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S Oyanagi

Publications and source records attributed to S Oyanagi.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1983

Distribution of intracytoplasmic acidophilic granule-containing neurons in the human brain.

Using four autopsied brains, we studied the anatomic locations of the intracytoplasmic acidophilic granule (IAG)-containing neurons. These neurons occurred in the hypothalamus, zona incerta, insular cortex, and the other 23 nuclei. However, IAGs were not observed in neurons of the Ammon's horn, thalamus, dentate nucleus, or in Purkinje cells of the cerebellum. The distribution of IAG-containing neurons does not exactly correspond to that of the neuromelanin- or monoamine-forming neurons. There is, however, a striking parallelism between the IAG-containing neurons map and the Lewy bodies map. It is suggested by the superimposition of both maps that IAG-containing neurons may have a certain metabolic relation to the formation of Lewy bodies.

Adult↗
PubMed1982

Light- and electron-microscopic studies of intracytoplasmic acidophilic granules in the human locus ceruleus and substantia nigra.

Using the brains of 30 patients with mental and neurologic disorders, we studied the intracytoplasmic acidophilic granules in neurons of the substantia nigra and locus ceruleus by light and electron microscopy. The granules were present in all 30 brains, including those with no recognizable pathologic change, there was no correlation between their appearance and the age, sex, disease of, or the medication received by, the patients. In four electron-microscopically examined brains, we noted many small, round electron-dense bodies in the perikarya and neuronal processes of the substantia nigra and locus ceruleus. The bodies were packed tightly within a double membrane; in shape, size, and distribution in the neuronal cytoplasm, they corresponded to acidophilic granules. Some mitochondrial matrices contained one or more similar, but smaller inclusion bodies; large bodies pushed aside the mitochondrial cristae. We conclude that the acidophilic granules represent high developed forms of mitochondrial inclusions.

Adolescent↗
PubMed1981

Nasu-Hakola's disease (membranous lipodystrophy). A case report.

An autopsy case of Nasu-Hakola's disease (membranous lipodystrophy) was reported. A 29-year-old Japanese woman whose younger sister had been affected with typical Nasu-Hakola's disease with skeletal and neuropsychiatric syndromes and membrano-cystic lesions in the bones developed forgetfulness and lack of initiative. The clinical features were characterized by diminished drive, apathy, euphoria, disturbance of attention, amnestic syndrome, and gait disturbance. The clinical course of her illness was 8 years. The neuropathologic examination revealed marked symmetrical gliosis of the cerebral white matter (sclerosing leukodystrophy) predominantly in the frontal and temporal lobes with slight or moderate demyelination (dissociation glio-myelinique) and widespread axonal changes such as fragmentation and spheroid in the white matter of the cerebral hemisphere, cerebellum, basal ganglia, and brain stem. The ultrastructure of spheroids showed neurofilamentous accumulation. We discussed the importance of axonal changes with regard to the pathogenesis and etiogenesis of the disease.

Adult↗
PubMed1981

Pallido-nigro-luysial atrophy with massive appearance of corpora amylacea in the CNS.

A case of pallido-nigro-luysial atrophy, characterized by symptoms typical of progressive supranuclear palsy, presented (1) severe symmetrical abiotrophic degeneration of the globus pallidus, substantia nigra, and subthalamic nucleus and (2) widespread accumulations of corpora amylacea in the CNS. The former is thought to be consistent with pallido-nigro-luysial atrophy and we regard it as a combined system degeneration of both the pallido-nigral and the pallido-luysial systems. The significance of the latter is quite obscure. As far as we know, only three cases of pallido-nigro-luysial atrophy have been reported. However, there is no reported case of this disorder with such widespread and massive accumulations of corpora amylacea as in our case.

Aged↗
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↗