Idazoxan, an alpha‐2 antagonist, and L‐DOPA‐induced dyskinesias in patients with Parkinson's disease
Identifieur interne : 001B47 ( Istex/Corpus ); précédent : 001B46; suivant : 001B48Idazoxan, an alpha‐2 antagonist, and L‐DOPA‐induced dyskinesias in patients with Parkinson's disease
Auteurs : O. Rascol ; I. Arnulf ; H. Peyro-Saint Paul ; C. Brefel-Courbon ; M. Vidailhet ; C. Thalamas ; A. M. Bonnet ; S. Descombes ; B. Bejjani ; N. Fabre ; J. L. Montastruc ; Y. AgidSource :
- Movement Disorders [ 0885-3185 ] ; 2001-07.
English descriptors
Abstract
Dyskinesia is a frequent and disabling side effect in patients with Parkinson's disease treated with chronic dopatherapy. Preclinical data in the 1‐methyl‐4‐phenyl‐1,2,3,6,‐tetrahydropyridine (MPTP) monkey suggest that alpha‐2 antagonists may reduce dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia. We assessed, in a pilot randomised placebo‐controlled study, the effects of single oral doses (10 mg, 20 mg, and 40 mg) of idazoxan, an alpha‐2 antagonist, on motor parkinsonian disability and L‐DOPA‐induced dyskinesia following an acute oral challenge of L‐DOPA in 18 patients with Parkinson's disease. The severity of L‐DOPA‐induced dyskinesia improved after 20 mg idazoxan pretreatment, while there was no concommittant deterioration in the antiparkinsonian response to L‐DOPA. These results suggest that blocking alpha‐2 receptors in patients with Parkinson's disease might improve L‐DOPA‐induced dyskinesia without the cost of a return of parkinsonian symptomatology. Further studies are required to assess whether this property could have potential therapeutic applications in the long‐term management of dyskinetic patients with Parkinson's disease. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1143
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ISTEX:D45B693FEB760DA50DF70021526CB4914873B8E7Le document en format XML
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Preclinical data in the 1‐methyl‐4‐phenyl‐1,2,3,6,‐tetrahydropyridine (MPTP) monkey suggest that alpha‐2 antagonists may reduce dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia. We assessed, in a pilot randomised placebo‐controlled study, the effects of single oral doses (10 mg, 20 mg, and 40 mg) of idazoxan, an alpha‐2 antagonist, on motor parkinsonian disability and L‐DOPA‐induced dyskinesia following an acute oral challenge of L‐DOPA in 18 patients with Parkinson's disease. The severity of L‐DOPA‐induced dyskinesia improved after 20 mg idazoxan pretreatment, while there was no concommittant deterioration in the antiparkinsonian response to L‐DOPA. These results suggest that blocking alpha‐2 receptors in patients with Parkinson's disease might improve L‐DOPA‐induced dyskinesia without the cost of a return of parkinsonian symptomatology. Further studies are required to assess whether this property could have potential therapeutic applications in the long‐term management of dyskinetic patients with Parkinson's disease. © 2001 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>O. Rascol MD, PhD</name><affiliations><json:string>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</json:string></affiliations></json:item><json:item><name>I. Arnulf MD</name><affiliations><json:string>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</json:string></affiliations></json:item><json:item><name>H. Peyro‐Saint Paul MD</name><affiliations><json:string>Institut de recherche Pierre Fabre, Boulogne, France</json:string></affiliations></json:item><json:item><name>C. 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Agid MD, PhD</name><affiliations><json:string>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>idazoxan</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>α2 receptors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>L‐DOPA, dyskinesia</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Dyskinesia is a frequent and disabling side effect in patients with Parkinson's disease treated with chronic dopatherapy. Preclinical data in the 1‐methyl‐4‐phenyl‐1,2,3,6,‐tetrahydropyridine (MPTP) monkey suggest that alpha‐2 antagonists may reduce dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia. 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Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</affiliation></author><author><persName><forename type="first">C.</forename><surname>Thalamas</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</affiliation></author><author><persName><forename type="first">A.M.</forename><surname>Bonnet</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</affiliation></author><author><persName><forename type="first">S.</forename><surname>Descombes</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, 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Preclinical data in the 1‐methyl‐4‐phenyl‐1,2,3,6,‐tetrahydropyridine (MPTP) monkey suggest that alpha‐2 antagonists may reduce dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia. We assessed, in a pilot randomised placebo‐controlled study, the effects of single oral doses (10 mg, 20 mg, and 40 mg) of idazoxan, an alpha‐2 antagonist, on motor parkinsonian disability and L‐DOPA‐induced dyskinesia following an acute oral challenge of L‐DOPA in 18 patients with Parkinson's disease. The severity of L‐DOPA‐induced dyskinesia improved after 20 mg idazoxan pretreatment, while there was no concommittant deterioration in the antiparkinsonian response to L‐DOPA. These results suggest that blocking alpha‐2 receptors in patients with Parkinson's disease might improve L‐DOPA‐induced dyskinesia without the cost of a return of parkinsonian symptomatology. Further studies are required to assess whether this property could have potential therapeutic applications in the long‐term management of dyskinetic patients with Parkinson's disease. © 2001 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>idazoxan</term></item><item><term>α2 receptors</term></item><item><term>Parkinson's disease</term></item><item><term>L‐DOPA, dyskinesia</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-08-23">Received</change><change when="2001-01-15">Registration</change><change when="2001-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D45B693FEB760DA50DF70021526CB4914873B8E7/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>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</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. 