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S Oyanagi

Publications and source records attributed to S Oyanagi.

18 recordsLinked to original sources
PubMed1992

Presenile dementia with progressive supranuclear palsy tangles and Pick bodies: an unusual degenerative disorder involving the cerebral cortex, cerebral nuclei, and brain stem nuclei.

Degeneration of heterogeneous systems in the central nervous system, with widespread distribution of argyrophilic neuronal fibrillary inclusions, was found in a patient with presenile dementia. Atrophy was circumscribed in the frontal and temporal lobes. Neuronal loss was severe in the basal ganglia, subthalamic nucleus, and substantia nigra. Immunocytochemical study using anti-phosphorylated tau and anti-ubiquitin antibodies in conjunction with ultrastructural observations revealed two types of inclusions: neurofibrillary tangles (NFTs) of progressive supranuclear palsy (PSP) in the Edinger-Westphal nucleus, locus coeruleus, cerebellar dentate nucleus, inferior olivary nucleus, and posterior horn of the spinal cord; and Pick bodies (PBs) in the atrophied cerebral cortex and red nucleus. PSP-type NFTs and PBs have been demonstrated in a single case for the first time. Despite their pathognomonic significance in certain disorders, we suggest that these inclusions may reflect a form of cytoskeletal disorganization, which is not entirely restricted to a single disease entity.

Adult↗
PubMed1992

Ultrastructural and immunohistochemical study of degenerate neurite-bearing ghost tangles.

Some ghost tangles in the brains of Alzheimer patients were accompanied by many small argyrophilic structures which were electron microscopically confirmed to be degenerate neurites. In these ghost tangles, roughly dispersed 15 nm straight and occasional twisted tubules were penetrated by proliferated astrocytic processes. Immunohistochemically, these ghost tangles lost immunoreactivities to anti-NFT, -tau and -ubiquitin antibodies, but were thioflavine-S fluorescent, though antigenicity to beta-protein was not proved. This similarity in composition of degenerate neurite-bearing ghost tangles to senile plaques might be induced by the amyloid nature of tubules, which probably provokes the reaction of neuropils.

Aged↗
PubMed1989

Senile plaque-like structures: observation of a probably unknown type of senile plaque by periodic-acid methenamine silver (PAM) electron microscopy.

Numerous diffuse senile plaque-like structures (SPLSs) were found in the cerebral cortex from cases with dementia of the Alzheimer type by means of the methenamine-Bodian method. SPLSs varied in shape and size. They were never recognized in the original Bodian, PAS and Congo red preparations, but were positive with anti-beta-protein immunostaining and periodic-acid methenamine silver (PAM) methods, which are thought to specifically stain amyloid substance. With PAM electron microscopy, we found sparse aggregations of amorphous, often ramified, structures with fine granular silver deposits in SPLS. Routine electron microscopic examination on the same portion where SPLS were confirmed by PAM electron microscopy revealed amorphous, partially fibrous structures. These structures might be amyloid or amyloid-precursor substance. In SPLSs only a few degenerated neurites and astrocytic processes with glycogen granules were seen. We consider SPLSs to be a kind of senile plaque.

Adult↗
PubMed1988

Clinical and neuropathological study of a familial case of juvenile parkinsonism.

This is a detailed autopsy case of rare juvenile parkinsonism with dominant heredity. The patient displayed parkinsonian symptoms which began at the age of 24, and expired in a state of quadriplegia-in-flexion at 35. In the later stage, myoclonic jerks, epileptiform convulsions and dementia appeared. L-dopa was effective only in the early stages. The autopsy revealed severe degeneration and the formation of atypical Lewy bodies in the cerebral cortex, as well as typical lesions of idiopathic parkinsonism with a Lewy body formation in the brain stem. This case was considered to belong essentially to idiopathic parkinsonism. The pathology of juvenile parkinsonism is reviewed briefly.

Adult↗
PubMed1985

[An autopsy case with peculiar acidophilic bodies in the dentate nucleus and brain stem, associated with degeneration of the pyramidal-extrapyramidal systems].

Case S.S. 59 years of age, male. At the age of 25, he had admitted to sanatorium for 7 years because of pulmonary tuberculosis. After his discharge, at the age of 45, he had started complaining of depressive mood or the idea of suicide and admitted to a mental hospital. Psychiatric diagnosis was depression and slight mental retardation. Shortly after, his depressive mood was improved, but his hypochondriac attitude was unchanged. No tendency toward dementia was proven. At the age of 54, he became enable to walk. Neurologically, pyramidal and some sort of extrapyramidal signs, dysarthria, disturbance of swallowing, fecal and urinary incontinence became apparent. Laboratory data showed scarcely any abnormality. At the age of 59, he died of bronchopneumonia. Neuropathologically, moderate degeneration of dentate nucleus, slight degeneration of pyramidal tract from medulla oblongata to spinal cord, striatum, substantia nigra were found. Neither senile plaques nor neurofibrillary changes could be seen throughout central nervous system. The most important finding is the presence of peculiar acidophilic bodies. They are round or oval, 10 approximately 20 mu in diameter and distributed in dentate nucleus, oculomotor nucleus, central grey of midbrain, superior colliculus, putamen, pallidum, subthalamic nucleus, Zona incerta, hypothalamus, Locus coeruleus, reticular formation of midbrain and pons, pontine nucleus, raphe nucleus, vestibular nucleus, inferior olive in order of number of the bodies. These bodies are scattered in so-called ground substance, and have no relations to any cell bodies or cell processes.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Stem↗
PubMed1977

Multiple system degeneration and involving thalamus, reticular formation, pallido-nigral, pallido-luysian and dentato-rubral systems. A case report.

