Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study
Identifieur interne : 001604 ( Istex/Corpus ); précédent : 001603; suivant : 001605Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study
Auteurs : Masato Kanazawa ; Takayoshi Shimohata ; Yasuko Toyoshima ; Mari Tada ; Akiyoshi Kakita ; Takashi Morita ; Tetsutaro Ozawa ; Hitoshi Takahashi ; Masatoyo NishizawaSource :
- Movement Disorders [ 0885-3185 ] ; 2009-07-15.
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Abstract
The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22583
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Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kakita, Akiyoshi" sort="Kakita, Akiyoshi" uniqKey="Kakita A" first="Akiyoshi" last="Kakita">Akiyoshi Kakita</name><affiliation><mods:affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pathological Neuroscience, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, Niigata University, Niigata, Japan</mods:affiliation></affiliation></author><author><name sortKey="Morita, Takashi" sort="Morita, Takashi" uniqKey="Morita T" first="Takashi" last="Morita">Takashi Morita</name><affiliation><mods:affiliation>Department of Pathology, Shinrakuen Hospital, Niigata, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ozawa, Tetsutaro" sort="Ozawa, Tetsutaro" uniqKey="Ozawa T" first="Tetsutaro" last="Ozawa">Tetsutaro Ozawa</name><affiliation><mods:affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</mods:affiliation></affiliation></author><author><name sortKey="Takahashi, Hitoshi" sort="Takahashi, Hitoshi" uniqKey="Takahashi H" first="Hitoshi" last="Takahashi">Hitoshi Takahashi</name><affiliation><mods:affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nishizawa, Masatoyo" sort="Nishizawa, Masatoyo" uniqKey="Nishizawa M" first="Masatoyo" last="Nishizawa">Masatoyo Nishizawa</name><affiliation><mods:affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official 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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="2009-07-15">2009-07-15</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1312">1312</biblScope><biblScope unit="page" to="1318">1318</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">794DDA51BBCBE22D672130D09EA1D289879D5C07</idno><idno type="DOI">10.1002/mds.22583</idno><idno type="ArticleID">MDS22583</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>parkinsonian disorders</term><term>progressive supranuclear palsy</term><term>spinocerebellar ataxias</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Masato Kanazawa MD</name><affiliations><json:string>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Takayoshi Shimohata MD, PhD</name><affiliations><json:string>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Yasuko Toyoshima MD, PhD</name><affiliations><json:string>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Mari Tada MD</name><affiliations><json:string>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</json:string><json:string>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Akiyoshi Kakita MD, PhD</name><affiliations><json:string>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</json:string><json:string>Department of Pathological Neuroscience, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Takashi Morita MD, PhD</name><affiliations><json:string>Department of Pathology, Shinrakuen Hospital, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Tetsutaro Ozawa MD, PhD</name><affiliations><json:string>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Hitoshi Takahashi MD, PhD</name><affiliations><json:string>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Masatoyo Nishizawa MD, PhD</name><affiliations><json:string>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>progressive supranuclear palsy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>spinocerebellar ataxias</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>parkinsonian disorders</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society</abstract><qualityIndicators><score>6.141</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1452</abstractCharCount><pdfWordCount>3741</pdfWordCount><pdfCharCount>25798</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>200</abstractWordCount></qualityIndicators><title>Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study</title><genre><json:string>Serial article</json:string></genre><host><volume>24</volume><pages><total>7</total><last>1318</last><first>1312</first></pages><issn><json:string>0885-3185</json:string></issn><issue>9</issue><subject><json:item><value>Research 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xml:lang="en">Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2009</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: Nothing to report.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study</title><author><persName><forename type="first">Masato</forename><surname>Kanazawa</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation></author><author><persName><forename type="first">Takayoshi</forename><surname>Shimohata</surname><roleName type="degree">MD, PhD</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, Brain Research Institute, Niigata University, 1‐757 Asahimachi‐dori, Chuoku, Niigata, Niigata 951‐8585, Japan</p></note><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation></author><author><persName><forename type="first">Yasuko</forename><surname>Toyoshima</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation></author><author><persName><forename type="first">Mari</forename><surname>Tada</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation></author><author><persName><forename type="first">Akiyoshi</forename><surname>Kakita</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><affiliation>Department of Pathological Neuroscience, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, Niigata