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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ISTEX:84501A6996AFFE9686105A527412308DBB3FDBB7Le document en format XML
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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. 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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. 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