La maladie de Parkinson en France (serveur d'exploration)

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Interaction of noradrenergic pharmacological manipulation and subthalamic stimulation on movement initiation control in Parkinson's disease.

Identifieur interne : 001749 ( PubMed/Checkpoint ); précédent : 001748; suivant : 001750

Interaction of noradrenergic pharmacological manipulation and subthalamic stimulation on movement initiation control in Parkinson's disease.

Auteurs : Marion Albares [France] ; Stéphane Thobois [France] ; Emilie Favre [France] ; Emmanuel Broussolle [France] ; Gustavo Polo [France] ; Philippe Domenech [France] ; Philippe Boulinguez [France] ; Bénédicte Ballanger [France]

Source :

RBID : pubmed:25284704

English descriptors

Abstract

Slowness in movement initiation (akinesia) is a cardinal feature of Parkinson's disease (PD), which is still poorly understood. Notably, akinesia is restored by subthalamic nucleus deep brain stimulation (STN-DBS) but not fully reversed by current dopaminergic treatments. It was recently suggested that this disorder is of executive nature (related to inhibitory control of response) and of non-dopaminergic origin (possibly noradrenergic).

DOI: 10.1016/j.brs.2014.09.002
PubMed: 25284704


Affiliations:


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pubmed:25284704

Le document en format XML

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<term>Adrenergic alpha-2 Receptor Agonists (therapeutic use)</term>
<term>Aged</term>
<term>Clonidine (therapeutic use)</term>
<term>Combined Modality Therapy (methods)</term>
<term>Deep Brain Stimulation</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Movement (drug effects)</term>
<term>Movement (physiology)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson Disease (therapy)</term>
<term>Psychomotor Performance (drug effects)</term>
<term>Psychomotor Performance (physiology)</term>
<term>Reaction Time (drug effects)</term>
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<term>Parkinson Disease</term>
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<term>Parkinson Disease</term>
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<div type="abstract" xml:lang="en">Slowness in movement initiation (akinesia) is a cardinal feature of Parkinson's disease (PD), which is still poorly understood. Notably, akinesia is restored by subthalamic nucleus deep brain stimulation (STN-DBS) but not fully reversed by current dopaminergic treatments. It was recently suggested that this disorder is of executive nature (related to inhibitory control of response) and of non-dopaminergic origin (possibly noradrenergic).</div>
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<DateCreated>
<Year>2014</Year>
<Month>12</Month>
<Day>26</Day>
</DateCreated>
<DateCompleted>
<Year>2015</Year>
<Month>05</Month>
<Day>20</Day>
</DateCompleted>
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<Year>2016</Year>
<Month>05</Month>
<Day>18</Day>
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<Volume>8</Volume>
<Issue>1</Issue>
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<MedlineDate>2015 Jan-Feb</MedlineDate>
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<Title>Brain stimulation</Title>
<ISOAbbreviation>Brain Stimul</ISOAbbreviation>
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<ArticleTitle>Interaction of noradrenergic pharmacological manipulation and subthalamic stimulation on movement initiation control in Parkinson's disease.</ArticleTitle>
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<Abstract>
<AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Slowness in movement initiation (akinesia) is a cardinal feature of Parkinson's disease (PD), which is still poorly understood. Notably, akinesia is restored by subthalamic nucleus deep brain stimulation (STN-DBS) but not fully reversed by current dopaminergic treatments. It was recently suggested that this disorder is of executive nature (related to inhibitory control of response) and of non-dopaminergic origin (possibly noradrenergic).</AbstractText>
<AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To test the double hypothesis that: 1) the ability to control movement initiation is modified by noradrenergic neurotransmission modulation, and 2) this effect is mediated by the regulation of STN activity.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Sixteen STN-DBS PD patients were enrolled in a placebo-controlled study investigating the effects of noradrenergic attenuation by clonidine (∝2-adrenergic receptor agonist). Movement initiation latency was assessed by means of a cue-target reaction time task. Patients, who remained on their chronic dopaminergic medication, were tested on four sessions: two with placebo (ON- or OFF-DBS), and two with a 150 μg oral dose of clonidine (ON- or OFF-DBS).</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">In the OFF stimulation condition, patients were locked into a mode of control maintaining inappropriate response inhibition. This dysfunctional executive setting was overcome by STN-DBS. Clonidine, however, was found to impair specifically the ability to release inhibitory control in the ON-DBS state.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Overall our results suggest an important implication of the noradrenergic system in the pathophysiology of akinesia in PD. Reducing the noradrenergic "tonus" may even block the positive action of STN-DBS on akinesia, suggesting, at least by part, a noradrenergic-dependent STN-DBS efficiency.</AbstractText>
<CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
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<LastName>Albares</LastName>
<ForeName>Marion</ForeName>
<Initials>M</Initials>
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<Affiliation>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron, France.</Affiliation>
