Pain in multiple system atrophy
Identifieur interne : 002585 ( Main/Corpus ); précédent : 002584; suivant : 002586Pain in multiple system atrophy
Auteurs : F. Tison ; K. Wenning ; A. Volonte ; R. Poewe ; P. Henry ; P. QuinnSource :
- Journal of Neurology [ 0340-5354 ] ; 1996-02-01.
Abstract
Abstract: Pain is a recognized feature of idiopathic Parkinson’s disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (P=0.02), and by patients with levodopa-induced dyskinesias (P=0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.
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DOI: 10.1007/BF02444007
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pain in multiple system atrophy</title><author><name sortKey="Tison, F" sort="Tison, F" uniqKey="Tison F" first="F." last="Tison">F. Tison</name><affiliation><mods:affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Wenning, K" sort="Wenning, K" uniqKey="Wenning K" first="K." last="Wenning">K. Wenning</name><affiliation><mods:affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Volonte, A" sort="Volonte, A" uniqKey="Volonte A" first="A." last="Volonte">A. Volonte</name><affiliation><mods:affiliation>Department of Neurology, H.S. Raffaele, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Poewe, R" sort="Poewe, R" uniqKey="Poewe R" first="R." last="Poewe">R. Poewe</name><affiliation><mods:affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Henry, P" sort="Henry, P" uniqKey="Henry P" first="P." last="Henry">P. Henry</name><affiliation><mods:affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Quinn, P" sort="Quinn, P" uniqKey="Quinn P" first="P." last="Quinn">P. Quinn</name><affiliation><mods:affiliation>Institute of Neurology, University Department of Clinical Neurology, Queen Square, London, UK</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1007/BF02444007</idno><idno type="url">https://api.istex.fr/document/CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002585</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Pain in multiple system atrophy</title><author><name sortKey="Tison, F" sort="Tison, F" uniqKey="Tison F" first="F." last="Tison">F. Tison</name><affiliation><mods:affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Wenning, K" sort="Wenning, K" uniqKey="Wenning K" first="K." last="Wenning">K. Wenning</name><affiliation><mods:affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Volonte, A" sort="Volonte, A" uniqKey="Volonte A" first="A." last="Volonte">A. Volonte</name><affiliation><mods:affiliation>Department of Neurology, H.S. Raffaele, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Poewe, R" sort="Poewe, R" uniqKey="Poewe R" first="R." last="Poewe">R. Poewe</name><affiliation><mods:affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Henry, P" sort="Henry, P" uniqKey="Henry P" first="P." last="Henry">P. Henry</name><affiliation><mods:affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Quinn, P" sort="Quinn, P" uniqKey="Quinn P" first="P." last="Quinn">P. Quinn</name><affiliation><mods:affiliation>Institute of Neurology, University Department of Clinical Neurology, Queen Square, London, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology</title><title level="j" type="abbrev">J Neurol</title><idno type="ISSN">0340-5354</idno><idno type="eISSN">1432-1459</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1996-02-01">1996-02-01</date><biblScope unit="volume">243</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="153">153</biblScope><biblScope unit="page" to="156">156</biblScope></imprint><idno type="ISSN">0340-5354</idno></series><idno type="istex">CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389</idno><idno type="DOI">10.1007/BF02444007</idno><idno type="ArticleID">Art9</idno><idno type="ArticleID">BF02444007</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0340-5354</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Pain is a recognized feature of idiopathic Parkinson’s disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (P=0.02), and by patients with levodopa-induced dyskinesias (P=0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>F. Tison</name><affiliations><json:string>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</json:string></affiliations></json:item><json:item><name>G. K. Wenning</name><affiliations><json:string>Universitäts-Klinik für Neurologie, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>M. A. Volonte</name><affiliations><json:string>Department of Neurology, H.S. Raffaele, Milan, Italy</json:string></affiliations></json:item><json:item><name>W. R. Poewe</name><affiliations><json:string>Universitäts-Klinik für Neurologie, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>P. Henry</name><affiliations><json:string>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</json:string></affiliations></json:item><json:item><name>N. P. Quinn</name><affiliations><json:string>Institute of Neurology, University Department of Clinical Neurology, Queen Square, London, UK</json:string></affiliations></json:item></author><articleId><json:string>Art9</json:string><json:string>BF02444007</json:string></articleId><language><json:string>eng</json:string></language><abstract>Abstract: Pain is a recognized feature of idiopathic Parkinson’s disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (P=0.02), and by patients with levodopa-induced dyskinesias (P=0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.