title: Peculiar axonal debris with subsequent astrocytic response (foamy spheroid body). A topographic, light microscopic, immunohistochemical and electron microscopic study.
abstract: Foamy spheroid bodies (FSBs) are described, as newly identified pathological structures occurring in human brain. FSBs favoured the substantia nigra pars reticulata (SNPR) and/or globus pallidus (GP) in degenerative conditions especially postencephalitic parkinsonism, progressive supranuclear palsy, pallido-nigro-luysial atrophy and multiple system atrophy. No FSBs were observed anywhere in the presence of substantia nigra pars compacta (SNPC) degeneration, such as occurs in idiopathic Parkinson's disease, or luysio-pallidal system degeneration, such as found in dentato-rubro-pallido-luysial atrophy or Joseph's disease. FSBs were also occasionally identified in the substantia nigra (SN) and/or GP of aged persons. In addition to SN and GP lesions, FSBs were seen in diffuse axonal lesions of long fibre tracts (the corpus callosum, the superior cerebellar peduncle) after non-missile head injuries, and in peri-infarct lesions. Under the light microscope, FSBs appear as slightly eosinophilic, foamy and nearly round objects with vague outlines, measuring approximately 10-50 microns in diameter. Some FSBs contain coarse, eosinophilic clusters at their periphery. FSB stained black when stained by the Gallyas silver method. Some FSBs were immunohistochemically positive for synaptophysin and 68 kDa neurofilament. Glial fibrillary acidic protein-positive fibres were observed alongside and/or inside some FSBs. Electron microscopically, FSBs were found to consist of collections of neuritic debris containing a variety of dense bodies and a small number of both mitochondria and neurofilaments. Some such collections were surrounded by astrocytic processes. These findings strongly suggest that FSBs are collections of small axonal debris destined for removal by astrocytes in due course. A variety of factors (degeneration of the SNPR and/or the GP, injury, infarction, ageing) seemed to be responsible for the histogenesis of FSBs.
authors.affiliation: Department of Clinical Neuropathology, Tokyo Metropolitan Institute for Neurosciences, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Arai
authors.forename: S
authors.initials: S
authors.lastname: Yagishita
authors.forename: K
authors.initials: K
authors.lastname: Misugi
authors.forename: M
authors.initials: M
authors.lastname: Oda
authors.forename: K
authors.initials: K
authors.lastname: Kosaka
authors.forename: T
authors.initials: T
authors.lastname: Mizutani
authors.forename: Y
authors.initials: Y
authors.lastname: Morimatsu
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001253:Astrocytes / Q000473:pathology / Q000648:ultrastructure*; D001369:Axons / Q000648:ultrastructure*; D001479:Basal Ganglia / Q000473:pathology / Q000648:ultrastructure; D001921:Brain / Q000473:pathology* / Q000648:ultrastructure; D005260:Female; D005917:Globus Pallidus / Q000473:pathology / Q000648:ultrastructure; D006801:Humans; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009410:Nerve Degeneration; D009419:Nerve Tissue Proteins / Q000032:analysis*; D015388:Organelles / Q000648:ultrastructure*; D013378:Substantia Nigra / Q000473:pathology / Q000648:ultrastructure
chemical_list: D009419:Nerve Tissue Proteins