Clinical correlates of similar pathologies in parkinsonian syndromes
Identifieur interne : 001063 ( Main/Corpus ); précédent : 001062; suivant : 001064Clinical correlates of similar pathologies in parkinsonian syndromes
Auteurs : Yun Ju Christine Song ; Yue Huang ; Glenda Margaret HallidaySource :
- Movement Disorders [ 0885-3185 ] ; 2011-02-15.
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- KwdEn :
Abstract
Background:: There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features. Methods:: Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point‐counting method was used to evaluate subregional volumes, and α‐synuclein and phospho‐tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features. Results:: All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian‐plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus. Discussion:: This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23336
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Clinical correlates of similar pathologies in parkinsonian syndromes</title><author><name sortKey="Song, Yun Ju Christine" sort="Song, Yun Ju Christine" uniqKey="Song Y" first="Yun Ju Christine" last="Song">Yun Ju Christine Song</name><affiliation><mods:affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</mods:affiliation></affiliation></author><author><name sortKey="Huang, Yue" sort="Huang, Yue" uniqKey="Huang Y" first="Yue" last="Huang">Yue Huang</name><affiliation><mods:affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</mods:affiliation></affiliation></author><author><name sortKey="Halliday, Glenda Margaret" sort="Halliday, Glenda Margaret" uniqKey="Halliday G" first="Glenda Margaret" last="Halliday">Glenda Margaret Halliday</name><affiliation><mods:affiliation>Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23336</idno><idno type="url">https://api.istex.fr/document/50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001063</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Clinical correlates of similar pathologies in parkinsonian syndromes</title><author><name sortKey="Song, Yun Ju Christine" sort="Song, Yun Ju Christine" uniqKey="Song Y" first="Yun Ju Christine" last="Song">Yun Ju Christine Song</name><affiliation><mods:affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</mods:affiliation></affiliation></author><author><name sortKey="Huang, Yue" sort="Huang, Yue" uniqKey="Huang Y" first="Yue" last="Huang">Yue Huang</name><affiliation><mods:affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</mods:affiliation></affiliation></author><author><name sortKey="Halliday, Glenda Margaret" sort="Halliday, Glenda Margaret" uniqKey="Halliday G" first="Glenda Margaret" last="Halliday">Glenda Margaret Halliday</name><affiliation><mods:affiliation>Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</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="2011-02-15">2011-02-15</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="499">499</biblScope><biblScope unit="page" to="506">506</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32</idno><idno type="DOI">10.1002/mds.23336</idno><idno type="ArticleID">MDS23336</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>atrophy</term><term>clinical features</term><term>multiple system atrophy</term><term>pathological severity</term><term>progressive supranuclear palsy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background:: There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features. Methods:: Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point‐counting method was used to evaluate subregional volumes, and α‐synuclein and phospho‐tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features. Results:: All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian‐plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus. Discussion:: This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Yun Ju Christine Song PhD</name><affiliations><json:string>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</json:string></affiliations></json:item><json:item><name>Yue Huang PhD</name><affiliations><json:string>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</json:string></affiliations></json:item><json:item><name>Glenda Margaret Halliday PhD</name><affiliations><json:string>Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>clinical features</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>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pathological severity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>progressive supranuclear palsy</value></json:item></subject><articleId><json:string>MDS23336</json:string></articleId><language><json:string>eng</json:string></language><abstract>Background:: There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features. Methods:: Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point‐counting method was used to evaluate subregional volumes, and α‐synuclein and phospho‐tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features. Results:: All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian‐plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus. Discussion:: This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.525</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1688</abstractCharCount><pdfWordCount>4669</pdfWordCount><pdfCharCount>29375</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>238</abstractWordCount></qualityIndicators><title>Clinical correlates of similar pathologies in parkinsonian syndromes</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>8</total><last>506</last><first>499</first></pages><issn><json:string>0885-3185</json:string></issn><issue>3</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23336</json:string></doi><id>50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Clinical correlates of similar pathologies in parkinsonian syndromes</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note>Author Roles and Disclosures</note><note type="content">*Relevant conflicts of interest/financial disclosures: Tissues were received from the Sydney Brain Bank, which is supported by the National Health and Medical Research Council of Australia (Enabling Grant #282933), Neuroscience Research Australia and the University of New South Wales. Y.J.C. Song was an Australian Postgraduate and Parkinson's NSW Scholar and G.M. Halliday is a Senior Principal Research Fellow of the National Health and Medical Research Council of Australia. Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Clinical correlates of similar pathologies in parkinsonian syndromes</title><author><persName><forename type="first">Yun Ju Christine</forename><surname>Song</surname></persName><roleName type="degree">PhD</roleName><affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</affiliation></author><author><persName><forename type="first">Yue</forename><surname>Huang</surname></persName><roleName type="degree">PhD</roleName><affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</affiliation></author><author><persName><forename type="first">Glenda Margaret</forename><surname>Halliday</surname></persName><roleName type="degree">PhD</roleName><note type="correspondence"><p>Correspondence: Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</p></note><affiliation>Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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="2011-02-15"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="499">499</biblScope><biblScope unit="page" to="506">506</biblScope></imprint></monogr><idno type="istex">50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32</idno><idno type="DOI">10.1002/mds.23336</idno><idno type="ArticleID">MDS23336</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background:: There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features. Methods:: Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point‐counting