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Y Morimatsu

Publications and source records attributed to Y Morimatsu.

At least 37 records · Page 2Linked to original sources
PubMed1994

[Penetration of the esophageal and gastric ulcers to the cardioaortic system following hiatus hernia: a lethal complication in the severely-handicapped].

Among the severely-handicapped, hiatus hernia (HH) and/or gastroesophageal regurgitation (GER) are not uncommon. We report here three patients with HH and/or GER. Two of them died of massive hemorrhage in the alimentary tract from the heart or the thoracic aorta due to penetration of the gastric or esophageal ulcer. The third patient died of pneumonia, but autopsy proved multiple esophageal ulcers, one of which reached the wall of the brachiocephalic artery without penetration. We propose that proper treatment for HH and/or GER is required for the severely-handicapped, including surgical intervention, before their general conditions become worse and decompensatory.

Adult↗
PubMed1993

Foamy spheroid bodies in the globus pallidus and the substantia nigra pars reticulata: an investigation on regional distribution in 56 cases without neurodegenerative diseases.

In order to clarify the sites of predilection for foamy spheroid bodies (FSBs) their regional distribution was studied in 56 persons (30-98 years) without neurodegenerative diseases. Variable amounts of FSBs were observed in approximately 30% of cases and favoured the rostro-ventral parts of the globus pallidus (GP), including the ventral pallidum, and/or the substantia nigra pars reticulata (SNr). The results strongly suggest that FSBs develop during aging and are a hitherto undescribed pathological hallmark for degeneration of the GP and the SNr.

Adult↗
PubMed1993

[The cranial MRI in severe cerebral palsy: a comparative study with clinical data].

The magnetic resonance examination was performed in 38 patients with severe cerebral palsy (CP; 15 males and 23 females) who had both motor delay (unable to move anywhere) and mental retardation (I. Q or D. Q below 30). Neuroimaging findings were compared with the CP type, etiology, and grade of understanding of language. Cranial magnetic resonance imagings (MRI) in CP were divided into five types. Type 1 : nine predominantly showed cyst-liked ventricles and periventricular hyperintensity on T2-weighted imaging (PVH) and only scarred basal ganglia and thalamus were visible. All suffered from neonatal asphyxia and the clinical type was rigospastic tetraplegia (RST). Type 2: eleven predominantly showed PVH and hyperintensity on T2-weighted (HT2) in basal ganglia and thalamus. All suffered from neonatal asphyxia and the clinical type was RST or rigospastic diplegia. Type 3: five showed PVH and three had cortical atrophy. All suffered from neonatal asphyxia and the clinical type was spastic diplegia. Type 4: four predominantly showed HT 2 in putamen and thalamus. Three had cortical atrophy. All suffered from neonatal asphyxia. The clinical type was athetotic CP (ATH). Type 5: nine predominantly showed HT 2 in globus pallidus. Four had cortical atrophy and two had hippocampal atrophy. All suffered from neonatal jaundice and the clinical type was ATH. All patients who suffered from neonatal asphyxia and spastic CP had MRI in PVH. All patients who suffered from neonatal asphyxia and ATH showed HT 2 in putamen and thalamus. Almost patients who suffered neonatal jaundice and ATH showed HT 2 in globus pallidus. With athetotic CP, cases with atrophy of the cerebral cortex or/and hippocampus were lower grade of understanding of language than no atrophy of both. The result of studies of MRI are in agreement with neuropathological findings.

Adolescent↗
PubMed1992

Peculiar axonal debris with subsequent astrocytic response (foamy spheroid body). A topographic, light microscopic, immunohistochemical and electron microscopic study.

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.

Adult↗
PubMed1992

Immunohistochemical expression of microtubule-associated protein 5 (MAP5) in glial cells in multiple system atrophy.

