Abnormal reciprocal inhibition between antagonist muscles in Parkinson's disease.
Identifieur interne : 001318 ( PubMed/Corpus ); précédent : 001317; suivant : 001319Abnormal reciprocal inhibition between antagonist muscles in Parkinson's disease.
Auteurs : S. Meunier ; S. Pol ; J L Houeto ; M. VidailhetSource :
- Brain : a journal of neurology [ 0006-8950 ] ; 2000.
English descriptors
- KwdEn :
- Adult, Aged, Antiparkinson Agents (therapeutic use), Electric Stimulation, Electromyography, Female, Forearm (innervation), H-Reflex, Humans, Male, Median Nerve (physiology), Median Nerve (physiopathology), Middle Aged, Motor Activity (physiology), Motor Neurons (physiology), Muscle, Skeletal (innervation), Muscle, Skeletal (physiology), Muscle, Skeletal (physiopathology), Neural Pathways (physiology), Neural Pathways (physiopathology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Radial Nerve (physiology), Radial Nerve (physiopathology), Reference Values, Wrist Joint (physiology), Wrist Joint (physiopathology).
- MESH :
- chemical , therapeutic use : Antiparkinson Agents.
- drug therapy : Parkinson Disease.
- innervation : Forearm, Muscle, Skeletal.
- physiology : Median Nerve, Motor Activity, Motor Neurons, Muscle, Skeletal, Neural Pathways, Radial Nerve, Wrist Joint.
- physiopathology : Median Nerve, Muscle, Skeletal, Neural Pathways, Parkinson Disease, Radial Nerve, Wrist Joint.
- Adult, Aged, Electric Stimulation, Electromyography, Female, H-Reflex, Humans, Male, Middle Aged, Reference Values.
Abstract
Disynaptic Ia reciprocal inhibition acts, at the spinal level, by actively inhibiting antagonist motor neurons and reducing the inhibition of agonist motor neurons. The deactivation of this pathway in Parkinson's disease is still debated. Disynaptic reciprocal inhibition of H reflexes in the forearm flexor muscles was examined in 15 control subjects and 16 treated parkinsonian patients at rest and at the onset of a voluntary wrist flexion. Two patients were reassessed 18 h after withdrawal of antiparkinsonian medication. At rest, the level of Ia reciprocal inhibition between the wrist antagonist muscles was not significantly different between patients and controls. In contrast, clear abnormalities of this inhibition were revealed by voluntary movements in the patients. In normal subjects, at the onset of a wrist flexion, Ia reciprocal inhibition showed a large decrease, and we argue that this decrease is supraspinal in origin. On the less affected sides of the patients the descending modulation was still present but lower than in controls; on the more affected sides this modulation had vanished almost completely. These movement-induced abnormalities of disynaptic Ia reciprocal inhibition were closely associated with Parkinson's disease but were probably not dependent on L-dopa. They could play a role in the disturbances of precise voluntary movements observed in Parkinson's disease.
PubMed: 10775546
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Vidailhet</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10775546</idno><idno type="pmid">10775546</idno><idno type="wicri:Area/PubMed/Corpus">001318</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001318</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Abnormal reciprocal inhibition between antagonist muscles in Parkinson's disease.</title><author><name sortKey="Meunier, S" sort="Meunier, S" uniqKey="Meunier S" first="S" last="Meunier">S. Meunier</name><affiliation><nlm:affiliation>Clinical Neurophysiology, Réeducation and INSERM U289, Hôpital de la Salpêtrière, France. sabine.meunier@psl.ap-hop-paris.fr</nlm:affiliation></affiliation></author><author><name sortKey="Pol, S" sort="Pol, S" uniqKey="Pol S" first="S" last="Pol">S. Pol</name></author><author><name sortKey="Houeto, J L" sort="Houeto, J L" uniqKey="Houeto J" first="J L" last="Houeto">J L Houeto</name></author><author><name sortKey="Vidailhet, M" sort="Vidailhet, M" uniqKey="Vidailhet M" first="M" last="Vidailhet">M. Vidailhet</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="ISSN">0006-8950</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Antiparkinson Agents (therapeutic use)</term><term>Electric Stimulation</term><term>Electromyography</term><term>Female</term><term>Forearm (innervation)</term><term>H-Reflex</term><term>Humans</term><term>Male</term><term>Median Nerve (physiology)</term><term>Median Nerve (physiopathology)</term><term>Middle Aged</term><term>Motor Activity (physiology)</term><term>Motor Neurons (physiology)</term><term>Muscle, Skeletal (innervation)</term><term>Muscle, Skeletal (physiology)</term><term>Muscle, Skeletal (physiopathology)</term><term>Neural Pathways (physiology)</term><term>Neural Pathways (physiopathology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Radial Nerve (physiology)</term><term>Radial Nerve (physiopathology)</term><term>Reference Values</term><term>Wrist Joint (physiology)</term><term>Wrist Joint (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Forearm</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Median Nerve</term><term>Motor Activity</term><term>Motor Neurons</term><term>Muscle, Skeletal</term><term>Neural Pathways</term><term>Radial Nerve</term><term>Wrist Joint</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Median