Atypical parkinsonism combining α‐synuclein inclusions and polyglucosan body disease
Identifieur interne : 005099 ( Main/Merge ); précédent : 005098; suivant : 005100Atypical parkinsonism combining α‐synuclein inclusions and polyglucosan body disease
Auteurs : Elsa Krim [France] ; Anne Vital [France] ; Frederic Macia [France] ; Farid Yekhlef [France] ; François Tison [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-02.
English descriptors
- KwdEn :
- Aged, Glial Fibrillary Acidic Protein (metabolism), Glucans (metabolism), Humans, Immunohistochemistry (methods), Inclusion Bodies (metabolism), Inclusion Bodies (pathology), Lewy Bodies (metabolism), Lewy Bodies (pathology), Male, Multiple System Atrophy (etiology), Multiple System Atrophy (pathology), Nerve Tissue Proteins (metabolism), Parkinsonian Disorders (complications), Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Review Literature as Topic, Staining and Labeling (methods), Synucleins, adult polyglucosan body disease, alpha-Synuclein, multiple system atrophy, parkinsonism, α‐synuclein inclusions.
- MESH :
- chemical , metabolism : Glial Fibrillary Acidic Protein, Glucans, Nerve Tissue Proteins.
- complications : Parkinsonian Disorders.
- etiology : Multiple System Atrophy.
- metabolism : Inclusion Bodies, Lewy Bodies, Parkinsonian Disorders.
- methods : Immunohistochemistry, Staining and Labeling.
- pathology : Inclusion Bodies, Lewy Bodies, Multiple System Atrophy, Parkinsonian Disorders.
- Aged, Humans, Male, Review Literature as Topic, Synucleins, alpha-Synuclein.
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
Url:
DOI: 10.1002/mds.20285
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<term>Lewy Bodies</term>
<term>Multiple System Atrophy</term>
<term>Parkinsonian Disorders</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Humans</term>
<term>Male</term>
<term>Review Literature as Topic</term>
<term>Synucleins</term>
<term>alpha-Synuclein</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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 alpha-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.</div>
</front>
</TEI>
</PubMed>
</double>
</record>
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