An immunohistochemical study focusing on glial cells was performed using monoclonal antibodies against microtubule-associated proteins (MAP1, MAP2 and MAP5), transferrin, leukocyte common antigen (LCA) and glial fibrillary acidic protein (GFAP) in 5 cases of multiple system atrophy (MSA) exhibiting olivopontocerebellar atrophy and striatonigral degeneration. An antibody to MAP5, a fetal antigen in developing brain, was strongly demonstrated in the glial cytoplasmic inclusions (GCIs) which have recently drawn a great deal of attention and were observed in all 5 cases of MSA. Moreover, MAP5-positive glial cells (MAP5-Gs) were present in significantly higher number than in the controls in various regions where GCIs were found, predominantly in putamen, substantia nigra, cerebellar white matter and internal capsule. LCA and transferrin, markers of microglia and oligodendroglia, respectively, were immunohistochemically detected in some MAP5-Gs. GFAP, on the other hand, was not expressed in MAP5-Gs at all. These findings suggest that MAP5-Gs consist of reactive microglia and oligodendroglia. Our study is the first to demonstrate immunohistochemical detection of MAP5 in glial pathological changes in MSA.

Aged↗
PubMed1992

A neuropathological study of a case of the Prader-Willi syndrome with an interstitial deletion of the proximal long arm of chromosome 15.

An autopsy case, a 6-month-old girl, with an interstitial deletion of the long arm of chromosome 15;del(15)(q11.1q12) was reported. Muscle hypotonia, poor sucking and intermittent ocular deviation were noticed soon after birth. She also exhibited external features peculiar to the Prader-Willi syndrome (PWS). The muscle hypotonia persisted and head control was not achieved. She died at the age of 6 months due to bronchopneumonia. G-banding analysis of prometaphase chromosomes revealed a deletion of chromosome 15. Bronchopneumonia of the lungs and fatty metamorphosis of the liver were found. Neuropathological anomalies recognized were; disturbed undulating structures, resembling cortical micropolygyria and pachygyria, in the dentate nucleus and the inferior olivary nucleus, grumose degeneration of the nerve cells in the dentate nucleus, and heterotopia of middle-sized neurons in the cerebellar white matter. No abnormalities were observed in the hypothalamus-pituitary system. In some autopsy cases of PWS, cerebellar lesions have been reported. These might be related to the muscle hypotonia in PWS.

Brain↗
PubMed1992

A neuropathological study of early onset Cockayne syndrome with chromosomal anomaly 47XXX.

We present the clinical and neuropathological findings in a female patient with early onset Cockayne syndrome and a chromosomal anomaly (47XXX). The girl was the only child of healthy, unrelated parents. She was born with a birth weight of 1,930 gm. She had progeroid facial features with bilateral cataracts. A diagnosis of 47XXX was made on the basis of a chromosomal study. Physical shortness became increasingly prominent while her weight remained stationary. Psychomotor retardation was noted, and she could never sit alone. A brain CT scan showed cerebral atrophy and calcification of the basal ganglia. Cultured skin fibroblast exhibited significant sensitivity to the ultraviolet light. She died from a chest infection at the age of 7 years and 4 months. Microscopically, the renal glomeruli showed diffuse sclerotic changes with thick capillary basement membranes. A neuropathological examination revealed a very small brain (295 gm), extensive myelin deficiency, gliosis in the white matter, and calcifications in the basal ganglia, and cerebral and cerebellar cortices. The loss of both Purkinje and granular cells was noticed in the cerebellar cortex. This is the first report of a case with the Cockayne syndrome and 47XXX, and the 47XXX in this patient seems to be coincidental.

Brain↗
PubMed1991

Clinical and neuropathological findings in severe athetoid cerebral palsy: a comparative study of globo-Luysian and thalamo-putaminal groups.

We divided cases of severe athetoid cerebral palsy originating perinatally into two groups neuropathologically, the "globo-Luysian group" (GL) and the "thalamo-putaminal group" (TP). The major abnormal sites in GL were the pallidum and subthalamic nucleus, and in TP the thalamus and putamen. The lesions in TP were more widespread and frequently accompanied by fibrillary gliosis in the central gray matter of the midbrain, and subthalamic nuclei were dominantly devastated. Concerning the etiology, GL and TP were related to perinatal severe jaundice and neonatal asphyxia, respectively. The patients in TP showed lower mental ability and suffered from more intractable convulsions than those in GL. In GL, rigidospasticity was frequently demonstrated with fluctuation of athetoid movements, while in TP various abnormalities of muscle tone were observed, with rather restricted athetosis.

Adolescent↗
PubMed1991

[Immunohistochemical study of glial cytoplasmic inclusion in multiple system atrophy].

