Oculomotor function in multiple system atrophy: Clinical and laboratory features in 30 patients
Identifieur interne : 001247 ( Istex/Corpus ); précédent : 001246; suivant : 001248Oculomotor function in multiple system atrophy: Clinical and laboratory features in 30 patients
Auteurs : Tim Anderson ; Linda Luxon ; Niall Quinn ; Susan Daniel ; C. David Marsden ; Adolfo BronsteinSource :
- Movement Disorders [ 0885-3185 ] ; 2008-05-15.
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Abstract
We reviewed the clinical and laboratory oculomotor features in 30 patients with probable multiple system atrophy (MSA), 22 with MSA‐P and 8 with MSA‐C. Six patients were also examined post mortem, MSA being confirmed in four and excluded in two (Parkinson's disease and progressive supranuclear palsy). Clinical examination showed the following abnormalities; excessive square wave jerks—21 of 30 patients; mild vertical supranuclear gaze palsy—8 of 30; gaze‐evoked nystagmus—12 of 30 patients, three of whom had no extraocular evidence of cerebellar dysfunction; positioning downbeat nystagmus—10 of 25; mild or moderate saccadic hypometria—22 of 30; impaired (“broken up”) smooth pursuit—28 of 30; reduced VOR suppression—16 of 24. Electro‐oculography and caloric testing did not add significant extra information. In patients presenting with an akinetic‐rigid syndrome it can be difficult to differentiate idiopathic Parkinson's disease from MSA‐P and other causes of atypical parkinsonism. Our findings suggest that the presence of excessive square wave jerks, mild – moderate hypometria of saccades, impaired VOR suppression, spontaneous nystagmus or positioning downbeat nystagmus may be oculomotor “red flags” or clues to the presence of MSA. Further, the presence of clinically slow saccades, or moderate‐to‐severe gaze restriction, suggests a diagnosis other than MSA. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.21999
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David Marsden</name><affiliation><mods:affiliation>Van Der Veer Institute for Parkinson's and Brain Research, Christchurch, New Zealand</mods:affiliation></affiliation></author><author><name sortKey="Bronstein, Adolfo" sort="Bronstein, Adolfo" uniqKey="Bronstein A" first="Adolfo" last="Bronstein">Adolfo Bronstein</name><affiliation><mods:affiliation>Department of Neuro‐otology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Neurosciences and Mental Health, Medicine, Imperial College, London, United Kingdom</mods:affiliation></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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-05-15">2008-05-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="977">977</biblScope><biblScope unit="page" to="984">984</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3D3FD14B982659679FAD68B5BA492EEFE0F0F699</idno><idno type="DOI">10.1002/mds.21999</idno><idno type="ArticleID">MDS21999</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>multiple system atrophy (MSA)</term><term>oculomotor</term><term>pathology</term><term>positioning downbeat nystagmus (pDBN)</term><term>saccades</term><term>vestibular</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We reviewed the clinical and laboratory oculomotor features in 30 patients with probable multiple system atrophy (MSA), 22 with MSA‐P and 8 with MSA‐C. Six patients were also examined post mortem, MSA being confirmed in four and excluded in two (Parkinson's disease and progressive supranuclear palsy). Clinical examination showed the following abnormalities; excessive square wave jerks—21 of 30 patients; mild vertical supranuclear gaze palsy—8 of 30; gaze‐evoked nystagmus—12 of 30 patients, three of whom had no extraocular evidence of cerebellar dysfunction; positioning downbeat nystagmus—10 of 25; mild or moderate saccadic hypometria—22 of 30; impaired (“broken up”) smooth pursuit—28 of 30; reduced VOR suppression—16 of 24. Electro‐oculography and caloric testing did not add significant extra information. In patients presenting with an akinetic‐rigid syndrome it can be difficult to differentiate idiopathic Parkinson's disease from MSA‐P and other causes of atypical parkinsonism. Our findings suggest that the presence of excessive square wave jerks, mild – moderate hypometria of saccades, impaired VOR suppression, spontaneous nystagmus or positioning downbeat nystagmus may be oculomotor “red flags” or clues to the presence of MSA. Further, the presence of clinically slow saccades, or moderate‐to‐severe gaze restriction, suggests a diagnosis other than MSA. