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Y Morimatsu

Publications and source records attributed to Y Morimatsu.

At least 55 records · Page 3Linked to original sources
PubMed1988

Paraneoplastic cortical cerebellar degeneration. A neuropathological study of an autopsy case in comparison with cortical cerebellar degeneration in alcoholics.

A case is described of paraneoplastic cortical cerebellar degeneration in a patient with a small cell carcinoma of the lung. Following therapy, clinical improvement of cerebellar ataxia had been observed. The most severe degeneration was found in the superior aspects of the vermis and in the anterior and simple lobes as well as in the inferior aspects of the hemisphere. In addition to this distribution of degenerative lesions, uneven loss of Purkinje cells was apparent. Such distribution patterns in this case were apparently compatible with those of alcoholic cortical cerebellar degeneration (ACD), although the lesions were less severe than in ACD. Furthermore, dendritic changes in the Purkinje cells including loss of the spiny branchlets, focal swelling of the dendrites, and disappearance of secondary and tertiary branches were remarkable. It is noteworthy that these cells showed various stages of degeneration before cell loss occurred. These data suggest that the degree of vulnerability varies among Purkinje cells, and that this could be related to the uneven loss of these cells. It is proposed that, although this case and cases of ACD have both similarities and differences in their neuropathological aspects, it is apparent that both conditions have some common morphopathogenetic factor.

Alcoholism↗
PubMed1987

Axonal polyglucosan body in the ventral posterolateral nucleus of the human thalamus in relation to ageing.

Axonal polyglucosan bodies in myelinated axons in the ventral posterolateral nucleus of the human thalamus (VPL) are described. These axonal inclusions were distributed exclusively in the dorsolateral part of the caudal VPL, and their arrangement may be associated with fibres originating from the gracile nucleus. They were not observed in patients under age of 50, and appeared to increase in number and size with advancing age. It is suggested that axonal polyglucosan bodies are an ageing phenomenon of the secondary sensory fibres.

Adolescent↗
PubMed1987

[Morphometry of the brainstem with transverse section of the upper pons].

The authors developed new method of morphometry in the brainstem, which used transverse section of the upper pons. After fixation with formalin, the brainstem was separated from the cerebrum and the cerebellum. Both junctions of midbrain-pons and pons-medulla were cut and then the pons was horizontally separated into four slices. The oral surface of the second slice from oral side, in which the central portion of the locus ceruleus is located, was measured with computed digitizer after enlarging the picture. The authors measured the total size of the slice in the pons (Total S), the tegmentum size (Teg S), the total length (Total L), the tegmentum length (Teg L) and so on. The tegmentum was separated from the base along the ventral line of the medial leminiscus. In the study of 23 control cases (16 to 77 year old, 13 male and 10 female, all were Japanese), Total S (563 +/- 85 mm) and Teg S (136 +/- 19 mm) ranged to some extent, while the percentage of the tegmentum size to the total size (Teg S/Total S X 100: %Teg S) distributed in narrow range (24.4 +/- 2.3%), which was considered to be an appropriate index to reveal normal structure of the upper pons. The percentage of the tegmentum length to the total length (%Teg L) was also an appropriate and a simple index. Using this method to stained preparation, it was confirmed that the tegmentum size of such cases with olivopontocerebellar atrophy or infantile spasms were significantly small.

Adolescent↗
PubMed1986

A case report of infantile striatal necrosis with an acute onset.

We report here an autopsy case, an 8-year-old boy diagnosed as having infantile striatal necrosis, characterized by a preceding febrile illness followed by acute encephalopathy with abrupt obtundation, seizures and dystonia, with remarkable improvement of the disturbed consciousness and intelligence after TRH-T therapy. These clinical symptoms were linked with bilateral necrosis of the striata on CT scanning. The presented case belonged to a newly described subgroup of the heredogenous disorders that produce necrosis of the putamina in children.

Basal Ganglia Diseases↗
PubMed1986

Neuropathology of the brainstem in age-dependent epileptic encephalopathy--especially of cases with infantile spasms.

Twenty-two autopsy cases with developmental disabilities with history of infantile spasms were studied with special regard to brainstem lesions. Eleven out of 22 cases were considered to be of prenatal origin, ten cases were perinatal and one case had suffered from acute encephalopathy at six months of age. Some common pathological findings were noticed throughout the cases despite their various etiologies; small size of the brainstem tegmentum, spongy state in and around the central tegmental tract, localized periaqueductal glial scar. Control study on another autopsy series of 76 cases with developmental disabilities showed a close connection between these findings in the brainstem tegmentum and history of infantile spasms.