method was used to evaluate subregional volumes, and α‐synuclein and phospho‐tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features. Results:: All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian‐plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus. Discussion:: This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>atrophy</term></item><item><term>clinical features</term></item><item><term>multiple system atrophy</term></item><item><term>Parkinson's disease</term></item><item><term>pathological severity</term></item><item><term>progressive supranuclear palsy</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="2008-11-25">Received</change><change when="2010-06-07">Registration</change><change when="2011-02-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32/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="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/mds.v26.3</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="2011-02-15">15 February 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="230" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23336</doi><idGroup><id type="unit" value="MDS23336"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2008-11-25"></event><event type="manuscriptRevised" date="2009-07-27"></event><event type="manuscriptAccepted" date="2010-06-07"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2012-01-12"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-01-21"></event><event type="publishedOnlineFinalForm" date="2011-03-31"></event><event type="firstOnline" date="2011-01-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">499</numbering><numbering type="pageLast">506</numbering></numberingGroup><correspondenceTo>Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23336.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="41"></count><count type="wordTotal" number="6169"></count></countGroup><titleGroup><title type="main" xml:lang="en">Clinical correlates of similar pathologies in parkinsonian syndromes<link href="#fn4"></link></title><title type="short" xml:lang="en">Parkinsonian Clinicopathological Correlations</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yun Ju Christine</givenNames><familyName>Song</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yue</givenNames><familyName>Huang</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" corresponding="yes" affiliationRef="#corr1"><personName><givenNames>Glenda Margaret</givenNames><familyName>Halliday</familyName><degrees>PhD</degrees></personName><contactDetails><email>g.halliday@neura.edu.au</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="AU" type="organization"><unparsedAffiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</unparsedAffiliation></affiliation><affiliation xml:id="corr1" countryCode="AU"><unparsedAffiliation>Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">atrophy</keyword><keyword xml:id="kwd2">clinical features</keyword><keyword xml:id="kwd3">multiple system atrophy</keyword><keyword xml:id="kwd4">Parkinson's disease</keyword><keyword xml:id="kwd5">pathological severity</keyword><keyword xml:id="kwd6">progressive supranuclear palsy</keyword></keywordGroup><supportingInformation><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23336:MDS_23336_sm_authorroles"></mediaResource><caption>Author Roles and Disclosures</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Background:</title><p>There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features.</p></section><section xml:id="abs1-2"><title type="main">Methods:</title><p>Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point‐counting method was used to evaluate subregional volumes, and α‐synuclein and phospho‐tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features.</p></section><section xml:id="abs1-3"><title type="main">Results:</title><p>All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian‐plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus.</p></section><section xml:id="abs1-4"><title type="main">Discussion:</title><p>This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease. © 2011 Movement Disorder Society</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn4"><p><b>Relevant conflicts of interest/financial disclosures:</b> Tissues were received from the Sydney Brain Bank, which is supported by the National Health and Medical Research Council of Australia (Enabling Grant #282933), Neuroscience Research Australia and the University of New South Wales. Y.J.C. Song was an Australian Postgraduate and Parkinson's NSW Scholar and G.M. Halliday is a Senior Principal Research Fellow of the National Health and Medical Research Council of Australia. Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Clinical correlates of similar pathologies in parkinsonian syndromes</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Parkinsonian Clinicopathological Correlations</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Clinical correlates of similar pathologies in parkinsonian syndromes</title></titleInfo><name type="personal"><namePart type="given">Yun Ju Christine</namePart><namePart type="family">Song</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yue</namePart><namePart type="family">Huang</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neuroscience Research Australia and the University of New South Wales, Randwick, New South Wales, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Glenda Margaret</namePart><namePart type="family">Halliday</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</affiliation><description>Correspondence: Neuroscience Research Australia, Barker Street, Randwick, New South Wales 2031, Australia</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-02-15</dateIssued><dateCaptured encoding="w3cdtf">2008-11-25</dateCaptured><dateValid encoding="w3cdtf">2010-06-07</dateValid><copyrightDate encoding="w3cdtf">2011</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">2</extent><extent unit="tables">2</extent><extent unit="references">41</extent><extent unit="words">6169</extent></physicalDescription><abstract lang="en">Background:: There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features. Methods:: Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point‐counting method was used to evaluate subregional volumes, and α‐synuclein and phospho‐tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features. Results:: All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian‐plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus. Discussion:: This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease. © 2011 Movement Disorder Society</abstract><note type="additional physical form">Author Roles and Disclosures</note><note type="content">*Relevant conflicts of interest/financial disclosures: Tissues were received from the Sydney Brain Bank, which is supported by the National Health and Medical Research Council of Australia (Enabling Grant #282933), Neuroscience Research Australia and the University of New South Wales. Y.J.C. Song was an Australian Postgraduate and Parkinson's NSW Scholar and G.M. Halliday is a Senior Principal Research Fellow of the National Health and Medical Research Council of Australia. Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>atrophy</topic><topic>clinical features</topic><topic>multiple system atrophy</topic><topic>Parkinson's disease</topic><topic>pathological severity</topic><topic>progressive supranuclear palsy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>499</start><end>506</end><total>8</total></extent></part></relatedItem><identifier type="istex">50EE935819BAD6E0B6FD0918EC5E814F3C0A6D32</identifier><identifier type="DOI">10.1002/mds.23336</identifier><identifier type="ArticleID">MDS23336</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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