Autonomic dysfunction in different subtypes of multiple system atrophy
Identifieur interne : 000D73 ( Istex/Corpus ); précédent : 000D72; suivant : 000D74Autonomic dysfunction in different subtypes of multiple system atrophy
Auteurs : Claudia Schmidt ; Birgit Herting ; Silke Prieur ; Susann Junghanns ; Katherine Schweitzer ; Christoph Globas ; Ludger Schöls ; Heinz Reichmann ; Daniela Berg ; Tjalf ZiemssenSource :
- Movement Disorders [ 0885-3185 ] ; 2008-09-15.
English descriptors
Abstract
Multiple system atrophy (MSA) can clinically be divided into the cerebellar (MSA‐C) and the parkinsonian (MSA‐P) variant. However, till now, it is unknown whether autonomic dysfunction in these two entities differs regarding severity and profile. We compared the pattern of autonomic dysfunction in 12 patients with MSA‐C and 26 with MSA‐P in comparison with 27 age‐ and sex‐matched healthy controls using a standard battery of autonomic function tests and a structured anamnesis of the autonomic nervous system. MSA‐P patients complained significantly more often about the symptoms of autonomic dysfunctions than MSA‐C patients, especially regarding vasomotor, secretomotor, and gastrointestinal subsystems. However, regarding cardiovascular, sudomotor pupil, urogenital, and sleep subsystems, there were no significant quantitative or qualitative differences as analyzed by autonomic anamnesis and testing. Our results suggest that there are only minor differences in the pattern of autonomic dysfunction between the two clinical MSA phenotypes. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.22187
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ISTEX:725C3392D497BA6250201A73255EA228FF648036Le document en format XML
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However, till now, it is unknown whether autonomic dysfunction in these two entities differs regarding severity and profile. We compared the pattern of autonomic dysfunction in 12 patients with MSA‐C and 26 with MSA‐P in comparison with 27 age‐ and sex‐matched healthy controls using a standard battery of autonomic function tests and a structured anamnesis of the autonomic nervous system. MSA‐P patients complained significantly more often about the symptoms of autonomic dysfunctions than MSA‐C patients, especially regarding vasomotor, secretomotor, and gastrointestinal subsystems. However, regarding cardiovascular, sudomotor pupil, urogenital, and sleep subsystems, there were no significant quantitative or qualitative differences as analyzed by autonomic anamnesis and testing. Our results suggest that there are only minor differences in the pattern of autonomic dysfunction between the two clinical MSA phenotypes. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Claudia Schmidt MD</name><affiliations><json:string>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</json:string></affiliations></json:item><json:item><name>Birgit Herting MD</name><affiliations><json:string>Parkinson Research group, Department of Neurology, University of Dresden, Germany</json:string></affiliations></json:item><json:item><name>Silke Prieur</name><affiliations><json:string>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</json:string></affiliations></json:item><json:item><name>Susann Junghanns MD</name><affiliations><json:string>Parkinson Research group, Department of Neurology, University of Dresden, Germany</json:string></affiliations></json:item><json:item><name>Katherine Schweitzer MD</name><affiliations><json:string>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Christoph Globas MD</name><affiliations><json:string>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Ludger Schöls MD</name><affiliations><json:string>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Heinz Reichmann MD</name><affiliations><json:string>Parkinson Research group, Department of Neurology, University of Dresden, Germany</json:string></affiliations></json:item><json:item><name>Daniela Berg MD</name><affiliations><json:string>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Tjalf Ziemssen MD</name><affiliations><json:string>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>autonomic nervous system</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>multiple system atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autonomic dysfunction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MSA subtypes</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Multiple system atrophy (MSA) can clinically be divided into the cerebellar (MSA‐C) and the parkinsonian (MSA‐P) variant. However, till now, it is unknown whether autonomic dysfunction in these two entities differs regarding severity and profile. We compared the pattern of autonomic dysfunction in 12 patients with MSA‐C and 26 with MSA‐P in comparison with 27 age‐ and sex‐matched healthy controls using a standard battery of autonomic function tests and a structured anamnesis of the autonomic nervous system. MSA‐P patients complained significantly more often about the symptoms of autonomic dysfunctions than MSA‐C patients, especially regarding vasomotor, secretomotor, and gastrointestinal subsystems. However, regarding cardiovascular, sudomotor pupil, urogenital, and sleep subsystems, there were no significant quantitative or qualitative differences as analyzed by autonomic anamnesis and testing. 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type="first">Tjalf</forename><surname>Ziemssen</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Autonomic and Neuroendocrinological Laboratory, Department of Neurology, University of Technology Dresden, Fetscherstraβe 74, D‐01307 Dresden, Germany</p></note><affiliation>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</affiliation></author></analytic><monogr><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. 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However, till now, it is unknown whether autonomic dysfunction in these two entities differs regarding severity and profile. We compared the pattern of autonomic dysfunction in 12 patients with MSA‐C and 26 with MSA‐P in comparison with 27 age‐ and sex‐matched healthy controls using a standard battery of autonomic function tests and a structured anamnesis of the autonomic nervous system. MSA‐P patients complained significantly more often about the symptoms of autonomic dysfunctions than MSA‐C patients, especially regarding vasomotor, secretomotor, and gastrointestinal subsystems. However, regarding cardiovascular, sudomotor pupil, urogenital, and sleep subsystems, there were no significant quantitative or qualitative differences as analyzed by autonomic anamnesis and testing. Our results suggest that there are only minor differences in the pattern of autonomic dysfunction between the two clinical MSA phenotypes. © 2008 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>autonomic nervous system</term></item><item><term>multiple system atrophy</term></item><item><term>autonomic