Haruo Watanabe

ENCEPHALOMYELOPATHY DUE TO AN ORGANIC MERCURY COMPOUND.

OUR INTEREST in the toxicity of organic metal compounds was stimulated by reports of organic tin intoxication in 19551 and the “Minamata disease,” presumably caused by organic mercury compound,2 which was reported in 1957.3 An excellent review on the clinical, histopathologic, and epidemiologic aspects of this disease has been published.4 A few reports concerning the intoxication of man by organomercury compounds indicate the cause to be the inspiration of the fumes of agricultural drugs in most cases. In 1940, Hunter and associates5 reported 4 cases of intoxication by methylmercury phosphate or nitrate. Fourteen years later, Hunter and Russell6 described detailed histopathologic findings in the brain of one of the patients in the previously reported cases. The microscopic changes in the brain were most pronounced in the occipital pole region of the cerebrum and palleocerebellum. Constriction of the visual fields may be attributed to atrophy of the area striata and, according to their statement, the ataxia could be correlated with changes in the cerebellar cortex. Brown7 reported clinical and autopsy findings in a case of phenylmercury acetate intoxication which showed a clinical picture resembling amyotrophic lateral sclerosis. Microscopic findings showed degeneration of motor cells in the anterior horn and the lateral column of the spinal cord, without changes in the brain. Kantarjians also pointed out the clinical resemblance to amyotrophic lateral sclerosis in 11 cases of definite ethylmercury ptoluene sulfonanilide intoxication. This paper is a report of 3 cases of intoxication caused by the application of a solution containing organic mercury compound for the treatment of a widespread fungus skin infection.

Studies on hepatocerebral disease: III. Hepatolenticular degeneration in Japan, with studies on copper metabolism

Age in Years Fig. 1. Age and sex of patients in Japan with Wilson’s disease in accord with American and European studies, that a disturbance of copper metabolism also plays a major role in the pathogenesis of Wilson’s disease in Japan. Similar but rare cases with clinicopathologic findings suggestive of Wilson’s disease but without an abnormality of copper metabolism have also been seen. Wilson’s disease used to be considered a very rare disease in Japan. However, much interest was aroused in this disease recently, and 62 cases have been reported in the past ten years. The inference is well grounded that many more unreported cases must be present in this countrv. The distribution of the patients showed no pnrticular grouping, and the cases were found in almost all sections of Japan. The heredity of 43 families was investigated in regard to this condition. Familial occurrence of the disease or blood relationship between father and mother of the patient was demonstrated in 15 families, or 35%. In the latter cases, most marriages were between cousins.