Group I nonreciprocal inhibition in primary restless legs syndrome.
Identifieur interne : 002462 ( PubMed/Curation ); précédent : 002461; suivant : 002463Group I nonreciprocal inhibition in primary restless legs syndrome.
Auteurs : Cesa Scaglione [Italie] ; Roberto Vetrugno ; Giuseppe Plazzi ; Giovanni Rizzo ; Federica Provini ; Pasquale Montagna ; Paolo MartinelliSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Electrophysiology, H-Reflex (physiology), Humans, Intralaminar Thalamic Nuclei (physiopathology), Motor Neurons (physiology), Nerve Net (physiopathology), Neural Inhibition (physiology), Questionnaires, Restless Legs Syndrome (diagnosis), Restless Legs Syndrome (physiopathology), Reticular Formation (physiopathology), Spinal Nerves (physiopathology).
- MESH :
- diagnosis : Restless Legs Syndrome.
- physiology : H-Reflex, Motor Neurons, Neural Inhibition.
- physiopathology : Intralaminar Thalamic Nuclei, Nerve Net, Restless Legs Syndrome, Reticular Formation, Spinal Nerves.
- Electrophysiology, Humans, Questionnaires.
Abstract
Electrophysiological investigations of restless legs syndrome (RLS) have found spinal circuits impinging on motoneurones. We evaluated the H reflex threshold, latency, the Hmax/Mmax ratio, and the short latency autogenic inhibition in 7 patients with RLS and 10 age-matched controls by testing the excitability changes in soleus H reflex Ib interneuron function. A significant reduction in Ib inhibition at 4 (P = 0.043), 5 (P = 0.007), and 6 ms (P = 0.001) of H reflex conditioning interstimulus interval was found in RLS patients. Data support the hypothesis that altered group I nonreciprocal inhibition is implicated in enhancing the spinal circuitry excitability of RLS, and are consistent with the view of an abnormal supraspinal drive to spinal interneurons in RLS.
DOI: 10.1002/mds.21794
PubMed: 17987650
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We evaluated the H reflex threshold, latency, the Hmax/Mmax ratio, and the short latency autogenic inhibition in 7 patients with RLS and 10 age-matched controls by testing the excitability changes in soleus H reflex Ib interneuron function. A significant reduction in Ib inhibition at 4 (P = 0.043), 5 (P = 0.007), and 6 ms (P = 0.001) of H reflex conditioning interstimulus interval was found in RLS patients. Data support the hypothesis that altered group I nonreciprocal inhibition is implicated in enhancing the spinal circuitry excitability of RLS, and are consistent with the view of an abnormal supraspinal drive to spinal interneurons in RLS.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17987650</PMID><DateCreated><Year>2008</Year><Month>01</Month><Day>31</Day></DateCreated><DateCompleted><Year>2008</Year><Month>04</Month><Day>14</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>1</Issue><PubDate><Year>2008</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Group I nonreciprocal inhibition in primary restless legs syndrome.</ArticleTitle><Pagination><MedlinePgn>96-100</MedlinePgn></Pagination><Abstract><AbstractText>Electrophysiological investigations of restless legs syndrome (RLS) have found spinal circuits impinging on motoneurones. We evaluated the H reflex threshold, latency, the Hmax/Mmax ratio, and the short latency autogenic inhibition in 7 patients with RLS and 10 age-matched controls by testing the excitability changes in soleus H reflex Ib interneuron function. A significant reduction in Ib inhibition at 4 (P = 0.043), 5 (P = 0.007), and 6 ms (P = 0.001) of H reflex conditioning interstimulus interval was found in RLS patients. Data support the hypothesis that altered group I nonreciprocal inhibition is implicated in enhancing the spinal circuitry excitability of RLS, and are consistent with the view of an abnormal supraspinal drive to spinal interneurons in RLS.</AbstractText><CopyrightInformation>2007 Movement Disorder Society</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Scaglione</LastName><ForeName>Cesa</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy. cesa.scaglione@unibo.it</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vetrugno</LastName><ForeName>Roberto</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Plazzi</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Rizzo</LastName><ForeName>Giovanni</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Provini</LastName><ForeName>Federica</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Montagna</LastName><ForeName>Pasquale</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Martinelli</LastName><ForeName>Paolo</ForeName><Initials>P</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>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004594">Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006181">H-Reflex</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020646">Intralaminar Thalamic Nuclei</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009046">Motor Neurons</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009415">Nerve Net</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009433">Neural Inhibition</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011795">Questionnaires</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012148">Restless Legs Syndrome</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012154">Reticular Formation</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013127">Spinal Nerves</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>11</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>4</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>11</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21794</ArticleId><ArticleId IdType="pubmed">17987650</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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