Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial
Identifieur interne : 000250 ( Main/Corpus ); précédent : 000249; suivant : 000251Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial
Auteurs : Ira Shoulson ; David Oakes ; Stanley Fahn ; Anthony Lang ; J. William Langston ; Peter Lewitt ; C. Warren Olanow ; John B. Penney ; Caroline Tanner ; Karl Kieburtz ; Alice RudolphSource :
- Annals of Neurology [ 0364-5134 ] ; 2002-05.
Abstract
Deprenyl (selegiline) delays the need for levodopa therapy in patients with early Parkinson's disease, but the long‐term benefits of this treatment remain unclear. During 1987 to 1988, 800 patients with early Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments, or a placebo and were then placed on active deprenyl (10mg/day). A second, independent randomization was carried out in early 1993 for 368 subjects who by that time had required levodopa and who had consented to continuing the deprenyl treatment (D subjects) or changing to a matching placebo (P subjects) under double‐blind conditions. The first development of wearing off, dyskinesias, or on–off motor fluctuations was the prespecified primary outcome measure. During the average 2‐year follow‐up, there were no differences between the treatment groups with respect to the primary outcome measure (hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; p = 0.38), withdrawal from the study, death, or adverse events. Although 34% of D subjects developed dyskinesias and only 19% of P subjects did (p = 0.006), only 16% of D subjects developed freezing of gait but 29% of P subjects did (p = 0.0003). Decline in motor performance was less in D subjects than P subjects. Levodopa‐treated Parkinson's disease patients who had been treated with deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.
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DOI: 10.1002/ana.10191
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Penney</name></author><author><name sortKey="Tanner, Caroline" sort="Tanner, Caroline" uniqKey="Tanner C" first="Caroline" last="Tanner">Caroline Tanner</name><affiliation><mods:affiliation>Parkinson's Institute, Sunnyvale, CA</mods:affiliation></affiliation></author><author><name sortKey="Kieburtz, Karl" sort="Kieburtz, Karl" uniqKey="Kieburtz K" first="Karl" last="Kieburtz">Karl Kieburtz</name><affiliation><mods:affiliation>University of Rochester Medical Center, Rochester, NY</mods:affiliation></affiliation></author><author><name sortKey="Rudolph, Alice" sort="Rudolph, Alice" uniqKey="Rudolph A" first="Alice" last="Rudolph">Alice Rudolph</name><affiliation><mods:affiliation>University of Rochester Medical Center, Rochester, NY</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-05">2002-05</date><biblScope unit="volume">51</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="604">604</biblScope><biblScope unit="page" to="612">612</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">7C5BBF056B2C59C8EC40B42446B6F5512D575A77</idno><idno type="DOI">10.1002/ana.10191</idno><idno type="ArticleID">ANA10191</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Deprenyl (selegiline) delays the need for levodopa therapy in patients with early Parkinson's disease, but the long‐term benefits of this treatment remain unclear. During 1987 to 1988, 800 patients with early Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments, or a placebo and were then placed on active deprenyl (10mg/day). A second, independent randomization was carried out in early 1993 for 368 subjects who by that time had required levodopa and who had consented to continuing the deprenyl treatment (D subjects) or changing to a matching placebo (P subjects) under double‐blind conditions. The first development of wearing off, dyskinesias, or on–off motor fluctuations was the prespecified primary outcome measure. During the average 2‐year follow‐up, there were no differences between the treatment groups with respect to the primary outcome measure (hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; p = 0.38), withdrawal from the study, death, or adverse events. Although 34% of D subjects developed dyskinesias and only 19% of P subjects did (p = 0.006), only 16% of D subjects developed freezing of gait but 29% of P subjects did (p = 0.0003). Decline in motor performance was less in D subjects than P subjects. Levodopa‐treated Parkinson's disease patients who had been treated with deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ira Shoulson MD</name><affiliations><json:string>University of Rochester Medical Center, Rochester, NY</json:string></affiliations></json:item><json:item><name>David Oakes PhD</name><affiliations><json:string>University of Rochester Medical Center, Rochester, NY</json:string></affiliations></json:item><json:item><name>Stanley Fahn MD</name><affiliations><json:string>Columbia–Presbyterian Medical Center, New York, NY</json:string></affiliations></json:item><json:item><name>Anthony Lang MD</name><affiliations><json:string>Toronto Western Hospital, Toronto, ON</json:string></affiliations></json:item><json:item><name>J. William Langston MD</name><affiliations><json:string>Parkinson's Institute, Sunnyvale, CA</json:string></affiliations></json:item><json:item><name>Peter LeWitt MD</name><affiliations><json:string>Sinai Hospital, Detroit, MI</json:string></affiliations></json:item><json:item><name>C. Warren Olanow MD</name><affiliations><json:string>Mt. Sinai School of Medicine, New York, NY</json:string></affiliations></json:item><json:item><name>John B. Penney MD</name></json:item><json:item><name>Caroline Tanner MD, PhD</name><affiliations><json:string>Parkinson's Institute, Sunnyvale, CA</json:string></affiliations></json:item><json:item><name>Karl Kieburtz MD</name><affiliations><json:string>University of Rochester Medical Center, Rochester, NY</json:string></affiliations></json:item><json:item><name>Alice Rudolph