Levodopa‐induced dyskinesias in Parkinson's disease: Is sensitization reversible?
Identifieur interne : 001455 ( Istex/Corpus ); précédent : 001454; suivant : 001456Levodopa‐induced dyskinesias in Parkinson's disease: Is sensitization reversible?
Auteurs : Boulos-Paul Bejjani ; Isabelle Arnulf ; Sophie Demeret ; Philippe Damier ; Anne-Marie Bonnet ; Jean-Luc Houeto ; Yves AgidSource :
- Annals of Neurology [ 0364-5134 ] ; 2000-05.
Abstract
Levodopa‐induced dyskinesias (LIDs) in patients with Parkinson's disease are considered to result from the severity of dopaminergic denervation in the striatum, which is an irrevocable phenomenon, and sensitization induced by long‐term intermittent administration of levodopa. Taking advantage of the 64% reduction of levodopa treatment allowed in 12 Parkinson's disease patients by continuous high‐frequency stimulation of the subthalamic nucleus, we evaluated the severity of parkinsonian motor disability and LIDs during two levodopa challenges performed before the surgical implantation of the stimulation electrodes and after 8.8 months of continuous bilateral subthalamic nucleus stimulation that was interrupted 2 hours before the levodopa test. Motor disability during the “off” and “on” drug periods was unchanged. The severity of LIDs during the “on” period and dystonia during the “off” period decreased by 54% and 62%, respectively. The reduced severity of LIDs in the absence of subthalamic nucleus stimulation demonstrates that the sensitization phenomenon resulting from long‐term intermittent levodopa administration is partially reversible. Ann Neurol 2000;47:655–658
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DOI: 10.1002/1531-8249(200005)47:5<655::AID-ANA16>3.0.CO;2-#
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France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité des troubles du mouvement, Hôpital Notre‐Dame des Secous, Byblos, Lebanon</mods:affiliation></affiliation></author><author><name sortKey="Arnulf, Isabelle" sort="Arnulf, Isabelle" uniqKey="Arnulf I" first="Isabelle" last="Arnulf">Isabelle Arnulf</name><affiliation><mods:affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Centre d'Investigation Clinique, Groupe‐Hospitalier Pitié‐Salpêtrière, 47‐83 Boulevard de l'Hôpital, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Demeret, Sophie" sort="Demeret, Sophie" uniqKey="Demeret S" first="Sophie" last="Demeret">Sophie Demeret</name><affiliation><mods:affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Damier, Philippe" sort="Damier, Philippe" uniqKey="Damier P" first="Philippe" last="Damier">Philippe Damier</name><affiliation><mods:affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Bonnet, Anne Arie" sort="Bonnet, Anne Arie" uniqKey="Bonnet A" first="Anne-Marie" last="Bonnet">Anne-Marie Bonnet</name><affiliation><mods:affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Houeto, Jean Uc" sort="Houeto, Jean Uc" uniqKey="Houeto J" first="Jean-Luc" last="Houeto">Jean-Luc Houeto</name><affiliation><mods:affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation><mods:affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</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>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2000-05">2000-05</date><biblScope unit="volume">47</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="655">655</biblScope><biblScope unit="page" to="658">658</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno 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Taking advantage of the 64% reduction of levodopa treatment allowed in 12 Parkinson's disease patients by continuous high‐frequency stimulation of the subthalamic nucleus, we evaluated the severity of parkinsonian motor disability and LIDs during two levodopa challenges performed before the surgical implantation of the stimulation electrodes and after 8.8 months of continuous bilateral subthalamic nucleus stimulation that was interrupted 2 hours before the levodopa test. Motor disability during the “off” and “on” drug periods was unchanged. The severity of LIDs during the “on” period and dystonia during the “off” period decreased by 54% and 62%, respectively. The reduced severity of LIDs in the absence of subthalamic nucleus stimulation demonstrates that the sensitization phenomenon resulting from long‐term intermittent levodopa administration is partially reversible. Ann Neurol 2000;47:655–658</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Boulos‐Paul Bejjani MD</name><affiliations><json:string>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</json:string><json:string>Unité des troubles du mouvement, Hôpital Notre‐Dame des Secous, Byblos, Lebanon</json:string></affiliations></json:item><json:item><name>Isabelle Arnulf MD</name><affiliations><json:string>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</json:string><json:string>Centre d'Investigation Clinique, Groupe‐Hospitalier Pitié‐Salpêtrière, 47‐83 Boulevard de