A pathological study of prolonged cases of Minamata disease. With particular reference to 83 autopsy cses.

This study consists of 83 autopsy cases including 64 prolonged cases of Minamata disease. Lesions were severe in the prolonged cases with an acute onset, while they tended to be mild in those with chronic onset. Cerebral cortex showed loss of nerve cells in many of the former, with the cortex often being in a loosening or spongy state, while the thinning-out or decrease of neurons not exceeding 30% of all cells was frequent in the latter. Glial reaction was also intense in the former, but relatively weak in the latter; gradual loss of degenerative neurons without glial reaction was not rare. A given selectivity was found in the localization of lesions of the cerebral cortex, but it was not so conspicuous in those with a chronic onset as in those with an acute onset. Secondary changes corresponding to the lesions of the cortex appeared in the medulla. Cerebellar lesions in the chronic onset cases, as compared with those in the acute onset ones, were milder. The selectively localized area was diminished; the nodulus, uvula and lingula of the vermis and the medial surface of the semilunar lobules were the most likely to be damaged. Of the spinal peripheral nerves, damages to the spinal sensory nerve were found, which were more predominant than those to the motor nerve system, and in which was noted prominent regeneration and repair. The deposited mercury found in organs tended to remain in the nervous system and the kidneys during the prolonged course of this disease, and the prolonged accumulation of mercury in the nervous system appeared to have an influence on the pathogenesis of chronic Minamata disease.