Effectiveness of piracetam in cortical myoclonus
Identifieur interne : 001B54 ( Istex/Corpus ); précédent : 001B53; suivant : 001B55Effectiveness of piracetam in cortical myoclonus
Auteurs : P. Brown ; M. J. Steiger ; P. D. Thompson ; J. C. Rothwell ; B. L. Day ; M. Salama ; T. Waegemans ; MarsdenSource :
- Movement Disorders [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
Abstract
Twenty‐one patients with disabling spontaneous, reflex, or action myoclonus due to various causes, who had shown apparent clinical improvement on introduction of piracetam, entered a placebo‐controlled double‐blind crossover trial of piracetam (2.4– 16.8 g daily). All but one patient had electrophysiological evidence of cortical myoclonus. Patients were randomly allocated to a 14‐ day course of piracetam followed by identical placebo, or placebo followed by piracetam. Nineteen patients received piracetam/placebo in addition to their routine antimyoclonic treatment (carbamazepine, clonazepam, phenytoin, primidone, sodium valproate, or tryptophan plus isocarboxazid, alone or in combination) and two received piracetam/placebo as monotherapy. All patients were rated at the end of each treatment phase using stimulus sensitivity, motor, writing, functional disability, global assessment, and visual analogue scales. Ten of the 21 patients had to be rescued from the placebo phase of the trial because of a severe and intolerable exacerbation of their myoclonus. No patients required rescue from the piracetam phase of the double‐blind trial. When the 21 patients were considered together, there was a significant improvement in motor, writing, functional disability, global assessment, and visual analogue scores during treatment with piracetam compared with placebo. The total rating score also improved significantly with piracetam, by a median of 22%. Piracetam, usually in combination with other antimyoclonic drugs, is a useful treatment for myoclonus of cortical origin.
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DOI: 10.1002/mds.870080112
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<p>Twenty‐one patients with disabling spontaneous, reflex, or action myoclonus due to various causes, who had shown apparent clinical improvement on introduction of piracetam, entered a placebo‐controlled double‐blind crossover trial of piracetam (2.4– 16.8 g daily). All but one patient had electrophysiological evidence of cortical myoclonus. Patients were randomly allocated to a 14‐ day course of piracetam followed by identical placebo, or placebo followed by piracetam. Nineteen patients received piracetam/placebo in addition to their routine antimyoclonic treatment (carbamazepine, clonazepam, phenytoin, primidone, sodium valproate, or tryptophan plus isocarboxazid, alone or in combination) and two received piracetam/placebo as monotherapy. All patients were rated at the end of each treatment phase using stimulus sensitivity, motor, writing, functional disability, global assessment, and visual analogue scales. Ten of the 21 patients had to be rescued from the placebo phase of the trial because of a severe and intolerable exacerbation of their myoclonus. No patients required rescue from the piracetam phase of the double‐blind trial. When the 21 patients were considered together, there was a significant improvement in motor, writing, functional disability, global assessment, and visual analogue scores during treatment with piracetam compared with placebo. The total rating score also improved significantly with piracetam, by a median of 22%. Piracetam, usually in combination with other antimyoclonic drugs, is a useful treatment for myoclonus of cortical origin.</p>
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<!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Effectiveness of piracetam in cortical myoclonus</title>
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<titleInfo type="abbreviated" lang="en"><title>PIRACETAM IN CORTICAL MYOCLONUS</title>
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<name type="personal"><namePart type="given">P.</namePart>
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<name type="personal"><namePart type="given">M. J.</namePart>
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<name type="personal"><namePart type="given">P. D.</namePart>
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<abstract lang="en">Twenty‐one patients with disabling spontaneous, reflex, or action myoclonus due to various causes, who had shown apparent clinical improvement on introduction of piracetam, entered a placebo‐controlled double‐blind crossover trial of piracetam (2.4– 16.8 g daily). All but one patient had electrophysiological evidence of cortical myoclonus. Patients were randomly allocated to a 14‐ day course of piracetam followed by identical placebo, or placebo followed by piracetam. Nineteen patients received piracetam/placebo in addition to their routine antimyoclonic treatment (carbamazepine, clonazepam, phenytoin, primidone, sodium valproate, or tryptophan plus isocarboxazid, alone or in combination) and two received piracetam/placebo as monotherapy. All patients were rated at the end of each treatment phase using stimulus sensitivity, motor, writing, functional disability, global assessment, and visual analogue scales. Ten of the 21 patients had to be rescued from the placebo phase of the trial because of a severe and intolerable exacerbation of their myoclonus. No patients required rescue from the piracetam phase of the double‐blind trial. When the 21 patients were considered together, there was a significant improvement in motor, writing, functional disability, global assessment, and visual analogue scores during treatment with piracetam compared with placebo. The total rating score also improved significantly with piracetam, by a median of 22%. Piracetam, usually in combination with other antimyoclonic drugs, is a useful treatment for myoclonus of cortical origin.</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>Piracetam</topic>
<topic>Cortical myoclonus</topic>
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<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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<identifier type="ISSN">0885-3185</identifier>
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<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
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<part><date>1993</date>
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