[Event-related desynchronization and Parkinson disease. Importance in the analysis of the phase of preparation for movement].
Identifieur interne : 001419 ( PubMed/Corpus ); précédent : 001418; suivant : 001420[Event-related desynchronization and Parkinson disease. Importance in the analysis of the phase of preparation for movement].
Auteurs : L. Defebvre ; P. Derambure ; J L Bourriez ; A. Destée ; J D GuieuSource :
- Neurophysiologie clinique = Clinical neurophysiology [ 0987-7053 ] ; 1999.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- physiology : Movement, Volition.
- physiopathology : Parkinson Disease.
- Case-Control Studies, Cortical Synchronization, Electroencephalography, Humans, Middle Aged.
Abstract
This study was aimed at determining the spatiotemporal distribution of event-related desynchronization (ERD) during self-paced voluntary movement in order to establish the interest of this method for the analysis of movement programming in Parkinson's disease. Desynchronization of mu rhythm was recorded 2 s before to 0.5 s after right then left self-paced voluntary wrist flexions from 11 leads covering the primary sensorimotor cortex (central), supplementary motor area (frontocentral) and parietal cortex (parietocentral). Recordings were obtained from ten control subjects, ten patients treated for Parkinson's disease (bilateral symptoms) and 20 patients presenting with right or left hemiparkinsonism before and after chronic administration of L-dopa. In the control group, ERD started over the contralateral primary sensorimotor cortex 1,750 ms before movement and was bilateral just before performance of the movement. In both treated and de novo Parkinson's disease groups, decrease in ERD latency (1,000 to 1,250 ms before movement) was only observed when movements were performed with the akinetic hand and corresponded to a decrease in motor cortical activity. This confirmed that programming of movement is affected in Parkinson's disease. Earlier ERD with central ipsilateral distribution were also observed, suggesting that other cortical areas might be activated to compensate for dysfunction of movement programming and to increase the level of cortical activity required for performance of the movement. The administration of L-dopa to de novo hemiparkinsonians patients resulted in increased ERD latency over contralateral and ipsilateral central areas. As in the treated Parkinson's disease group, frontocentral ERD could also be recorded. L-dopa would thus partially restore the affected motor programmation and modulate cortical activation in both supplementary motor area and primary motor cortex, the later receiving more afferences from basal ganglia.
PubMed: 10093819
Links to Exploration step
pubmed:10093819Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">[Event-related desynchronization and Parkinson disease. Importance in the analysis of the phase of preparation for movement].</title>
<author><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. Defebvre</name>
<affiliation><nlm:affiliation>Service de neurophysiologie clinique, CHRU de Lille, France.</nlm:affiliation>
</affiliation>
</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="Destee, A" sort="Destee, A" uniqKey="Destee A" first="A" last="Destée">A. Destée</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>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="1999">1999</date>
<idno type="RBID">pubmed:10093819</idno>
<idno type="pmid">10093819</idno>
<idno type="wicri:Area/PubMed/Corpus">001419</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001419</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">[Event-related desynchronization and Parkinson disease. Importance in the analysis of the phase of preparation for movement].</title>
<author><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. Defebvre</name>
<affiliation><nlm:affiliation>Service de neurophysiologie clinique, CHRU de Lille, France.</nlm:affiliation>
</affiliation>
</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="Destee, A" sort="Destee, A" uniqKey="Destee A" first="A" last="Destée">A. Destée</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>
</analytic>
<series><title level="j">Neurophysiologie clinique = Clinical neurophysiology</title>
<idno type="ISSN">0987-7053</idno>
<imprint><date when="1999" type="published">1999</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (therapeutic use)</term>
<term>Case-Control Studies</term>
<term>Cortical Synchronization</term>
<term>Electroencephalography</term>
<term>Humans</term>
<term>Levodopa (therapeutic use)</term>
<term>Middle Aged</term>
<term>Movement (physiology)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Volition (physiology)</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>
<term>Volition</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Case-Control Studies</term>
<term>Cortical Synchronization</term>
<term>Electroencephalography</term>
<term>Humans</term>
<term>Middle Aged</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">This study was aimed at determining the spatiotemporal distribution of event-related desynchronization (ERD) during self-paced voluntary movement in order to establish the interest of this method for the analysis of movement programming in Parkinson's disease. Desynchronization of mu rhythm was recorded 2 s before to 0.5 s after right then left self-paced voluntary wrist flexions from 11 leads covering the primary sensorimotor cortex (central), supplementary motor area (frontocentral) and parietal cortex (parietocentral). Recordings were obtained from ten control subjects, ten patients treated for Parkinson's disease (bilateral symptoms) and 20 patients presenting with right or left hemiparkinsonism before and after chronic administration of L-dopa. In the control group, ERD started over the contralateral primary sensorimotor cortex 1,750 ms before movement and was bilateral just before performance of the movement. In both treated and de novo Parkinson's disease groups, decrease in ERD latency (1,000 to 1,250 ms before movement) was only observed when movements were performed with the akinetic hand and corresponded to a decrease in motor cortical activity. This confirmed that programming of movement is affected in Parkinson's disease. Earlier ERD with central ipsilateral distribution were also observed, suggesting that other cortical areas might be activated to compensate for dysfunction of movement programming and to increase the level of cortical activity required for performance of the movement. The administration of L-dopa to de novo hemiparkinsonians patients resulted in increased ERD latency over contralateral and ipsilateral central areas. As in the treated Parkinson's disease group, frontocentral ERD could also be recorded. L-dopa would thus partially restore the affected motor programmation and modulate cortical activation in both supplementary motor area and primary motor cortex, the later receiving more afferences from basal ganglia.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10093819</PMID>
