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H Ishino

Publications and source records attributed to H Ishino.

At least 19 recordsLinked to original sources
PubMed1992

[An autopsy case of ataxic form of Creutzfeldt-Jakob disease].

An autopsy case of ataxic form of Creutzfeldt-Jakob disease (Brownell and Oppenheimer, 1965) was reported. The patient, a 71-year-old male, noticed ataxic gait at the beginning of June in 1988, and was admitted to the Hiroshima City Hospital for the neurological examination at the end of June. He showed ataxia of the left arm and legs and diplopia. Gradually he became delirious at night. On July 16, tremor-like involuntary movement of the left hand was noticed. On July 20, he became somnolent and doubly incontinent. Myoclonus and paratonic rigidity were also observed. The EEG showed periodic synchronous discharge on July 25. The brain CT and MRI were normal. He became apallic gradually and died on October 28. The duration of illness was 5 months. At autopsy, brain weighed 1000gr. Cerebral atrophy and slight enlargement of the ventricles were observed. The cerebellum was also slightly atrophic. Histologically, the destruction of the cerebral cortical layer, slight sieve-like spongy state of the neuropil, slight neuronal loss of the thalamus and sieve-like spongy state of the striatum were observed. The cerebellar lesion was the most severe, where granular cell loss and gliosis of the cortex were observed.

Aged↗
PubMed1991

Genetic factors regulate the rise in blood pressure in F2 generation crossed between stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats.

1. There was no significant difference between the systolic blood pressure (SBP) of offspring derived from SHRSP mother and WKY father and the SBP of offspring derived from WKY mother and SHRSP father at the developing stage (5-13 weeks of age). 2. The degree of genetic determinations of SBP in stroke-prone spontaneously hypertensive rat (SHRSP) at 5, 7, 10 and 13 weeks of age, determined by genetic crosses between SHRSP and WKY, was 73.9, 70.8, 50.2 and 55.3% respectively. 3. Significant correlations between SBP at 5 and 7 weeks, 7 and 10 weeks, 10 and 13 weeks, also at 5 and 13 weeks of age in F2 generation crossed between SHRSP and WKY were observed. SBP falling at or above the 80th percentile group in F2 generation at 5 weeks of age were constantly higher than SBP falling at or below the 20th percentile group from 7 weeks of age onwards. 4. These results indicate that there exists 'tracking phenomenon of SBP in SHRSP' and that genetic factors regulate the rise in SBP. Tracking of SBP in F2 generation gives us new methodological insight into hypertensive mechanism in SHR.

Animals↗
PubMed1990

Relative frequencies of dementia of the Alzheimer type and vascular dementia in Japanese nursing homes.

We have studied neuropathologically 200 aged nursing home residents (101 men and 99 women) autopsied between 1976 and 1985. Seventy-three of the 200 showed dementia during life, that is, 27% and 55% of the residents in nursing homes and special nursing homes, respectively. The relative frequencies of SDAT and VD in nursing homes as a whole were the same (34%). The relative frequencies of SDAT and VD in special nursing homes, where usually high concentrations of VD have been noted, were 21% and 52%, respectively. A comparison of the results of our special nursing homes (SDAT:VD = 1:2.5) and nursing homes as a whole (SDAT:VD = 1:1) with those of Barnes and Raskind (SDAT:VD = 2:1) and Rovner et al. (SDAT:VD = 3:1) showed that the frequencies of VD in Japanese nursing homes are considerably higher than those in their American counterparts.

Aged↗
PubMed1990

[Cases of numerous diffuse plaques in the neocortex but without severe senile changes in the hippocampus].

Using modified Bielschowsky method, we studied neuropathologically 159 aged subjects autopsied during the period from 1976 to 1988, of which we found 19 cases (average age at death: 82.6 ys) with numerous diffuse plaques in the frontal and temporal neocortex and no severe senile changes in H1-H3 of Ammon's horn (dp group). Amyloid angiopathy had been excluded and one case was excluded because of considerable cerebrovascular lesions. The dp group was divided into 8 demented (average age at death: 86.0 ys) and 10 nondemented patients (average age at death: 79.7 ys). We compared the number, type, and ratio of types of senile plaques in the frontal cortex, temporal cortex, and putamen of the demented and nondemented groups, and obtained the following results: (1) Eight (14%) of the 59 nondemented and 8 (40%) of the 20 demented cases in which no severe senile changes in the neocortex and hippocampus had been detected by Bodian stain showed numerous diffuse plaques in the neocortex when the modified Bielschowsky method was used. (2) The ratio of classic and primitive plaques to diffuse plaques in the frontal cortex was the same in both groups, but the nondemented group had exclusively diffuse plaques in the temporal cortex. (3) In the putamen 2 nondemented cases (20%) and 6 demented cases (75%) had exclusively diffuse plaques. We considered that classic and primitive plaques are more closely related to dementia than are diffuse plaques in the temporal lobe in cases without severe senile changes in the hippocampus.

Aged↗
PubMed1990

[A case of Binswanger disease with numerous diffuse plaques in the neocortex].