PhD</name><affiliations><json:string>University of Rochester Medical Center, Rochester, NY</json:string></affiliations></json:item></author><articleId><json:string>ANA10191</json:string></articleId><language><json:string>eng</json:string></language><abstract>Deprenyl (selegiline) delays the need for levodopa therapy in patients with early Parkinson's disease, but the long‐term benefits of this treatment remain unclear. During 1987 to 1988, 800 patients with early Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments, or a placebo and were then placed on active deprenyl (10mg/day). A second, independent randomization was carried out in early 1993 for 368 subjects who by that time had required levodopa and who had consented to continuing the deprenyl treatment (D subjects) or changing to a matching placebo (P subjects) under double‐blind conditions. The first development of wearing off, dyskinesias, or on–off motor fluctuations was the prespecified primary outcome measure. During the average 2‐year follow‐up, there were no differences between the treatment groups with respect to the primary outcome measure (hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; p = 0.38), withdrawal from the study, death, or adverse events. Although 34% of D subjects developed dyskinesias and only 19% of P subjects did (p = 0.006), only 16% of D subjects developed freezing of gait but 29% of P subjects did (p = 0.0003). Decline in motor performance was less in D subjects than P subjects. Levodopa‐treated Parkinson's disease patients who had been treated with deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.</abstract><qualityIndicators><score>7.806</score><pdfVersion>1.2</pdfVersion><pdfPageSize>605 x 786 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1642</abstractCharCount><pdfWordCount>4806</pdfWordCount><pdfCharCount>31535</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>254</abstractWordCount></qualityIndicators><title>Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial</title><corporate><json:item><name>the Parkinson Study Group</name></json:item></corporate><genre><json:string>article</json:string></genre><host><volume>51</volume><publisherId><json:string>ANA</json:string></publisherId><pages><total>9</total><last>612</last><first>604</first></pages><issn><json:string>0364-5134</json:string></issn><issue>5</issue><subject><json:item><value>Original Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8249</json:string></eissn><title>Annals of Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><publicationDate>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1002/ana.10191</json:string></doi><id>7C5BBF056B2C59C8EC40B42446B6F5512D575A77</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/7C5BBF056B2C59C8EC40B42446B6F5512D575A77/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/7C5BBF056B2C59C8EC40B42446B6F5512D575A77/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/7C5BBF056B2C59C8EC40B42446B6F5512D575A77/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><availability><p>WILEY</p></availability><date>2002</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial</title><author><orgName>the Parkinson Study Group</orgName></author><author><persName><forename type="first">Ira</forename><surname>Shoulson</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Department of Neurology, University of Rochester Medical Center, 1351 Mt. Hope Avenue, Suite 212, Rochester, NY 14620</p></note><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation></author><author><persName><forename type="first">David</forename><surname>Oakes</surname></persName><roleName type="degree">PhD</roleName><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation></author><author><persName><forename type="first">Stanley</forename><surname>Fahn</surname></persName><roleName type="degree">MD</roleName><affiliation>Columbia–Presbyterian Medical Center, New York, NY</affiliation></author><author><persName><forename type="first">Anthony</forename><surname>Lang</surname></persName><roleName type="degree">MD</roleName><affiliation>Toronto Western Hospital, Toronto, ON</affiliation></author><author><persName><forename type="first">J. William</forename><surname>Langston</surname></persName><roleName type="degree">MD</roleName><affiliation>Parkinson's Institute, Sunnyvale, CA</affiliation></author><author><persName><forename type="first">Peter</forename><surname>LeWitt</surname></persName><roleName type="degree">MD</roleName><affiliation>Sinai Hospital, Detroit, MI</affiliation></author><author><persName><forename type="first">C. Warren</forename><surname>Olanow</surname></persName><roleName type="degree">MD</roleName><affiliation>Mt. Sinai School of Medicine, New York, NY</affiliation></author><author><persName><forename type="first">John B.</forename><surname>Penney</surname></persName><roleName type="degree">MD</roleName></author><author><persName><forename type="first">Caroline</forename><surname>Tanner</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Parkinson's Institute, Sunnyvale, CA</affiliation></author><author><persName><forename type="first">Karl</forename><surname>Kieburtz</surname></persName><roleName type="degree">MD</roleName><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation></author><author><persName><forename type="first">Alice</forename><surname>Rudolph</surname></persName><roleName type="degree">PhD</roleName><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-05"></date><biblScope unit="volume">51</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="604">604</biblScope><biblScope unit="page" to="612">612</biblScope></imprint></monogr><idno type="istex">7C5BBF056B2C59C8EC40B42446B6F5512D575A77</idno><idno type="DOI">10.1002/ana.10191</idno><idno type="ArticleID">ANA10191</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Deprenyl (selegiline) delays the need for levodopa therapy in patients with early Parkinson's disease, but