Executive impairments and dysfunction of inhibitory control in Parkinson's disease
Identifieur interne : 000403 ( Hal/Curation ); précédent : 000402; suivant : 000404Executive impairments and dysfunction of inhibitory control in Parkinson's disease
Auteurs : Emilie Favre [France]Source :
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Abstract
Executive impairments in Parkinson’s disease are debilitating and have no satisfying therapeutic option. This is partly due to the fact that executive functions are difficult to investigate from cognitive, neuro-functional and neurochemical standpoints. Here, we build on recent theoretical and methodological improvements to revisit executive impairments. We are interested in a function that consists in locking in advance movement initiation mechanisms in the face of uncertainty: proactive control of non-selective inhibition of action. Our leading hypothesis is that dysfunction of proactive inhibitory control could generate widespread and heterogeneous executive impairments. We thus: 1) tried to relate clinical markers of the disease to behavioral indexes of proactive control impairment; 2) identified the associated cerebral dysfunctions by means of advanced electroencephalographic methods and manipulation of deep brain stimulation of the subthalamic nucleus; and 3) investigated the neurochemical origin of this function. Our results suggest that impulsivity is not the only outcome of inhibitory impairment. Disorder of proactive inhibitory control may also account for hypo-productive behaviors such as akinesia. Results also indicate that this mechanism is of non-dopaminergic origin and relies on medial frontal and subthalamic activity. This work opens the way for new therapeutic approaches for Parkinson’s disease as well as a better understanding of clinical symptoms observed in others diseases
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stimulation</term><term>Dopamine</term><term>Dysexecutive syndrome</term><term>Impulsivity</term><term>Inhibition</term><term>Parkinson’s disease</term><term>Proactive control</term></keywords><keywords scheme="mix" xml:lang="fr"><term>Akinésie</term><term>Contrôle proactif</term><term>Impulsivité</term><term>Maladie de Parkinson</term><term>Stimulation cérébrale profonde</term><term>Syndrome dysexécutif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Executive impairments in Parkinson’s disease are debilitating and have no satisfying therapeutic option. This is partly due to the fact that executive functions are difficult to investigate from cognitive, neuro-functional and neurochemical standpoints. Here, we build on recent theoretical and methodological improvements to revisit executive impairments. We are interested in a function that consists in locking in advance movement initiation mechanisms in the face of uncertainty: proactive control of non-selective inhibition of action. Our leading hypothesis is that dysfunction of proactive inhibitory control could generate widespread and heterogeneous executive impairments. We thus: 1) tried to relate clinical markers of the disease to behavioral indexes of proactive control impairment; 2) identified the associated cerebral dysfunctions by means of advanced electroencephalographic methods and manipulation of deep brain stimulation of the subthalamic nucleus; and 3) investigated the neurochemical origin of this function. Our results suggest that impulsivity is not the only outcome of inhibitory impairment. Disorder of proactive inhibitory control may also account for hypo-productive behaviors such as akinesia. Results also indicate that this mechanism is of non-dopaminergic origin and relies on medial frontal and subthalamic activity. This work opens the way for new therapeutic approaches for Parkinson’s disease as well as a better understanding of clinical symptoms observed in others diseases</div></front></TEI><hal api="V3"><titleStmt><title xml:lang="en">Executive impairments and dysfunction of inhibitory control in Parkinson's disease</title><title xml:lang="fr">Troubles exécutifs et dysfonctionnement du contrôle inhibiteur dans la maladie de Parkinson</title><author role="aut"><persName><forename type="first">Emilie</forename><surname>Favre</surname></persName><idno type="halauthorid">1223102</idno><idno type="IdRef">http://www.idref.fr/188444947</idno><affiliation ref="#struct-24477"></affiliation></author><editor role="depositor"><persName><forename>ABES</forename><surname>STAR</surname></persName><email type="md5">f5aa7f563b02bb6adbba7496989af39a</email><email type="domain">abes.fr</email></editor></titleStmt><editionStmt><edition n="v1" type="current"><date type="whenSubmitted">2015-09-28 15:47:06</date><date type="whenModified">2015-09-30 01:00:17</date><date type="whenReleased">2015-09-29 14:23:24</date><date type="whenProduced">2015-05-29</date><date type="whenEndEmbargoed">2015-09-28</date><ref type="file" target="https://tel.archives-ouvertes.fr/tel-01206212/document"><date notBefore="2015-09-28"></date></ref><ref type="file" subtype="author" n="1" target="https://tel.archives-ouvertes.fr/tel-01206212/file/TH2015FavreEmilie.pdf"><date notBefore="2015-09-28"></date></ref></edition><respStmt><resp>contributor</resp><name key="131274"><persName><forename>ABES</forename><surname>STAR</surname></persName><email type="md5">f5aa7f563b02bb6adbba7496989af39a</email><email type="domain">abes.fr</email></name></respStmt></editionStmt><publicationStmt><distributor>CCSD</distributor><idno type="halId">tel-01206212</idno><idno type="halUri">https://tel.archives-ouvertes.fr/tel-01206212</idno><idno type="halBibtex">favre:tel-01206212</idno><idno type="halRefHtml">Neurosciences [q-bio.NC]. Université Claude Bernard - Lyon I, 2015. Français. <NNT : 2015LYO10076></idno><idno