Document Detail


The distribution and dynamic density of oligodendroglial cytoplasmic inclusions (GCIs) in multiple system atrophy: a correlation between the density of GCIs and the degree of involvement of striatonigral and olivopontocerebellar systems.
MedLine Citation:
PMID:  9194897     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The distribution and dynamic density of oligodendroglial cytoplasmic inclusions (GCIs) were studied based on 30 cases of multiple system atrophy (MSA), including striatonigral degeneration (SND), olivopontocerebellar atrophy (OPCA) and Shy-Drager syndrome. GCIs were widely spread throughout the central nervous system, including the striatonigral and olivopontocerebellar systems. Inclusion-bearing cells appeared to be oligodendrocytes which usually had larger and lighter nuclei than those of normal-looking oligodendrocytes. The distribution of GCIs was similar in all cases, irrespective of the degrees of OPCA and SND, but the frequency of GCIs varied from case to case. We classified all the cases into two categories based on the degree of neuropathological changes of SND (mild and severe) and, independently, into three groups based on that of OPCA (minimal, moderate and severe), i.e., a total of six groups. An association between the frequency of GCIs and the severity of the lesions was obtained. For example, many GCIs were seen the cerebellar white matter in the cases in which OPCA was not histologically confirmed. More GCIs were seen in the cases with moderate OPCA. In the cases with severe OPCA, GCIs were rarer and smaller, in proportion to the devastation of fibers; no GCIs were seen in the cases with more severe OPCA. The incidence of GCIs showed a positive correlation to the severity of OPCA but not that of SND in the corticopontine tracts, of both OPCA and SND in the pyramidal tracts, and of SND but not of OPCA in the pencil fibers of the putamen. It is suggested that GCIs may represent either a change synchronous with neuronal degeneration or a phenomenon preceding neuronal changes, especially in the cerebellar white matter. Thus, they may represent the early changes in MSA and may be a useful neuropathological hallmark for diagnosis of MSA, even in cases with minimal OPCA and SND.
Authors:
M Inoue; S Yagishita; M Ryo; K Hasegawa; N Amano; M Matsushita
Related Documents :
16535807 - Storage and retrieval of snop-coded pathologic diagnoses using offsite computing and op...
2549797 - Giant axonal neuropathy. a review.
16757847 - Sminet-2: description of an internet-based surveillance system for communicable disease...
17424757 - Persistent systemic air embolism and delayed pulmonary hemorrhage after weaning from ca...
23371877 - Palatal rugae and their role in forensic odontology.
10646437 - Pediatric spinal cord injuries: a case presentation.
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Acta neuropathologica     Volume:  93     ISSN:  0001-6322     ISO Abbreviation:  Acta Neuropathol.     Publication Date:  1997 Jun 
Date Detail:
Created Date:  1997-08-05     Completed Date:  1997-08-05     Revised Date:  2007-11-09    
Medline Journal Info:
Nlm Unique ID:  0412041     Medline TA:  Acta Neuropathol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  585-91     Citation Subset:  IM    
Affiliation:
Division of Pathology, Kanagawa Rehabilitation Center, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Aged
Atrophy
Autonomic Nervous System Diseases / pathology*
Cerebellar Diseases / pathology*
Corpus Striatum / pathology*
Female
Humans
Inclusion Bodies / pathology*
Male
Middle Aged
Oligodendroglia / pathology*
Olivopontocerebellar Atrophies / pathology
Pons / pathology*
Shy-Drager Syndrome / pathology
Spinocerebellar Degenerations / pathology
Substantia Nigra / pathology*

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Ultrastructural concomitants of hypoxia-induced angiogenesis.
Next Document:  Increase in oxidative key enzymes in a case of muscle ubiquinol-cytochrome c reductase deficiency.