<DateCreated><Year>1999</Year>
<Month>05</Month>
<Day>04</Day>
</DateCreated>
<DateCompleted><Year>1999</Year>
<Month>05</Month>
<Day>04</Day>
</DateCompleted>
<DateRevised><Year>2013</Year>
<Month>11</Month>
<Day>21</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Print">0987-7053</ISSN>
<JournalIssue CitedMedium="Print"><Volume>29</Volume>
<Issue>1</Issue>
<PubDate><Year>1999</Year>
<Month>Feb</Month>
</PubDate>
</JournalIssue>
<Title>Neurophysiologie clinique = Clinical neurophysiology</Title>
<ISOAbbreviation>Neurophysiol Clin</ISOAbbreviation>
</Journal>
<ArticleTitle>[Event-related desynchronization and Parkinson disease. Importance in the analysis of the phase of preparation for movement].</ArticleTitle>
<Pagination><MedlinePgn>71-89</MedlinePgn>
</Pagination>
<Abstract><AbstractText>This study was aimed at determining the spatiotemporal distribution of event-related desynchronization (ERD) during self-paced voluntary movement in order to establish the interest of this method for the analysis of movement programming in Parkinson's disease. Desynchronization of mu rhythm was recorded 2 s before to 0.5 s after right then left self-paced voluntary wrist flexions from 11 leads covering the primary sensorimotor cortex (central), supplementary motor area (frontocentral) and parietal cortex (parietocentral). Recordings were obtained from ten control subjects, ten patients treated for Parkinson's disease (bilateral symptoms) and 20 patients presenting with right or left hemiparkinsonism before and after chronic administration of L-dopa. In the control group, ERD started over the contralateral primary sensorimotor cortex 1,750 ms before movement and was bilateral just before performance of the movement. In both treated and de novo Parkinson's disease groups, decrease in ERD latency (1,000 to 1,250 ms before movement) was only observed when movements were performed with the akinetic hand and corresponded to a decrease in motor cortical activity. This confirmed that programming of movement is affected in Parkinson's disease. Earlier ERD with central ipsilateral distribution were also observed, suggesting that other cortical areas might be activated to compensate for dysfunction of movement programming and to increase the level of cortical activity required for performance of the movement. The administration of L-dopa to de novo hemiparkinsonians patients resulted in increased ERD latency over contralateral and ipsilateral central areas. As in the treated Parkinson's disease group, frontocentral ERD could also be recorded. L-dopa would thus partially restore the affected motor programmation and modulate cortical activation in both supplementary motor area and primary motor cortex, the later receiving more afferences from basal ganglia.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Defebvre</LastName>
<ForeName>L</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Service de neurophysiologie clinique, CHRU de Lille, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Derambure</LastName>
<ForeName>P</ForeName>
<Initials>P</Initials>
</Author>
<Author ValidYN="Y"><LastName>Bourriez</LastName>
<ForeName>J L</ForeName>
<Initials>JL</Initials>
</Author>
<Author ValidYN="Y"><LastName>Destée</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
</Author>
<Author ValidYN="Y"><LastName>Guieu</LastName>
<ForeName>J D</ForeName>
<Initials>JD</Initials>
</Author>
</AuthorList>
<Language>fre</Language>
<PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType>
<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<VernacularTitle>Désynchronisation liée à l'événement et maladie de Parkinson. Intérêt dans l'analyse de la phase de préparation au mouvement.</VernacularTitle>
</Article>
<MedlineJournalInfo><Country>France</Country>
<MedlineTA>Neurophysiol Clin</MedlineTA>
<NlmUniqueID>8804532</NlmUniqueID>
<ISSNLinking>0987-7053</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>46627O600J</RegistryNumber>
<NameOfSubstance UI="D007980">Levodopa</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003344" MajorTopicYN="Y">Cortical Synchronization</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004569" MajorTopicYN="N">Electroencephalography</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009068" MajorTopicYN="N">Movement</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014836" MajorTopicYN="N">Volition</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year>
<Month>3</Month>
<Day>27</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>1999</Year>
<Month>3</Month>
<Day>27</Day>
<Hour>0</Hour>
<Minute>1</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>1999</Year>
<Month>3</Month>
<Day>27</Day>
<Hour>0</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">10093819</ArticleId>
<ArticleId IdType="pii">S0987705399800422</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001419 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001419 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonFranceV1 |flux= PubMed |étape= Corpus |type= RBID |clé= pubmed:10093819 |texte= [Event-related desynchronization and Parkinson disease. Importance in the analysis of the phase of preparation for movement]. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:10093819" \ | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \ | NlmPubMed2Wicri -a ParkinsonFranceV1
This area was generated with Dilib version V0.6.29. |