La maladie de Parkinson en France (serveur d'exploration)

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Effect of L-dopa on the pattern of movement-related (de)synchronisation in advanced Parkinson's disease

Identifieur interne : 003266 ( Main/Curation ); précédent : 003265; suivant : 003267

Effect of L-dopa on the pattern of movement-related (de)synchronisation in advanced Parkinson's disease

Auteurs : D. Devos [France] ; E. Labyt [France] ; P. Derambure [France] ; J. L. Bourriez [France] ; F. Cassim [France] ; J. D. Guieu [France] ; A. Destee [France] ; L. Defebvre [France]

Source :

RBID : Pascal:04-0328230

Descripteurs français

English descriptors

Abstract

Dès le début de la maladie de Parkinson (MP), l'altération de la préparation motrice pourrait être révélée par un délai excessif de désynchronisation du rythme mu liée au mouvement, qui pourrait correspondre à une activation anormale du cortex sensorimoteur primaire (SMP) controlatéral. Après le mouvement, une réduction d'amplitude de la synchronisation du rythme bêta a été observée au niveau de la même région par rapport à des sujets contrôles et pourrait être en rapport avec une altération de la désactivation corticale. En analysant la (dé)synchronisation liée à l'événement, nous avons évalué la progression de ces anomalies chez le parkinsonien évolué et l'effet de la L-dopa sur celles-ci. Sous L-dopa, le score UPDRS III diminuait en moyenne de 60 %. La latence de désynchronisation centrale controlatérale pendant la préparation et la désynchronisation centrale bilatérale pendant l'exécution du mouvement augmentaient significativement sous L-dopa, avec parallèlement une diminution de la latence de désynchronisation frontocentrale. De même, la synchronisation bêta centrale controlatérale augmentait après le mouvement sous L-dopa. Ces changements de paramètres semblaient inversement corrélés à la bradykinésie. La latence de désynchronisation du rythme mu et l'amplitude de synchronisation du rythme bêta sont davantage diminuées dans la MP évoluée par rapport aux stades précoces, suggérant une détérioration de l'activation et de la désactivation corticale avec l'évolution de la maladie. La L-dopa restaure partiellement le pattern anormal de (dé)synchronisation des rythmes mu et bêta couvrant le cortex SMP.

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Pascal:04-0328230

Le document en format XML

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<term>Electroencephalography</term>
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<term>Humans</term>
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<div type="abstract" xml:lang="fr">Dès le début de la maladie de Parkinson (MP), l'altération de la préparation motrice pourrait être révélée par un délai excessif de désynchronisation du rythme mu liée au mouvement, qui pourrait correspondre à une activation anormale du cortex sensorimoteur primaire (SMP) controlatéral. Après le mouvement, une réduction d'amplitude de la synchronisation du rythme bêta a été observée au niveau de la même région par rapport à des sujets contrôles et pourrait être en rapport avec une altération de la désactivation corticale. En analysant la (dé)synchronisation liée à l'événement, nous avons évalué la progression de ces anomalies chez le parkinsonien évolué et l'effet de la L-dopa sur celles-ci. Sous L-dopa, le score UPDRS III diminuait en moyenne de 60 %. La latence de désynchronisation centrale controlatérale pendant la préparation et la désynchronisation centrale bilatérale pendant l'exécution du mouvement augmentaient significativement sous L-dopa, avec parallèlement une diminution de la latence de désynchronisation frontocentrale. De même, la synchronisation bêta centrale controlatérale augmentait après le mouvement sous L-dopa. Ces changements de paramètres semblaient inversement corrélés à la bradykinésie. La latence de désynchronisation du rythme mu et l'amplitude de synchronisation du rythme bêta sont davantage diminuées dans la MP évoluée par rapport aux stades précoces, suggérant une détérioration de l'activation et de la désactivation corticale avec l'évolution de la maladie. La L-dopa restaure partiellement le pattern anormal de (dé)synchronisation des rythmes mu et bêta couvrant le cortex SMP.</div>
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</author>
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<region type="old region">Nord-Pas-de-Calais</region>
<settlement type="city">Lille</settlement>
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<sZ>7 aut.</sZ>
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<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="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L." last="Defebvre">L. Defebvre</name>
<affiliation wicri:level="3">
<inist:fA14 i1="01">
<s1>Department of Neurology, EA2683, Lille University Medical Centre</s1>
<s2>Lille</s2>
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<region type="region">Hauts-de-France</region>
<region type="old region">Nord-Pas-de-Calais</region>
<settlement type="city">Lille</settlement>
</placeName>
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<title level="j" type="main">Neurophysiologie clinique : (Paris)</title>
<title level="j" type="abbreviated">Neurophysiol. clin. : (Paris)</title>
<idno type="ISSN">0987-7053</idno>
<imprint>
<date when="2003">2003</date>
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<title level="j" type="main">Neurophysiologie clinique : (Paris)</title>
<title level="j" type="abbreviated">Neurophysiol. clin. : (Paris)</title>
<idno type="ISSN">0987-7053</idno>
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<keywords scheme="KwdEn" xml:lang="en">
<term>Advanced stage</term>
<term>Desynchronization</term>
<term>Levodopa</term>
<term>Motion</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Parkinson maladie</term>
<term>Lévodopa</term>
<term>Stade avancé</term>
<term>Système nerveux pathologie</term>
<term>Désynchronisation</term>
<term>Mouvement</term>
</keywords>
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<div type="abstract" xml:lang="fr">Dès le début de la maladie de Parkinson (MP), l'altération de la préparation motrice pourrait être révélée par un délai excessif de désynchronisation du rythme mu liée au mouvement, qui pourrait correspondre à une activation anormale du cortex sensorimoteur primaire (SMP) controlatéral. Après le mouvement, une réduction d'amplitude de la synchronisation du rythme bêta a été observée au niveau de la même région par rapport à des sujets contrôles et pourrait être en rapport avec une altération de la désactivation corticale. En analysant la (dé)synchronisation liée à l'événement, nous avons évalué la progression de ces anomalies chez le parkinsonien évolué et l'effet de la L-dopa sur celles-ci. Sous L-dopa, le score UPDRS III diminuait en moyenne de 60 %. La latence de désynchronisation centrale controlatérale pendant la préparation et la désynchronisation centrale bilatérale pendant l'exécution du mouvement augmentaient significativement sous L-dopa, avec parallèlement une diminution de la latence de désynchronisation frontocentrale. De même, la synchronisation bêta centrale controlatérale augmentait après le mouvement sous L-dopa. Ces changements de paramètres semblaient inversement corrélés à la bradykinésie. La latence de désynchronisation du rythme mu et l'amplitude de synchronisation du rythme bêta sont davantage diminuées dans la MP évoluée par rapport aux stades précoces, suggérant une détérioration de l'activation et de la désactivation corticale avec l'évolution de la maladie. La L-dopa restaure partiellement le pattern anormal de (dé)synchronisation des rythmes mu et bêta couvrant le cortex SMP.</div>
</front>
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<name sortKey="Devos, D" sort="Devos, D" uniqKey="Devos D" first="D" last="Devos">D. Devos</name>
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</author>
<author>
<name sortKey="Bourriez, J L" sort="Bourriez, J L" uniqKey="Bourriez J" first="J L" last="Bourriez">J L Bourriez</name>
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<author>
<name sortKey="Cassim, F" sort="Cassim, F" uniqKey="Cassim F" first="F" last="Cassim">F. Cassim</name>
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<name sortKey="Destee, A" sort="Destee, A" uniqKey="Destee A" first="A" last="Destée">A. Destée</name>
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<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>
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<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>
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