</abstract><qualityIndicators><score>5.189</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 784 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1283</abstractCharCount><pdfWordCount>2753</pdfWordCount><pdfCharCount>16092</pdfCharCount><pdfPageCount>4</pdfPageCount><abstractWordCount>203</abstractWordCount></qualityIndicators><title>Pain in multiple system atrophy</title><genre><json:string>research-article</json:string></genre><host><volume>243</volume><pages><last>156</last><first>153</first></pages><issn><json:string>0340-5354</json:string></issn><issue>2</issue><subject><json:item><value>Neurosciences</value></json:item><json:item><value>Neuroradiology</value></json:item><json:item><value>Neurology</value></json:item></subject><journalId><json:string>415</json:string></journalId><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1432-1459</json:string></eissn><title>Journal of Neurology</title><publicationDate>1996</publicationDate><copyrightDate>1996</copyrightDate></host><publicationDate>1996</publicationDate><copyrightDate>1996</copyrightDate><doi><json:string>10.1007/BF02444007</json:string></doi><id>CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Pain in multiple system atrophy</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><availability><p>SPRINGER</p></availability><date>1995-05-23</date></publicationStmt><notesStmt><note>Original Communication</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Pain in multiple system atrophy</title><author corresp="yes"><persName><forename type="first">F.</forename><surname>Tison</surname></persName><affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</affiliation></author><author><persName><forename type="first">G.</forename><surname>Wenning</surname></persName><affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</affiliation></author><author><persName><forename type="first">M.</forename><surname>Volonte</surname></persName><affiliation>Department of Neurology, H.S. Raffaele, Milan, Italy</affiliation></author><author><persName><forename type="first">W.</forename><surname>Poewe</surname></persName><affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</affiliation></author><author><persName><forename type="first">P.</forename><surname>Henry</surname></persName><affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</affiliation></author><author><persName><forename type="first">N.</forename><surname>Quinn</surname></persName><affiliation>Institute of Neurology, University Department of Clinical Neurology, Queen Square, London, UK</affiliation></author></analytic><monogr><title level="j">Journal of Neurology</title><title level="j" type="abbrev">J Neurol</title><idno type="JournalID">415</idno><idno type="pISSN">0340-5354</idno><idno type="eISSN">1432-1459</idno><idno type="IssueArticleCount">20</idno><idno type="VolumeIssueCount">10</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1996-02-01"></date><biblScope unit="volume">243</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="153">153</biblScope><biblScope unit="page" to="156">156</biblScope></imprint></monogr><idno type="istex">CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389</idno><idno type="DOI">10.1007/BF02444007</idno><idno type="ArticleID">Art9</idno><idno type="ArticleID">BF02444007</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995-05-23</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Pain is a recognized feature of idiopathic Parkinson’s disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (P=0.02), and by patients with levodopa-induced dyskinesias (P=0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Neurosciences</term></item><item><term>Neuroradiology</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-05-23">Created</change><change when="1996-02-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" 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Type="Secondary">Neurology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo TocLevels="0" VolumeType="Regular"><VolumeIDStart>243</VolumeIDStart><VolumeIDEnd>243</VolumeIDEnd><VolumeIssueCount>10</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>2</IssueIDStart><IssueIDEnd>2</IssueIDEnd><IssueArticleCount>20</IssueArticleCount><IssueHistory><CoverDate><Year>1996</Year><Month>2</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1996</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art9"><ArticleInfo ArticleType="OriginalPaper" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>BF02444007</ArticleID><ArticleDOI>10.1007/BF02444007</ArticleDOI><ArticleSequenceNumber>9</ArticleSequenceNumber><ArticleTitle Language="En">Pain in multiple system atrophy</ArticleTitle><ArticleCategory>Original Communication</ArticleCategory><ArticleFirstPage>153</ArticleFirstPage><ArticleLastPage>156</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2006</Year><Month>6</Month><Day>9</Day></RegistrationDate><Received><Year>1995</Year><Month>5</Month><Day>23</Day></Received><Revised><Year>1995</Year><Month>7</Month><Day>6</Day></Revised><Accepted><Year>1995</Year><Month>7</Month><Day>10</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1996</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>415</JournalID><VolumeIDStart>243</VolumeIDStart><VolumeIDEnd>243</VolumeIDEnd><IssueIDStart>2</IssueIDStart><IssueIDEnd>2</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>F.