Corticobasal syndrome with novel argyrophilic glial inclusions
Identifieur interne : 001D68 ( Istex/Corpus ); précédent : 001D67; suivant : 001D69Corticobasal syndrome with novel argyrophilic glial inclusions
Auteurs : Gregory A. Rippon ; S. M. Staugaitis ; Steven S. M. Chin ; James E. Goldman ; K. MarderSource :
- Movement Disorders [ 0885-3185 ] ; 2005-05.
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Abstract
A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20396
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Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Gregory A. Rippon MD</name><affiliations><json:string>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</json:string><json:string>Gertrude H. Sergievsky Center, Columbia University, New York, New York, USA</json:string><json:string>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA</json:string></affiliations></json:item><json:item><name>S.M. 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Marder MD, MPH</name><affiliations><json:string>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</json:string><json:string>Gertrude H. Sergievsky Center, Columbia University, New York, New York, USA</json:string><json:string>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA</json:string><json:string>Department of Psychiatry, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>corticobasal degeneration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>corticobasal syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glial inclusions</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuropathology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>degenerative disorders</value></json:item></subject><language><json:string>eng</json:string></language><abstract>A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. 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Sergievsky Center, Columbia University College of Physicians and Surgeons, 622 W. 168th Street, New York, NY 10032</p></note><affiliation>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</affiliation><affiliation>Gertrude H. 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Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. 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Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley" registered="yes">10.1002/mds.v20:5</doi><numberingGroup><numbering type="journalVolume" number="20">20</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2005-05">May 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="100" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.20396</doi><idGroup><id type="unit" value="MDS20396"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Brief Report with Video</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2005 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2004-04-30"></event><event type="manuscriptRevised" date="2004-07-26"></event><event type="manuscriptAccepted" date="2004-08-05"></event><event type="publishedOnlineEarlyUnpaginated" date="2005-02-22"></event><event type="firstOnline" date="2005-02-22"></event><event type="publishedOnlineFinalForm" date="2005-04-28"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></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">598</numbering><numbering type="pageLast">602</numbering></numberingGroup><correspondenceTo>Gertrude H. Sergievsky Center, Columbia University College of Physicians and Surgeons, 622 W. 168th Street, New York, NY 10032</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS20396.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="25"></count><count type="wordTotal" number="3045"></count></countGroup><titleGroup><title type="main" xml:lang="en">Corticobasal syndrome with novel argyrophilic glial inclusions</title><title type="short" xml:lang="en">CBS With Novel Oligodendroglial Inclusions</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2 #af3" corresponding="yes"><personName><givenNames>Gregory A.</givenNames><familyName>Rippon</familyName><degrees>MD</degrees></personName><contactDetails><email>grippon@sergievsky.cpmc.columbia.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af4"><personName><givenNames>S.M.</givenNames><familyName>Staugaitis</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3 #af5"><personName><givenNames>Steven S.M.</givenNames><familyName>Chin</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3 #af5"><personName><givenNames>James E.</givenNames><familyName>Goldman</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af2 #af3 #af6"><personName><givenNames>K.</givenNames><familyName>Marder</familyName><degrees>MD, MPH</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Gertrude H. Sergievsky Center, Columbia University, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurosciences, Cleveland Clinic Foundation, Cleveland, Ohio, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Pathology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Department of Psychiatry, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">corticobasal degeneration</keyword><keyword xml:id="kwd2">corticobasal syndrome</keyword><keyword xml:id="kwd3">glial inclusions</keyword><keyword xml:id="kwd4">neuropathology</keyword><keyword xml:id="kwd5">degenerative disorders</keyword></keywordGroup><supportingInformation><p> This article includes Supplementary Video, available online at <url href="http://www.interscience.wiley.com/jpages/0885-3185/suppmat"> http://www.interscience.wiley.com/jpages/0885‐3185/suppmat </url> . </p></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Corticobasal syndrome with novel argyrophilic glial inclusions</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CBS With Novel Oligodendroglial Inclusions</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Corticobasal syndrome with novel argyrophilic glial inclusions</title></titleInfo><name type="personal"><namePart type="given">Gregory A.</namePart><namePart type="family">Rippon</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</affiliation><affiliation>Gertrude H. Sergievsky Center, Columbia University, New York, New York, USA</affiliation><affiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA</affiliation><description>Correspondence: Gertrude H. Sergievsky Center, Columbia University College of Physicians and Surgeons, 622 W. 168th Street, New York, NY 10032</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.M.</namePart><namePart type="family">Staugaitis</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurosciences, Cleveland Clinic Foundation, Cleveland, Ohio, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Steven S.M.</namePart><namePart type="family">Chin</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA</affiliation><affiliation>Department of Pathology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">James E.</namePart><namePart type="family">Goldman</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA</affiliation><affiliation>Department of Pathology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Marder</namePart><namePart type="termsOfAddress">MD, MPH</namePart><affiliation>Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</affiliation><affiliation>Gertrude H. Sergievsky Center, Columbia University, New York, New York, USA</affiliation><affiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA</affiliation><affiliation>Department of Psychiatry, Columbia University College of Physicians and Surgeons, Columbia University, New York, New York, USA</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">2005-05</dateIssued><dateCaptured encoding="w3cdtf">2004-04-30</dateCaptured><dateValid encoding="w3cdtf">2004-08-05</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="references">25</extent><extent unit="words">3045</extent></physicalDescription><abstract lang="en">A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>corticobasal degeneration</topic><topic>corticobasal syndrome</topic><topic>glial inclusions</topic><topic>neuropathology</topic><topic>degenerative 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><note type="content"> This article includes Supplementary Video, available online at http://www.interscience.wiley.com/jpages/0885‐3185/suppmat .</note><subject><genre>article category</genre><topic>Brief Report with Video</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>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>598</start><end>602</end><total>5</total></extent></part></relatedItem><identifier type="istex">32F8EA69F6D8D6CDA861CBF1801566B9FA9D60E6</identifier><identifier type="DOI">10.1002/mds.20396</identifier><identifier type="ArticleID">MDS20396</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 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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