Impaired heteronymous somatosensory motor cortical inhibition in dystonia
Identifieur interne : 000905 ( Istex/Corpus ); précédent : 000904; suivant : 000906Impaired heteronymous somatosensory motor cortical inhibition in dystonia
Auteurs : Laura Bertolasi ; Silvia Romito ; Michele Tinazzi ; Niccol Rizzuto ; Alberto PrioriSource :
- Movement Disorders [ 0885-3185 ] ; 2003-11.
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- KwdEn :
Abstract
A typical pathophysiological abnormality in dystonia is cocontraction of antagonist muscles, with impaired reciprocal inhibitory mechanisms in the spinal cord. Recent experimental data have shown that inhibitory interactions between antagonist muscles have also a parallel control at the level of the sensorimotor cortex. The aim of this work was to study heteronymous effects of a median nerve stimulus on the corticospinal projections to forearm muscles in dystonia. We used the technique of antagonist cortical inhibition, which assesses the conditioning effect of median nerve afferent input on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in ipsilateral forearm extensor muscles at rest. Nine healthy subjects and 10 patients with torsion dystonia participated in the study. MEPs and somatosensory evoked potentials were normal in patients. In healthy subjects, median nerve stimulation at 15‐ to 18‐msec intervals inhibited the test MEPs in forearm extensors. In dystonic patients, median nerve stimulation delivered at the same conditioning–test intervals elicited significantly less inhibition of the test MEP. On the whole, these data suggest an impaired sensory–motor integration in dystonia and, more specifically, the decreased antagonistic cortical inhibition could suggest that functional interactions between antagonist muscles are primarily impaired at the cortical level. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10514
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<front><div type="abstract" xml:lang="en">A typical pathophysiological abnormality in dystonia is cocontraction of antagonist muscles, with impaired reciprocal inhibitory mechanisms in the spinal cord. Recent experimental data have shown that inhibitory interactions between antagonist muscles have also a parallel control at the level of the sensorimotor cortex. The aim of this work was to study heteronymous effects of a median nerve stimulus on the corticospinal projections to forearm muscles in dystonia. We used the technique of antagonist cortical inhibition, which assesses the conditioning effect of median nerve afferent input on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in ipsilateral forearm extensor muscles at rest. Nine healthy subjects and 10 patients with torsion dystonia participated in the study. MEPs and somatosensory evoked potentials were normal in patients. In healthy subjects, median nerve stimulation at 15‐ to 18‐msec intervals inhibited the test MEPs in forearm extensors. In dystonic patients, median nerve stimulation delivered at the same conditioning–test intervals elicited significantly less inhibition of the test MEP. On the whole, these data suggest an impaired sensory–motor integration in dystonia and, more specifically, the decreased antagonistic cortical inhibition could suggest that functional interactions between antagonist muscles are primarily impaired at the cortical level. © 2003 Movement Disorder Society</div>
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<!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Impaired heteronymous somatosensory motor cortical inhibition in dystonia</title>
</titleInfo>
<titleInfo type="abbreviated" lang="en"><title>Cortical Reciprocal Inhibition in Dystonia</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Impaired heteronymous somatosensory motor cortical inhibition in dystonia</title>
</titleInfo>
<name type="personal"><namePart type="given">Laura</namePart>
<namePart type="family">Bertolasi</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurological Sciences and Vision, Section of Neurology, University of Verona, Verona, Italy</affiliation>
<description>Correspondence: Dipartimento di Scienze Neurologiche e della Visione, Sez. di Neurologia, Università degli Studi di Verona, Ospedale Policlinico, P.le L.A. Scuro 10, 37134 Verona, Italy</description>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Silvia</namePart>
<namePart type="family">Romito</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurological Sciences and Vision, Section of Neurology, University of Verona, Verona, Italy</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Michele</namePart>
<namePart type="family">Tinazzi</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurological Sciences and Vision, Section of Neurology, University of Verona, Verona, Italy</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Niccoló</namePart>
<namePart type="family">Rizzuto</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurological Sciences and Vision, Section of Neurology, University of Verona, Verona, Italy</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Alberto</namePart>
<namePart type="family">Priori</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Institute of Neurology, University of Milano, IRCCS, Ospedale Maggiore Policlinico, Milano, 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">2003-11</dateIssued>
<dateCaptured encoding="w3cdtf">2002-07-22</dateCaptured>
<dateValid encoding="w3cdtf">2003-04-14</dateValid>
<copyrightDate encoding="w3cdtf">2003</copyrightDate>
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<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="figures">2</extent>
<extent unit="tables">1</extent>
<extent unit="references">32</extent>
<extent unit="words">4666</extent>
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<abstract lang="en">A typical pathophysiological abnormality in dystonia is cocontraction of antagonist muscles, with impaired reciprocal inhibitory mechanisms in the spinal cord. Recent experimental data have shown that inhibitory interactions between antagonist muscles have also a parallel control at the level of the sensorimotor cortex. The aim of this work was to study heteronymous effects of a median nerve stimulus on the corticospinal projections to forearm muscles in dystonia. We used the technique of antagonist cortical inhibition, which assesses the conditioning effect of median nerve afferent input on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in ipsilateral forearm extensor muscles at rest. Nine healthy subjects and 10 patients with torsion dystonia participated in the study. MEPs and somatosensory evoked potentials were normal in patients. In healthy subjects, median nerve stimulation at 15‐ to 18‐msec intervals inhibited the test MEPs in forearm extensors. In dystonic patients, median nerve stimulation delivered at the same conditioning–test intervals elicited significantly less inhibition of the test MEP. On the whole, these data suggest an impaired sensory–motor integration in dystonia and, more specifically, the decreased antagonistic cortical inhibition could suggest that functional interactions between antagonist muscles are primarily impaired at the cortical level. © 2003 Movement Disorder Society</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>antagonist cortical inhibition</topic>
<topic>dystonia</topic>
<topic>motor cortex</topic>
<topic>transcranial brain stimulation</topic>
<topic>muscle afferents</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>11</number>
</detail>
<extent unit="pages"><start>1367</start>
<end>1373</end>
<total>7</total>
</extent>
</part>
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<identifier type="istex">B1C4F11AB2EE568A0E66A3AE07592BCAFBCBA29F</identifier>
<identifier type="DOI">10.1002/mds.10514</identifier>
<identifier type="ArticleID">MDS10514</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Movement Disorder Society</accessCondition>
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<recordContentSource>WILEY</recordContentSource>
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