Between October 1972 and October 1973, the first nationwide survey of the multiple sclerosis group of diseases in Japan was performed by the Multiple Sclerosis Research Committee of Japan, supported by the Japan Ministry of Health and Welfare. Reports on 1,084 patients with the multiple sclerosis group were collected: 509 patients with multiple sclerosis, 82 with Devic's disease, 357 with "multiple sclerosis possible," and 136 with "other or unclassified demyelinating diseases." The natural history in the present nationwide series of multiple sclerosis patients showed considerable similarity to that of patients in Western countries, suggesting that multiple sclerosis in Japan is essentially the same as that in the Western countries. However, the previously reported special characteristics of Japanese multiple sclerosis patients, namely, a higher rate of visual impairment at onset, a higher rate of optic nerve involvement during the course of illness, and a higher rate of Devic's disease, were reconfirmed in the present series.
Serum fatty acid compositions were determined in 21 Japanese patients with multiple sclerosis and 14 neurological controls. No statistical difference was found either for linoleic acid or for arachidonic acid between the 2 groups. It may be that neither serum linoleic acid nor arachidonic acid is inevitably associated with the pathogenesis of multiple sclerosis.
Circadian variations of plasma cortisol were studied in four different groups of subjects; 17 patients with prolonged coma, 3 patient with tetraplegia with alert consciousness and without body movement, 4 patients with stabilized chronic infection with alert consciousness and with normal body movement, and control subjects consisting of 7 healthy volunteers and 5 patients with various neuromuscular disease without disturbance of con sciousness, motor dysfunction or infection. The maximum level of plasma cortisol attained during the circadian variations was low in prolonged coma, whereas the minimum level was high in prolonged coma, as compared to other three groups. The amplitudes between the maximum and the minimum level were significantly smaller in prolonged coma than in control (p<0.005). The tendency that the maximum level appeared at early morning and the minimum at late evening was similarly observed in both prolonged coma and control groups suggesting that there is no phase shift of the circadian rhythm of cortisol in prolonged coma. The responses of plasma TSH to synthetic TSH-releasing hormone or those of plasma cortisol to ACTH were not different between prolonged coma and control, suggesting that the reduced amplitude in prolonged coma is not attributed to the function of the patients' pituitary and/or adrenal cortex. Also, there were no differences in diurnal variations in plasma glucose or non-esterified fatty acid between the prolonged coma and control, nevertheless the former was fed with liquid food via a i asal tube. Therefore, highly significant reduction of the amplitude of circadian variation of cortisol in prolonged coma may not be due to exogenous factors, such as a poverty of body movement, complications due to chronic infec tion, or tube feeding. The results seem to suggest that the reduced amplitude of the circadian variations in plasma cortisol may have relation to the unconsciousness of prolonged coma due to severe damage to the central nervous system.
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