Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive symptom
Identifieur interne : 001352 ( Main/Corpus ); précédent : 001351; suivant : 001353Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive symptom
Auteurs : Virginie Czernecki ; Michael Schüpbach ; Sadek Yaici ; Richard Lévy ; Eric Bardinet ; Jérôme Yelnik ; Bruno Dubois ; Yves AgidSource :
- Movement Disorders [ 0885-3185 ] ; 2008-05-15.
English descriptors
Abstract
To evaluate the effects of the dopamine D2‐D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery‐Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS‐III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1–18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0–78%). Mood also improved (75 ± 31%; range 0–100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2‐D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo‐limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.21949
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ISTEX:ED91C023356D1D4FFF7501D9DD48101CF35B1793Le document en format XML
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We suggest that apathy, which was compensated for by an enhancement of D2‐D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo‐limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Virginie Czernecki PhD</name><affiliations><json:string>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</json:string><json:string>INSERM Unit 610, Paris, France</json:string></affiliations></json:item><json:item><name>Michael Schüpbach MD</name><affiliations><json:string>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</json:string><json:string>Department of Neurology, University Hospital, Bern, Switzerland</json:string></affiliations></json:item><json:item><name>Sadek Yaici MD</name><affiliations><json:string>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</json:string></affiliations></json:item><json:item><name>Richard Lévy MD, PhD</name><affiliations><json:string>INSERM Unit 610, Paris, France</json:string></affiliations></json:item><json:item><name>Eric Bardinet PhD</name><affiliations><json:string>CNRS‐UPR640, CHU Pitié‐Salpêtrière, Université Pierre et Marie Curie‐Paris 6, Paris, France</json:string></affiliations></json:item><json:item><name>Jérôme Yelnik PhD</name><affiliations><json:string>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</json:string></affiliations></json:item><json:item><name>Bruno Dubois MD, PhD</name><affiliations><json:string>INSERM Unit 610, Paris, France</json:string></affiliations></json:item><json:item><name>Yves Agid MD, PhD</name><affiliations><json:string>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>subthalamic stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>apathy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopaminergic agonist</value></json:item></subject><articleId><json:string>MDS21949</json:string></articleId><language><json:string>eng</json:string></language><abstract>To evaluate the effects of the dopamine D2‐D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery‐Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS‐III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1–18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0–78%). Mood also improved (75 ± 31%; range 0–100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2‐D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo‐limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively. © 2008 Movement Disorder Society</abstract><qualityIndicators><score>5.724</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1370</abstractCharCount><pdfWordCount>3312</pdfWordCount><pdfCharCount>22018</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>201</abstractWordCount></qualityIndicators><title>Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive 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Center d'Investigation Clinique, Hôpital de la Salpêtrière, 47‐83 boulevard de l'Hôpital, 75013 Paris, France</p></note><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation><affiliation>INSERM Unit 610, Paris, France</affiliation></author><author><persName><forename type="first">Michael</forename><surname>Schüpbach</surname></persName><roleName type="degree">MD</roleName><note type="biography">Virginie Czerecki and Michael Schüpbach contributed equally to this work.</note><affiliation>Virginie Czerecki and Michael Schüpbach contributed equally to this work.</affiliation><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation><affiliation>Department of Neurology, University Hospital, Bern, Switzerland</affiliation></author><author><persName><forename type="first">Sadek</forename><surname>Yaici</surname></persName><roleName type="degree">MD</roleName><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation></author><author><persName><forename type="first">Richard</forename><surname>Lévy</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>INSERM Unit 610, Paris, France</affiliation></author><author><persName><forename type="first">Eric</forename><surname>Bardinet</surname></persName><roleName type="degree">PhD</roleName><affiliation>CNRS‐UPR640, CHU Pitié‐Salpêtrière, Université Pierre et Marie Curie‐Paris 6, Paris, France</affiliation></author><author><persName><forename type="first">Jérôme</forename><surname>Yelnik</surname></persName><roleName type="degree">PhD</roleName><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation></author><author><persName><forename type="first">Bruno</forename><surname>Dubois</surname></persName><roleName type="degree">MD, 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We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery‐Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS‐III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1–18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0–78%). Mood also improved (75 ± 31%; range 0–100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2‐D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo‐limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively. © 2008 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson disease</term></item><item><term>subthalamic stimulation</term></item><item><term>apathy</term></item><item><term>dopaminergic agonist</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-11-21">Received</change><change when="2007-12-24">Registration</change><change when="2008-05-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/ED91C023356D1D4FFF7501D9DD48101CF35B1793/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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href="file:MDS.MDS21949.