Recently, glial cytoplasmic inclusion (GCI) has been demonstrated to be argyrophilic cytoplasmic body by silver staining in the oligodendroglia of patients with multiple system atrophy. We observed such GCIs in all 20 cases of multiple system atrophy. No GCI was noticed in all 6 cases of hereditary spinocerebellar degenerations. Immunohistochemically, GCI was stained positively with antibodies to ubiquitin, alpha-tubulin, and beta-tubulin, of which characteristics is consistent with previous reports. In addition, GCI was first demonstrated to react with an antibody to microtubule-associated protein-1B(5), which is one of the proteins of cytoskeleton organization and a component of cross-bridges between microtubular assembly. The result suggests strong relationship between the formation of the OCI and immunohistochemical expression of MAP-1B(5).

Antibodies, Monoclonal↗
PubMed1990

Senile dementia of Alzheimer type characterized by laminar neuronal loss exclusively in the hippocampus, parahippocampus and medial occipitotemporal cortex.

Seven cases of senile dementia of Alzheimer type (SDAT) with unusual clinico-pathological findings are reported. The patients showed neuronal loss in laminar pattern, with gliosis exclusively confined to the CA1 of the hippocampus, the area of the hippocampal gyrus (entorhinal cortex) and medial occipitotemporal cortex. This change was more pronounced in the oral region. The subcortical white matter showed more pronounced fibrillary gliosis than loss of myelin. Both Alzheimer's neurofibrillary tangles and senile plaques were less marked than those usually seen in SDAT. The mental disturbance started after the age of 65 in all patients. The main clinical feature was marked character change in addition to disturbance of cognitive function. Cranial computed tomography showed marked dilatation of the oral portion of the inferior horn of the lateral ventricle in the early stage. It was apparent that although the cases in this group could be incorporated within in the spectrum of SDAT, they could also be considered to represent a variant of SDAT. This group could contribute to an understanding of the clinico-pathological spectrum of SDAT as well as indicating ways of managing such patients.

Aged↗
PubMed1990

Non-missile head injury: report of a patient surviving for 6 years.

A female patient with non-missile head injury is described. She showed slight improvement in her level of consciousness, and survived for 6 1/2 years after injury. At autopsy, the white matter lesions were localized rather than diffuse in distribution. In addition to lesions in the corpus callosum, anterior commissure and dorsolateral quadrant of the rostral brain stem, those in the parasagittal cerebral white matter, and in the hilus of the dentate nucleus and superior cerebellar peduncle were considered to be due to primary axonal injury. A cavity in the frontal white matter was remarkable in that there was no evidence to indicate expansion of the lesion due to haemorrhage. These features suggested that the injurious physical forces had acted parallel to the direction of the axons.

Accidents, Traffic↗
PubMed1990

[Alzheimer's neurofibrillary tangles in a 52-year-old patient with severe brain damage].

A woman, who had been developmentally delayed since her birth, further deteriorated after she got an episode of high fever of unknown origin at 2 years of age. At the age of 52 years, she died of liver cancer after a long-standing HB virus carrier state. Neuropathological examination revealed brain atrophy, narrowed white matter, myelin pallor, fibrillary gliosis and status marmoratus of the thalamus. These findings suggested the primary cause of the brain pathology in this case to be a developmental destructive process which should have taken place in the early stage of brain development. In addition, neurofibrillary tangles (NFT) were noticed in the hippocampus, locus ceruleus and nucleus basalis of Meynert, but no senile plaques were found anywhere. These NFT changes seemed to be closely resembling to those of the Fukuyama type congenital muscular dystrophy. But the reason why NFT occur in this case is still obscure and probably different from that in the Down syndrome or in physiological senility.

Brain↗
PubMed1990

[A clinical study of death in profound mental retardation with motor disturbance].

Among 848 cases of profound mental retardation with motor disturbance admitted to Metropolitan Medical Center of Severely Handicapped in the last 20 years, 98 died. The 94 cases whose cause of death was determined were clinically investigated. There was no difference in sex, and 72% of the patients died before the age of 15 years. Half of the patients died of pneumonia; sudden death occurred in 9, and ileus in 8. These three were thought to be the most important and characteristic causes of death in severely handicapped patients. In recent years, deaths due to pneumonia have decreased and those due to ileus have disappeared, but deaths due to malignant neoplasm have begun to be recognized. There were also some deaths from intracranial hemorrhage in young children, and some deaths from tracheal bleeding in those who had tracheal tubes. These two were also important causes of death in the patients. Sudden death had certain characteristics: most cases were adolescent or young patients with mixed quadriplegia who were sensitive to environmental changes and often showed marked hypertonia by athetosis, and in addition, all of their acute changes occurred between 5 and 8 a.m. or between 6 and 9 p.m.

