Deleterious plasticity in Parkinson’s disease from akinesia to hyperkinesia
Identifieur interne : 000743 ( Main/Exploration ); précédent : 000742; suivant : 000744Deleterious plasticity in Parkinson’s disease from akinesia to hyperkinesia
Auteurs : Alice Poisson [France]Source :
Descripteurs français
English descriptors
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Abstract
Mirror movements and akinesia can be both found during Parkinson’s disease. Although very different, they may both reflect an abnormal cerebral plasticity during the disease and the perturbation of the motor inhibitory control. This work reveals that mirror movements are linked to a1/ disruption of the reactive inhibitory control and 2/ to the overactivation of numerous cortical areas. The latter could be the result of a compensatory recruitment aiming at improving the movement. But they could as well reflect a deleterious loss of cerebral activation specificity during Parkinson’s disease. The second experience shows that in healthy subject, the proactive inhibitory control is underpinned by the noradrenergic system. Last but not least the third part of this work reveals an abnormal implementation of the proactive inhibitory control in Parkinson’s disease and suggests its involvement in akinesia. Brought together these results suggest that an abnormal plasticity phenomenon underlies the mirror movements and the akinesia in Parkinson’s disease. More precisely, we observed a default of the reactive inhibitory control associated to mirror movements in Parkinson’s disease and an excess of proactive inhibitory control that seems to be linked to akinesia. The finding of an adrenergic modulation of the proactive inhibitory control opens the fields for the development of noradrenergic therapeutics in akinesia
Url:
Affiliations:
- France
- Auvergne-Rhône-Alpes, Rhône-Alpes
- Grenoble, Lyon
- Université Claude Bernard Lyon 1, Université Joseph Fourier, Université de Grenoble, Université de Lyon
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Le document en format XML
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Fourier</orgName><orgName type="institution" wicri:auto="newGroup">Université de Grenoble</orgName><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName><orgName type="university">Université Claude Bernard Lyon 1</orgName><orgName type="institution" wicri:auto="newGroup">Université de Lyon</orgName></affiliation></author></analytic></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>Akinesia</term><term>FMRI</term><term>Mirror movements</term><term>Parkinson’s disease</term></keywords><keywords scheme="mix" xml:lang="fr"><term>Akinésie</term><term>IRMf</term><term>Locus coeruleus</term><term>Maladie de Parkinson</term><term>Mouvements en miroir</term><term>Noradrénaline</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mirror movements and akinesia can be both found during Parkinson’s disease. Although very different, they may both reflect an abnormal cerebral plasticity during the disease and the perturbation of the motor inhibitory control. This work reveals that mirror movements are linked to a1/ disruption of the reactive inhibitory control and 2/ to the overactivation of numerous cortical areas. The latter could be the result of a compensatory recruitment aiming at improving the movement. But they could as well reflect a deleterious loss of cerebral activation specificity during Parkinson’s disease. The second experience shows that in healthy subject, the proactive inhibitory control is underpinned by the noradrenergic system. Last but not least the third part of this work reveals an abnormal implementation of the proactive inhibitory control in Parkinson’s disease and suggests its involvement in akinesia. Brought together these results suggest that an abnormal plasticity phenomenon underlies the mirror movements and the akinesia in Parkinson’s disease. More precisely, we observed a default of the reactive inhibitory control associated to mirror movements in Parkinson’s disease and an excess of proactive inhibitory control that seems to be linked to akinesia. The finding of an adrenergic modulation of the proactive inhibitory control opens the fields for the development of noradrenergic therapeutics in akinesia</div></front></TEI><affiliations><list><country><li>France</li></country><region><li>Auvergne-Rhône-Alpes</li><li>Rhône-Alpes</li></region><settlement><li>Grenoble</li><li>Lyon</li></settlement><orgName><li>Université Claude Bernard Lyon 1</li><li>Université Joseph Fourier</li><li>Université de Grenoble</li><li>Université de Lyon</li></orgName></list><tree><country name="France"><region name="Auvergne-Rhône-Alpes"><name sortKey="Poisson, Alice" sort="Poisson, Alice" uniqKey="Poisson A" first="Alice" last="Poisson">Alice Poisson</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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