Atypical parkinsonism combining α‐synuclein inclusions and polyglucosan body disease
Identifieur interne : 003152 ( Istex/Corpus ); précédent : 003151; suivant : 003153Atypical parkinsonism combining α‐synuclein inclusions and polyglucosan body disease
Auteurs : Elsa Krim ; Anne Vital ; Frederic Macia ; Farid Yekhlef ; François TisonSource :
- Movement Disorders [ 0885-3185 ] ; 2005-02.
English descriptors
- KwdEn :
Abstract
Adult polyglucosan body disease (APGBD) is a rare disorder affecting the central and peripheral nervous systems and in which parkinsonism is unusual. A 71‐year‐old man presented levodopa‐unresponsive parkinsonism with urinary incontinence and recurrent syncopes of 6 years standing masquerading as atypical parkinsonism of the multiple system atrophy (MSA‐P) type. Brain histopathology demonstrated massive accumulation of polyglucosan bodies particularly in the putamen. In addition, there were dense α‐synuclein–positive cytoplasmic oligodendroglial inclusions in the pons and in the middle cerebellar peduncle. These inclusions may be either due to the chance association of MSA‐P with APGBD, or pathologically related to APGBD. © 2004 Movement Disorder Society
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DOI: 10.1002/mds.20285
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<front><div type="abstract" xml:lang="en">Adult polyglucosan body disease (APGBD) is a rare disorder affecting the central and peripheral nervous systems and in which parkinsonism is unusual. A 71‐year‐old man presented levodopa‐unresponsive parkinsonism with urinary incontinence and recurrent syncopes of 6 years standing masquerading as atypical parkinsonism of the multiple system atrophy (MSA‐P) type. Brain histopathology demonstrated massive accumulation of polyglucosan bodies particularly in the putamen. In addition, there were dense α‐synuclein–positive cytoplasmic oligodendroglial inclusions in the pons and in the middle cerebellar peduncle. These inclusions may be either due to the chance association of MSA‐P with APGBD, or pathologically related to APGBD. © 2004 Movement Disorder Society</div>
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<affiliation>Service de Neurologie, Centre Hospitalier Universitaire de Bordeaux, France</affiliation>
<description>Correspondence: Service de Neurologie, Hôpital Haut‐Lévèque, CHU de Bordeaux, Avenue de Magellan, 33604 Pessac, France</description>
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<place><placeTerm type="text">Hoboken</placeTerm>
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<dateIssued encoding="w3cdtf">2005-02</dateIssued>
<dateCaptured encoding="w3cdtf">2003-11-17</dateCaptured>
<dateValid encoding="w3cdtf">2004-02-16</dateValid>
<copyrightDate encoding="w3cdtf">2005</copyrightDate>
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<language><languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="figures">3</extent>
<extent unit="tables">1</extent>
<extent unit="references">36</extent>
<extent unit="words">2358</extent>
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<abstract lang="en">Adult polyglucosan body disease (APGBD) is a rare disorder affecting the central and peripheral nervous systems and in which parkinsonism is unusual. A 71‐year‐old man presented levodopa‐unresponsive parkinsonism with urinary incontinence and recurrent syncopes of 6 years standing masquerading as atypical parkinsonism of the multiple system atrophy (MSA‐P) type. Brain histopathology demonstrated massive accumulation of polyglucosan bodies particularly in the putamen. In addition, there were dense α‐synuclein–positive cytoplasmic oligodendroglial inclusions in the pons and in the middle cerebellar peduncle. These inclusions may be either due to the chance association of MSA‐P with APGBD, or pathologically related to APGBD. © 2004 Movement Disorder Society</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>adult polyglucosan body disease</topic>
<topic>α‐synuclein inclusions</topic>
<topic>multiple system atrophy</topic>
<topic>parkinsonism</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>
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<subject><genre>article category</genre>
<topic>Brief Report</topic>
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<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>2</number>
</detail>
<extent unit="pages"><start>200</start>
<end>204</end>
<total>5</total>
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<identifier type="istex">84501A6996AFFE9686105A527412308DBB3FDBB7</identifier>
<identifier type="DOI">10.1002/mds.20285</identifier>
<identifier type="ArticleID">MDS20285</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2004 Movement Disorder Society</accessCondition>
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