Apathy following subthalamic stimulation in Parkinson disease: a dopamine responsive symptom.
Identifieur interne : 000005 ( Hal/Corpus ); précédent : 000004; suivant : 000006Apathy 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.
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-Asberg 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.
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DOI: 10.1002/mds.21949
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Hal:hal-00805452Le document en format XML
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Paris 6</orgName><orgName type="acronym">UPMC</orgName><desc><address><addrLine>4 place Jussieu - 75005 Paris</addrLine><country key="FR"></country></address><ref type="url">http://www.upmc.fr/</ref></desc></org></tutelle><tutelle name="U975" active="#struct-300002" type="direct"><org type="institution" xml:id="struct-300002" status="VALID"><orgName>INSERM</orgName><desc><address><country key="FR"></country></address></desc></org></tutelle><tutelle name="UMR7225" active="#struct-441569" type="direct"><org type="institution" xml:id="struct-441569" status="VALID"><idno type="IdRef">02636817X</idno><idno type="ISNI">0000000122597504</idno><orgName>Centre National de la Recherche Scientifique</orgName><orgName type="acronym">CNRS</orgName><date type="start">1939-10-19</date><desc><address><country key="FR"></country></address><ref type="url">http://www.cnrs.fr/</ref></desc></org></tutelle></tutelles></hal:affiliation></affiliation></author><author><name sortKey="Dubois, Bruno" sort="Dubois, Bruno" uniqKey="Dubois B" first="Bruno" last="Dubois">Bruno Dubois</name><affiliation><hal:affiliation type="laboratory" xml:id="struct-81470" status="OLD"><orgName>Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière [Paris]</orgName><orgName type="acronym">CRICM</orgName><desc><address><addrLine>GH Pitié-Salpêtrière 47, boulevard de l'Hôpital 75651 Paris cedex 13</addrLine><country key="FR"></country></address><ref type="url">http://www.cricm.upmc.fr/</ref></desc><listRelation><relation active="#struct-93591" type="direct"></relation><relation name="U975" active="#struct-300002" type="direct"></relation><relation name="UMR7225" active="#struct-441569" type="direct"></relation></listRelation><tutelles><tutelle active="#struct-93591" type="direct"><org type="institution" xml:id="struct-93591" status="VALID"><orgName>Université Pierre et Marie Curie - 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75651 PARIS Cedex 13</addrLine><country key="FR"></country></address></desc><listRelation><relation active="#struct-300068" type="direct"></relation><relation active="#struct-300887" type="direct"></relation></listRelation><tutelles><tutelle active="#struct-300068" type="direct"><org type="institution" xml:id="struct-300068" status="VALID"><orgName>Assistance publique - Hôpitaux de Paris (AP-HP)</orgName><desc><address><country key="FR"></country></address></desc></org></tutelle><tutelle active="#struct-300887" type="direct"><org type="institution" xml:id="struct-300887" status="INCOMING"><orgName>Hôpital Pitié-Salpêtrière</orgName><desc><address><country key="FR"></country></address></desc></org></tutelle></tutelles></hal:affiliation></affiliation></author></analytic><idno type="DOI">10.1002/mds.21949</idno><series><title level="j">Movement Disorders</title><idno type="ISSN">0885-3185</idno><imprint><date type="datePub">2008-05-15</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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-Asberg 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.</div></front></TEI><hal api="V3"><titleStmt><title xml:lang="en">Apathy following subthalamic stimulation in Parkinson disease: a dopamine responsive symptom.</title><author role="aut"><persName><forename type="first">Virginie</forename><surname>Czernecki</surname></persName><email></email><idno type="halauthor">362796</idno><affiliation ref="#struct-188430"></affiliation><affiliation ref="#struct-81470"></affiliation></author><author role="aut"><persName><forename type="first">Michael</forename><surname>Schüpbach</surname></persName><email></email><idno type="halauthor">831798</idno><affiliation ref="#struct-3037"></affiliation></author><author role="aut"><persName><forename type="first">Sadek</forename><surname>Yaici</surname></persName><email></email><idno type="halauthor">831836</idno></author><author role="aut"><persName><forename type="first">Richard</forename><surname>Lévy</surname></persName><email></email><idno type="halauthor">89614</idno><affiliation ref="#struct-252026"></affiliation><affiliation ref="#struct-2968"></affiliation></author><author role="aut"><persName><forename type="first">Eric</forename><surname>Bardinet</surname></persName><email></email><idno type="halauthor">98501</idno><affiliation ref="#struct-81470"></affiliation><affiliation ref="#struct-218549"></affiliation><affiliation ref="#struct-106232"></affiliation></author><author role="aut"><persName><forename