</AffiliationInfo>
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<LastName>Thobois</LastName>
<ForeName>Stéphane</ForeName>
<Initials>S</Initials>
<AffiliationInfo>
<Affiliation>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron, France; Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France.</Affiliation>
</AffiliationInfo>
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<LastName>Broussolle</LastName>
<ForeName>Emmanuel</ForeName>
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<Affiliation>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron, France; Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France.</Affiliation>
</AffiliationInfo>
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<LastName>Polo</LastName>
<ForeName>Gustavo</ForeName>
<Initials>G</Initials>
<AffiliationInfo>
<Affiliation>Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France.</Affiliation>
</AffiliationInfo>
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<LastName>Domenech</LastName>
<ForeName>Philippe</ForeName>
<Initials>P</Initials>
<AffiliationInfo>
<Affiliation>Laboratoire de Neurosciences Cognitives, ENS/INSERM-U960, Paris, France; Innovation Thérapeutique Fonctionnelle, Service de Neurochirurgie, CHU Henri Mondor, Creteil, France.</Affiliation>
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</Author>
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<LastName>Boulinguez</LastName>
<ForeName>Philippe</ForeName>
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<AffiliationInfo>
<Affiliation>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron, France.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Ballanger</LastName>
<ForeName>Bénédicte</ForeName>
<Initials>B</Initials>
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<Affiliation>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron, France. Electronic address: benedicte.ballanger@isc.cnrs.fr.</Affiliation>
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<PublicationType UI="D018848">Controlled Clinical Trial</PublicationType>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<Year>2014</Year>
<Month>09</Month>
<Day>15</Day>
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<Country>United States</Country>
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<NameOfSubstance UI="D003000">Clonidine</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList>
<MeshHeading>
<DescriptorName UI="D058647" MajorTopicYN="N">Adrenergic alpha-2 Receptor Agonists</DescriptorName>
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<MeshHeading>
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<MeshHeading>
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<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading>
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<QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName>
</MeshHeading>
<MeshHeading>
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</MeshHeading>
<MeshHeading>
<DescriptorName UI="D011930" MajorTopicYN="N">Reaction Time</DescriptorName>
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</MeshHeading>
<MeshHeading>
<DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName>
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</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Akinesia</Keyword>
<Keyword MajorTopicYN="N">Executive control</Keyword>
<Keyword MajorTopicYN="N">Noradrenaline</Keyword>
<Keyword MajorTopicYN="N">Reaction time</Keyword>
<Keyword MajorTopicYN="N">STN-DBS</Keyword>
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</MedlineCitation>
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<Year>2014</Year>
<Month>03</Month>
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<Year>2014</Year>
<Month>08</Month>
<Day>11</Day>
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<PubMedPubDate PubStatus="accepted">
<Year>2014</Year>
<Month>09</Month>
<Day>04</Day>
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<Year>2014</Year>
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<Month>10</Month>
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</PubMedPubDate>
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<Year>2015</Year>
<Month>5</Month>
<Day>21</Day>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
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<affiliations>
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<country>
<li>France</li>
</country>
<region>
<li>Île-de-France</li>
</region>
<settlement>
<li>Créteil</li>
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<country name="France">
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<name sortKey="Albares, Marion" sort="Albares, Marion" uniqKey="Albares M" first="Marion" last="Albares">Marion Albares</name>
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<name sortKey="Ballanger, Benedicte" sort="Ballanger, Benedicte" uniqKey="Ballanger B" first="Bénédicte" last="Ballanger">Bénédicte Ballanger</name>
<name sortKey="Boulinguez, Philippe" sort="Boulinguez, Philippe" uniqKey="Boulinguez P" first="Philippe" last="Boulinguez">Philippe Boulinguez</name>
<name sortKey="Broussolle, Emmanuel" sort="Broussolle, Emmanuel" uniqKey="Broussolle E" first="Emmanuel" last="Broussolle">Emmanuel Broussolle</name>
<name sortKey="Domenech, Philippe" sort="Domenech, Philippe" uniqKey="Domenech P" first="Philippe" last="Domenech">Philippe Domenech</name>
<name sortKey="Favre, Emilie" sort="Favre, Emilie" uniqKey="Favre E" first="Emilie" last="Favre">Emilie Favre</name>
<name sortKey="Polo, Gustavo" sort="Polo, Gustavo" uniqKey="Polo G" first="Gustavo" last="Polo">Gustavo Polo</name>
<name sortKey="Thobois, Stephane" sort="Thobois, Stephane" uniqKey="Thobois S" first="Stéphane" last="Thobois">Stéphane Thobois</name>
</country>
</tree>
</affiliations>
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