Auditory startle response in cervical dystonia
Identifieur interne : 001866 ( Istex/Corpus ); précédent : 001865; suivant : 001867Auditory startle response in cervical dystonia
Auteurs : Jörg Müller ; Markus Kofler ; Gregor K. Wenning ; Klaus Seppi ; Josep Valls-Solé ; Werner PoeweSource :
- Movement Disorders [ 0885-3185 ] ; 2003-12.
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- KwdEn :
Abstract
The excitability of brainstem neurons is abnormally enhanced in patients with cervical dystonia (CD), but the extend of such abnormality is not known. We examined whether patients with CD showed abnormalities in the auditory startle response (ASR), a brainstem reflex elicited by an unexpected loud stimulus. Thirteen patients with CD were investigated 3 months after botulinum toxin treatment. Thirteen healthy volunteers served as controls. ASRs were elicited by binaural high‐intensity auditory stimuli. Reflex electromyographic (EMG) activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. We found that ASR onset latencies were similar for patients and controls. CD patients had significantly lower ASR probabilities than controls (P = 0.007). ASR area under the curve was significantly smaller in CD patients (P = 0.017). Similar to controls, patients showed a significant habituation of ASR (P < 0.001, each); however, CD patients showed a prolonged tonic or phasic EMG activity after the initial ASR that was not observed in controls. Normal latencies and recruitment pattern indicate a preserved organization of intrinsic neural pathways mediating ASR in CD. Reduced ASR probability and magnitude as well as prolonged EMG activity after the proper startle response corroborate and extend previous findings on brainstem dysfunction in CD. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10609
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Wenning</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Seppi, Klaus" sort="Seppi, Klaus" uniqKey="Seppi K" first="Klaus" last="Seppi">Klaus Seppi</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Valls Ole, Josep" sort="Valls Ole, Josep" uniqKey="Valls Ole J" first="Josep" last="Valls-Solé">Josep Valls-Solé</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Barcelona, Barcelona, Spain</mods:affiliation></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:CD908077747990C3567804B6B95A1689771218B5</idno><date when="2003" year="2003">2003</date><idno type="doi">10.1002/mds.10609</idno><idno type="url">https://api.istex.fr/document/CD908077747990C3567804B6B95A1689771218B5/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001866</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Auditory startle response in cervical dystonia</title><author><name sortKey="Muller, Jorg" sort="Muller, Jorg" uniqKey="Muller J" first="Jörg" last="Müller">Jörg Müller</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Kofler, Markus" sort="Kofler, Markus" uniqKey="Kofler M" first="Markus" last="Kofler">Markus Kofler</name><affiliation><mods:affiliation>Department of Neurology, Hospital Hochzirl, Austria</mods:affiliation></affiliation></author><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Seppi, Klaus" sort="Seppi, Klaus" uniqKey="Seppi K" first="Klaus" last="Seppi">Klaus Seppi</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Valls Ole, Josep" sort="Valls Ole, Josep" uniqKey="Valls Ole J" first="Josep" last="Valls-Solé">Josep Valls-Solé</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Barcelona, Barcelona, Spain</mods:affiliation></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><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. 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We examined whether patients with CD showed abnormalities in the auditory startle response (ASR), a brainstem reflex elicited by an unexpected loud stimulus. Thirteen patients with CD were investigated 3 months after botulinum toxin treatment. Thirteen healthy volunteers served as controls. ASRs were elicited by binaural high‐intensity auditory stimuli. Reflex electromyographic (EMG) activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. We found that ASR onset latencies were similar for patients and controls. CD patients had significantly lower ASR probabilities than controls (P = 0.007). ASR area under the curve was significantly smaller in CD patients (P = 0.017). Similar to controls, patients showed a significant habituation of ASR (P < 0.001, each); however, CD patients showed a prolonged tonic or phasic EMG activity after the initial ASR that was not observed in controls. Normal latencies and recruitment pattern indicate a preserved organization of intrinsic neural pathways mediating ASR in CD. Reduced ASR probability and magnitude as well as prolonged EMG activity after the proper startle response corroborate and extend previous findings on brainstem dysfunction in CD. © 2003 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Jörg Müller MD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Markus Kofler MD</name><affiliations><json:string>Department of Neurology, Hospital Hochzirl, Austria</json:string></affiliations></json:item><json:item><name>Gregor K. Wenning MD, PhD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Klaus Seppi MD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Josep Valls‐Solé MD, PhD</name><affiliations><json:string>Department of Neurology, University Hospital Barcelona, Barcelona, Spain</json:string></affiliations></json:item><json:item><name>Werner Poewe MD</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>auditory startle response</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cervical dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>brainstem reflex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pedunculopontine nucleus (PPN)</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The excitability of brainstem neurons is abnormally enhanced in patients with cervical dystonia (CD), but the extend of such abnormality is not known. We examined whether patients with CD showed abnormalities in the auditory startle response (ASR), a brainstem reflex elicited by an unexpected loud stimulus. Thirteen patients with CD were investigated 3 months after botulinum toxin treatment. Thirteen healthy volunteers served as controls. ASRs were elicited by binaural high‐intensity auditory stimuli. Reflex electromyographic (EMG) activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. We found that ASR onset latencies were similar for patients and controls. CD patients had significantly lower ASR probabilities than controls (P = 0.007). ASR area under the curve was significantly smaller in CD patients (P = 0.017). Similar to controls, patients showed a significant habituation of ASR (P > 0.001, each); however, CD patients showed a prolonged tonic or phasic EMG activity after the initial ASR that was not observed in controls. Normal latencies and recruitment pattern indicate a preserved organization of intrinsic neural pathways mediating ASR in CD. 