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Biomedical subjects

K Isaki

Publications and source records attributed to K Isaki.

67 records · Page 4Linked to original sources
PubMed1981

Fine structure of experimental epileptogenic focus produced by intracerebral implantation of cobalt-gelatin stick in rabbits.

The experimental epileptogenic focus produced by cobalt-gelatin stick implantation in the cerebral cortex of rabbits has been studied by electron microscopy. Since our cobalt focus was latent, the bemegride maneuver was intravenously performed to identify the cobalt lesion of the cortex as an epileptogenic focus. The cobalt lesion comprised three different zones. Of the three zones, the reactive zone showed a glio-mesenchymal scar and prominent ultrastructural changes. The major change of this zone was found in the neurons, neuropils and astrocytes. Electron-lucent neurons deprived of the usual neuropils surrounding them, widening of extracellular spaces and swollen dendrites in neuropils, and proliferating astrocytes were observed constantly throughout the experimental period. These findings may be significant for the genesis of this type of epilepsy.

Animals↗
PubMed1979

Amyotrophic lateral sclerosis with temporal lobe atrophy.

Clinical and neuropathological findings are reported on a 48-year-old man who developed progressive bulbar palsy, muscle atrophy of four extremities, and hyperreflexia. Duration of the illness was about 19 months. Moderate personality changes were observed during his hospitalization. Neuropathological examination revealed the presence of an ALS: severe loss of the large motoneurons in the spinal anterior horns, and degeneration of the corticospinal tract, more prominent on the left side. The hypoglossal, the facial, and the motor trigeminal nuclei were also involved, but the oculomotor, the trochlear and the abducens nuclei were well preserved. There was bilateral, but more pronounced on the right, atrophy of the temporal poles consistent with the lesions of the temporal types of Pick's disease. This case indicates the simultaneous occurrence of degenerative diseases of the CNS, and the correspondence of laterality between the temporal lobe and the spinal cord may suggest a common etiology of these two types of disease processes.

Amyotrophic Lateral Sclerosis↗
PubMed1979

First autopsy report of a multiple sclerosis case in Hokuriku District of Japan.

The first autopsy of a case of multiple sclerosis from the District of Hokuriku was reported. The patient, a 50-year-old house-wife, born in Toyama Prefecture, had noticed a paresthesia of her face, fatigue, numbness and weakness in the right limbs, dimness of vision and gait disturbance at ave 44. Furthermore, in the course of the disease, she had suffered from visual disorder, tetraplegia, hyperreflexia, pyramidal signs and cerebellar syndroms such as dysarthria, nystagmus, intention tremor and ataxia. She also showed symptoms of euphoria and dementia. After a course of six years she died of bronchopneumonia. Remissions and exacerbations were noted four times during her clinical history. Histopathologically, there were many recent and old demyelinating lesions of varying sizes and shapes in all parts of the central nervous system, namely the cerebrum, brainstem, spinal cord and optic nerve. In contrast to the clinical symptoms, the cerebellum itself revealed less plaques than the other areas of the brain. According to the observed distributions of the lesions, our case can be classified as belonging to the optico-cerebro-spinal type in the Ikuta and Zimmerman classification. The demyelinated lesions were characterized by a perivenular distribution of the plaques, lack of tissue necrosis, paucity of inflammatory reaction and marked fibrous gliosis of varying degrees.

Bronchopneumonia↗
PubMedDate not supplied

Serial cerebral MRI with FLAIR sequences in acute carbon monoxide poisoning.

In a patient with acute carbon monoxide (CO) poisoning in whom no delayed sequelae have been observed, MRI was performed serially from the time of exposure. When few clear findings were noted on conventional T2-weighted spin echo (SE) imaging, distinct hyperintense areas in the deep cerebral white matter were already evident on fluid attenuated inversion recovery (FLAIR) pulse imaging. These abnormal findings appeared to reflect a disease process differing from the acute phase disturbance of consciousness, namely the course of a gradually progressive demyelination. Neither serial intelligence tests nor single photon emission CT (SPECT) studies of regional cerebral blood flow conducted in the same period revealed any abnormalities. These results suggest that, in the subclinical phase in which there are few significant findings on T2-weighted SE imaging or SPECT, insidious demyelinating changes are already apparent on FLAIR imaging and that FLAIR imaging may thus be useful in the early diagnosis of the interval form of CO poisoning.

Adult↗
PubMedDate not supplied

Cerebellar dentate nucleus in Alzheimer's disease with myoclonus.

Although myoclonus commonly occurs in a later stage of Alzheimer's disease (AD), the pathological basis of this symptom is still unclear. In order to elucidate the neuropathological substrate of myoclonus in AD, we quantitatively assessed neuronal density and volume, with a discrimination between small and large neurons, at the rostral and caudal parts in the cerebellar dentate nucleus of 8 AD patients with myoclonus, 10 AD patients without myoclonus and 9 controls, using stereological probes. The neuronal numerical density of the large neurons at the rostral part and of total counts (rostral and caudal parts) in the myoclonic AD group were significantly greater than in the nonmyoclonic AD group. There were no significant differences in the density of small neurons between the two AD groups. The ratio of small neurons to large neurons (S/L ratio) of total counts was significantly lower in AD with myoclonus than in AD without myoclonus. The mean neuronal volume of the large neurons at the rostral part was significantly greater in myoclonic AD than in nonmyoclonic AD. Conversely, the volume of the small neurons at the rostral part was significantly lower in myoclonic AD than in nonmyoclonic AD. This study, for the first time, shows an increase in mean volume of large neurons and a decrease in mean volume of small neurons as well as a change in the S/L ratio in the dentate nucleus in AD with myoclonus. An imbalance in the S/L ratio as well as morphological changes of these neurons in the dentate nucleus may contribute to the pathological substrate of myoclonus in AD.

