Interaction of noradrenergic pharmacological manipulation and subthalamic stimulation on movement initiation control in Parkinson's disease.
Identifieur interne : 005981 ( Main/Curation ); précédent : 005980; suivant : 005982Interaction 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
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Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon</wicri:regionArea><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion></affiliation></author><author><name sortKey="Favre, Emilie" sort="Favre, Emilie" uniqKey="Favre E" first="Emilie" last="Favre">Emilie Favre</name><affiliation wicri:level="1"><nlm: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.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>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</wicri:regionArea><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion></affiliation></author><author><name sortKey="Broussolle, Emmanuel" sort="Broussolle, Emmanuel" uniqKey="Broussolle E" first="Emmanuel" last="Broussolle">Emmanuel Broussolle</name><affiliation wicri:level="1"><nlm: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.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>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</wicri:regionArea><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion></affiliation></author><author><name sortKey="Polo, Gustavo" sort="Polo, Gustavo" uniqKey="Polo G" first="Gustavo" last="Polo">Gustavo Polo</name><affiliation wicri:level="1"><nlm:affiliation>Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon</wicri:regionArea><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion><wicri:noRegion>Hospices Civils de Lyon</wicri:noRegion></affiliation></author><author><name sortKey="Domenech, Philippe" sort="Domenech, Philippe" uniqKey="Domenech P" first="Philippe" last="Domenech">Philippe Domenech</name><affiliation wicri:level="3"><nlm:affiliation>Laboratoire de Neurosciences Cognitives, ENS/INSERM-U960, Paris, France; Innovation Thérapeutique Fonctionnelle, Service de Neurochirurgie, CHU Henri Mondor, Creteil, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neurosciences Cognitives, ENS/INSERM-U960, Paris, France; Innovation Thérapeutique Fonctionnelle, Service de Neurochirurgie, CHU Henri Mondor, Creteil</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Créteil</settlement></placeName></affiliation></author><author><name sortKey="Boulinguez, Philippe" sort="Boulinguez, Philippe" uniqKey="Boulinguez P" first="Philippe" last="Boulinguez">Philippe Boulinguez</name><affiliation wicri:level="1"><nlm:affiliation>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron</wicri:regionArea><wicri:noRegion>Bron</wicri:noRegion><wicri:noRegion>Bron</wicri:noRegion></affiliation></author><author><name sortKey="Ballanger, Benedicte" sort="Ballanger, Benedicte" uniqKey="Ballanger B" first="Bénédicte" last="Ballanger">Bénédicte Ballanger</name><affiliation wicri:level="1"><nlm: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.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université de Lyon, F-69622, Lyon, France; Université Lyon 1, Villeurbanne, France; CNRS, UMR5229, Centre de Neuroscience Cognitive, Bron</wicri:regionArea><wicri:noRegion>Bron</wicri:noRegion><wicri:noRegion>Bron</wicri:noRegion></affiliation></author></analytic><series><title level="j">Brain stimulation</title><idno type="eISSN">1876-4754</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><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><term>Subthalamic Nucleus (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Adrenergic alpha-2 Receptor Agonists</term><term>Clonidine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Movement</term><term>Psychomotor Performance</term><term>Reaction Time</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Combined Modality Therapy</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Movement</term><term>Psychomotor Performance</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Deep Brain Stimulation</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><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></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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