Nerve</term><term>Muscle, Skeletal</term><term>Neural Pathways</term><term>Parkinson Disease</term><term>Radial Nerve</term><term>Wrist Joint</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Electric Stimulation</term><term>Electromyography</term><term>Female</term><term>H-Reflex</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Reference Values</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Disynaptic Ia reciprocal inhibition acts, at the spinal level, by actively inhibiting antagonist motor neurons and reducing the inhibition of agonist motor neurons. The deactivation of this pathway in Parkinson's disease is still debated. Disynaptic reciprocal inhibition of H reflexes in the forearm flexor muscles was examined in 15 control subjects and 16 treated parkinsonian patients at rest and at the onset of a voluntary wrist flexion. Two patients were reassessed 18 h after withdrawal of antiparkinsonian medication. At rest, the level of Ia reciprocal inhibition between the wrist antagonist muscles was not significantly different between patients and controls. In contrast, clear abnormalities of this inhibition were revealed by voluntary movements in the patients. In normal subjects, at the onset of a wrist flexion, Ia reciprocal inhibition showed a large decrease, and we argue that this decrease is supraspinal in origin. On the less affected sides of the patients the descending modulation was still present but lower than in controls; on the more affected sides this modulation had vanished almost completely. These movement-induced abnormalities of disynaptic Ia reciprocal inhibition were closely associated with Parkinson's disease but were probably not dependent on L-dopa. They could play a role in the disturbances of precise voluntary movements observed in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10775546</PMID><DateCreated><Year>2000</Year><Month>06</Month><Day>06</Day></DateCreated><DateCompleted><Year>2000</Year><Month>06</Month><Day>06</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-8950</ISSN><JournalIssue CitedMedium="Print"><Volume>123 ( Pt 5)</Volume><PubDate><Year>2000</Year><Month>May</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Abnormal reciprocal inhibition between antagonist muscles in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1017-26</MedlinePgn></Pagination><Abstract><AbstractText>Disynaptic Ia reciprocal inhibition acts, at the spinal level, by actively inhibiting antagonist motor neurons and reducing the inhibition of agonist motor neurons. The deactivation of this pathway in Parkinson's disease is still debated. Disynaptic reciprocal inhibition of H reflexes in the forearm flexor muscles was examined in 15 control subjects and 16 treated parkinsonian patients at rest and at the onset of a voluntary wrist flexion. Two patients were reassessed 18 h after withdrawal of antiparkinsonian medication. At rest, the level of Ia reciprocal inhibition between the wrist antagonist muscles was not significantly different between patients and controls. In contrast, clear abnormalities of this inhibition were revealed by voluntary movements in the patients. In normal subjects, at the onset of a wrist flexion, Ia reciprocal inhibition showed a large decrease, and we argue that this decrease is supraspinal in origin. On the less affected sides of the patients the descending modulation was still present but lower than in controls; on the more affected sides this modulation had vanished almost completely. These movement-induced abnormalities of disynaptic Ia reciprocal inhibition were closely associated with Parkinson's disease but were probably not dependent on L-dopa. They could play a role in the disturbances of precise voluntary movements observed in Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meunier</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Clinical Neurophysiology, Réeducation and INSERM U289, Hôpital de la Salpêtrière, France. sabine.meunier@psl.ap-hop-paris.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pol</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Houeto</LastName><ForeName>J L</ForeName><Initials>JL</Initials></Author><Author ValidYN="Y"><LastName>Vidailhet</LastName><ForeName>M</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><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="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004576" 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UI="D009043" MajorTopicYN="N">Motor Activity</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009046" MajorTopicYN="N">Motor Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="N">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000294" MajorTopicYN="N">innervation</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009434" MajorTopicYN="N">Neural Pathways</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</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="D011826" MajorTopicYN="N">Radial Nerve</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012016" MajorTopicYN="N">Reference Values</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014955" MajorTopicYN="N">Wrist Joint</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>4</Month><Day>25</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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