Soleus H‐reflex tests in dystonia
Identifieur interne : 001144 ( Istex/Corpus ); précédent : 001143; suivant : 001145Soleus H‐reflex tests in dystonia
Auteurs : Koelman ; R. B. Willemse ; L. J. Bour ; A. A. J. Hilgevoord ; J. D. Speelman ; B. W. Ongerboer De VisseSource :
- Movement Disorders [ 0885-3185 ] ; 1995-01.
English descriptors
- KwdEn :
Abstract
Vibratory inhibition, the homonymous recovery curve and the ratio of the maximal H‐reflex to direct muscle potential (H/M ratio) of the soleus H‐reflex were assessed in 10 patients with leg dystonia and in six patients with arm or neck dystonia. The results were compared with those obtained in 48 healthy control subjects. H‐reflex variables most helpful for the discrimination of patients and healthy subjects were identified. In patients with leg dystonia, vibratory inhibition was less marked than in control subjects, whereas late facilitation of the recovery curve was increased. In patients with leg dystonia, area values of test reflexes in the late facilitatory phase of the recovery curve exceeded peak‐peak values, in contrast to findings in control subjects. This finding may be attributable to less synchronization of enhanced test reflexes in dystonia than in the control condition. In differentiating patients with leg dystonia from control subjects, a combination of parameters of vibratory inhibition and the late facilitatory phase of the recovery curve appeared most useful. In patients with arm or neck dystonia and in the unaffected legs of hemidystonic patients, soleus H‐reflex test results were in the normal range. Abnormalities in the results of the soleus H‐reflex tests we used appear to be related to the presence of clinical signs in the extremity under examination and not to the severity of features.
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DOI: 10.1002/mds.870100109
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The results were compared with those obtained in 48 healthy control subjects. H‐reflex variables most helpful for the discrimination of patients and healthy subjects were identified. In patients with leg dystonia, vibratory inhibition was less marked than in control subjects, whereas late facilitation of the recovery curve was increased. In patients with leg dystonia, area values of test reflexes in the late facilitatory phase of the recovery curve exceeded peak‐peak values, in contrast to findings in control subjects. This finding may be attributable to less synchronization of enhanced test reflexes in dystonia than in the control condition. In differentiating patients with leg dystonia from control subjects, a combination of parameters of vibratory inhibition and the late facilitatory phase of the recovery curve appeared most useful. In patients with arm or neck dystonia and in the unaffected legs of hemidystonic patients, soleus H‐reflex test results were in the normal range. Abnormalities in the results of the soleus H‐reflex tests we used appear to be related to the presence of clinical signs in the extremity under examination and not to the severity of features.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Koelman</name><affiliations><json:string>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</json:string></affiliations></json:item><json:item><name>R. B. Willemse</name><affiliations><json:string>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</json:string></affiliations></json:item><json:item><name>L. J. Bour</name><affiliations><json:string>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</json:string></affiliations></json:item><json:item><name>A. A. J. Hilgevoord</name><affiliations><json:string>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</json:string></affiliations></json:item><json:item><name>J. D. Speelman</name><affiliations><json:string>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</json:string></affiliations></json:item><json:item><name>B. W. 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In patients with leg dystonia, vibratory inhibition was less marked than in control subjects, whereas late facilitation of the recovery curve was increased. In patients with leg dystonia, area values of test reflexes in the late facilitatory phase of the recovery curve exceeded peak‐peak values, in contrast to findings in control subjects. This finding may be attributable to less synchronization of enhanced test reflexes in dystonia than in the control condition. In differentiating patients with leg dystonia from control subjects, a combination of parameters of vibratory inhibition and the late facilitatory phase of the recovery curve appeared most useful. In patients with arm or neck dystonia and in the unaffected legs of hemidystonic patients, soleus H‐reflex test results were in the normal range. 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D.</forename><surname>Speelman</surname></persName><affiliation>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</affiliation></author><author><persName><forename type="first">B. W. Ongerboer</forename><surname>de Visse</surname></persName><affiliation>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-01"></date><biblScope unit="vol">10</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="44">44</biblScope><biblScope unit="page" to="50">50</biblScope></imprint></monogr><idno type="istex">8CF9D423F57D2245B141641C607BB65634380B9A</idno><idno type="DOI">10.1002/mds.870100109</idno><idno type="ArticleID">MDS870100109</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Vibratory inhibition, the homonymous recovery curve and the ratio of the maximal H‐reflex to direct muscle potential (H/M ratio) of the soleus H‐reflex were assessed in 10 patients with leg dystonia and in six patients with arm or neck dystonia. The results were compared with those obtained in 48 healthy control subjects. H‐reflex variables most helpful for the discrimination of patients and healthy subjects were identified. In patients with leg dystonia, vibratory inhibition was less marked than in control subjects, whereas late facilitation of the recovery curve was increased. In patients with leg dystonia, area values of test reflexes in the late facilitatory phase of the recovery curve exceeded peak‐peak values, in contrast to findings in control subjects. This finding may be attributable to less synchronization of enhanced test reflexes in dystonia than in the control condition. In differentiating patients with leg dystonia from control subjects, a combination of parameters of vibratory inhibition and the late facilitatory phase of the recovery curve appeared most useful. In patients with arm or neck dystonia and in the unaffected legs of hemidystonic patients, soleus H‐reflex test results were in the normal range. Abnormalities in the results of the soleus H‐reflex tests we used appear to be related to the presence of clinical signs in the extremity under examination and not to the severity of features.