The clinical features and prognosis of chronic posthypoxic myoclonus
Identifieur interne : 002989 ( Istex/Corpus ); précédent : 002988; suivant : 002990The clinical features and prognosis of chronic posthypoxic myoclonus
Auteurs : Werhahn ; Brown ; P. D. Thompson ; C. D. MarsdenSource :
- Movement Disorders [ 0885-3185 ] ; 1997-03.
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Abstract
The clinical and neurophysiologic features of 14 patients with chronic posthypoxic myoclonus are presented. Patients were first seen a mean of 2.5 years (range, 2 to 105 months) after the hypoxic event and followed up for 3.7 years (range, 7 to 84 months) thereafter. All patients had had a cardiorespiratory arrest, most caused by an acute asthmatic attack (11 cases). All patients had multifocal action myoclonus. Eleven patients had additional stimulus‐sensitive myoclonus. There was late improvement in the myoclonic syndrome and the level of disability in all but one patient. Three patients were eventually able to discontinue antimyoclonic medication, and five patients were able to walk unaided. Cognitive deficits were found in seven patients and were usually mild. Other neurologic deficits were rare. Electrophysiologic investigation confirmed cortical action myoclonus in every case, although this could be combined with cortical reflex myoclonus, an exaggerated startle response, or brainstem reticular reflex myoclonus. We conclude that posthypoxic myoclonus typically consists of multifocal cortical action myoclonus that improves with time. It is only rarely associated with severe additional neurologic deficit.
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DOI: 10.1002/mds.870120212
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Patients were first seen a mean of 2.5 years (range, 2 to 105 months) after the hypoxic event and followed up for 3.7 years (range, 7 to 84 months) thereafter. All patients had had a cardiorespiratory arrest, most caused by an acute asthmatic attack (11 cases). All patients had multifocal action myoclonus. Eleven patients had additional stimulus‐sensitive myoclonus. There was late improvement in the myoclonic syndrome and the level of disability in all but one patient. Three patients were eventually able to discontinue antimyoclonic medication, and five patients were able to walk unaided. Cognitive deficits were found in seven patients and were usually mild. Other neurologic deficits were rare. Electrophysiologic investigation confirmed cortical action myoclonus in every case, although this could be combined with cortical reflex myoclonus, an exaggerated startle response, or brainstem reticular reflex myoclonus. We conclude that posthypoxic myoclonus typically consists of multifocal cortical action myoclonus that improves with time. It is only rarely associated with severe additional neurologic deficit.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Werhahn</name><affiliations><json:string>MRC Human Movement and Balance Unit, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England</json:string><json:string>Current Address: Ludwig‐Maximilians Universität, Klinikum Grosshadern, Neurologische Klinik, Marchioninistr. 15, D—81377 München, Germany</json:string></affiliations></json:item><json:item><name>Dr. Brown</name><affiliations><json:string>MRC Human Movement and Balance Unit, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England</json:string></affiliations></json:item><json:item><name>P. D. 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All patients had had a cardiorespiratory arrest, most caused by an acute asthmatic attack (11 cases). All patients had multifocal action myoclonus. Eleven patients had additional stimulus‐sensitive myoclonus. There was late improvement in the myoclonic syndrome and the level of disability in all but one patient. Three patients were eventually able to discontinue antimyoclonic medication, and five patients were able to walk unaided. Cognitive deficits were found in seven patients and were usually mild. Other neurologic deficits were rare. Electrophysiologic investigation confirmed cortical action myoclonus in every case, although this could be combined with cortical reflex myoclonus, an exaggerated startle response, or brainstem reticular reflex myoclonus. We conclude that posthypoxic myoclonus typically consists of multifocal cortical action myoclonus that improves with time. 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D.</givenNames><familyName>Marsden</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>MRC Human Movement and Balance Unit, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England</unparsedAffiliation></affiliation><affiliation xml:id="curr1" countryCode="DE"><unparsedAffiliation>Ludwig‐Maximilians Universität, Klinikum Grosshadern, Neurologische Klinik, Marchioninistr. 