A case of Binswanger disease with numerous diffuse plaques in the neocortex was reported. This male patient had a previous history of hypertension and myocardial infarction. From the age of 60, he developed dysarthria, bradykinesia, marche à petit pas and falling down. Neurological examination at his first admission disclosed muscular rigidity and increased jaw and deep tendon reflexes, but dementia was not found. Brain CT showed moderate brain atrophy and EEG consisted of slow wave dysrhythmia. He was diagnosed of Parkinsonism and treatment started without effects. During his second admission for the treatment of myocardial infarction, at the age of 64, delirium developed. Progressive dementia began and finally he was confined to bed. From the age of 69, spontaneous speech became almost lost. Contracture of the extremities, increased deep tendon reflexes and force grasping were noted. Brain CT showed symmetrical low attenuation in the frontal and parietal white matter with moderate dilatation of the lateral ventricles. At the age of 70, he died of general prostration about ten years after the initial symptoms. Neuropathological findings: Macroscopic findings: The brain weighed 1300 g. Atherosclerotic changes of the large arteries at the base of the brain were moderate. Coronal sections of the brain showed moderate enlargement of the lateral ventricles with multiple small lacunes in the basal ganglia. Microscopic findings: Bilateral diffuse demyelination of the white matter with sparing of the U-fibers was noted. Holzer stain revealed fibrillary gliosis in the left parietal and occipital white matter. Marked adventitial fibrosis of the deep white matter arteries and terminal stages of hyalinosis of the perforating arteries were found. Basal ganglia showed status lacunaris. Bilateral pyramidal tracts were atrophic secondly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

[A case of bilateral necrosis of the basal ganglia after hypotensive shocks].

We reported a case with bilateral necrosis of the basal ganglia after hypotensive shocks. The patient was a 69-year-old woman, who fell into a hypotensive shock (B.P. below 40 mmHg) of unknown origin during examination of her bladder cancer and was admitted into CCU. After admission, hypotensive shocks were repeated four times (B.P. below 50 mmHg each time). Neurological examination revealed a left spastic hemiplegia. Brain CT on 10th day showed bilaterally low density areas around the basal ganglia and a diagnosis of brain infarction was made. She gradually presented quadriplegia and symptomatic changes from pyramidal to extrapyramidal signs. Brain CT on 24th day showed bilateral hemorrhagic infarction of the basal ganglia with enhanced effect. On 79th day, she again fell into shock and died. Neuropathological examination of the brain was as follows. 1) laminar necrosis of the deep layers of the cerebral cortex, 2) bilateral necrosis of the hippocampal Sommer sector, 3) bilateral necrosis of the caudate nucleus, putamen and pallidum with neuronal loss and infiltration of fat granule cells, 4) sparing of the internal capsules, 5) bilateral necrosis of the reticular zone of the substantia nigra, 6) foci of fresh necrosis and loss of Purkinje cells in the cerebellum. These lesions are consistent with those of selective vulnerability in hypoxia as described by Scholz et al. An extensive distribution of cerebral as well as basal ganglia necrosis in this case was caused by repeated shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1983

Joseph disease in a non-Portuguese family.

We studied four patients with Joseph disease in a Japanese family. There were two clinical types in the family. One was characterized by pyramidal and cerebellar signs with or without extrapyramidal signs; the other, by cerebellar signs, loss of tendon reflexes, and peripheral sensory loss. The family tree indicated autosomal-dominant inheritance. Neuropathologic examination revealed marked degeneration of the substantia nigra, dentate nuclei, Clarke column, and anterior horn cells of the spinal cord. This is the first report of pathologically proven Joseph disease in a non-Portuguese family.

Adult↗
PubMed1976

Frequency of Alzheimer's neurofibrillary tangles in the cerebral cortex in progressive supranuclear palsy (subcortical argyrophilic dystrophy).

The frequency of Alzheimer's neurofibrillary tangles was studied, employing large sections of the cerebral hemispheres, in the cerebral cortex in 2 cases of progressive supranuclear palsy. The majority of the neurofibrillary tangles were found in the smaller nerve cells of the third layer. The typical triangular form was rare, and most of them showed argyrophilic neurofibrillary filaments which coiled around the well-preserved nucleus. We concluded that their occurrence in the cerebral cortex is one of the morphological manifestations of the disease process.

Aged↗
PubMed1976

Effect of flupenthixol on depression with special reference to combination use with tricyclic antidepressants. An uncontrolled pilot study with 45 patients.

In an open, uncontrolled trial flupenthixol was administered to 45 patients with endogenous depression. The drug was markedly effective in eight patients, effective in nine patients, fairly effective in 12 patients, and ineffective or aggravating in 16 patients. Four patients showed transient manic symptoms. Dosage was 1-3 mg daily. In 36 patients flupenthixol was used in combination with previously administered tricyclic antidepressants, and in nine patients it was used alone. Clinical effect was quickly apparent. It appeared within 1 week in 63% and within 2 weeks in 93% of subjects. Side-effects were observed in 13 patients: insomnia, five patients; slight extrapyramidal symptoms, nine patients. Sedative-hypnogenic effects were rarely seen. In 71% of 17 patients in whom the drug was found to be markedly effective or effective, flupenthixol's influence on psychomotor retardation was particularly striking. Other clear benefits were relief of depressive mood, psychic anxiety, and agitation. It is recommended that flupenthixol is given, as supplementary medication, to patients (1) whose depressive symptoms other than psychomotor retardation have already improved with current tricyclic antidepressants, and (2) in whom, before antidepressant medication, psychomotor retardation is a principal feature.

Adolescent↗