Prolonged cortical silent period but normal sensorimotor plasticity in spinocerebellar ataxia 6
Identifieur interne : 001370 ( Istex/Corpus ); précédent : 001369; suivant : 001371Prolonged cortical silent period but normal sensorimotor plasticity in spinocerebellar ataxia 6
Auteurs : James T. H. Teo ; Susanne A. Schneider ; Binith J. Cheeran ; Miguel Fernandez-Del-Olmo ; Paola Giunti ; John C. Rothwell ; Kailash P. BhatiaSource :
- Movement Disorders [ 0885-3185 ] ; 2008-02-15.
English descriptors
Abstract
Spinocerebellar ataxia 6 (SCA6) is a hereditary disease characterized by a trinucleotide repeat expansion in the CACNA1A gene and late‐onset bilateral cerebellar atrophy. It is unclear if there is significant pathology outside of the cerebellum. We used transcranial magnetic stimulation to assess sensorimotor cortical circuits and cortical plasticity in 8 SCA6 patients and 8 age‐matched controls. Behavioral performance was assessed using a rhythmic tapping task. Neurophysiological measures of SCA6 patients showed a prolonged cortical silent period (CSP) but normal MEP recruitment curve, short‐latency afferent inhibition, long‐latency afferent inhibition and ipsilateral silent period. Paired‐associative stimulation induction also increased motor‐evoked potentials normally. SCA6 patients had greater variability with cued rhythmic tapping than normals and deteriorated when the cue was removed; in comparison, normal subjects had similar variability between cued and uncued rhythmic tapping. Analysis using a Wing–Kristofferson timing model indicated that both clock variance and motor delay variance were abnormal. Conclusion. In SCA6, the circuits for sensorimotor integration and the mechanisms for LTP‐like plasticity in the sensorimotor cortex are unimpaired. A prolonged CSP in SCA6 just like in other cerebellar atrophies would suggest that this neurophysiological change typifies cerebellar dysfunction. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21847
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Rothwell</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</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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It is unclear if there is significant pathology outside of the cerebellum. We used transcranial magnetic stimulation to assess sensorimotor cortical circuits and cortical plasticity in 8 SCA6 patients and 8 age‐matched controls. Behavioral performance was assessed using a rhythmic tapping task. Neurophysiological measures of SCA6 patients showed a prolonged cortical silent period (CSP) but normal MEP recruitment curve, short‐latency afferent inhibition, long‐latency afferent inhibition and ipsilateral silent period. Paired‐associative stimulation induction also increased motor‐evoked potentials normally. SCA6 patients had greater variability with cued rhythmic tapping than normals and deteriorated when the cue was removed; in comparison, normal subjects had similar variability between cued and uncued rhythmic tapping. Analysis using a Wing–Kristofferson timing model indicated that both clock variance and motor delay variance were abnormal. Conclusion. In SCA6, the circuits for sensorimotor integration and the mechanisms for LTP‐like plasticity in the sensorimotor cortex are unimpaired. A prolonged CSP in SCA6 just like in other cerebellar atrophies would suggest that this neurophysiological change typifies cerebellar dysfunction. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>James T.H. Teo MA, MRCP, MPhil</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</json:string></affiliations></json:item><json:item><name>Susanne A. Schneider MD</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</json:string></affiliations></json:item><json:item><name>Binith J. Cheeran MRCP, MPhil</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</json:string></affiliations></json:item><json:item><name>Miguel Fernandez‐del‐Olmo PhD</name><affiliations><json:string>INEF Galicia, Institute of Physical Education and Sport, A Coruña, Spain</json:string></affiliations></json:item><json:item><name>Paola Giunti MD, PhD</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</json:string></affiliations></json:item><json:item><name>John C. Rothwell PhD</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</json:string></affiliations></json:item><json:item><name>Kailash P. Bhatia MD, DM, FRCP</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>spinocerebellar ataxia 6</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>transcranial magnetic stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cerebellum</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>plasticity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>timing</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Spinocerebellar ataxia 6 (SCA6) is a hereditary disease characterized by a trinucleotide repeat expansion in the CACNA1A gene and late‐onset bilateral cerebellar atrophy. It is unclear if there is significant pathology outside of the cerebellum. We used transcranial magnetic stimulation to assess sensorimotor cortical circuits and cortical plasticity in 8 SCA6 patients and 8 age‐matched controls. Behavioral performance was assessed using a rhythmic tapping task. Neurophysiological measures of SCA6 patients showed a prolonged cortical silent period (CSP) but normal MEP recruitment curve, short‐latency afferent inhibition, long‐latency afferent inhibition and ipsilateral silent period. Paired‐associative stimulation induction also increased motor‐evoked potentials normally. SCA6 patients had greater variability with cued rhythmic tapping than normals and deteriorated when the cue was removed; in comparison, normal subjects had similar variability between cued and uncued rhythmic tapping. Analysis using a Wing–Kristofferson timing model indicated that both clock variance and motor delay variance were abnormal. Conclusion. In SCA6, the circuits for sensorimotor integration and the mechanisms for LTP‐like plasticity in the sensorimotor cortex are unimpaired. 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It is unclear if there is significant pathology outside of the cerebellum. We used transcranial magnetic stimulation to assess sensorimotor cortical circuits and cortical plasticity in 8 SCA6 patients and 8 age‐matched controls. Behavioral performance was assessed using a rhythmic tapping task. Neurophysiological measures of SCA6 patients showed a prolonged cortical silent period (CSP) but normal MEP recruitment curve, short‐latency afferent inhibition, long‐latency afferent inhibition and ipsilateral silent period. Paired‐associative stimulation induction also increased motor‐evoked potentials normally. SCA6 patients had greater variability with cued rhythmic tapping than normals and deteriorated when the cue was removed; in comparison, normal subjects had similar variability between cued and uncued rhythmic tapping. Analysis using a Wing–Kristofferson timing model indicated that both clock variance and motor delay variance were abnormal. Conclusion. In SCA6, the circuits for sensorimotor integration and the mechanisms for LTP‐like plasticity in the sensorimotor cortex are unimpaired. 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P.</givenNames><familyName>Bhatia</familyName><degrees>MD, DM, FRCP</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="ES" type="organization"><unparsedAffiliation>INEF Galicia, Institute of Physical Education and Sport, A Coruña, Spain</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">spinocerebellar ataxia 6</keyword><keyword xml:id="kwd2">transcranial magnetic stimulation</keyword><keyword xml:id="kwd3">cerebellum</keyword><keyword xml:id="kwd4">plasticity</keyword><keyword xml:id="kwd5">timing</keyword></keywordGroup><fundingInfo><fundingAgency>Wellington Fund, London</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Brain Research Trust, London</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Xunta de Galicia, Spain</fundingAgency><fundingNumber>PGIDIT06PXIB160333PR</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Spinocerebellar ataxia 6 (SCA6) is a hereditary disease characterized by a trinucleotide repeat expansion in the CACNA1A gene and late‐onset bilateral cerebellar atrophy. It is unclear if there is significant pathology outside of the cerebellum. We used transcranial magnetic stimulation to assess sensorimotor cortical circuits and cortical plasticity in 8 SCA6 patients and 8 age‐matched controls. Behavioral performance was assessed using a rhythmic tapping task. Neurophysiological measures of SCA6 patients showed a prolonged cortical silent period (CSP) but normal MEP recruitment curve, short‐latency afferent inhibition, long‐latency afferent inhibition and ipsilateral silent period. Paired‐associative stimulation induction also increased motor‐evoked potentials normally. SCA6 patients had greater variability with cued rhythmic tapping than normals and deteriorated when the cue was removed; in comparison, normal subjects had similar variability between cued and uncued rhythmic tapping. Analysis using a Wing–Kristofferson timing model indicated that both clock variance and motor delay variance were abnormal. <i>Conclusion.