l'Hôpital, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Sophie Demeret MD</name><affiliations><json:string>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>Philippe Damier MD, PhD</name><affiliations><json:string>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>Anne‐Marie Bonnet MD</name><affiliations><json:string>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>Jean‐Luc Houeto MD</name><affiliations><json:string>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</json:string></affiliations></json:item><json:item><name>Yves Agid MD, PhD</name><affiliations><json:string>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</json:string></affiliations></json:item></author><articleId><json:string>ANA16</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>shortCommunication</json:string></originalGenre><abstract>Levodopa‐induced dyskinesias (LIDs) in patients with Parkinson's disease are considered to result from the severity of dopaminergic denervation in the striatum, which is an irrevocable phenomenon, and sensitization induced by long‐term intermittent administration of levodopa. Taking advantage of the 64% reduction of levodopa treatment allowed in 12 Parkinson's disease patients by continuous high‐frequency stimulation of the subthalamic nucleus, we evaluated the severity of parkinsonian motor disability and LIDs during two levodopa challenges performed before the surgical implantation of the stimulation electrodes and after 8.8 months of continuous bilateral subthalamic nucleus stimulation that was interrupted 2 hours before the levodopa test. Motor disability during the “off” and “on” drug periods was unchanged. The severity of LIDs during the “on” period and dystonia during the “off” period decreased by 54% and 62%, respectively. The reduced severity of LIDs in the absence of subthalamic nucleus stimulation demonstrates that the sensitization phenomenon resulting from long‐term intermittent levodopa administration is partially reversible. 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reversible?</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><availability><p>Copyright © 2000 American Neurological Association</p></availability><date>2000</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Levodopa‐induced dyskinesias in Parkinson's disease: Is sensitization reversible?</title><author xml:id="author-1"><persName><forename type="first">Boulos‐Paul</forename><surname>Bejjani</surname></persName><roleName type="degree">MD</roleName><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>Unité des troubles du mouvement, Hôpital Notre‐Dame des Secous, Byblos, Lebanon</affiliation></author><author xml:id="author-2"><persName><forename type="first">Isabelle</forename><surname>Arnulf</surname></persName><roleName type="degree">MD</roleName><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>Centre d'Investigation Clinique, Groupe‐Hospitalier Pitié‐Salpêtrière, 47‐83 Boulevard de l'Hôpital, 75013 Paris, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">Sophie</forename><surname>Demeret</surname></persName><roleName type="degree">MD</roleName><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">Philippe</forename><surname>Damier</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">Anne‐Marie</forename><surname>Bonnet</surname></persName><roleName type="degree">MD</roleName><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">Jean‐Luc</forename><surname>Houeto</surname></persName><roleName type="degree">MD</roleName><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation></author><author xml:id="author-7"><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</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>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2000-05"></date><biblScope unit="volume">47</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="655">655</biblScope><biblScope unit="page" to="658">658</biblScope></imprint></monogr><idno type="istex">5CE0B636D2EF00B187B8F047BD971320415C5B67</idno><idno type="DOI">10.1002/1531-8249(200005)47:5<655::AID-ANA16>3.0.CO;2-#</idno><idno type="ArticleID">ANA16</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2000</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Levodopa‐induced dyskinesias (LIDs) in patients with Parkinson's disease are considered to result from the severity of dopaminergic denervation in the striatum, which is an irrevocable phenomenon, and sensitization induced by long‐term intermittent administration of levodopa. Taking advantage of the 64% reduction of levodopa treatment allowed in 12 Parkinson's disease patients by continuous high‐frequency stimulation of the subthalamic nucleus, we evaluated the severity of parkinsonian motor disability and LIDs during two levodopa challenges performed before the surgical implantation of the stimulation electrodes and after 8.8 months of continuous bilateral subthalamic nucleus stimulation that was interrupted 2 hours before the levodopa test. Motor disability during the “off” and “on” drug periods was unchanged. The severity of LIDs during the “on” period and dystonia during the “off” period decreased by 54% and 62%, respectively. The reduced severity of LIDs in the absence of subthalamic nucleus stimulation demonstrates that the sensitization phenomenon resulting from long‐term intermittent levodopa administration is partially reversible. 