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Biomedical subjects

H Tanabe

Publications and source records attributed to H Tanabe.

At least 361 records · Page 20Linked to original sources
PubMed1983

A clinico-pathological study of chronic hereditary motor neuropathy.

Forty cases of chronic hereditary motor neuropathy (CHMN) were divided into five categories according to the distribution of muscle atrophy; they were proximal, facioscapulohumeral, bulbospinal, distal and scapuloperoneal forms. Their clinical features and laboratory data were analysed, and muscle biopsies from 32 of them were studied by histological, histochemical and electron microscopical methods. An attempt at quantitative assessment of the histological changes was also made. All muscle biopsies showed a mixture of neurogenic and 'myopathic' changes in varying proportions. They showed more 'myopathic' changes than Werdnig-Hoffmann's disease, amyotrophic lateral sclerosis and other neurogenic atrophies except Charcot-Marie-Tooth disease. There was marked variation in the average number of atrophied muscle fibers contained in grouped atrophy. Frequently, deranged internal structure of the muscle fibres was revealed both by histochemical and electron microscopical methods. Based on the evidence of heterogeneity of CHMN in respect of genetics, clinical features and histological changes, it was speculated that CHMN represents a group of diseases which involves primarily different parts of the motor units.

Adolescent↗
PubMed1983

[Bilateral crossed visuomotor ataxia--a case report].

We observed a 55 y.o. right-handed woman, who was suspected of splenium tumor (glioblastoma?) by CT scan and presented bilateral crossed visuomotor ataxia proposed by Rondot et al. Left unilateral apraxia and agraphia were not found, but left unilateral hemialexia was evident by tachistoscopic examinations. In regard to bilateral crossed visuomotor ataxia, we suggested that at least there might be three possible hypotheses about its realization mechanism. (1) Callosal lesion might disconnect heterotopical fibers which runs from one occipital lobe to another frontal lobe. (2) Integrated information of visual and proprioceptive inputs in the parieto-occipital regions could not be transferred mutually to other side of the brain. (3) Functional dissociation between visual perception of "moving" and that of "position" might be the cause of this symptom. Former could be transferred via subcallosal pathway, but latter not transferred due to the callosal lesion. Hypothesis (1) could not explain, at least, "positive aspects" of this symptom, and which hypothesis is most probable might not be decided at present, because anatomical evidence and patho-plastic mechanism are not yet clarified.

Ataxia↗
PubMed1982

[Broca's area and Broca's aphasia: based on the observations of two cases with the lesions involving Broca's area].

Recently, the relation between Broca's area and Broca's aphasia has come into notice again. We investigated two right-handed patients without Broca's aphasia in spite of the presence of lesions involving Broca's area after hemorrhagic infarction. In addition, the clinical findings, the clinical courses and the sites of lesions of two cases were quite similar as follows. They showed no motor deficits and no other abnormal neurological findings from the beginning of the strokes. From the near muteness in the initial stage, speech began to improve gradually. And then, they demonstrated so called transcortical motor aphasia. Namely, repetition and reading aloud were excellent and articulations were normal without phonetic disintegration and dysprosody in contrast to the sparse and limited spontaneous speech. Comprehension was well preserved. Anomia was present and the ability to generate word lists was so poor that, for instance, only two animal names were listed in one minute. Mild to moderate agraphia was present. Agrammatism and buccofacial apraxia were not associated. Afterwards, the two patients showed rapid amelioration. About one month later after the stroke, only a slight difficulty in word finding and mild agraphia remained. In both cases, the lesions confined predominantly to the cortical and subcortical areas in the left posterior part of both the third and the second frontal gyri were confirmed by computerized tomography. According to the evidence from our two cases and to the literature, it may be concluded that the lesion restricted to the posterior part of the third and second frontal gyri in the dominant hemisphere produces a subtype of transcortical motor aphasia and that the lesion restricted to the posterior part of the third frontal gyrus (Broca's area) does not lead to phonetic disintegration.

Aged↗