Somatosensory disinhibition in dystonia
Identifieur interne : 000090 ( Istex/Curation ); précédent : 000089; suivant : 000091Somatosensory disinhibition in dystonia
Auteurs : Emma Frasson [Italie] ; Alberto Priori [Italie] ; Laura Bertolasi [Italie] ; Francois Mauguière [France] ; Antonio Fiaschi [Italie] ; Michele Tinazzi [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2001-07.
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Abstract
Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1142
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wicri:level="1"><mods:affiliation>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona, Italy</mods:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Scienze Neurologiche e Della Visione, Sez. di Neurologia e Sez. di Neurologia Riabilitativa, Verona</wicri:regionArea></affiliation></author><author><name sortKey="Priori, Alberto" sort="Priori, Alberto" uniqKey="Priori A" first="Alberto" last="Priori">Alberto Priori</name><affiliation wicri:level="1"><mods:affiliation>Istituto di Clinica Neurologica, Università di Milano, IRCCS Ospedale Maggiore di Milano, Italy</mods:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Istituto di Clinica Neurologica, Università di Milano, IRCCS Ospedale Maggiore di Milano</wicri:regionArea></affiliation></author><author><name sortKey="Bertolasi, Laura" sort="Bertolasi, Laura" uniqKey="Bertolasi L" first="Laura" last="Bertolasi">Laura 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Verona</wicri:regionArea></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. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-07">2001-07</date><biblScope unit="vol">16</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="674">674</biblScope><biblScope unit="page" to="682">682</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E0941C5106E2E0B09507D76E8F291750C93241BE</idno><idno type="DOI">10.1002/mds.1142</idno><idno type="ArticleID">MDS1142</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>dystonia</term><term>paired stimulation</term><term>recovery cycle</term><term>somatosensory evoked potentials</term><term>somatosensory system</term><term>upper limb SEPs</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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