type="halRef">Neurosciences [q-bio.NC]. Université Claude Bernard - Lyon I, 2015. Français. <NNT : 2015LYO10076></idno></publicationStmt><seriesStmt><idno type="stamp" n="STAR">STAR - Dépôt national des thèses électroniques</idno><idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno></seriesStmt><notesStmt></notesStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Executive impairments and dysfunction of inhibitory control in Parkinson's disease</title><title xml:lang="fr">Troubles exécutifs et dysfonctionnement du contrôle inhibiteur dans la maladie de Parkinson</title><author role="aut"><persName><forename type="first">Emilie</forename><surname>Favre</surname></persName><idno type="halauthorid">1223102</idno><idno type="IdRef">http://www.idref.fr/188444947</idno><affiliation ref="#struct-24477"></affiliation></author></analytic><monogr><idno type="nnt">2015LYO10076</idno><imprint><date type="dateDefended">2015-05-29</date></imprint><authority type="institution">Université Claude Bernard - Lyon I</authority><authority type="school">École Doctorale Neurosciences et Cognition (NSCo)</authority><authority type="supervisor">Philippe Boulinguez</authority><authority type="jury">Stéphane Christophe Thobois [Président]</authority><authority type="jury">Kathy Dujardin [Rapporteur]</authority><authority type="jury">Philippe Allain [Rapporteur]</authority><authority type="jury">Serge Pinto</authority><authority type="jury">George Andrew Michael</authority></monogr></biblStruct></sourceDesc><profileDesc><langUsage><language ident="fr">French</language></langUsage><textClass><keywords scheme="author"><term xml:lang="en">Dysexecutive syndrome</term><term xml:lang="en">Proactive control</term><term xml:lang="en">Inhibition</term><term xml:lang="en">Parkinson’s disease</term><term xml:lang="en">Akinesia</term><term xml:lang="en">Impulsivity</term><term xml:lang="en">Dopamine</term><term xml:lang="en">Deep brain stimulation</term><term xml:lang="fr">Syndrome dysexécutif</term><term xml:lang="fr">Contrôle proactif</term><term xml:lang="fr">Maladie de Parkinson</term><term xml:lang="fr">Akinésie</term><term xml:lang="fr">Impulsivité</term><term xml:lang="fr">Stimulation cérébrale profonde</term></keywords><classCode scheme="halDomain" n="sdv.neu">Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]</classCode><classCode scheme="halTypology" n="THESE">Theses</classCode></textClass><abstract xml:lang="en">Executive impairments in Parkinson’s disease are debilitating and have no satisfying therapeutic option. This is partly due to the fact that executive functions are difficult to investigate from cognitive, neuro-functional and neurochemical standpoints. Here, we build on recent theoretical and methodological improvements to revisit executive impairments. We are interested in a function that consists in locking in advance movement initiation mechanisms in the face of uncertainty: proactive control of non-selective inhibition of action. Our leading hypothesis is that dysfunction of proactive inhibitory control could generate widespread and heterogeneous executive impairments. We thus: 1) tried to relate clinical markers of the disease to behavioral indexes of proactive control impairment; 2) identified the associated cerebral dysfunctions by means of advanced electroencephalographic methods and manipulation of deep brain stimulation of the subthalamic nucleus; and 3) investigated the neurochemical origin of this function. Our results suggest that impulsivity is not the only outcome of inhibitory impairment. Disorder of proactive inhibitory control may also account for hypo-productive behaviors such as akinesia. Results also indicate that this mechanism is of non-dopaminergic origin and relies on medial frontal and subthalamic activity. This work opens the way for new therapeutic approaches for Parkinson’s disease as well as a better understanding of clinical symptoms observed in others diseases</abstract><abstract xml:lang="fr">Les troubles exécutifs de la maladie de Parkinson sont invalidants et sans solution thérapeutique satisfaisante. La raison est liée au fait que les fonctions exécutives sont difficiles à appréhender, tant au niveau de leur modélisation cognitive qu'anatomo-fonctionnelle ou neurochimique. Ici, nous nous appuyons sur des avancées théoriques et méthodologiques récentes pour revisiter ces troubles exécutifs. Nous nous intéressons à une fonction, récemment mise en évidence, destinée à verrouiller par anticipation le déclenchement de toute action en situation d'incertitude : le contrôle proactif de l'inhibition non sélective de l'action. Notre hypothèse directrice est que son dysfonctionnement est susceptible de générer une grande variété de troubles exécutifs. Nous avons : 1) recherché les liens entre marqueurs cliniques et troubles du contrôle proactif ; 2) identifié les dysfonctionnements cérébraux associés au moyen de méthodes électroencéphalographiques innovantes combinées à l'enregistrement des effets de la stimulation du noyau sous-thalamique ; et 3) sondé l'origine neurochimique de cette fonction. Nos résultats suggèrent qu'un dysfonctionnement de l'inhibition proactive n'engendre pas uniquement des troubles impulsifs mais explique également des comportements hypo-productifs comme l'akinésie. Ils indiquent que ces troubles ne sont pas d'origine dopaminergique et qu'ils sont liés au dysfonctionnement de l'activité du cortex frontal médian et du noyau sous-thalamique. Ces travaux ouvrent la voie à de nouvelles perspectives thérapeutiques pour la maladie de Parkinson et à une meilleure appréhension de la clinique d'autres pathologies</abstract></profileDesc></hal></record>Pour manipuler ce document sous Unix (Dilib)
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