the long‐term benefits of this treatment remain unclear. During 1987 to 1988, 800 patients with early Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments, or a placebo and were then placed on active deprenyl (10mg/day). A second, independent randomization was carried out in early 1993 for 368 subjects who by that time had required levodopa and who had consented to continuing the deprenyl treatment (D subjects) or changing to a matching placebo (P subjects) under double‐blind conditions. The first development of wearing off, dyskinesias, or on–off motor fluctuations was the prespecified primary outcome measure. During the average 2‐year follow‐up, there were no differences between the treatment groups with respect to the primary outcome measure (hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; p = 0.38), withdrawal from the study, death, or adverse events. Although 34% of D subjects developed dyskinesias and only 19% of P subjects did (p = 0.006), only 16% of D subjects developed freezing of gait but 29% of P subjects did (p = 0.0003). Decline in motor performance was less in D subjects than P subjects. Levodopa‐treated Parkinson's disease patients who had been treated with deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-06-06">Received</change><change when="2002-01-19">Registration</change><change when="2002-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/7C5BBF056B2C59C8EC40B42446B6F5512D575A77/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>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8249</doi><issn type="print">0364-5134</issn><issn type="electronic">1531-8249</issn><idGroup><id type="product" value="ANA"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="ANNALS OF NEUROLOGY">Annals of Neurology</title><title type="short">Ann Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley" registered="yes">10.1002/ana.v51:5</doi><numberingGroup><numbering type="journalVolume" number="51">51</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2002-05">May 2002</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="11" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ana.10191</doi><idGroup><id type="unit" value="ANA10191"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2002 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2001-06-06"></event><event type="manuscriptRevised" date="2002-01-10"></event><event type="manuscriptAccepted" date="2002-01-19"></event><event type="firstOnline" date="2002-04-23"></event><event type="publishedOnlineFinalForm" date="2002-04-23"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:FullText result:FullText" date="2011-02-24"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">604</numbering><numbering type="pageLast">612</numbering></numberingGroup><correspondenceTo>Department of Neurology, University of Rochester Medical Center, 1351 Mt. Hope Avenue, Suite 212, Rochester, NY 14620</correspondenceTo><objectNameGroup><objectName elementName="appendix">APPENDIX</objectName></objectNameGroup><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA10191.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="5"></count><count type="referenceTotal" number="23"></count><count type="wordTotal" number="5558"></count></countGroup><titleGroup><title type="main" xml:lang="en">Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial</title><title type="short" xml:lang="en">Impact of Sustained Deprenyl Treatment</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Ira</givenNames><familyName>Shoulson</familyName><degrees>MD</degrees></personName><contactDetails><email>ishoulson@mct.rochester.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>David</givenNames><familyName>Oakes</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Stanley</givenNames><familyName>Fahn</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Anthony</givenNames><familyName>Lang</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>J. William</givenNames><familyName>Langston</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Peter</givenNames><familyName>LeWitt</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af6"><personName><givenNames>C. Warren</givenNames><familyName>Olanow</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" noteRef="#fn1"><personName><givenNames>John B.</givenNames><familyName>Penney</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Caroline</givenNames><familyName>Tanner</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Karl</givenNames><familyName>Kieburtz</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Alice</givenNames><familyName>Rudolph</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au12" creatorRole="author" noteRef="#fn2"><groupName>the Parkinson Study Group </groupName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>University of Rochester Medical Center, Rochester, NY</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Columbia–Presbyterian Medical Center, New York, NY</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Toronto Western Hospital, Toronto, ON</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Parkinson's Institute, Sunnyvale, CA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Sinai Hospital, Detroit, MI</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Mt. Sinai School of Medicine, New York, NY</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Deprenyl (selegiline) delays the need for levodopa therapy in patients with early Parkinson's disease, but the long‐term benefits of this treatment remain unclear. During 1987 to 1988, 800 patients with early Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments, or a placebo and were then placed on active deprenyl (10mg/day). A second, independent randomization was carried out in early 1993 for 368 subjects who by that time had required levodopa and who had consented to continuing the deprenyl treatment (D subjects) or changing to a matching placebo (P subjects) under double‐blind conditions. The first development of wearing off, dyskinesias, or on–off motor fluctuations was the prespecified primary outcome measure. During the average 2‐year follow‐up, there were no differences between the treatment groups with respect to the primary outcome measure (hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; <i>p</i> = 0.38), withdrawal from the study, death, or adverse events. Although 34% of D subjects developed dyskinesias and only 19% of P subjects did (<i>p</i> = 0.006), only 16% of D subjects developed freezing of gait but 29% of P subjects did (<i>p</i> = 0.0003). Decline in motor performance was less in D subjects than P subjects. Levodopa‐treated Parkinson's disease patients who had been treated with deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Deceased.