type="first">Jérôme</forename><surname>Yelnik</surname></persName><email></email><idno type="halauthor">404202</idno><affiliation ref="#struct-81470"></affiliation><affiliation ref="#struct-2623"></affiliation></author><author role="aut"><persName><forename type="first">Bruno</forename><surname>Dubois</surname></persName><email></email><idno type="halauthor">89615</idno><affiliation ref="#struct-81470"></affiliation></author><author role="aut"><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><email></email><idno type="halauthor">217013</idno><affiliation ref="#struct-43171"></affiliation></author><editor role="depositor"><persName><forename>Olivier</forename><surname>Colliot</surname></persName><email>olivier.colliot@upmc.fr</email></editor></titleStmt><editionStmt><edition n="v1" type="current"><date type="whenSubmitted">2013-03-27 19:52:42</date><date type="whenModified">2013-04-04 10:26:30</date><date type="whenReleased">2013-03-27 19:52:42</date><date type="whenProduced">2008-05-15</date></edition><respStmt><resp>contributor</resp><name key="180860"><persName><forename>Olivier</forename><surname>Colliot</surname></persName><email>olivier.colliot@upmc.fr</email></name></respStmt></editionStmt><publicationStmt><distributor>CCSD</distributor><idno type="halId">hal-00805452</idno><idno type="halUri">https://hal.inria.fr/hal-00805452</idno><idno type="halBibtex">czernecki:hal-00805452</idno><idno type="halRefHtml">Movement Disorders, Wiley, 2008, 23 (7), pp.964-9. <10.1002/mds.21949></idno><idno type="halRef">Movement Disorders, Wiley, 2008, 23 (7), pp.964-9. <10.1002/mds.21949></idno></publicationStmt><seriesStmt><idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno><idno type="stamp" n="ONERA">ONERA - Office National d'Études et de Recherches Aérospatiales</idno><idno type="stamp" n="UPMC">Université Pierre et Marie Curie</idno><idno type="stamp" n="ICM" p="UPMC">Institut du Cerveau et de la Moëlle Epinière</idno></seriesStmt><notesStmt><note type="audience" n="2">International</note><note type="popular" n="0">No</note><note type="peer" n="1">Yes</note></notesStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Apathy following subthalamic stimulation in Parkinson disease: a dopamine responsive symptom.</title><author role="aut"><persName><forename type="first">Virginie</forename><surname>Czernecki</surname></persName><idno type="halAuthorId">362796</idno><affiliation ref="#struct-188430"></affiliation><affiliation ref="#struct-81470"></affiliation></author><author role="aut"><persName><forename type="first">Michael</forename><surname>Schüpbach</surname></persName><idno type="halAuthorId">831798</idno><affiliation ref="#struct-3037"></affiliation></author><author role="aut"><persName><forename type="first">Sadek</forename><surname>Yaici</surname></persName><idno type="halAuthorId">831836</idno></author><author role="aut"><persName><forename type="first">Richard</forename><surname>Lévy</surname></persName><idno type="halAuthorId">89614</idno><affiliation ref="#struct-252026"></affiliation><affiliation ref="#struct-2968"></affiliation></author><author role="aut"><persName><forename type="first">Eric</forename><surname>Bardinet</surname></persName><idno type="halAuthorId">98501</idno><affiliation ref="#struct-81470"></affiliation><affiliation ref="#struct-218549"></affiliation><affiliation ref="#struct-106232"></affiliation></author><author role="aut"><persName><forename type="first">Jérôme</forename><surname>Yelnik</surname></persName><idno type="halAuthorId">404202</idno><affiliation ref="#struct-81470"></affiliation><affiliation ref="#struct-2623"></affiliation></author><author role="aut"><persName><forename type="first">Bruno</forename><surname>Dubois</surname></persName><idno type="halAuthorId">89615</idno><affiliation ref="#struct-81470"></affiliation></author><author role="aut"><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><idno type="halAuthorId">217013</idno><affiliation ref="#struct-43171"></affiliation></author></analytic><monogr><idno type="halJournalId" status="VALID">17211</idno><idno type="issn">0885-3185</idno><idno type="eissn">1531-8257</idno><title level="j">Movement Disorders</title><imprint><publisher>Wiley</publisher><biblScope unit="volume">23</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="pp">964-9</biblScope><date type="datePub">2008-05-15</date></imprint></monogr><idno type="doi">10.1002/mds.21949</idno><idno type="pubmed">18398913</idno></biblStruct></sourceDesc><profileDesc><langUsage><language ident="en">English</language></langUsage><textClass><classCode scheme="halDomain" n="info.info-im">Computer Science [cs]/Medical Imaging</classCode><classCode scheme="halTypology" n="ART">Journal articles</classCode></textClass><abstract xml: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-Asberg 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.</abstract></profileDesc></hal></record>Pour manipuler ce document sous Unix (Dilib)
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