15, D—81377 München, Germany</unparsedAffiliation></affiliation><affiliation xml:id="curr2" countryCode="AU"><unparsedAffiliation>University Department of Medicine and Department of Neurology, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Postanoxia</keyword><keyword xml:id="kwd2">Myoclonus</keyword><keyword xml:id="kwd3">Lance</keyword><keyword xml:id="kwd4">Adams syndrome</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The clinical and neurophysiologic features of 14 patients with chronic posthypoxic myoclonus are presented. Patients were first seen a mean of 2.5 years (range, 2 to 105 months) after the hypoxic event and followed up for 3.7 years (range, 7 to 84 months) thereafter. All patients had had a cardiorespiratory arrest, most caused by an acute asthmatic attack (11 cases). All patients had multifocal action myoclonus. Eleven patients had additional stimulus‐sensitive myoclonus. There was late improvement in the myoclonic syndrome and the level of disability in all but one patient. Three patients were eventually able to discontinue antimyoclonic medication, and five patients were able to walk unaided. Cognitive deficits were found in seven patients and were usually mild. Other neurologic deficits were rare. Electrophysiologic investigation confirmed cortical action myoclonus in every case, although this could be combined with cortical reflex myoclonus, an exaggerated startle response, or brainstem reticular reflex myoclonus. We conclude that posthypoxic myoclonus typically consists of multifocal cortical action myoclonus that improves with time. It is only rarely associated with severe additional neurologic deficit.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>The clinical features and prognosis of chronic posthypoxic myoclonus</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CHRONIC POSTHYPOXIC MYOCLONUS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The clinical features and prognosis of chronic posthypoxic myoclonus</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Werhahn</namePart><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England</affiliation><affiliation>Current Address: Ludwig‐Maximilians Universität, Klinikum Grosshadern, Neurologische Klinik, Marchioninistr. 15, D—81377 München, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Brown</namePart><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England</affiliation><description>Correspondence: MRC Human Movement & Balance Unit, Institute of Neurology, Queen Square, London WC1N 3BG, U</description><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, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England</affiliation><affiliation>Current Address: University Department of Medicine and Department of Neurology, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. D.</namePart><namePart type="family">Marsden</namePart><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, England</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">1997-03</dateIssued><dateCaptured encoding="w3cdtf">1996-01-12</dateCaptured><dateValid encoding="w3cdtf">1996-05-01</dateValid><copyrightDate encoding="w3cdtf">1997</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">1</extent><extent unit="references">14</extent></physicalDescription><abstract lang="en">The clinical and neurophysiologic features of 14 patients with chronic posthypoxic myoclonus are presented. Patients were first seen a mean of 2.5 years (range, 2 to 105 months) after the hypoxic event and followed up for 3.7 years (range, 7 to 84 months) thereafter. All patients had had a cardiorespiratory arrest, most caused by an acute asthmatic attack (11 cases). All patients had multifocal action myoclonus. Eleven patients had additional stimulus‐sensitive myoclonus. There was late improvement in the myoclonic syndrome and the level of disability in all but one patient. Three patients were eventually able to discontinue antimyoclonic medication, and five patients were able to walk unaided. Cognitive deficits were found in seven patients and were usually mild. Other neurologic deficits were rare. Electrophysiologic investigation confirmed cortical action myoclonus in every case, although this could be combined with cortical reflex myoclonus, an exaggerated startle response, or brainstem reticular reflex myoclonus. We conclude that posthypoxic myoclonus typically consists of multifocal cortical action myoclonus that improves with time. It is only rarely associated with severe additional neurologic deficit.</abstract><subject lang="en"><genre>Keywords</genre><topic>Postanoxia</topic><topic>Myoclonus</topic><topic>Lance</topic><topic>Adams syndrome</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</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>1997</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>216</start><end>220</end><total>5</total></extent></part></relatedItem><identifier type="istex">205E8C7933849A39B9EFA82F96F67AFD03F8EA32</identifier><identifier type="DOI">10.1002/mds.870120212</identifier><identifier type="ArticleID">MDS870120212</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 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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