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number="1"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="38"></count><count type="wordTotal" number="3663"></count></countGroup><titleGroup><title type="main" xml:lang="en">Idazoxan, an alpha‐2 antagonist, and L‐DOPA‐induced dyskinesias in patients with Parkinson's disease</title><title type="short" xml:lang="en">Idazoxan in Dyskinetic PD Patients</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>O.</givenNames><familyName>Rascol</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>rascol@cict.fr</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>I.</givenNames><familyName>Arnulf</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>H.</givenNames><familyName>Peyro‐Saint Paul</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C.</givenNames><familyName>Brefel‐Courbon</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>M.</givenNames><familyName>Vidailhet</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C.</givenNames><familyName>Thalamas</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>A.M.</givenNames><familyName>Bonnet</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>S.</givenNames><familyName>Descombes</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" 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xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Institut de recherche Pierre Fabre, Boulogne, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">idazoxan</keyword><keyword xml:id="kwd2">α2 receptors</keyword><keyword xml:id="kwd3">Parkinson's disease</keyword><keyword xml:id="kwd4">L‐DOPA, dyskinesia</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Dyskinesia is a frequent and disabling side effect in patients with Parkinson's disease treated with chronic dopatherapy. Preclinical data in the 1‐methyl‐4‐phenyl‐1,2,3,6,‐tetrahydropyridine (MPTP) monkey suggest that alpha‐2 antagonists may reduce dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia. We assessed, in a pilot randomised placebo‐controlled study, the effects of single oral doses (10 mg, 20 mg, and 40 mg) of idazoxan, an alpha‐2 antagonist, on motor parkinsonian disability and L‐DOPA‐induced dyskinesia following an acute oral challenge of L‐DOPA in 18 patients with Parkinson's disease. The severity of L‐DOPA‐induced dyskinesia improved after 20 mg idazoxan pretreatment, while there was no concommittant deterioration in the antiparkinsonian response to L‐DOPA. These results suggest that blocking alpha‐2 receptors in patients with Parkinson's disease might improve L‐DOPA‐induced dyskinesia without the cost of a return of parkinsonian symptomatology. Further studies are required to assess whether this property could have potential therapeutic applications in the long‐term management of dyskinetic patients with Parkinson's disease. © 2001 Movement Disorder Society.</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>Idazoxan, an alpha‐2 antagonist, and L‐DOPA‐induced dyskinesias in patients with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Idazoxan in Dyskinetic PD Patients</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Idazoxan, an alpha‐2 antagonist, and L‐DOPA‐induced dyskinesias in patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">O.</namePart><namePart type="family">Rascol</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</affiliation><description>Correspondence: Laboratoire de Pharmacologie Médicale et Clinique, Faculté de Médecine, 37 Allées Jules Guesde 31073 Toulouse Cedex, France</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Arnulf</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Peyro‐Saint Paul</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institut de recherche Pierre Fabre, Boulogne, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Brefel‐Courbon</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Vidailhet</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Thalamas</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.M.</namePart><namePart type="family">Bonnet</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Descombes</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Bejjani</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Clinical Investigation Centre and INSERM U289, University Hospital of Pitie‐Salpetriere, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Fabre</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.L.</namePart><namePart type="family">Montastruc</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre and INSERM U455, University Hospital, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Agid</namePart><namePart type="termsOfAddress">MD, 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unit="words">3663</extent></physicalDescription><abstract lang="en">Dyskinesia is a frequent and disabling side effect in patients with Parkinson's disease treated with chronic dopatherapy. Preclinical data in the 1‐methyl‐4‐phenyl‐1,2,3,6,‐tetrahydropyridine (MPTP) monkey suggest that alpha‐2 antagonists may reduce dihydroxyphenylalanine (L‐DOPA)‐induced dyskinesia. We assessed, in a pilot randomised placebo‐controlled study, the effects of single oral doses (10 mg, 20 mg, and 40 mg) of idazoxan, an alpha‐2 antagonist, on motor parkinsonian disability and L‐DOPA‐induced dyskinesia following an acute oral challenge of L‐DOPA in 18 patients with Parkinson's disease. The severity of L‐DOPA‐induced dyskinesia improved after 20 mg idazoxan pretreatment, while there was no concommittant deterioration in the antiparkinsonian response to L‐DOPA. These results suggest that blocking alpha‐2 receptors in patients with Parkinson's disease might improve L‐DOPA‐induced dyskinesia without the cost of a return of parkinsonian symptomatology. Further studies are required to assess whether this property could have potential therapeutic applications in the long‐term management of dyskinetic patients with Parkinson's disease. © 2001 Movement Disorder Society.</abstract><subject lang="en"><genre>Keywords</genre><topic>idazoxan</topic><topic>α2 receptors</topic><topic>Parkinson's disease</topic><topic>L‐DOPA, 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. 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