University, Niigata, Japan</affiliation></author><author><persName><forename type="first">Takashi</forename><surname>Morita</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Pathology, Shinrakuen Hospital, Niigata, Japan</affiliation></author><author><persName><forename type="first">Tetsutaro</forename><surname>Ozawa</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, 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We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>progressive supranuclear palsy</term></item><item><term>spinocerebellar ataxias</term></item><item><term>Parkinson's disease</term></item><item><term>parkinsonian disorders</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="2008-09-24">Received</change><change when="2009-03-09">Registration</change><change when="2009-07-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/794DDA51BBCBE22D672130D09EA1D289879D5C07/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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href="file:MDS.MDS22583.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="4"></count><count type="referenceTotal" number="26"></count><count type="wordTotal" number="5345"></count></countGroup><titleGroup><title type="main" xml:lang="en">Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study<link href="#fn1"></link></title><title type="short" xml:lang="en">PSP: A Distinct Phenotype with Cerebellar Ataxia</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Masato</givenNames><familyName>Kanazawa</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Takayoshi</givenNames><familyName>Shimohata</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email normalForm="t-shimo@bri.niigata-u.ac.jp">t‐shimo@bri.niigata‐u.ac.jp</email></contactDetails></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Yasuko</givenNames><familyName>Toyoshima</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Mari</givenNames><familyName>Tada</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Akiyoshi</givenNames><familyName>Kakita</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Takashi</givenNames><familyName>Morita</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tetsutaro</givenNames><familyName>Ozawa</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Hitoshi</givenNames><familyName>Takahashi</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Masatoyo</givenNames><familyName>Nishizawa</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="JP" type="organization"><unparsedAffiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="JP" type="organization"><unparsedAffiliation>Department of Pathological Neuroscience, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, Niigata University, Niigata, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="JP" type="organization"><unparsedAffiliation>Department of Pathology, Shinrakuen Hospital, Niigata, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">progressive supranuclear palsy</keyword><keyword xml:id="kwd2">spinocerebellar ataxias</keyword><keyword xml:id="kwd3">Parkinson's disease</keyword><keyword xml:id="kwd4">parkinsonian disorders</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: Nothing to report.</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>Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PSP: A Distinct Phenotype with Cerebellar Ataxia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study</title></titleInfo><name type="personal"><namePart type="given">Masato</namePart><namePart type="family">Kanazawa</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takayoshi</namePart><namePart type="family">Shimohata</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><description>Correspondence: Department of Neurology, Brain Research Institute, Niigata University, 1‐757 Asahimachi‐dori, Chuoku, Niigata, Niigata 951‐8585, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yasuko</namePart><namePart type="family">Toyoshima</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mari</namePart><namePart type="family">Tada</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Akiyoshi</namePart><namePart type="family">Kakita</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><affiliation>Department of Pathological Neuroscience, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Morita</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, Shinrakuen Hospital, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tetsutaro</namePart><namePart type="family">Ozawa</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hitoshi</namePart><namePart type="family">Takahashi</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masatoyo</namePart><namePart type="family">Nishizawa</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan</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">2009-07-15</dateIssued><dateCaptured encoding="w3cdtf">2008-09-24</dateCaptured><dateValid encoding="w3cdtf">2009-03-09</dateValid><copyrightDate encoding="w3cdtf">2009</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">4</extent><extent unit="references">26</extent><extent unit="words">5345</extent></physicalDescription><abstract lang="en">The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><subject lang="en"><genre>Keywords</genre><topic>progressive supranuclear palsy</topic><topic>spinocerebellar ataxias</topic><topic>Parkinson's disease</topic><topic>parkinsonian disorders</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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1312</start><end>1318</end><total>7</total></extent></part></relatedItem><identifier type="istex">794DDA51BBCBE22D672130D09EA1D289879D5C07</identifier><identifier type="DOI">10.1002/mds.22583</identifier><identifier type="ArticleID">MDS22583</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 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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