</p></note><note xml:id="fn2"><p>Members of the Parkinson Study Group who participated in this study are listed in the <link href="#app1">Appendix</link> on page 610.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Impact of Sustained Deprenyl Treatment</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Impact of sustained deprenyl (selegiline) in levodopa‐treated Parkinson's disease: A randomized placebo‐controlled extension of the deprenyl and tocopherol antioxidative therapy of parkinsonism trial</title></titleInfo><name type="personal"><namePart type="given">Ira</namePart><namePart type="family">Shoulson</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation><description>Correspondence: Department of Neurology, University of Rochester Medical Center, 1351 Mt. Hope Avenue, Suite 212, Rochester, NY 14620</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Oakes</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stanley</namePart><namePart type="family">Fahn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Columbia–Presbyterian Medical Center, New York, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anthony</namePart><namePart type="family">Lang</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Toronto Western Hospital, Toronto, ON</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. William</namePart><namePart type="family">Langston</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson's Institute, Sunnyvale, CA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">LeWitt</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sinai Hospital, Detroit, MI</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. Warren</namePart><namePart type="family">Olanow</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Mt. Sinai School of Medicine, New York, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John B.</namePart><namePart type="family">Penney</namePart><namePart type="termsOfAddress">MD</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Caroline</namePart><namePart type="family">Tanner</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Parkinson's Institute, Sunnyvale, CA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karl</namePart><namePart type="family">Kieburtz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alice</namePart><namePart type="family">Rudolph</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>University of Rochester Medical Center, Rochester, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="corporate"><namePart>the Parkinson Study Group</namePart><description>University of Rochester Medical Center, Rochester, NYColumbia–Presbyterian Medical Center, New York, NYToronto Western Hospital, Toronto, ONParkinson's Institute, Sunnyvale, CASinai Hospital, Detroit, MIMt. Sinai School of Medicine, New York, NY</description></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-05</dateIssued><dateCaptured encoding="w3cdtf">2001-06-06</dateCaptured><dateValid encoding="w3cdtf">2002-01-19</dateValid><copyrightDate encoding="w3cdtf">2002</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">3</extent><extent unit="tables">5</extent><extent unit="references">23</extent><extent unit="words">5558</extent></physicalDescription><abstract lang="en">Deprenyl (selegiline) delays the need for levodopa therapy in patients with early Parkinson's disease, but the long‐term benefits of this treatment remain unclear. During 1987 to 1988, 800 patients with early Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments, or a placebo and were then placed on active deprenyl (10mg/day). A second, independent randomization was carried out in early 1993 for 368 subjects who by that time had required levodopa and who had consented to continuing the deprenyl treatment (D subjects) or changing to a matching placebo (P subjects) under double‐blind conditions. The first development of wearing off, dyskinesias, or on–off motor fluctuations was the prespecified primary outcome measure. During the average 2‐year follow‐up, there were no differences between the treatment groups with respect to the primary outcome measure (hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; p = 0.38), withdrawal from the study, death, or adverse events. Although 34% of D subjects developed dyskinesias and only 19% of P subjects did (p = 0.006), only 16% of D subjects developed freezing of gait but 29% of P subjects did (p = 0.0003). Decline in motor performance was less in D subjects than P subjects. Levodopa‐treated Parkinson's disease patients who had been treated with deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>51</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>604</start><end>612</end><total>9</total></extent></part></relatedItem><identifier type="istex">7C5BBF056B2C59C8EC40B42446B6F5512D575A77</identifier><identifier type="DOI">10.1002/ana.10191</identifier><identifier type="ArticleID">ANA10191</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Wiley‐Liss, Inc.</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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