Group I nonreciprocal inhibition in primary restless legs syndrome
Identifieur interne : 002C37 ( Istex/Corpus ); précédent : 002C36; suivant : 002C38Group I nonreciprocal inhibition in primary restless legs syndrome
Auteurs : Cesa Scaglione ; Roberto Vetrugno ; Giuseppe Plazzi ; Giovanni Rizzo ; Federica Provini ; Pasquale Montagna ; Paolo MartinelliSource :
- Movement Disorders [ 0885-3185 ] ; 2008-01.
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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. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21794
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ISTEX:800D55DF8E337FB8DA5DF27DB4FE9BE2F6EB35B7Le document en format XML
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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. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Cesa Scaglione MD, PhD</name><affiliations><json:string>Department of Neurological Sciences, University of Bologna, Bologna, Italy</json:string></affiliations></json:item><json:item><name>Roberto Vetrugno MD, PhD</name><affiliations><json:string>Department of Neurological Sciences, University of Bologna, Bologna, Italy</json:string></affiliations></json:item><json:item><name>Giuseppe Plazzi MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bologna, Bologna, Italy</json:string></affiliations></json:item><json:item><name>Giovanni Rizzo MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bologna, Bologna, Italy</json:string></affiliations></json:item><json:item><name>Federica Provini MD, PhD</name><affiliations><json:string>Department of Neurological Sciences, University of Bologna, Bologna, Italy</json:string></affiliations></json:item><json:item><name>Pasquale Montagna MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bologna, Bologna, Italy</json:string></affiliations></json:item><json:item><name>Paolo Martinelli MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bologna, Bologna, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>restless legs syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>spinal reflex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Ib inhibition</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>reticular formation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>nucleus reticularis giganto‐cellularis</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Electrophysiological investigations of restless legs syndrome (RLS) have found spinal circuits impinging on motoneurones. 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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. © 2007 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>restless legs syndrome</term></item><item><term>spinal reflex</term></item><item><term>Ib inhibition</term></item><item><term>reticular formation</term></item><item><term>nucleus reticularis giganto‐cellularis</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-05-31">Received</change><change when="2007-09-30">Registration</change><change when="2008-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/800D55DF8E337FB8DA5DF27DB4FE9BE2F6EB35B7/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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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 (<i>P</i> = 0.043), 5 (<i>P</i> = 0.007), and 6 ms (<i>P</i> = 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. © 2007 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Group I nonreciprocal inhibition in primary restless legs syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Ib Autogenic Inhibition in RLS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Group I nonreciprocal inhibition in primary restless legs syndrome</title></titleInfo><name type="personal"><namePart type="given">Cesa</namePart><namePart type="family">Scaglione</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy</affiliation><description>Correspondence: Dipartimento di Scienze Neurologiche, Via Ugo Foscolo 7, 40123 Bologna</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roberto</namePart><namePart type="family">Vetrugno</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Giuseppe</namePart><namePart type="family">Plazzi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Giovanni</namePart><namePart type="family">Rizzo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Federica</namePart><namePart type="family">Provini</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pasquale</namePart><namePart type="family">Montagna</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paolo</namePart><namePart type="family">Martinelli</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bologna, Bologna, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2008-01</dateIssued><dateCaptured encoding="w3cdtf">2007-05-31</dateCaptured><dateValid encoding="w3cdtf">2007-09-30</dateValid><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">1</extent><extent unit="references">29</extent><extent unit="words">3321</extent></physicalDescription><abstract lang="en">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. © 2007 Movement Disorder Society</abstract><note type="funding">MURST - No. RFo (ex 60%) 2005–2006; </note><note type="funding">Fondazione Cassa di Risparmio‐Bologna, Italy</note><subject lang="en"><genre>Keywords</genre><topic>restless legs syndrome</topic><topic>spinal reflex</topic><topic>Ib inhibition</topic><topic>reticular formation</topic><topic>nucleus reticularis giganto‐cellularis</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>96</start><end>100</end><total>5</total></extent></part></relatedItem><identifier type="istex">800D55DF8E337FB8DA5DF27DB4FE9BE2F6EB35B7</identifier><identifier type="DOI">10.1002/mds.21794</identifier><identifier type="ArticleID">MDS21794</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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