Adolescent↗
PubMed1985

Neuropathological study and chemico-pathological correlation in sibling cases of Sanfilippo syndrome type B.

Pathological and biochemical studies of two sibling cases (18-year-old girl and 16-year-old boy) with Sanfilippo syndrome type B are presented. Pathological study revealed distended neurons and neuronal processes with inclusions throughout the CNS and the visceral organs, and neuronal loss and corresponding gliosis. The authors paid particular attention to atrophic changes in the thalamus and to "dissociation gliomyélinique" in the cerebral white matter. Histochemistry and electron microscopy revealed regional differences in stored materials. Biochemical studies revealed an accumulation of glycosaminoglycans in the CNS and abnormalities in the lipid metabolism in the brain and visceral organs. A protein assay of the cerebrum showed increased glial fibrillary acidic protein and low levels of myelin basic protein in the white matter.

Adolescent↗
PubMed1985

[A case of toxic leucoencephalopathy induced by 5FU derivatives].

A case of toxic leucoencephalopathy induced by 5 FU derivatives is reported. A 46-year-old woman was diagnosed as having breast cancer, and radical mastectomy was performed on May, 1982. After operation, she was given irradiation and 5FU derivative (tegafur or carmofur) 600 mg and Nolvadex 20 mg (tamoxifen citrate) were administered every day. After taking the medication for a month, she began to stagger and developed a tremor in both arms. She was admitted to our hospital on August 16, because she showed evidence of dysarthria and memory disturbance in addition to her initial complaints. Soon after admission, she developed akinetic mutism, and metastasis in the brain stem was suspected. In spite of her severe condition, she was given radiation over the posterior fossa and continued the medication. On September 22, CT disclosed low density area in the centrum semiovale bilaterally. She died of DIC on November 30. An autopsy was performed. The brain weight was 1110 g and the outer surface of the brain was normal. In frontal cut surfaces stained with K.B., bilateral degeneration of the centrum semiovale was apparent. Microscopically, the degree of myelin degeneration was stronger than that of axon, and numerous fatty granular cells were found in the degenerated area. There were no bizarre shaped astrocytes, inclusion body or cellular infiltration. Fibrillary gliosis was scanty. No metastasis was found in the central nervous system or other organs. Based on these pathological findings and clinical history, toxic leucoencephalopathy induced by 5 FU derivatives was suggested.

Antineoplastic Agents↗
PubMed1984

Necrotizing leukoencephalopathy and treated multiple myeloma. An autopsy case without intrathecal chemotherapy or irradiation of the brain.

A 48-year-old woman with multiple myeloma, developed progressive neurological disturbances one year after the bone marrow remission. There was neither intrathecal chemotherapy nor brain irradiation. She received cyclophosphamide, phenylalanine mustard, urethane, and prednisolone intravenously or orally. At postmortem examination the cerebral hemispheres had a conspicuous destruction of white matter, consistent with a necrotizing leukoencephalopathy with focal and diffuse demyelination. No myeloma cells were found in the nervous system. Alzheimer type II glias and abnormal glias closely resembling Alzheimer type I glia were numerous in the affected white matter. No oligodendroglias with intranuclear inclusions were found. No virus particles were detected by electron microscope. The neuropathological changes had features similar to those seen in leukoencephalopathy with intrathecal administration of methotrexate. The glial abnormality, the most striking feature in the present case, strongly suggests toxic and metabolic disturbances. It appears that the leukoencephalopathy of the present case developed on the more complicated etiopathogenesis. However, it would be emphasized that the side-effects of the drugs could be considered as one of the etiologica factors causing the glial abnormality.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1983

Chronic recurrent demyelinating encephalomyelitis associated with hemophagocytic lymphohistiocytosis.

A man aged 31 with remittent fever, leukopenia, polyuria, and splenomegaly in addition to chronic and recurrent episodes of neurologic abnormalities was examined pathologically. A chronic type of perivenous encephalomyelitis was found in the CNS, and chronic inflammatory lesions were noticed in the infundibulo-hypophyseal system and also in the peripheral nerves. Moreover, hemophagocytic lymphohistiocytosis predominated in the reticuloendothelial system. This seemed to be the first adult case of demyelinating disease with hemophagocytic lymphohistiocytosis.

Adult↗