A trial of dextromethorphan in parkinsonian patients with motor response complications
Identifieur interne : 002A80 ( Istex/Corpus ); précédent : 002A79; suivant : 002A81A trial of dextromethorphan in parkinsonian patients with motor response complications
Auteurs : Leo Verhagen Metman ; Pierre J. Blanchet ; Pep N Van Den Munckhof ; Paolo Del Dotto ; Remco Natté ; Thomas N. ChaseSource :
- Movement Disorders [ 0885-3185 ] ; 1998-05.
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- KwdEn :
Abstract
The effects of the NMDA antagonist dextromethorphan (DM) on levodopa‐associated dyskinesias and motor fluctuations were studied in patients with advanced Parkinson's disease. During initial open‐label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60–120 mg/day). The 12 remaining patients either experinced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double‐blind, placebo‐controlled, crossover study with two 2‐week arms separted by 1 week wash‐out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% accfording to UPDRS interviews, without compromising the anti‐Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. Although the narrow therapeutic index of DM limits its clinical usefulness, these findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate levodopa‐associated motor complications.
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DOI: 10.1002/mds.870130307
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During initial open‐label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60–120 mg/day). The 12 remaining patients either experinced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double‐blind, placebo‐controlled, crossover study with two 2‐week arms separted by 1 week wash‐out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% accfording to UPDRS interviews, without compromising the anti‐Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. Although the narrow therapeutic index of DM limits its clinical usefulness, these findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate levodopa‐associated motor complications.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Leo Verhagen Metman MD</name><affiliations><json:string>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</json:string></affiliations></json:item><json:item><name>Pierre J. 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Chase MD</name><affiliations><json:string>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>NMDA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glutamate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Motor complications</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The effects of the NMDA antagonist dextromethorphan (DM) on levodopa‐associated dyskinesias and motor fluctuations were studied in patients with advanced Parkinson's disease. During initial open‐label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60–120 mg/day). The 12 remaining patients either experinced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double‐blind, placebo‐controlled, crossover study with two 2‐week arms separted by 1 week wash‐out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% accfording to UPDRS interviews, without compromising the anti‐Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. 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During initial open‐label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60–120 mg/day). The 12 remaining patients either experinced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double‐blind, placebo‐controlled, crossover study with two 2‐week arms separted by 1 week wash‐out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% accfording to UPDRS interviews, without compromising the anti‐Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. Although the narrow therapeutic index of DM limits its clinical usefulness, these findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate levodopa‐associated motor complications.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>NMDA</term></item><item><term>Glutamate</term></item><item><term>Motor complications</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-08-19">Received</change><change when="1997-12-07">Registration</change><change when="1998-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6678D223545AE509A9A53066038F609551C223B3/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="tocForm">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/mds.v13:3</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="1998-05">May 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="7" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870130307</doi><idGroup><id type="unit" value="MDS870130307"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1998 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1997-08-19"></event><event type="manuscriptRevised" date="1997-12-04"></event><event type="manuscriptAccepted" date="1997-12-07"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.3.2 mode:FullText" date="2014-06-23"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.3.2 mode:FullText" date="2014-06-23"></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">414</numbering><numbering type="pageLast">417</numbering></numberingGroup><correspondenceTo>The National Institutes of Health, Building 10, Room 5C104, 10 Center Dr. MSC 1406, Bethesda, MD 20892‐1406, U.S.A.===</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870130307.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="21"></count></countGroup><titleGroup><title type="main" xml:lang="en">A trial of dextromethorphan in parkinsonian patients with motor response complications</title><title type="short" xml:lang="en">DEXTROMETHORPHAN IN ADVANCED PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Leo Verhagen</givenNames><familyName>Metman</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Pierre J.</givenNames><familyName>Blanchet</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Pepÿn</givenNames><familyName>van den Munckhof</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Paolo Del</givenNames><familyName>Dotto</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Remco</givenNames><familyName>Natté</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Thomas N.</givenNames><familyName>Chase</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">NMDA</keyword><keyword xml:id="kwd2">Glutamate</keyword><keyword xml:id="kwd3">Motor complications</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The effects of the NMDA antagonist dextromethorphan (DM) on levodopa‐associated dyskinesias and motor fluctuations were studied in patients with advanced Parkinson's disease. During initial open‐label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60–120 mg/day). The 12 remaining patients either experinced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double‐blind, placebo‐controlled, crossover study with two 2‐week arms separted by 1 week wash‐out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% accfording to UPDRS interviews, without compromising the anti‐Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. Although the narrow therapeutic index of DM limits its clinical usefulness, these findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate levodopa‐associated motor complications.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>A trial of dextromethorphan in parkinsonian patients with motor response complications</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>DEXTROMETHORPHAN IN ADVANCED PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>A trial of dextromethorphan in parkinsonian patients with motor response complications</title></titleInfo><name type="personal"><namePart type="given">Leo Verhagen</namePart><namePart type="family">Metman</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre J.</namePart><namePart type="family">Blanchet</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pepÿn</namePart><namePart type="family">van den Munckhof</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paolo Del</namePart><namePart type="family">Dotto</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Remco</namePart><namePart type="family">Natté</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas N.</namePart><namePart type="family">Chase</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.</affiliation><description>Correspondence: The National Institutes of Health, Building 10, Room 5C104, 10 Center Dr. MSC 1406, Bethesda, MD 20892‐1406, U.S.A.===</description><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">1998-05</dateIssued><dateCaptured encoding="w3cdtf">1997-08-19</dateCaptured><dateValid encoding="w3cdtf">1997-12-07</dateValid><copyrightDate encoding="w3cdtf">1998</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="tables">1</extent><extent unit="references">21</extent></physicalDescription><abstract lang="en">The effects of the NMDA antagonist dextromethorphan (DM) on levodopa‐associated dyskinesias and motor fluctuations were studied in patients with advanced Parkinson's disease. During initial open‐label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60–120 mg/day). The 12 remaining patients either experinced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double‐blind, placebo‐controlled, crossover study with two 2‐week arms separted by 1 week wash‐out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% accfording to UPDRS interviews, without compromising the anti‐Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. Although the narrow therapeutic index of DM limits its clinical usefulness, these findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate levodopa‐associated motor complications.</abstract><subject lang="en"><genre>Keywords</genre><topic>NMDA</topic><topic>Glutamate</topic><topic>Motor complications</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>414</start><end>417</end><total>4</total></extent></part></relatedItem><identifier type="istex">6678D223545AE509A9A53066038F609551C223B3</identifier><identifier type="DOI">10.1002/mds.870130307</identifier><identifier type="ArticleID">MDS870130307</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 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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