[STUDY OF THE ETIOLOGY OF AMYOTROPHIC LATERAL SCLEROSIS].
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Biomedical subjects
Publications and source records attributed to N V KONOVALOV.
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Although various hypotheses have been put out as to the etiology of amyotrophic lateral sclerosis, they do not seem to date to have been substantiated by experimental evidence. As the incidental outcome of studies on possible carcinogenic processes, the authors of this paper have obtained experimental data indicating the possibility of reproducing amyotrophic lateral sclerosis in monkeys by administering extracts from the spinal cord of persons who have died of the disease. The illness in monkeys is marked by a long incubation period, which may be of five years or more, and it is very similar to the disease in man in its clinical and pathological picture. The experimental evidence strongly suggests that this disease is of virus origin. The virus-like agent discovered has been passaged twice in monkeys without consequent attenuation; it is not pathogenic for mice and other laboratory animals.The authors point out that, before final conclusions can be drawn, serological and immunological confirmation is required. Research is now proceeding to that end.
A recent report from the Tuberculosis Chemotherapy Centre, Madras, showed that a vitamin-B-complex preparation containing a small amount of pyridoxine (as well as aneurine hydrochloride, riboflavine, nicotinamide, panthenol and cyanocobalamin) was effective in the treatment of peripheral neuropathy caused by daily high-dosage (12.5-15.2 mg/kg body-weight) isoniazid therapy of pulmonary tuberculosis. The present report gives results which show that the B-complex preparation is fully effective in preventing peripheral neuropathy in patients receiving the same high dosage of isoniazid, and that this is due to the small pyridoxine content of only 6 mg daily, and not to any of its other constituents. The low cost of this small dose of pyridoxine makes high-dosage isoniazid therapy, given in combination with other drugs or alone, a possible proposition in developing countries.Studies in the Centre have produced clear evidence that there is an increase in the frequency of peripheral neuropathy when the dosage of isoniazid is increased from 7.8-9.6 mg/kg body-weight to 12.5-15.6 mg/kg daily, and that its incidence is higher among slow than among rapid inactivators of isoniazid.The studies also show that increasing the dosage of isoniazid when given alone from a moderate daily dosage of 7.8-9.6 mg/kg to the high daily dosage of 12.5-15.6 mg/kg has not materially altered the radiographic or the bacteriological response to treatment.
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