PATHOLOGY OF MINAMATA DISEASE

Minamata disease, or methylmercury poisoning, was first discovered in 1956 around Minamata Bay, Kumamoto Prefecture, Japan. a similar epidem ic occurred in 1965 along the Agano River, Niigata Prefecture, Japan. The neuropathology of Minamata disease has been well studied; this rev iew focuses on human cases of Minamata disease in Kumamoto Prefecture. Nervous system lesions associated with Minamata disease have a charac teristic distribution. In the cerebral cortex, the calcarine cortex wa s found to be involved in all cases of Minamata disease, particularly along the calcarine fissure. The destruction of nerve tissue was promi nent in the anterior portions of the calcarine cortex. Occasionally, t he centrifugal route from the visual and visual association areas (int ernal sagittal stratum) showed secondary degeneration in prolonged cas es after acute onset. Postcentral, precentral, and temporal transverse cortices showed similar changes, though they were less severe. Intens e lesions in the precentral cortex caused the development of secondary bilateral degeneration of the pyramidal tracts. In the cerebellum, th e lesions occurred deeper in the hemisphere. The granule cell populati on was most affected. In the peripheral nerves, sensory nerves were mo re affected than motor nerves. Secondary degeneration of Goll's tracts was occasionally seen in prolonged or chronic cases.