Aged↗
PubMedDate not supplied

Striatonigral degeneration combined with olivopontocerebellar atrophy with subcortical dementia and hallucinatory state.

We present an autopsied case of striatonigral degeneration (SND) combined with olivopontocerebellar atrophy (OPCA) with subcortical dementia and hallucinatory state. A Japanese woman without a remarkable family history showed hand tremor at the age of 35 years, followed by bradykinesia, muscle rigidity, orthostatic hypotension, neurogenic bladder and pyramidal signs. No obvious cerebellar symptoms were found. Various antiparkinsonian drugs were administered, but were not markedly effective for the parkinsonism. She developed a mild dementia characterized by mild memory disturbance with preservation of orientation, slowing of thought processes, emotional lability toward sadness, impaired ability to manipulate acquired knowledge and poor calculating, and by the absence of aphasia, apraxia and agnosia. The features in this patient were consistent with those seen in subcortical dementia. She also had auditory hallucinations. MRI revealed hypointense T2 signals in the putamina and substantia nigra. T1-weighted MRI demonstrated atrophy of both the pons and cerebellum in addition to atrophy of the putamina and substantia nigra. EEG showed slowing of background activity. She died of cardiac failure at the age of 47. Autopsy disclosed brain stem tegmental atrophy, SND, OPCA and many glial cytoplasmic inclusions in the central nervous system, but well-preserved cerebrum. We discuss the relationship between the psychiatric symptoms and pathologic findings of brain stem tegmentum.

Autopsy↗
PubMedDate not supplied

Microglial and astrocytic change in brains of Creutzfeldt-Jakob disease: an immunocytochemical and quantitative study.

AIM: The relationship between microglial cells and astrocytes in brains from patients with Creutzfeldt-Jakob disease (CJD) was immunohistochemically and quantitatively studied. MATERIALS AND METHODS: CJD cases, including three with subacute spongiform encephalopathy (SSE), three with panencephalopathic type of CJD (PECJD) and six normal controls were examined. Microglial cells were preferentially labeled by monoclonal anti-KP1 (CD68) antibody and astrocytes by polyclonal anti-glial fibrillary acidic protein (GFAP) antibody. Two cytokines were labeled by polyclonal anti-tumor necrosis factor-alpha (TNF-alpha) and polyclonal interleukin-1alpha (IL1alpha). RESULTS: In the CJD brains, microglial cell density was significantly higher in the white matter than in the cerebral cortex. In contrast, astrocyte density was significantly higher in the cortex than in the white matter. In the PECJD cases, many hypertrophic microglial cells were clustered along the margin of the demyelinated white matter whereas severely demyelinated white matter contained few microglial cells. The microglial cells were also located in vacuoles in myelinated fibers of the internal capsule in the PECJD cases, which resembled myelinopathic alteration in vacuolar myelopathy. The GFAP-positive astrocytes proliferated much more numerously in the severely demyelinated white matter. The densities of astrocytes and microglial cells showed a significantly negative correlation in the cerebral cortex. The density of the white matter microglia did not differ between the PECJD and SSE cases. TNF-alpha and IL1alpha were expressed by microglial cells, but the TNF-alpha-positive microglial cells were very few in both SSE and PECJD cases. A subset of IL1alpha-positive microglia was found in the SSE case white matter, although the number of KP 1-positive microglial cells greatly surpassed the number of IL1alpha-positive ones. CONCLUSION: These results imply that microglia are increased in number before demyelination and become hypertrophic while phagocytosing myelin in PECJD, and that the negative correlation between the density of microglia and astrocytes is not regulated by either cytokine.

Adult↗
PubMedDate not supplied

Corticobasal degeneration: an autopsy case clinically diagnosed as progressive supranuclear palsy.

We report an autopsy case diagnosed clinically as progressive supranuclear palsy (PSP), but neuropathologically confirmed as corticobasal degeneration (CBD). A 56-year-old Japanese woman slowly developed parkinsonism, dementia, character change, followed by vertical gaze palsy and dystonia. Brain MRI demonstrated diffuse cerebral atrophy with severe shrinkage of the brain stem tegmentum. The SPECT images using 123I-IMP disclosed symmetrical hypoperfusion in the frontal lobes. She died of respiratory failure at the age of 71. Gross inspection of the brain showed diffuse, symmetrical atrophy of the cerebrum and marked atrophy of the Luysian body, globus pallidus, substantia nigra and nuclei of the brain stem tegmentum. Microscopically, neuronal loss and fibrillary gliosis were observed in the Luysian body, globus pallidus, substantia nigra and nuclei of the brain stem tegmentum. The cerebellar dentate nucleus showed mild neuronal loss with some grumose degeneration. Neurofibrillary tangles were found only in the Luysian body, substantia nigra and raphe nuclei, whilst tau-positive inclusions were observed more extensively. Astrocytic plaques and swollen achromatic neurones were found in the postcentral gyrus. There were no tuft-shaped astrocytes in the brain. The clinicopathological similarities and differences between PSP and CBD are discussed.

Aged↗