</i> In SCA6, the circuits for sensorimotor integration and the mechanisms for LTP‐like plasticity in the sensorimotor cortex are unimpaired. A prolonged CSP in SCA6 just like in other cerebellar atrophies would suggest that this neurophysiological change typifies cerebellar dysfunction. © 2007 Movement Disorder Society</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>Prolonged cortical silent period but normal sensorimotor plasticity in spinocerebellar ataxia 6</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Prolonged Cortical Silent Period in SCA6</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Prolonged cortical silent period but normal sensorimotor plasticity in spinocerebellar ataxia 6</title></titleInfo><name type="personal"><namePart type="given">James T.H.</namePart><namePart type="family">Teo</namePart><namePart type="termsOfAddress">MA, MRCP, MPhil</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</affiliation><description>Correspondence: Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susanne A.</namePart><namePart type="family">Schneider</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Binith J.</namePart><namePart type="family">Cheeran</namePart><namePart type="termsOfAddress">MRCP, MPhil</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Miguel</namePart><namePart type="family">Fernandez‐del‐Olmo</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>INEF Galicia, Institute of Physical Education and Sport, A Coruña, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Giunti</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John C.</namePart><namePart type="family">Rothwell</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kailash P.</namePart><namePart type="family">Bhatia</namePart><namePart type="termsOfAddress">MD, DM, FRCP</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom</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">2008-02-15</dateIssued><dateCaptured encoding="w3cdtf">2007-07-25</dateCaptured><dateValid encoding="w3cdtf">2007-10-17</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">4</extent><extent unit="tables">1</extent><extent unit="references">42</extent><extent unit="words">4581</extent></physicalDescription><abstract lang="en">Spinocerebellar ataxia 6 (SCA6) is a hereditary disease characterized by a trinucleotide repeat expansion in the CACNA1A gene and late‐onset bilateral cerebellar atrophy. It is unclear if there is significant pathology outside of the cerebellum. We used transcranial magnetic stimulation to assess sensorimotor cortical circuits and cortical plasticity in 8 SCA6 patients and 8 age‐matched controls. Behavioral performance was assessed using a rhythmic tapping task. Neurophysiological measures of SCA6 patients showed a prolonged cortical silent period (CSP) but normal MEP recruitment curve, short‐latency afferent inhibition, long‐latency afferent inhibition and ipsilateral silent period. Paired‐associative stimulation induction also increased motor‐evoked potentials normally. SCA6 patients had greater variability with cued rhythmic tapping than normals and deteriorated when the cue was removed; in comparison, normal subjects had similar variability between cued and uncued rhythmic tapping. Analysis using a Wing–Kristofferson timing model indicated that both clock variance and motor delay variance were abnormal. Conclusion. In SCA6, the circuits for sensorimotor integration and the mechanisms for LTP‐like plasticity in the sensorimotor cortex are unimpaired. A prolonged CSP in SCA6 just like in other cerebellar atrophies would suggest that this neurophysiological change typifies cerebellar dysfunction. © 2007 Movement Disorder Society</abstract><note type="funding">Wellington Fund, London</note><note type="funding">Brain Research Trust, London</note><note type="funding">Xunta de Galicia, Spain - No. PGIDIT06PXIB160333PR; </note><subject lang="en"><genre>Keywords</genre><topic>spinocerebellar ataxia 6</topic><topic>transcranial magnetic stimulation</topic><topic>cerebellum</topic><topic>plasticity</topic><topic>timing</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>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>3</number></detail><extent unit="pages"><start>378</start><end>385</end><total>8</total></extent></part></relatedItem><identifier type="istex">CDF3AD383FDF30909F27F19A7CEE3B9A1DFE7366</identifier><identifier type="DOI">10.1002/mds.21847</identifier><identifier type="ArticleID">MDS21847</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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