Prolonged cortical silent period but normal sensorimotor plasticity in spinocerebellar ataxia 6
Identifieur interne : 002672 ( Main/Exploration ); précédent : 002671; suivant : 002673Prolonged cortical silent period but normal sensorimotor plasticity in spinocerebellar ataxia 6
Auteurs : James T. H. Teo [Royaume-Uni] ; Susanne A. Schneider [Royaume-Uni] ; Binith J. Cheeran [Royaume-Uni] ; Miguel Fernandez-Del-Olmo [Espagne] ; Paola Giunti [Royaume-Uni] ; John C. Rothwell [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-02-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adult, Aged, Case-Control Studies, Cerebellum, Electric Stimulation (methods), Evoked Potentials, Motor, Evoked Potentials, Somatosensory, Female, Humans, Male, Middle Aged, Motor Cortex (physiopathology), Nervous system diseases, Neural Inhibition (physiology), Neural Inhibition (radiation effects), Neuronal Plasticity, Plasticity, Reaction Time, Silent period, Somatosensory Cortex (physiopathology), Spinocerebellar Ataxias (pathology), Spinocerebellar Ataxias (physiopathology), Spinocerebellar ataxia, Timing, Transcranial Magnetic Stimulation (methods), Transcranial magnetic stimulation, cerebellum, plasticity, spinocerebellar ataxia 6, timing, transcranial magnetic stimulation.
- MESH :
- methods : Electric Stimulation, Transcranial Magnetic Stimulation.
- pathology : Spinocerebellar Ataxias.
- physiology : Neural Inhibition.
- physiopathology : Motor Cortex, Somatosensory Cortex, Spinocerebellar Ataxias.
- radiation effects : Neural Inhibition.
- Adult, Aged, Case-Control Studies, Evoked Potentials, Motor, Evoked Potentials, Somatosensory, Female, Humans, Male, Middle Aged, Neuronal Plasticity, Reaction Time.
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
Url:
DOI: 10.1002/mds.21847
Affiliations:
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H." last="Teo">James T. H. Teo</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG</wicri:regionArea><wicri:noRegion>London WC1N 3BG</wicri:noRegion></affiliation></author><author><name sortKey="Schneider, Susanne A" sort="Schneider, Susanne A" uniqKey="Schneider S" first="Susanne A." last="Schneider">Susanne A. Schneider</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG</wicri:regionArea><wicri:noRegion>London WC1N 3BG</wicri:noRegion></affiliation></author><author><name sortKey="Cheeran, Binith J" sort="Cheeran, Binith J" uniqKey="Cheeran B" first="Binith J." last="Cheeran">Binith J. Cheeran</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG</wicri:regionArea><wicri:noRegion>London WC1N 3BG</wicri:noRegion></affiliation></author><author><name sortKey="Fernandez El Lmo, Miguel" sort="Fernandez El Lmo, Miguel" uniqKey="Fernandez El Lmo M" first="Miguel" last="Fernandez-Del-Olmo">Miguel Fernandez-Del-Olmo</name><affiliation wicri:level="1"><country xml:lang="fr">Espagne</country><wicri:regionArea>INEF Galicia, Institute of Physical Education and Sport, A Coruña</wicri:regionArea><wicri:noRegion>A Coruña</wicri:noRegion></affiliation></author><author><name sortKey="Giunti, Paola" sort="Giunti, Paola" uniqKey="Giunti P" first="Paola" last="Giunti">Paola Giunti</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG</wicri:regionArea><wicri:noRegion>London WC1N 3BG</wicri:noRegion></affiliation></author><author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. 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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-02-15">2008-02-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="378">378</biblScope><biblScope unit="page" to="385">385</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">CDF3AD383FDF30909F27F19A7CEE3B9A1DFE7366</idno><idno type="DOI">10.1002/mds.21847</idno><idno type="ArticleID">MDS21847</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Case-Control Studies</term><term>Cerebellum</term><term>Electric Stimulation (methods)</term><term>Evoked Potentials, Motor</term><term>Evoked Potentials, Somatosensory</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Motor Cortex (physiopathology)</term><term>Nervous system diseases</term><term>Neural Inhibition (physiology)</term><term>Neural Inhibition (radiation effects)</term><term>Neuronal Plasticity</term><term>Plasticity</term><term>Reaction Time</term><term>Silent period</term><term>Somatosensory Cortex (physiopathology)</term><term>Spinocerebellar Ataxias (pathology)</term><term>Spinocerebellar Ataxias (physiopathology)</term><term>Spinocerebellar ataxia</term><term>Timing</term><term>Transcranial Magnetic Stimulation (methods)</term><term>Transcranial magnetic stimulation</term><term>cerebellum</term><term>plasticity</term><term>spinocerebellar ataxia 6</term><term>timing</term><term>transcranial magnetic stimulation</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Electric Stimulation</term><term>Transcranial Magnetic Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Spinocerebellar Ataxias</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neural Inhibition</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Motor Cortex</term><term>Somatosensory Cortex</term><term>Spinocerebellar Ataxias</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Neural Inhibition</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Case-Control Studies</term><term>Evoked Potentials, Motor</term><term>Evoked Potentials, Somatosensory</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neuronal Plasticity</term><term>Reaction Time</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Ataxie spinocérébelleuse</term><term>Cervelet</term><term>Pathologie du système nerveux</term><term>Plasticité</term><term>Période muette</term><term>Stimulation magnétique transcrânienne</term><term>Timing</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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</div></front></TEI><affiliations><list><country><li>Espagne</li><li>Royaume-Uni</li></country></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Teo, James T H" sort="Teo, James T H" uniqKey="Teo J" first="James T. H." last="Teo">James T. H. Teo</name></noRegion><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name><name sortKey="Cheeran, Binith J" sort="Cheeran, Binith J" uniqKey="Cheeran B" first="Binith J." last="Cheeran">Binith J. Cheeran</name><name sortKey="Giunti, Paola" sort="Giunti, Paola" uniqKey="Giunti P" first="Paola" last="Giunti">Paola Giunti</name><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. Rothwell</name><name sortKey="Schneider, Susanne A" sort="Schneider, Susanne A" uniqKey="Schneider S" first="Susanne A." last="Schneider">Susanne A. Schneider</name></country><country name="Espagne"><noRegion><name sortKey="Fernandez El Lmo, Miguel" sort="Fernandez El Lmo, Miguel" uniqKey="Fernandez El Lmo M" first="Miguel" last="Fernandez-Del-Olmo">Miguel Fernandez-Del-Olmo</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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