[Minamata disease: a neuropathological viewpoint].

Minamata disease (methylmercury poisoning) was first officially discovered around Minamata Bay in the Kumamoto Prefecture on May 1st, 1956. This year, a commemoration marking fifty years since this discovery of Minamata disease will be held in Minamata City. Over the years, new facts have gradually surfaced, especially after 1995, with the resolution of the political problems surrounding Minamata disease. For example, it was recently reported that large amounts of methylmercury were generated by the chemical processes of the Chisso acetaldehyde plant and later dumped directly into Minamata Bay. This report revealed the August 1951 switch from using manganese dioxide to ferric sulfide as a reaction promoter to maintain the activity of the Hg catalyst. As a result of this switch, the amount of methylmercury generated in the process rapidly increased. Thus, the true cause of the acute onset of Minamata disease in patients with a high-dose contamination of methylmercury was made clear. The severe contamination by methylmercury continued until 1968, when the plant finally stopped discharging its waste water into Minamata Bay. In 1996, the National Institute for Minamata Disease started an experimental study of methylmercury poisoning using the common marmoset. Results from this study showed that the lesions characteristic of the central nervous system in cases of acute methylmercury poisoning were promoted by brain edema, while those of the peripheral nerves were caused by axonal degeneration. Peripheral nerves were regenerated in two animals after two and a half years. Lesions characteristic of Minamata disease are systematically found throughout the nervous system. These lesions are found in the calcarine areas of occipital lobes, the pre- and post-central lobes, and the temporal transverse gyri. Milder and more diffuse lesions are also found in the cerebrum, where secondary degeneration of the central parts of white matter and internal sagittal stratum are due to primary damage of neurons. Purkinje and granular cells decrease in number in the cerebellum depending on the dose of methylmercury and the duration of methylmercury exposure. In the spinal cord, there is no primary change, but secondary degeneration is found on pyramidal tracts due to damage of the motor neurons of the precentral cortices. Additionally, secondary degeneration of Goll's tract is seen due to the primary degeneration of sensory nerve fibers including ganglion cells, sciatic nerves, and sural nerves. The experiments on the methylmercury-treated common marmosets provided every feature of pathological change found in the nervous system in human autopsy cases, depending on the dose of methylmercury.