</GivenName><FamilyName>Tison</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>G.</GivenName><GivenName>K.</GivenName><FamilyName>Wenning</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>M.</GivenName><GivenName>A.</GivenName><FamilyName>Volonte</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>W.</GivenName><GivenName>R.</GivenName><FamilyName>Poewe</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><FamilyName>Henry</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>N.</GivenName><GivenName>P.</GivenName><FamilyName>Quinn</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Départment de Neurologie</OrgDivision><OrgName>Hôpital Pellegrin</OrgName><OrgAddress><Street>Place Amélie Raba-Léon</Street><Postcode>F-33076</Postcode><City>Bordeaux Cedex</City><Country>France</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>Universitäts-Klinik für Neurologie</OrgName><OrgAddress><City>Innsbruck</City><Country>Austria</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Neurology</OrgDivision><OrgName>H.S. Raffaele</OrgName><OrgAddress><City>Milan</City><Country>Italy</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Institute of Neurology</OrgDivision><OrgName>University Department of Clinical Neurology</OrgName><OrgAddress><Street>Queen Square</Street><City>London</City><Country>UK</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>Pain is a recognized feature of idiopathic Parkinson’s disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (<Emphasis Type="Italic">P</Emphasis>=0.02), and by patients with levodopa-induced dyskinesias (<Emphasis Type="Italic">P</Emphasis>=0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Multiple system atrophy</Keyword><Keyword>Pain</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Pain in multiple system atrophy</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Pain in multiple system atrophy</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">F.</namePart><namePart type="family">Tison</namePart><affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="given">K.</namePart><namePart type="family">Wenning</namePart><affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="given">A.</namePart><namePart type="family">Volonte</namePart><affiliation>Department of Neurology, H.S. Raffaele, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="given">R.</namePart><namePart type="family">Poewe</namePart><affiliation>Universitäts-Klinik für Neurologie, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Henry</namePart><affiliation>Départment de Neurologie, Hôpital Pellegrin, Place Amélie Raba-Léon, F-33076, Bordeaux Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="given">P.</namePart><namePart type="family">Quinn</namePart><affiliation>Institute of Neurology, University Department of Clinical Neurology, Queen Square, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1995-05-23</dateCreated><dateIssued encoding="w3cdtf">1996-02-01</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Abstract: Pain is a recognized feature of idiopathic Parkinson’s disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (P=0.02), and by patients with levodopa-induced dyskinesias (P=0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.</abstract><note>Original Communication</note><relatedItem type="host"><titleInfo><title>Journal of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1996-02-01</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Neurosciences</topic><topic>Neuroradiology</topic><topic>Neurology</topic></subject><identifier type="ISSN">0340-5354</identifier><identifier type="eISSN">1432-1459</identifier><identifier type="JournalID">415</identifier><identifier type="IssueArticleCount">20</identifier><identifier type="VolumeIssueCount">10</identifier><part><date>1996</date><detail type="volume"><number>243</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="pages"><start>153</start><end>156</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1996</recordOrigin></recordInfo></relatedItem><identifier type="istex">CEE31C3B3B54F59DD0E8D8B5F1CB09E3FAB2C389</identifier><identifier type="DOI">10.1007/BF02444007</identifier><identifier type="ArticleID">Art9</identifier><identifier type="ArticleID">BF02444007</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1996</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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