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We examined whether patients with CD showed abnormalities in the auditory startle response (ASR), a brainstem reflex elicited by an unexpected loud stimulus. Thirteen patients with CD were investigated 3 months after botulinum toxin treatment. Thirteen healthy volunteers served as controls. ASRs were elicited by binaural high‐intensity auditory stimuli. Reflex electromyographic (EMG) activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. We found that ASR onset latencies were similar for patients and controls. CD patients had significantly lower ASR probabilities than controls (P = 0.007). ASR area under the curve was significantly smaller in CD patients (P = 0.017). Similar to controls, patients showed a significant habituation of ASR (P < 0.001, each); however, CD patients showed a prolonged tonic or phasic EMG activity after the initial ASR that was not observed in controls. Normal latencies and recruitment pattern indicate a preserved organization of intrinsic neural pathways mediating ASR in CD. Reduced ASR probability and magnitude as well as prolonged EMG activity after the proper startle response corroborate and extend previous findings on brainstem dysfunction in CD. © 2003 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>auditory startle response</term></item><item><term>cervical dystonia</term></item><item><term>brainstem reflex</term></item><item><term>pedunculopontine nucleus (PPN)</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-02-05">Received</change><change when="2003-06-16">Registration</change><change when="2003-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CD908077747990C3567804B6B95A1689771218B5/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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We examined whether patients with CD showed abnormalities in the auditory startle response (ASR), a brainstem reflex elicited by an unexpected loud stimulus. Thirteen patients with CD were investigated 3 months after botulinum toxin treatment. Thirteen healthy volunteers served as controls. ASRs were elicited by binaural high‐intensity auditory stimuli. Reflex electromyographic (EMG) activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. We found that ASR onset latencies were similar for patients and controls. CD patients had significantly lower ASR probabilities than controls (<i>P</i> = 0.007). ASR area under the curve was significantly smaller in CD patients (<i>P</i> = 0.017). Similar to controls, patients showed a significant habituation of ASR (<i>P</i> < 0.001, each); however, CD patients showed a prolonged tonic or phasic EMG activity after the initial ASR that was not observed in controls. Normal latencies and recruitment pattern indicate a preserved organization of intrinsic neural pathways mediating ASR in CD. Reduced ASR probability and magnitude as well as prolonged EMG activity after the proper startle response corroborate and extend previous findings on brainstem dysfunction in CD. © 2003 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>Auditory startle response in cervical dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Auditory Startle Response in Cervical Dystonia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Auditory startle response in cervical dystonia</title></titleInfo><name type="personal"><namePart type="given">Jörg</namePart><namePart type="family">Müller</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Markus</namePart><namePart type="family">Kofler</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Hospital Hochzirl, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregor K.</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus</namePart><namePart type="family">Seppi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Josep</namePart><namePart type="family">Valls‐Solé</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Hospital Barcelona, Barcelona, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Innsbruck, Austria</affiliation><description>Correspondence: Department of Neurology, University Hospital Innsbruck, Austria, Anichstr. 35, A‐6020 Innsbruck, Austria</description><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">2003-12</dateIssued><dateCaptured encoding="w3cdtf">2003-02-05</dateCaptured><dateValid encoding="w3cdtf">2003-06-16</dateValid><copyrightDate encoding="w3cdtf">2003</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">1</extent><extent unit="references">34</extent><extent unit="words">3168</extent></physicalDescription><abstract lang="en">The excitability of brainstem neurons is abnormally enhanced in patients with cervical dystonia (CD), but the extend of such abnormality is not known. We examined whether patients with CD showed abnormalities in the auditory startle response (ASR), a brainstem reflex elicited by an unexpected loud stimulus. Thirteen patients with CD were investigated 3 months after botulinum toxin treatment. Thirteen healthy volunteers served as controls. ASRs were elicited by binaural high‐intensity auditory stimuli. Reflex electromyographic (EMG) activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. We found that ASR onset latencies were similar for patients and controls. CD patients had significantly lower ASR probabilities than controls (P = 0.007). ASR area under the curve was significantly smaller in CD patients (P = 0.017). Similar to controls, patients showed a significant habituation of ASR (P < 0.001, each); however, CD patients showed a prolonged tonic or phasic EMG activity after the initial ASR that was not observed in controls. Normal latencies and recruitment pattern indicate a preserved organization of intrinsic neural pathways mediating ASR in CD. Reduced ASR probability and magnitude as well as prolonged EMG activity after the proper startle response corroborate and extend previous findings on brainstem dysfunction in CD. © 2003 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>auditory startle response</topic><topic>cervical dystonia</topic><topic>brainstem reflex</topic><topic>pedunculopontine nucleus (PPN)</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>Brief Report</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>2003</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>1522</start><end>1526</end><total>5</total></extent></part></relatedItem><identifier type="istex">CD908077747990C3567804B6B95A1689771218B5</identifier><identifier type="DOI">10.1002/mds.10609</identifier><identifier type="ArticleID">MDS10609</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 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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