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Soleus H‐reflex</term></item><item><term>Dystonia</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-05-26">Registration</change><change when="1995-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/8CF9D423F57D2245B141641C607BB65634380B9A/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Ongerboer</givenNames><familyName>de Visse</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="NL" type="organization"><unparsedAffiliation>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Soleus H‐reflex</keyword><keyword xml:id="kwd2">Dystonia</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Vibratory inhibition, the homonymous recovery curve and the ratio of the maximal H‐reflex to direct muscle potential (H/M ratio) of the soleus H‐reflex were assessed in 10 patients with leg dystonia and in six patients with arm or neck dystonia. The results were compared with those obtained in 48 healthy control subjects. H‐reflex variables most helpful for the discrimination of patients and healthy subjects were identified. In patients with leg dystonia, vibratory inhibition was less marked than in control subjects, whereas late facilitation of the recovery curve was increased. In patients with leg dystonia, area values of test reflexes in the late facilitatory phase of the recovery curve exceeded peak‐peak values, in contrast to findings in control subjects. This finding may be attributable to less synchronization of enhanced test reflexes in dystonia than in the control condition. In differentiating patients with leg dystonia from control subjects, a combination of parameters of vibratory inhibition and the late facilitatory phase of the recovery curve appeared most useful. In patients with arm or neck dystonia and in the unaffected legs of hemidystonic patients, soleus H‐reflex test results were in the normal range. Abnormalities in the results of the soleus H‐reflex tests we used appear to be related to the presence of clinical signs in the extremity under examination and not to the severity of features.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Soleus H‐reflex tests in dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SOLEUS H‐REFLEX TESTS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Soleus H‐reflex tests in dystonia</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Koelman</namePart><affiliation>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</affiliation><description>Correspondence: Department of Clinical Neurophysiology (D2), Academic Medical Centre, Meibergdreef 9, 1105 AZ‐Amsterdam, the Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. 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J.</namePart><namePart type="family">Hilgevoord</namePart><affiliation>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. D.</namePart><namePart type="family">Speelman</namePart><affiliation>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B. W. Ongerboer</namePart><namePart type="family">de Visse</namePart><affiliation>Clinical Neurophysiology Unit, Department of Neurology, Graduate School Neurosciences Amsterdam, Academic Medical Centre, Amsterdam, the Netherlands</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">1995-01</dateIssued><dateValid encoding="w3cdtf">1994-05-26</dateValid><copyrightDate encoding="w3cdtf">1995</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">3</extent><extent unit="tables">1</extent><extent unit="references">29</extent></physicalDescription><abstract lang="en">Vibratory inhibition, the homonymous recovery curve and the ratio of the maximal H‐reflex to direct muscle potential (H/M ratio) of the soleus H‐reflex were assessed in 10 patients with leg dystonia and in six patients with arm or neck dystonia. The results were compared with those obtained in 48 healthy control subjects. H‐reflex variables most helpful for the discrimination of patients and healthy subjects were identified. In patients with leg dystonia, vibratory inhibition was less marked than in control subjects, whereas late facilitation of the recovery curve was increased. In patients with leg dystonia, area values of test reflexes in the late facilitatory phase of the recovery curve exceeded peak‐peak values, in contrast to findings in control subjects. This finding may be attributable to less synchronization of enhanced test reflexes in dystonia than in the control condition. In differentiating patients with leg dystonia from control subjects, a combination of parameters of vibratory inhibition and the late facilitatory phase of the recovery curve appeared most useful. In patients with arm or neck dystonia and in the unaffected legs of hemidystonic patients, soleus H‐reflex test results were in the normal range. Abnormalities in the results of the soleus H‐reflex tests we used appear to be related to the presence of clinical signs in the extremity under examination and not to the severity of features.</abstract><subject lang="en"><genre>Keywords</genre><topic>Soleus H‐reflex</topic><topic>Dystonia</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>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>1995</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>44</start><end>50</end><total>7</total></extent></part></relatedItem><identifier type="istex">8CF9D423F57D2245B141641C607BB65634380B9A</identifier><identifier type="DOI">10.1002/mds.870100109</identifier><identifier type="ArticleID">MDS870100109</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1995 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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