Central nervous system lesions and segmental activity.
Identifieur interne : 001207 ( PubMed/Corpus ); précédent : 001206; suivant : 001208Central nervous system lesions and segmental activity.
Auteurs : Sabine Meunier ; Rose Katz ; Marion Simonetta-MoreauSource :
- Advances in experimental medicine and biology [ 0065-2598 ] ; 2002.
English descriptors
- KwdEn :
- MESH :
- physiology : Motor Neurons.
- physiopathology : Efferent Pathways, Parkinson Disease, Spinal Cord.
- Humans, Neural Inhibition.
Abstract
Study of activity in segmental pathways can help in understanding the pathophysiology of clinical disorders due to basal ganglia damage. Disynaptic Ia reciprocal inhibition (DI) acts by actively inhibiting antagonistic motoneurones and reducing the inhibition of agonist ones. During movement, activity of interneurones mediating DI is significantly modulated by descending inputs. In Parkinsonian patients, this descending modulation almost completely vanished. Lack of modulation was not dependent on L-DOPA as it occurred in treated patients and was not modified when patients were off medication. A potent heteronymous group II excitation of quadriceps MNs has been recently demonstrated in normal subjects after stimulation of the common peroneal nerve. This group II excitation was significantly enhanced in the rigid lower limb of Parkinsonian patients. We propose that enhanced group II excitation could contribute to rigidity in PD and result from a change in a tonic noradrenergic descending inhibitory control from locus coeruleus.
PubMed: 12171125
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pubmed:12171125Le document en format XML
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Disynaptic Ia reciprocal inhibition (DI) acts by actively inhibiting antagonistic motoneurones and reducing the inhibition of agonist ones. During movement, activity of interneurones mediating DI is significantly modulated by descending inputs. In Parkinsonian patients, this descending modulation almost completely vanished. Lack of modulation was not dependent on L-DOPA as it occurred in treated patients and was not modified when patients were off medication. A potent heteronymous group II excitation of quadriceps MNs has been recently demonstrated in normal subjects after stimulation of the common peroneal nerve. This group II excitation was significantly enhanced in the rigid lower limb of Parkinsonian patients. We propose that enhanced group II excitation could contribute to rigidity in PD and result from a change in a tonic noradrenergic descending inhibitory control from locus coeruleus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12171125</PMID><DateCreated><Year>2002</Year><Month>08</Month><Day>12</Day></DateCreated><DateCompleted><Year>2003</Year><Month>03</Month><Day>12</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0065-2598</ISSN><JournalIssue CitedMedium="Print"><Volume>508</Volume><PubDate><Year>2002</Year></PubDate></JournalIssue><Title>Advances in experimental medicine and biology</Title><ISOAbbreviation>Adv. Exp. Med. Biol.</ISOAbbreviation></Journal><ArticleTitle>Central nervous system lesions and segmental activity.</ArticleTitle><Pagination><MedlinePgn>309-13</MedlinePgn></Pagination><Abstract><AbstractText>Study of activity in segmental pathways can help in understanding the pathophysiology of clinical disorders due to basal ganglia damage. Disynaptic Ia reciprocal inhibition (DI) acts by actively inhibiting antagonistic motoneurones and reducing the inhibition of agonist ones. During movement, activity of interneurones mediating DI is significantly modulated by descending inputs. In Parkinsonian patients, this descending modulation almost completely vanished. Lack of modulation was not dependent on L-DOPA as it occurred in treated patients and was not modified when patients were off medication. A potent heteronymous group II excitation of quadriceps MNs has been recently demonstrated in normal subjects after stimulation of the common peroneal nerve. This group II excitation was significantly enhanced in the rigid lower limb of Parkinsonian patients. We propose that enhanced group II excitation could contribute to rigidity in PD and result from a change in a tonic noradrenergic descending inhibitory control from locus coeruleus.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meunier</LastName><ForeName>Sabine</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratoire de Neurophysiologie Clinique, Hĵpital de la Salpêtrière, Paris, France. meunier@chups.jussieu.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Katz</LastName><ForeName>Rose</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Simonetta-Moreau</LastName><ForeName>Marion</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Adv Exp Med Biol</MedlineTA><NlmUniqueID>0121103</NlmUniqueID><ISSNLinking>0065-2598</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D004525" MajorTopicYN="N">Efferent Pathways</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009046" MajorTopicYN="N">Motor Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009433" MajorTopicYN="N">Neural Inhibition</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013116" MajorTopicYN="N">Spinal Cord</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>8</Month><Day>13</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>3</Month><Day>13</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>8</Month><Day>13</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12171125</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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