Parkinson's disease therapeutics</title><author><persName><forename type="first">Olivier</forename><surname>Rascol</surname></persName><roleName type="degree">MD, PhD</roleName><note type="correspondence"><p>Correspondence: Department of Clinical Pharmacology, Faculty of Medicine, 37 Allées J Guesde, 31000 Toulouse, France</p></note><affiliation>Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III, Toulouse, France</affiliation></author><author><persName><forename type="first">Andres</forename><surname>Lozano</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurosurgery, University of Toronto, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Matthew</forename><surname>Stern</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA</affiliation></author><author><persName><forename type="first">Werner</forename><surname>Poewe</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria</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="2011-05"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1072">1072</biblScope><biblScope unit="page" to="1082">1082</biblScope></imprint></monogr><idno type="istex">A1E9CDE32413AB1BF3B0752267721A147AA6986D</idno><idno type="DOI">10.1002/mds.23714</idno><idno type="ArticleID">MDS23714</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In the mid‐1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>treatment</term></item><item><term>levodopa</term></item><item><term>dopamine agonists</term></item><item><term>catecholmethyltransferase inhibitors</term></item><item><term>monoamine oxidase B inhibitors</term></item><item><term>deep brain stimulation</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="2010-12-13">Received</change><change when="2011-02-22">Registration</change><change when="2011-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/A1E9CDE32413AB1BF3B0752267721A147AA6986D/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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A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 <i>Movement</i> Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Olivier Rascol has received honoraria for consultancy and lecture fees from Abbott, Addex, Boehringer Ingelheim, Eisai, GlaxosmithKline, Impax Pharmaceuticals, Lundbeck, Merck Serono, <i>Movement</i> Disorders Society, Novartis, Oxford Biomedica, Schering‐Plough, Servier, Teva Neuroscience, UCB and XenoPort. Andres Lozano is a consultant for Medtronic and Boston Scientific. Matthew Stern is a consultant for Adamas, Ipsen, Teva, Medtronic, and Schering‐Plough. Werner Poewe has received honoraria for consultancy and lecture fees from Astra Zeneca, Teva, Novartis, GSK, Boehringer‐Ingelheim, UCB, Orion Pharma, and Merck Serono in relation to clinical drug development programs for Parkinson's disease.</p></note><note xml:id="fn2"><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>Milestones in Parkinson's disease therapeutics</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Milestones in PD Therapeutics</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Milestones in Parkinson's disease therapeutics</title></titleInfo><name type="personal"><namePart type="given">Olivier</namePart><namePart type="family">Rascol</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III, Toulouse, France</affiliation><description>Correspondence: Department of Clinical Pharmacology, Faculty of Medicine, 37 Allées J Guesde, 31000 Toulouse, France</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andres</namePart><namePart type="family">Lozano</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosurgery, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matthew</namePart><namePart type="family">Stern</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria</affiliation><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">2011-05</dateIssued><dateCaptured encoding="w3cdtf">2010-12-13</dateCaptured><dateValid encoding="w3cdtf">2011-02-22</dateValid><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">2</extent><extent unit="references">130</extent><extent unit="words">9701</extent></physicalDescription><abstract lang="en">In the mid‐1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Olivier Rascol has received honoraria for consultancy and lecture fees from Abbott, Addex, Boehringer Ingelheim, Eisai, GlaxosmithKline, Impax Pharmaceuticals, Lundbeck, Merck Serono, Movement Disorders Society, Novartis, Oxford Biomedica, Schering‐Plough, Servier, Teva Neuroscience, UCB and XenoPort. Andres Lozano is a consultant for Medtronic and Boston Scientific. Matthew Stern is a consultant for Adamas, Ipsen, Teva, Medtronic, and Schering‐Plough. Werner Poewe has received honoraria for consultancy and lecture fees from Astra Zeneca, Teva, Novartis, GSK, Boehringer‐Ingelheim, UCB, Orion Pharma, and Merck Serono in relation to clinical drug development programs for Parkinson's disease.</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>Parkinson's disease</topic><topic>treatment</topic><topic>levodopa</topic><topic>dopamine agonists</topic><topic>catecholmethyltransferase inhibitors</topic><topic>monoamine oxidase B inhibitors</topic><topic>deep brain stimulation</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>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>2011</date><detail type="title"><title>25th Anniversary</title></detail><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1072</start><end>1082</end><total>11</total></extent></part></relatedItem><identifier type="istex">A1E9CDE32413AB1BF3B0752267721A147AA6986D</identifier><identifier type="DOI">10.1002/mds.23714</identifier><identifier type="ArticleID">MDS23714</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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