Interaction of noradrenergic pharmacological manipulation and subthalamic stimulation on movement initiation control in Parkinson's disease.
Identifieur interne : 001528 ( Ncbi/Merge ); précédent : 001527; suivant : 001529Interaction 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 :
- Brain stimulation [ 1876-4754 ]
English descriptors
- KwdEn :
- Adrenergic alpha-2 Receptor Agonists (therapeutic use), Aged, Clonidine (therapeutic use), Combined Modality Therapy (methods), Deep Brain Stimulation, Female, Humans, Male, Middle Aged, Movement (drug effects), Movement (physiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Psychomotor Performance (drug effects), Psychomotor Performance (physiology), Reaction Time (drug effects), Subthalamic Nucleus (physiology).
- MESH :
- chemical , therapeutic use : Adrenergic alpha-2 Receptor Agonists, Clonidine.
- drug effects : Movement, Psychomotor Performance, Reaction Time.
- drug therapy : Parkinson Disease.
- methods : Combined Modality Therapy.
- physiology : Movement, Psychomotor Performance, Subthalamic Nucleus.
- physiopathology : Parkinson Disease.
- therapy : Parkinson Disease.
- Aged, Deep Brain Stimulation, Female, Humans, Male, Middle Aged.
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
Links toward previous steps (curation, corpus...)
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pubmed:25284704Le document en format XML
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<series><title level="j">Brain stimulation</title>
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<term>Combined Modality Therapy (methods)</term>
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<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>
<term>Subthalamic Nucleus (physiology)</term>
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<term>Clonidine</term>
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<term>Psychomotor Performance</term>
<term>Reaction Time</term>
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<front><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>
</front>
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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>
<DateRevised><Year>2016</Year>
<Month>05</Month>
<Day>18</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1876-4754</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>8</Volume>
<Issue>1</Issue>
<PubDate><MedlineDate>2015 Jan-Feb</MedlineDate>
</PubDate>
</JournalIssue>
<Title>Brain stimulation</Title>
<ISOAbbreviation>Brain Stimul</ISOAbbreviation>
</Journal>
<ArticleTitle>Interaction of noradrenergic pharmacological manipulation and subthalamic stimulation on movement initiation control in Parkinson's disease.</ArticleTitle>
<Pagination><MedlinePgn>27-35</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.brs.2014.09.002</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S1935-861X(14)00310-6</ELocationID>
<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>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Albares</LastName>
<ForeName>Marion</ForeName>
<Initials>M</Initials>
<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>
<Author ValidYN="Y"><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>
</Author>
<Author ValidYN="Y"><LastName>Favre</LastName>
<ForeName>Emilie</ForeName>
<Initials>E</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>
</Author>
<Author ValidYN="Y"><LastName>Broussolle</LastName>
<ForeName>Emmanuel</ForeName>
<Initials>E</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>
</Author>
<Author ValidYN="Y"><LastName>Polo</LastName>
<ForeName>Gustavo</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><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>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boulinguez</LastName>
<ForeName>Philippe</ForeName>
<Initials>P</Initials>
<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>
<Author ValidYN="Y"><LastName>Ballanger</LastName>
<ForeName>Bénédicte</ForeName>
<Initials>B</Initials>
<AffiliationInfo><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>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D018848">Controlled Clinical Trial</PublicationType>
<PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>09</Month>
<Day>15</Day>
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<MedlineTA>Brain Stimul</MedlineTA>
<NlmUniqueID>101465726</NlmUniqueID>
<ISSNLinking>1876-4754</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D058647">Adrenergic alpha-2 Receptor Agonists</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>MN3L5RMN02</RegistryNumber>
<NameOfSubstance UI="D003000">Clonidine</NameOfSubstance>
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</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D058647" MajorTopicYN="N">Adrenergic alpha-2 Receptor Agonists</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName>
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<QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName>
</MeshHeading>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009068" MajorTopicYN="N">Movement</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011597" MajorTopicYN="N">Psychomotor Performance</DescriptorName>
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<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011930" MajorTopicYN="N">Reaction Time</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</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>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year>
<Month>03</Month>
<Day>17</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2014</Year>
<Month>08</Month>
<Day>11</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2014</Year>
<Month>09</Month>
<Day>04</Day>
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<Month>10</Month>
<Day>7</Day>
<Hour>6</Hour>
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<PubMedPubDate PubStatus="pubmed"><Year>2014</Year>
<Month>10</Month>
<Day>7</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="medline"><Year>2015</Year>
<Month>5</Month>
<Day>21</Day>
<Hour>6</Hour>
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<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25284704</ArticleId>
<ArticleId IdType="pii">S1935-861X(14)00310-6</ArticleId>
<ArticleId IdType="doi">10.1016/j.brs.2014.09.002</ArticleId>
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<affiliations><list><country><li>France</li>
</country>
<region><li>Île-de-France</li>
</region>
<settlement><li>Créteil</li>
</settlement>
</list>
<tree><country name="France"><noRegion><name sortKey="Albares, Marion" sort="Albares, Marion" uniqKey="Albares M" first="Marion" last="Albares">Marion Albares</name>
</noRegion>
<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>
</record>
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