Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease.
Identifieur interne : 001075 ( PubMed/Corpus ); précédent : 001074; suivant : 001076Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease.
Auteurs : D. Devos ; E. Labyt ; F. Cassim ; J L Bourriez ; N. Reyns ; G. Touzet ; S. Blond ; J D Guieu ; P. Derambure ; A. Destée ; L. DefebvreSource :
- The European journal of neuroscience [ 0953-816X ] ; 2003.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (therapeutic use), Automatic Data Processing, Beta Rhythm (drug effects), Brain Mapping, Electric Stimulation (methods), Electroencephalography, Electromyography, Female, Functional Laterality, Humans, Hypokinesia (physiopathology), Hypokinesia (therapy), Levodopa (therapeutic use), Male, Middle Aged, Movement (drug effects), Movement (physiology), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Somatosensory Cortex (drug effects), Somatosensory Cortex (physiopathology), Subthalamic Nucleus (physiopathology).
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug effects : Beta Rhythm, Movement, Somatosensory Cortex.
- methods : Electric Stimulation.
- physiology : Movement.
- physiopathology : Hypokinesia, Parkinson Disease, Somatosensory Cortex, Subthalamic Nucleus.
- therapy : Hypokinesia, Parkinson Disease.
- Aged, Automatic Data Processing, Brain Mapping, Electroencephalography, Electromyography, Female, Functional Laterality, Humans, Male, Middle Aged.
Abstract
In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement-related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l-dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self-paced wrist flexion in four conditions according to the presence or not of stimulation and l-dopa. Compared to without treatment, the motor score improved by approximately 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l-dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l-dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement-related somatosensory processing at the end of the movement through the basal ganglia into the cortex.
PubMed: 14622221
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Reyns</name></author><author><name sortKey="Touzet, G" sort="Touzet, G" uniqKey="Touzet G" first="G" last="Touzet">G. Touzet</name></author><author><name sortKey="Blond, S" sort="Blond, S" uniqKey="Blond S" first="S" last="Blond">S. Blond</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="Derambure, P" sort="Derambure, P" uniqKey="Derambure P" first="P" last="Derambure">P. Derambure</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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:14622221</idno><idno type="pmid">14622221</idno><idno type="wicri:Area/PubMed/Corpus">001075</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001075</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease.</title><author><name sortKey="Devos, D" sort="Devos, D" uniqKey="Devos D" first="D" last="Devos">D. Devos</name><affiliation><nlm:affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France. d-devos@chru-lille.fr</nlm:affiliation></affiliation></author><author><name sortKey="Labyt, E" sort="Labyt, E" uniqKey="Labyt E" first="E" last="Labyt">E. Labyt</name></author><author><name sortKey="Cassim, F" sort="Cassim, F" uniqKey="Cassim F" first="F" last="Cassim">F. Cassim</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="Reyns, N" sort="Reyns, N" uniqKey="Reyns N" first="N" last="Reyns">N. Reyns</name></author><author><name sortKey="Touzet, G" sort="Touzet, G" uniqKey="Touzet G" first="G" last="Touzet">G. Touzet</name></author><author><name sortKey="Blond, S" sort="Blond, S" uniqKey="Blond S" first="S" last="Blond">S. Blond</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="Derambure, P" sort="Derambure, P" uniqKey="Derambure P" first="P" last="Derambure">P. Derambure</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">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antiparkinson Agents (therapeutic use)</term><term>Automatic Data Processing</term><term>Beta Rhythm (drug effects)</term><term>Brain Mapping</term><term>Electric Stimulation (methods)</term><term>Electroencephalography</term><term>Electromyography</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Hypokinesia (physiopathology)</term><term>Hypokinesia (therapy)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Movement (drug effects)</term><term>Movement (physiology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Somatosensory Cortex (drug effects)</term><term>Somatosensory Cortex (physiopathology)</term><term>Subthalamic Nucleus (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 effects" xml:lang="en"><term>Beta Rhythm</term><term>Movement</term><term>Somatosensory Cortex</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Electric Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Movement</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hypokinesia</term><term>Parkinson Disease</term><term>Somatosensory Cortex</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Hypokinesia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Automatic Data Processing</term><term>Brain Mapping</term><term>Electroencephalography</term><term>Electromyography</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement-related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l-dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self-paced wrist flexion in four conditions according to the presence or not of stimulation and l-dopa. Compared to without treatment, the motor score improved by approximately 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l-dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l-dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement-related somatosensory processing at the end of the movement through the basal ganglia into the cortex.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14622221</PMID><DateCreated><Year>2003</Year><Month>11</Month><Day>18</Day></DateCreated><DateCompleted><Year>2003</Year><Month>12</Month><Day>19</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0953-816X</ISSN><JournalIssue CitedMedium="Print"><Volume>18</Volume><Issue>7</Issue><PubDate><Year>2003</Year><Month>Oct</Month></PubDate></JournalIssue><Title>The European journal of neuroscience</Title><ISOAbbreviation>Eur. J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1884-8</MedlinePgn></Pagination><Abstract><AbstractText>In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement-related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l-dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self-paced wrist flexion in four conditions according to the presence or not of stimulation and l-dopa. Compared to without treatment, the motor score improved by approximately 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l-dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l-dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement-related somatosensory processing at the end of the movement through the basal ganglia into the cortex.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Devos</LastName><ForeName>D</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France. d-devos@chru-lille.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Labyt</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Cassim</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Bourriez</LastName><ForeName>J L</ForeName><Initials>JL</Initials></Author><Author ValidYN="Y"><LastName>Reyns</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Touzet</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Blond</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Guieu</LastName><ForeName>J D</ForeName><Initials>JD</Initials></Author><Author ValidYN="Y"><LastName>Derambure</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Destée</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Defebvre</LastName><ForeName>L</ForeName><Initials>L</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Eur J Neurosci</MedlineTA><NlmUniqueID>8918110</NlmUniqueID><ISSNLinking>0953-816X</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="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001330" MajorTopicYN="N">Automatic Data Processing</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001611" MajorTopicYN="N">Beta Rhythm</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001931" MajorTopicYN="N">Brain Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004569" MajorTopicYN="N">Electroencephalography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004576" MajorTopicYN="N">Electromyography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007839" MajorTopicYN="N">Functional Laterality</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018476" MajorTopicYN="N">Hypokinesia</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009068" MajorTopicYN="N">Movement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013003" MajorTopicYN="N">Somatosensory Cortex</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020531" MajorTopicYN="N">Subthalamic Nucleus</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>11</Month><Day>19</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>12</Month><Day>20</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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