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Biomedical subjects

S Inada

Publications and source records attributed to S Inada.

106 records · Page 6Linked to original sources
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Kimura's disease.

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Humans↗
PubMedDate not supplied

Rheumatoid arthritis associated with methotrexate-induced pneumonitis: improvement with i.v. cyclophosphamide therapy.

Pneumonitis is one of the most serious adverse effects associated with low-dose weekly methotrexate (MTX) therapy. Immediate cessation of MTX, and the introduction of oxygen therapy and glucocorticoids usually results in a dramatic improvement in the pulmonary toxicity. We report here a case of MTX-induced pneumonitis in a patient with rheumatoid arthritis (RA). Severe hypoxemia and interstitial infiltration in both lung fields did not respond to the withdrawal of MTX and the administration of oxygen and steroid pulse therapy. When intravenous cyclophosphamide (CYC) pulse therapy was initiated, however, rapid physiologic and radiographic improvement was seen. Our case suggests that CYC treatment may have a beneficial effect on MTX-induced pneumonitis that is resistant to steroid therapy.

Aged↗
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Electromyographic analysis of canine distemper myoclonus.

Canine distemper myoclonus was electromyographically analysed to throw more light upon the condition without invasive surgical intervention. Although myoclonus seemed to occur synchronously in many muscles, the onset of myoclonus appeared to be slightly earlier in one or two particular muscles and, furthermore, myoclonus did not arise temporally in descending or ascending order along the neuroaxis. Myoclonus-like discharges were evoked by tendon-tapping and this feature disappeared after cessation of myoclonus. In successive myoclonic bursts, a significant positive correlation was noted between the silent period and the subsequent discharge period, independently of the level of consciousness, i.e., the longer the silent period, the longer the subsequent episode of myoclonus. This correlation was re-established very early after recovery from anesthesia with halothane, when electroencephalograms showed slow waves. These results strongly indicate that the lower motor neurons may be the primary site responsible for the genesis of canine distemper myoclonus.

Animals↗
PubMedDate not supplied

Canine distemper myoclonus and sleep: observation of a case.

Evolution of myoclonus was analysed electromyographically throughout quiet wakefulness, NREM sleep and REM sleep in a dog with canine distemper myoclonus. Compared with quiet wakefulness, the frequency of myoclonus was decreased and the intensity of discharges in individual myoclonic bursts was also lowered during NREM sleep. When NREM sleep shifted to REM sleep, neither of these parameters was noticeably altered. However, as REM sleep continued, the former was increased markedly and the latter was further attenuated. In general, violent motor activity was concurrent in the limbs, trunk and/or head. Thus, the increase in the frequency of myoclonus seemed to be similar in nature to the phasic event during REM sleep. This indicated that lower motoneurons producing myoclonic discharges responded well to supraspinal influences. In successive myoclonic bursts, a significant and consistent positive correlation existed between the silent period and the subsequent discharge period throughout the three different levels of consciousness, that is, the longer the silent period, the longer the subsequent episode of myoclonus. Therefore, this feature may be intrinsic to myoclonic firing of lower motoneurons in canine distemper myoclonus. These findings may support the idea that hyperexcitability of the lower motoneurons is primarily responsible for the genesis of canine distemper myoclonus.

Animals↗