dysfunction</term></item><item><term>MSA subtypes</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-01-31">Received</change><change when="2008-05-22">Registration</change><change when="2008-09-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/725C3392D497BA6250201A73255EA228FF648036/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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affiliationRef="#af2"><personName><givenNames>Heinz</givenNames><familyName>Reichmann</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Daniela</givenNames><familyName>Berg</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Tjalf</givenNames><familyName>Ziemssen</familyName><degrees>MD</degrees></personName><contactDetails><email>Ziemssen@web.de</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Parkinson Research group, Department of Neurology, University of Dresden, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">autonomic nervous system</keyword><keyword xml:id="kwd2">multiple system atrophy</keyword><keyword xml:id="kwd3">autonomic dysfunction</keyword><keyword xml:id="kwd4">MSA subtypes</keyword></keywordGroup><supportingInformation><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds22187:mds_22187_sm"></mediaResource><caption>Short overview of semiquantitative anamnesis questionnaire, Dresden (70 items).</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Multiple system atrophy (MSA) can clinically be divided into the cerebellar (MSA‐C) and the parkinsonian (MSA‐P) variant. However, till now, it is unknown whether autonomic dysfunction in these two entities differs regarding severity and profile. We compared the pattern of autonomic dysfunction in 12 patients with MSA‐C and 26 with MSA‐P in comparison with 27 age‐ and sex‐matched healthy controls using a standard battery of autonomic function tests and a structured anamnesis of the autonomic nervous system. MSA‐P patients complained significantly more often about the symptoms of autonomic dysfunctions than MSA‐C patients, especially regarding vasomotor, secretomotor, and gastrointestinal subsystems. However, regarding cardiovascular, sudomotor pupil, urogenital, and sleep subsystems, there were no significant quantitative or qualitative differences as analyzed by autonomic anamnesis and testing. Our results suggest that there are only minor differences in the pattern of autonomic dysfunction between the two clinical MSA phenotypes. © 2008 Movement Disorder Society</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>Autonomic dysfunction in different subtypes of multiple system atrophy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Autonomic Dysfunction in MSA Subtypes</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Autonomic dysfunction in different subtypes of multiple system atrophy</title></titleInfo><name type="personal"><namePart type="given">Claudia</namePart><namePart type="family">Schmidt</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Birgit</namePart><namePart type="family">Herting</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson Research group, Department of Neurology, University of Dresden, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Silke</namePart><namePart type="family">Prieur</namePart><affiliation>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susann</namePart><namePart type="family">Junghanns</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson Research group, Department of Neurology, University of Dresden, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katherine</namePart><namePart type="family">Schweitzer</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christoph</namePart><namePart type="family">Globas</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ludger</namePart><namePart type="family">Schöls</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Heinz</namePart><namePart type="family">Reichmann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson Research group, Department of Neurology, University of Dresden, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniela</namePart><namePart type="family">Berg</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Disorders, Hertie Institute of Clinical Brain Research, University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tjalf</namePart><namePart type="family">Ziemssen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Autonomic and neuroendocrinological laboratory, University of Dresden, Germany</affiliation><description>Correspondence: Autonomic and Neuroendocrinological Laboratory, Department of Neurology, University of Technology Dresden, Fetscherstraβe 74, D‐01307 Dresden, Germany</description><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">2008-09-15</dateIssued><dateCaptured encoding="w3cdtf">2008-01-31</dateCaptured><dateValid encoding="w3cdtf">2008-05-22</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="tables">3</extent><extent unit="references">19</extent><extent unit="words">4976</extent></physicalDescription><abstract lang="en">Multiple system atrophy (MSA) can clinically be divided into the cerebellar (MSA‐C) and the parkinsonian (MSA‐P) variant. However, till now, it is unknown whether autonomic dysfunction in these two entities differs regarding severity and profile. We compared the pattern of autonomic dysfunction in 12 patients with MSA‐C and 26 with MSA‐P in comparison with 27 age‐ and sex‐matched healthy controls using a standard battery of autonomic function tests and a structured anamnesis of the autonomic nervous system. MSA‐P patients complained significantly more often about the symptoms of autonomic dysfunctions than MSA‐C patients, especially regarding vasomotor, secretomotor, and gastrointestinal subsystems. However, regarding cardiovascular, sudomotor pupil, urogenital, and sleep subsystems, there were no significant quantitative or qualitative differences as analyzed by autonomic anamnesis and testing. Our results suggest that there are only minor differences in the pattern of autonomic dysfunction between the two clinical MSA phenotypes. © 2008 Movement Disorder Society</abstract><note type="additional physical form">Short overview of semiquantitative anamnesis questionnaire, Dresden (70 items).</note><subject lang="en"><genre>Keywords</genre><topic>autonomic nervous system</topic><topic>multiple system atrophy</topic><topic>autonomic dysfunction</topic><topic>MSA subtypes</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>Brief Report</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>12</number></detail><extent unit="pages"><start>1766</start><end>1772</end><total>7</total></extent></part></relatedItem><identifier type="istex">725C3392D497BA6250201A73255EA228FF648036</identifier><identifier type="DOI">10.1002/mds.22187</identifier><identifier type="ArticleID">MDS22187</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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