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affiliationRef="#af1"><personName><givenNames>Yves</givenNames><familyName>Agid</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="LB" type="organization"><unparsedAffiliation>Unité des troubles du mouvement, Hôpital Notre‐Dame des Secous, Byblos, Lebanon</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Levodopa‐induced dyskinesias (LIDs) in patients with Parkinson's disease are considered to result from the severity of dopaminergic denervation in the striatum, which is an irrevocable phenomenon, and sensitization induced by long‐term intermittent administration of levodopa. Taking advantage of the 64% reduction of levodopa treatment allowed in 12 Parkinson's disease patients by continuous high‐frequency stimulation of the subthalamic nucleus, we evaluated the severity of parkinsonian motor disability and LIDs during two levodopa challenges performed before the surgical implantation of the stimulation electrodes and after 8.8 months of continuous bilateral subthalamic nucleus stimulation that was interrupted 2 hours before the levodopa test. Motor disability during the “off” and “on” drug periods was unchanged. The severity of LIDs during the “on” period and dystonia during the “off” period decreased by 54% and 62%, respectively. The reduced severity of LIDs in the absence of subthalamic nucleus stimulation demonstrates that the sensitization phenomenon resulting from long‐term intermittent levodopa administration is partially reversible. Ann Neurol 2000;47:655–658</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Levodopa‐induced dyskinesias in Parkinson's disease: Is sensitization reversible?</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Reversibility of LID</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa‐induced dyskinesias in Parkinson's disease: Is sensitization reversible?</title></titleInfo><name type="personal"><namePart type="given">Boulos‐Paul</namePart><namePart type="family">Bejjani</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>Unité des troubles du mouvement, Hôpital Notre‐Dame des Secous, Byblos, Lebanon</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Isabelle</namePart><namePart type="family">Arnulf</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><affiliation>Centre d'Investigation Clinique, Groupe‐Hospitalier Pitié‐Salpêtrière, 47‐83 Boulevard de l'Hôpital, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sophie</namePart><namePart type="family">Demeret</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Damier</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anne‐Marie</namePart><namePart type="family">Bonnet</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Luc</namePart><namePart type="family">Houeto</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Agid</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Centre d'Investigation Clinique, Fédération de Neurologie and INSERM U289, Groupe‐Hospitalier Pitié‐Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="shortCommunication"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2000-05</dateIssued><dateCaptured encoding="w3cdtf">1999-05-06</dateCaptured><dateValid encoding="w3cdtf">2000-01-04</dateValid><copyrightDate encoding="w3cdtf">2000</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">15</extent><extent unit="words">2736</extent></physicalDescription><abstract lang="en">Levodopa‐induced dyskinesias (LIDs) in patients with Parkinson's disease are considered to result from the severity of dopaminergic denervation in the striatum, which is an irrevocable phenomenon, and sensitization induced by long‐term intermittent administration of levodopa. Taking advantage of the 64% reduction of levodopa treatment allowed in 12 Parkinson's disease patients by continuous high‐frequency stimulation of the subthalamic nucleus, we evaluated the severity of parkinsonian motor disability and LIDs during two levodopa challenges performed before the surgical implantation of the stimulation electrodes and after 8.8 months of continuous bilateral subthalamic nucleus stimulation that was interrupted 2 hours before the levodopa test. Motor disability during the “off” and “on” drug periods was unchanged. The severity of LIDs during the “on” period and dystonia during the “off” period decreased by 54% and 62%, respectively. The reduced severity of LIDs in the absence of subthalamic nucleus stimulation demonstrates that the sensitization phenomenon resulting from long‐term intermittent levodopa administration is partially reversible. 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