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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ISTEX:BB6FBD1E67637226BCE673AD93997113E3721EBDLe document en format XML
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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.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>P. Brown</name><affiliations><json:string>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>M. J. Steiger</name><affiliations><json:string>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>P. D. Thompson</name><affiliations><json:string>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>J. C. Rothwell</name><affiliations><json:string>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>B. L. Day</name><affiliations><json:string>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>M. Salama</name><affiliations><json:string>CRC, Brussels, Brainel 'Alleud, Belgium</json:string></affiliations></json:item><json:item><name>T. Waegemans</name><affiliations><json:string>U.C.B. s.a. Pharmaceutical Sector, Brainel 'Alleud, Belgium</json:string></affiliations></json:item><json:item><name>Prof. Marsden</name><affiliations><json:string>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Piracetam</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cortical myoclonus</value></json:item></subject><language><json:string>eng</json:string></language><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%. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1993"></date><biblScope unit="vol">8</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="63">63</biblScope><biblScope unit="page" to="68">68</biblScope></imprint></monogr><idno type="istex">BB6FBD1E67637226BCE673AD93997113E3721EBD</idno><idno type="DOI">10.1002/mds.870080112</idno><idno type="ArticleID">MDS870080112</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><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></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Piracetam</term></item><item><term>Cortical myoclonus</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Review</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/BB6FBD1E67637226BCE673AD93997113E3721EBD/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Pharmaceutical Sector, Brainel 'Alleud, Belgium</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Piracetam</keyword><keyword xml:id="kwd2">Cortical myoclonus</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><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></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>Effectiveness of piracetam in cortical myoclonus</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PIRACETAM IN CORTICAL MYOCLONUS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effectiveness of piracetam in cortical myoclonus</title></titleInfo><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Brown</namePart><affiliation>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. J.</namePart><namePart type="family">Steiger</namePart><affiliation>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P. D.</namePart><namePart type="family">Thompson</namePart><affiliation>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. C.</namePart><namePart type="family">Rothwell</namePart><affiliation>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B. L.</namePart><namePart type="family">Day</namePart><affiliation>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Salama</namePart><affiliation>CRC, Brussels, Brainel 'Alleud, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Waegemans</namePart><affiliation>U.C.B. s.a. Pharmaceutical Sector, Brainel 'Alleud, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Prof.</namePart><namePart type="family">Marsden</namePart><affiliation>MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><description>Correspondence: University Department of Clinical Neurology, Institute of Neurology, Queen Square, London WC1N 3BG, England</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">reviewArticle</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</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">1</extent><extent unit="tables">4</extent><extent unit="references">16</extent></physicalDescription><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></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>Review</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>1993</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>63</start><end>68</end><total>6</total></extent></part></relatedItem><identifier type="istex">BB6FBD1E67637226BCE673AD93997113E3721EBD</identifier><identifier type="DOI">10.1002/mds.870080112</identifier><identifier type="ArticleID">MDS870080112</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1993 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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