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Tim Anderson MD</name><affiliations><json:string>Van Der Veer Institute for Parkinson's and Brain Research, Christchurch, New Zealand</json:string></affiliations></json:item><json:item><name>Linda Luxon MD</name><affiliations><json:string>Department of Neuro‐otology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Niall Quinn MD</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Susan Daniel MD</name><affiliations><json:string>Queen Square Brain Bank for Neurological Disorders, Institute of Neurology, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>C. David Marsden DSc</name><affiliations><json:string>Van Der Veer Institute for Parkinson's and Brain Research, Christchurch, New Zealand</json:string></affiliations></json:item><json:item><name>Adolfo Bronstein MD</name><affiliations><json:string>Department of Neuro‐otology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom</json:string><json:string>Division of Neurosciences and Mental Health, Medicine, Imperial College, London, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>multiple system atrophy (MSA)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oculomotor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>positioning downbeat nystagmus (pDBN)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>saccades</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>vestibular</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pathology</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We reviewed the clinical and laboratory oculomotor features in 30 patients with probable multiple system atrophy (MSA), 22 with MSA‐P and 8 with MSA‐C. Six patients were also examined post mortem, MSA being confirmed in four and excluded in two (Parkinson's disease and progressive supranuclear palsy). Clinical examination showed the following abnormalities; excessive square wave jerks—21 of 30 patients; mild vertical supranuclear gaze palsy—8 of 30; gaze‐evoked nystagmus—12 of 30 patients, three of whom had no extraocular evidence of cerebellar dysfunction; positioning downbeat nystagmus—10 of 25; mild or moderate saccadic hypometria—22 of 30; impaired (“broken up”) smooth pursuit—28 of 30; reduced VOR suppression—16 of 24. Electro‐oculography and caloric testing did not add significant extra information. In patients presenting with an akinetic‐rigid syndrome it can be difficult to differentiate idiopathic Parkinson's disease from MSA‐P and other causes of atypical parkinsonism. Our findings suggest that the presence of excessive square wave jerks, mild – moderate hypometria of saccades, impaired VOR suppression, spontaneous nystagmus or positioning downbeat nystagmus may be oculomotor “red flags” or clues to the presence of MSA. 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Six patients were also examined post mortem, MSA being confirmed in four and excluded in two (Parkinson's disease and progressive supranuclear palsy). Clinical examination showed the following abnormalities; excessive square wave jerks—21 of 30 patients; mild vertical supranuclear gaze palsy—8 of 30; gaze‐evoked nystagmus—12 of 30 patients, three of whom had no extraocular evidence of cerebellar dysfunction; positioning downbeat nystagmus—10 of 25; mild or moderate saccadic hypometria—22 of 30; impaired (“broken up”) smooth pursuit—28 of 30; reduced VOR suppression—16 of 24. Electro‐oculography and caloric testing did not add significant extra information. In patients presenting with an akinetic‐rigid syndrome it can be difficult to differentiate idiopathic Parkinson's disease from MSA‐P and other causes of atypical parkinsonism. Our findings suggest that the presence of excessive square wave jerks, mild – moderate hypometria of saccades, impaired VOR suppression, spontaneous nystagmus or positioning downbeat nystagmus may be oculomotor “red flags” or clues to the presence of MSA. Further, the presence of clinically slow saccades, or moderate‐to‐severe gaze restriction, suggests a diagnosis other than MSA. © 2008 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>multiple system atrophy (MSA)</term></item><item><term>oculomotor</term></item><item><term>positioning downbeat nystagmus (pDBN)</term></item><item><term>saccades</term></item><item><term>vestibular</term></item><item><term>pathology</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-10-12">Received</change><change when="2008-02-02">Registration</change><change when="2008-05-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3D3FD14B982659679FAD68B5BA492EEFE0F0F699/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Department of Neuro‐otology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="GB" type="organization"><unparsedAffiliation>Queen Square Brain Bank for Neurological Disorders, Institute of Neurology, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="GB" type="organization"><unparsedAffiliation>Division of Neurosciences and Mental Health, Medicine, Imperial College, London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">multiple system atrophy (MSA)</keyword><keyword xml:id="kwd2">oculomotor</keyword><keyword xml:id="kwd3">positioning downbeat nystagmus (pDBN)</keyword><keyword xml:id="kwd4">saccades</keyword><keyword xml:id="kwd5">vestibular</keyword><keyword xml:id="kwd6">pathology</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We reviewed the clinical and laboratory oculomotor features in 30 patients with probable multiple system atrophy (MSA), 22 with MSA‐P and 8 with MSA‐C. Six patients were also examined post mortem, MSA being confirmed in four and excluded in two (Parkinson's disease and progressive supranuclear palsy). Clinical examination showed the following abnormalities; excessive square wave jerks—21 of 30 patients; mild vertical supranuclear gaze palsy—8 of 30; gaze‐evoked nystagmus—12 of 30 patients, three of whom had no extraocular evidence of cerebellar dysfunction; positioning downbeat nystagmus—10 of 25; mild or moderate saccadic hypometria—22 of 30; impaired (“broken up”) smooth pursuit—28 of 30; reduced VOR suppression—16 of 24. Electro‐oculography and caloric testing did not add significant extra information. In patients presenting with an akinetic‐rigid syndrome it can be difficult to differentiate idiopathic Parkinson's disease from MSA‐P and other causes of atypical parkinsonism. Our findings suggest that the presence of excessive square wave jerks, mild – moderate hypometria of saccades, impaired VOR suppression, spontaneous nystagmus or positioning downbeat nystagmus may be oculomotor “red flags” or clues to the presence of MSA. Further, the presence of clinically slow saccades, or moderate‐to‐severe gaze restriction, suggests a diagnosis other than MSA. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn3"><p>Deceased; formerly Institute of Neurology, Queen Square, London, UK</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Oculomotor function in multiple system atrophy: Clinical and laboratory features in 30 patients</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Oculomotor Function in MSA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Oculomotor function in multiple system atrophy: Clinical and laboratory features in 30 patients</title></titleInfo><name type="personal"><namePart type="given">Tim</namePart><namePart type="family">Anderson</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Van Der Veer Institute for Parkinson's and Brain Research, Christchurch, New Zealand</affiliation><description>Correspondence: Van Der Veer Institute for Parkinson's and Brain Research, 16 St Asaph Street, Christchurch, New Zealand</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Linda</namePart><namePart type="family">Luxon</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuro‐otology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Niall</namePart><namePart type="family">Quinn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susan</namePart><namePart type="family">Daniel</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Queen Square Brain Bank for Neurological Disorders, Institute of Neurology, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">David Marsden</namePart><namePart type="termsOfAddress">DSc</namePart><affiliation>Van Der Veer Institute for Parkinson's and Brain Research, Christchurch, New Zealand</affiliation><description>Deceased; formerly Institute of Neurology, Queen Square, London, UK</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Adolfo</namePart><namePart type="family">Bronstein</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neuro‐otology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom</affiliation><affiliation>Division of Neurosciences and Mental Health, Medicine, Imperial College, London, United Kingdom</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">2008-05-15</dateIssued><dateCaptured encoding="w3cdtf">2006-10-12</dateCaptured><dateValid encoding="w3cdtf">2008-02-02</dateValid><copyrightDate encoding="w3cdtf">2008</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">2</extent><extent unit="references">47</extent><extent unit="words">5898</extent></physicalDescription><abstract lang="en">We reviewed the clinical and laboratory oculomotor features in 30 patients with probable multiple system atrophy (MSA), 22 with MSA‐P and 8 with MSA‐C. Six patients were also examined post mortem, MSA being confirmed in four and excluded in two (Parkinson's disease and progressive supranuclear palsy). Clinical examination showed the following abnormalities; excessive square wave jerks—21 of 30 patients; mild vertical supranuclear gaze palsy—8 of 30; gaze‐evoked nystagmus—12 of 30 patients, three of whom had no extraocular evidence of cerebellar dysfunction; positioning downbeat nystagmus—10 of 25; mild or moderate saccadic hypometria—22 of 30; impaired (“broken up”) smooth pursuit—28 of 30; reduced VOR suppression—16 of 24. Electro‐oculography and caloric testing did not add significant extra information. In patients presenting with an akinetic‐rigid syndrome it can be difficult to differentiate idiopathic Parkinson's disease from MSA‐P and other causes of atypical parkinsonism. Our findings suggest that the presence of excessive square wave jerks, mild – moderate hypometria of saccades, impaired VOR suppression, spontaneous nystagmus or positioning downbeat nystagmus may be oculomotor “red flags” or clues to the presence of MSA. Further, the presence of clinically slow saccades, or moderate‐to‐severe gaze restriction, suggests a diagnosis other than MSA. © 2008 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>multiple system atrophy (MSA)</topic><topic>oculomotor</topic><topic>positioning downbeat nystagmus (pDBN)</topic><topic>saccades</topic><topic>vestibular</topic><topic>pathology</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>Research 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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>977</start><end>984</end><total>8</total></extent></part></relatedItem><identifier type="istex">3D3FD14B982659679FAD68B5BA492EEFE0F0F699</identifier><identifier type="DOI">10.1002/mds.21999</identifier><identifier type="ArticleID">MDS21999</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 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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