An autopsy case of multiple system degeneration is characterized by the following; (1) progressive dementia and abnormal sleep patterns, followed by Parkinsonian symptoms with terminal akinetic mutism; (2) severe symmetrical degeneration in the thalamus, particularly nucl. medialis thalami, the reticular formation of the brain stem, also the pallidonigral, pallido-Luysian and dentato-rubral systems. As far as we known, there is no case in the literature, of combined system degeneration, which shows such a wide anatomical range of lesions as the present one. Clinico-pathological correlation between dementia and degeneration of the thalamus, and between abnormal sleep-consciousness mechanism and degeneration of the reticular formation are discussed. The extrapyramidal symptoms are discussed from the clinico-pathological aspect. In addition, peculiar eosinophilic bodies are described, which were most frequently found in the putamen.

Adult↗
PubMed1976

Presenile dementia with Alzheimer-, Pick- and Lewy-body changes.

An autopsy case of unclassifiable presenil dementia is reported. The outstanding pathological findings were as follows; 1. presence of senile plaques, neurofibrillary changes, Pick bodies, Hirano bodies, granulovacuolar degeneration of neurons, etc. 2. numerous Lewy bodies in the brain stem and diencephalon, 3. peculiar swollen neurons with intracytoplasmic, eosinophilic and argentophilic inclusions ("Lewy-like-bodies") in the cerebral cortices. Detailed study of the last mentioned inclusions indicates that they are almost identical to Lewy bodies, though there are some minor differences, in histochemical and electronmicroscopic findings. Nosologically, this case may represent either a combination of Alzheimer's disease, Pick's disease and idiopathic Parkinsonism with "Lewy-like-bodies" in the cerebral cortices, or a single disease. As far as we know, no similar case been reported.

Aged↗
PubMedDate not supplied

A fetal type of Minamata disease. An autopsy case report with special reference to the nervous system.

Our knowledge concerning the pathology of fetal cases of human Minamata disease (methylmercury poisoning) is relatively limited. We report here a case with description of the distribution of mercury in the systemic organs, and the ultrastructural changes of the nervous system after a survival of 29 yr. The patient was a female born in 1957, with a body wt of 3000 g, who died in 1987. She carried a diagnosis of cerebral palsy, and had a convulsion at age 3 yr. Mercury levels in her mother's hair were 101 micrograms/g at the time of examination in 1959. At autopsy, the body measured 43 cm and weighed 23 kg. The brain weighed 920 g and showed marked cerebral atrophy, mild neuronal loss in the calcarine, postcentral and precentral cortices, cerebellar atrophy, and segmental demyelination of peripheral nerves. Mercury granules were present in the brain, kidney, and liver. Ultrastructural examination of the calcarine, post- and precentral cortices, and cerebellar cortices, showed severe atrophy of nerve cells, with a decrease in rough ER and an increase in nuclear chromatin and preservation of mitochondria. Autophagosomes were increased in number. In addition, high electron density, globular and dense bodies, measuring 0.3-1.8 microns in diameter, were found, surrounded by limited membrane, within both cerebral and cerebellar neurons. In the cellebellum, synapses were well-preserved.

Adult↗
PubMedDate not supplied

Pseudo-intracellular collagen tangles in human spinal ganglia.

A new structure was found in the spinal ganglia of 6 out of 215 human autopsy cases with various disorders. It was composed of ballooned cells fully packed with fibrillar structures showing the same staining properties as collagen. Ultrastructurally the fibrillar structures were bundles of collagen fibres with a striation of about 70nm periodicity, and they were enclosed by the cell membrane invaginated in a very complex manner into the cytoplasm. This structure, which we named 'pseudo-intracellular collagen tangle', was considered to result from a disturbance in the releasing process of collagen fibre from fibroblasts. The aetiology of the structure is unknown, but it might represent one of regressive or senile changes in human spinal ganglia.

Aged↗
PubMedDate not supplied

Juvenile parkinsonism: a case with first clinical manifestation at the age of six years and with neuropathological findings suggesting a new pathogenesis.

A clinico-pathological study of a 39-year-old female with Juvenile parkinsonism was carried out. Although the clinical manifestations were consistent with parkinsonism, the pathological findings were significantly different. Pathological examination showed the lesion to be localized to the substantia nigra, the number of neurons to be abnormally low, the proportion of melanin-containing cells to be reduced, and a large number of immature cells to be present. No neuronal degeneration associated with gliosis or release of melanin granules, such as seen in Parkinson's disease, was observed. Neuropathological studies, including cytometry and comparison against normal controls in the distribution of melanin granules, suggested hypoplasia and poor neuronal maturation of the substantia nigra. Since neuromelanin is thought to be the result of normal dopamine metabolism, reduction of melanin-containing cells in this case suggests inadequate or abnormal dopamine metabolism. Thus, the clinical manifestation of parkinsonism in this case seems to be related to the small number of melanin-containing cells which implies the dopamine deficiency state.

Autopsy↗