Adolescent↗
PubMed1989

An autopsy case of atypical infantile motor neuron disease with hyaline intraneuronal inclusions.

We describe a 5-year-old boy who had had a progressive motor weakness with bulbar palsy and spasticity of the lower extremities since age 3 years and who died of bronchopneumonia after about two and a half years of the illness. Neuropathologic examination revealed combined degenerative processes in the upper and lower motor neurons, the spinocerebellar and olivocerebellar systems, and the ventral thalamic nuclei. Lewy body-like intraneuronal hyaline inclusions, which ultrastructurally showed irregular accumulations of trilaminar membranous profiles, were detected in the spinal anterior horn, Clarke's dorsal nucleus, facial nerve nucleus, inferior olivary nucleus, and substantia nigra. This case could be considered as a unique form in the group of the infantile motor neuron diseases associated with multi-systemic degenerations in the central nervous system.

Brain↗
PubMed1989

Histopathological study of alobar holoprosencephaly. 1. Abnormal laminar architecture of the telencephalic cortex.

Abnormal architecture of the telencephalic cortex was studied in six autopsy specimens of alobar holoprosencephaly by histopathological, electron microscopic and immunohistochemical methods. Several common abnormalities are described and their significance discussed. In all of the specimens, the cortices showed excessive thickness and abnormal lamination with a middle cellular layer and an external sparse layer, indicating disturbance of neuronal migration. Neurons of the external sparse layer were segmented into irregularly arranged groups, suggesting disturbance of tissue organization. In three specimens, the internal pyramidal layer contained numerous abnormal glomerular structures which consisted of fine dendrites and axons.

Abnormalities, Multiple↗
PubMed1989

Histopathological study of alobar holoprosencephaly. 2. Marginal glioneural heterotopia and other gliomesenchymal abnormalities.

Abnormalities of glial and mesenchymal elements were studied in six autopsy specimens of alobar holoprosencephaly by histopathological and immunohistochemical methods. Marginal glioneural heterotopia was observed in all of the specimens. It was most prominent in the prosencephalic base around the optic chiasm, and extensive in five specimens. The floor of the third ventricle was intermingled with excessive mesenchymal elements, and in three specimens the ventricular cavity was plugged by heterotopic nodules. In the cerebellum, dysplastic nodules were observed in two specimens. In the telencephalon, the marginal and subventricular layers were thickened. The pathological significance of these findings is discussed with their possible relationship to the pathomechanism of holoprosencephaly.

Abnormalities, Multiple↗
PubMed1988

Familial bulbo-spinal muscular atrophy associated with testicular atrophy and sensory neuropathy (Kennedy-Alter-Sung syndrome). Autopsy case report of two brothers.

Autopsy cases of two brothers with bulbo-spinal muscular atrophy associated with gynecomastia, testicular atrophy and sensory neuropathy are reported. The disease started with finger tremor, proximal muscle weakness and facial muscle twitching at the second and fourth decades, accompanied by bulbar signs and glove-stocking type sensory disturbance. Systemic neurogenic patterns and diminished sensory nerve action potential amplitudes were recorded by electrophysiological studies. A marked loss of myelinated fibers was noticed upon sural nerve biopsy. Gonadal hormone values were normal, except for elevated urinary estrogen. Postmortem examinations revealed a remarkable degeneration of the facial and hypoglossal nuclei, and the spinal cord motoneurons. The skeletal muscles and the tongue showed neurogenic muscular atrophy with fatty replacement. Testicular atrophy was prominent showing hyalinized seminiferous tubuli with nodular and diffuse Leydig cell hyperplasia, containing estrogen immunoreactive substance. These clinical and histological features seemed to be highly compatible with those of Kennedy-Alter-Sung type bulbo-spinal muscular atrophy. The involvement of sensory peripheral nerves, however, was a distinct feature of this family.

Aged↗