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="4000"></count></countGroup><titleGroup><title type="main" xml:lang="en">Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive symptom</title><title type="short" xml:lang="en">Apathy Following Subthalamic Stimulation in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes" noteRef="#fn1"><personName><givenNames>Virginie</givenNames><familyName>Czernecki</familyName><degrees>PhD</degrees></personName><contactDetails><email>czerneck@chups.jussieu.fr</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af3" noteRef="#fn1"><personName><givenNames>Michael</givenNames><familyName>Schüpbach</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Sadek</givenNames><familyName>Yaici</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Richard</givenNames><familyName>Lévy</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Eric</givenNames><familyName>Bardinet</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jérôme</givenNames><familyName>Yelnik</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Bruno</givenNames><familyName>Dubois</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" 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>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>INSERM Unit 610, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CH" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital, Bern, Switzerland</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>CNRS‐UPR640, CHU Pitié‐Salpêtrière, Université Pierre et Marie Curie‐Paris 6, Paris, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson disease</keyword><keyword xml:id="kwd2">subthalamic stimulation</keyword><keyword xml:id="kwd3">apathy</keyword><keyword xml:id="kwd4">dopaminergic agonist</keyword></keywordGroup><fundingInfo><fundingAgency>French Parkinson's Disease Association</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Swiss National Science Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Swiss Parkinson's Disease Association</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To evaluate the effects of the dopamine D2‐D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery‐Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS‐III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1–18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0–78%). Mood also improved (75 ± 31%; range 0–100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2‐D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo‐limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Virginie Czerecki and Michael Schüpbach contributed equally to this work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive symptom</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Apathy Following Subthalamic Stimulation in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive symptom</title></titleInfo><name type="personal"><namePart type="given">Virginie</namePart><namePart type="family">Czernecki</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation><affiliation>INSERM Unit 610, Paris, France</affiliation><description>Virginie Czerecki and Michael Schüpbach contributed equally to this work.</description><description>Correspondence: Center d'Investigation Clinique, Hôpital de la Salpêtrière, 47‐83 boulevard de l'Hôpital, 75013 Paris, France</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Schüpbach</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation><affiliation>Department of Neurology, University Hospital, Bern, Switzerland</affiliation><description>Virginie Czerecki and Michael Schüpbach contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sadek</namePart><namePart type="family">Yaici</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard</namePart><namePart type="family">Lévy</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>INSERM Unit 610, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eric</namePart><namePart type="family">Bardinet</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>CNRS‐UPR640, CHU Pitié‐Salpêtrière, Université Pierre et Marie Curie‐Paris 6, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jérôme</namePart><namePart type="family">Yelnik</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bruno</namePart><namePart type="family">Dubois</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>INSERM Unit 610, 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>Center d'Investigation Clinique, Fédération de Neurologie, INSERM Unit 679, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2008-05-15</dateIssued><dateCaptured encoding="w3cdtf">2007-11-21</dateCaptured><dateValid encoding="w3cdtf">2007-12-24</dateValid><copyrightDate encoding="w3cdtf">2008</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">3</extent><extent unit="references">33</extent><extent unit="words">4000</extent></physicalDescription><abstract lang="en">To evaluate the effects of the dopamine D2‐D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery‐Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS‐III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1–18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0–78%). Mood also improved (75 ± 31%; range 0–100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2‐D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo‐limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively. © 2008 Movement Disorder Society</abstract><note type="funding">French Parkinson's Disease Association</note><note type="funding">Swiss National Science Foundation</note><note type="funding">Swiss Parkinson's Disease Association</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson disease</topic><topic>subthalamic stimulation</topic><topic>apathy</topic><topic>dopaminergic agonist</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. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research 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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>964</start><end>969</end><total>6</total></extent></part></relatedItem><identifier type="istex">ED91C023356D1D4FFF7501D9DD48101CF35B1793</identifier><identifier type="DOI">10.1002/mds.21949</identifier><identifier type="ArticleID">MDS21949</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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