Effect of L-Dopa on the pattern of movement-related (de)synchronisation in advanced Parkinson's disease.
Identifieur interne : 000403 ( Ncbi/Curation ); précédent : 000402; suivant : 000404Effect of L-Dopa on the pattern of movement-related (de)synchronisation in advanced Parkinson's disease.
Auteurs : D. Devos [France] ; E. Labyt ; P. Derambure ; J L Bourriez ; F. Cassim ; J D Guieu ; A. Destée ; L. DefebvreSource :
- Neurophysiologie clinique = Clinical neurophysiology [ 0987-7053 ] ; 2003.
English descriptors
- KwdEn :
- Adult, Antiparkinson Agents (therapeutic use), Beta Rhythm, Biomechanical Phenomena, Cortical Synchronization, Electroencephalography, Electromyography, Female, Humans, Levodopa (therapeutic use), Male, Middle Aged, Movement (physiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology).
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- physiology : Movement.
- physiopathology : Parkinson Disease.
- Adult, Beta Rhythm, Biomechanical Phenomena, Cortical Synchronization, Electroencephalography, Electromyography, Female, Humans, Male, Middle Aged.
Abstract
In the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a delay of mu rhythm movement-related desynchronisation, suggesting hypoactivation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in the amplitude of beta rhythm movement-related synchronisation was observed over the same region. This decrease--not seen in control subjects--was thus thought to be related to an impairment in cortical deactivation. By monitoring movement-related (de)synchronisation, we aimed (i) to extend to advanced PD the observations made in less-advanced situations and (ii) to test the effect of acute L-Dopa on these abnormalities. The United Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% following acute L-Dopa administration, and we observed the following concurrent changes: a marked increase in mu desynchronisation pre-movement latency (thus reduced delay) during movement preparation over contralateral, central regions; an increase in mu desynchronisation during movement execution over bilateral central regions; a decrease in mu desynchronisation latency over bilateral frontocentral regions, and a significant increase in beta synchronisation over contralateral, central regions after movement. Changes of mu and beta rhythm parameters seemed to be inversely correlated with bradykinesia. Mu rhythm desynchronisation latency and beta synchronisation amplitude further decreased in advanced PD compared to earlier stages of the disease, suggesting greater impairment of cortical activation/deactivation as the disease progresses. L-Dopa partially restored the abnormal mu and beta rhythm cortical (de)synchronisation patterns over the PSM cortex.
PubMed: 14672820
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Labyt</name></author><author><name sortKey="Derambure, P" sort="Derambure, P" uniqKey="Derambure P" first="P" last="Derambure">P. Derambure</name></author><author><name sortKey="Bourriez, J L" sort="Bourriez, J L" uniqKey="Bourriez J" first="J L" last="Bourriez">J L Bourriez</name></author><author><name sortKey="Cassim, F" sort="Cassim, F" uniqKey="Cassim F" first="F" last="Cassim">F. Cassim</name></author><author><name sortKey="Guieu, J D" sort="Guieu, J D" uniqKey="Guieu J" first="J D" last="Guieu">J D Guieu</name></author><author><name sortKey="Destee, A" sort="Destee, A" uniqKey="Destee A" first="A" last="Destée">A. Destée</name></author><author><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. 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Devos</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, EA2683, Lille University Medical Centre, Lille, France. d-devos@chru-lille.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Neurology, EA2683, Lille University Medical Centre, Lille</wicri:regionArea><placeName><region type="region">Hauts-de-France</region><region type="old region">Nord-Pas-de-Calais</region><settlement type="city">Lille</settlement></placeName></affiliation></author><author><name sortKey="Labyt, E" sort="Labyt, E" uniqKey="Labyt E" first="E" last="Labyt">E. Labyt</name></author><author><name sortKey="Derambure, P" sort="Derambure, P" uniqKey="Derambure P" first="P" last="Derambure">P. Derambure</name></author><author><name sortKey="Bourriez, J L" sort="Bourriez, J L" uniqKey="Bourriez J" first="J L" last="Bourriez">J L Bourriez</name></author><author><name sortKey="Cassim, F" sort="Cassim, F" uniqKey="Cassim F" first="F" last="Cassim">F. Cassim</name></author><author><name sortKey="Guieu, J D" sort="Guieu, J D" uniqKey="Guieu J" first="J D" last="Guieu">J D Guieu</name></author><author><name sortKey="Destee, A" sort="Destee, A" uniqKey="Destee A" first="A" last="Destée">A. Destée</name></author><author><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. Defebvre</name></author></analytic><series><title level="j">Neurophysiologie clinique = Clinical neurophysiology</title><idno type="ISSN">0987-7053</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antiparkinson Agents (therapeutic use)</term><term>Beta Rhythm</term><term>Biomechanical Phenomena</term><term>Cortical Synchronization</term><term>Electroencephalography</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Movement (physiology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Movement</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Beta Rhythm</term><term>Biomechanical Phenomena</term><term>Cortical Synchronization</term><term>Electroencephalography</term><term>Electromyography</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">In the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a delay of mu rhythm movement-related desynchronisation, suggesting hypoactivation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in the amplitude of beta rhythm movement-related synchronisation was observed over the same region. This decrease--not seen in control subjects--was thus thought to be related to an impairment in cortical deactivation. By monitoring movement-related (de)synchronisation, we aimed (i) to extend to advanced PD the observations made in less-advanced situations and (ii) to test the effect of acute L-Dopa on these abnormalities. The United Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% following acute L-Dopa administration, and we observed the following concurrent changes: a marked increase in mu desynchronisation pre-movement latency (thus reduced delay) during movement preparation over contralateral, central regions; an increase in mu desynchronisation during movement execution over bilateral central regions; a decrease in mu desynchronisation latency over bilateral frontocentral regions, and a significant increase in beta synchronisation over contralateral, central regions after movement. Changes of mu and beta rhythm parameters seemed to be inversely correlated with bradykinesia. Mu rhythm desynchronisation latency and beta synchronisation amplitude further decreased in advanced PD compared to earlier stages of the disease, suggesting greater impairment of cortical activation/deactivation as the disease progresses. L-Dopa partially restored the abnormal mu and beta rhythm cortical (de)synchronisation patterns over the PSM cortex.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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