Review Article: Pathology of Minamata Disease

Abstract

Minamata disease, or methylmercury poisoning, was first discovered in 1956 around Minamata Bay, Kumamoto Prefecture, Japan. A similar epidemic occurred in 1965 along the Agano River, Niigata Prefecture, Japan. The neuropathology of Minamata disease has been well studied; this review focuses on human cases of Minamata disease in Kumamoto Prefecture. Nervous system lesions associated with Minamata disease have a characteristic distribution. In the cerebral cortex, the calcarine cortex was found to be involved in all cases of Minamata disease, particularly along the calcarine fissure. The destruction of nerve tissue was prominent in the anterior portions of the calcarine cortex. Occasionally, the centrifugal route from the visual and visual association areas (internal sagittal stratum) showed secondary degeneration in prolonged cases after acute onset. Postcentral, precentral, and temporal transverse cortices showed similar changes, though they were less severe. Intense lesions in the precentral cortex caused the development of secondary bilateral degeneration of the pyramidal tracts. In the cerebellum, the lesions occurred deeper in the hemisphere. The granule cell population was most affected. In the peripheral nerves, sensory nerves were more affected than motor nerves. Secondary degeneration of Goll's tracts was occasionally seen in prolonged or chronic cases.

Increased expression of aquaporin-4 with methylmercury exposure in the brain of the common marmoset

“…AQP11 was found in Purkinje cells, hippocampal neurons of CA1 and CA2 and cerebral cortical neurons in the rat (Gorelick et al, 2006). The characteristic cerebellar alteration caused by MeHg poisoning in Minamata disease was the loss of granule cells with the presence of relatively well-preserved Purkinje cells (Eto, 1997). In some cases of MeHg-exposed common marmosets, granule cells and Purkinje cells were lost focally in the cerebellum with a proliferation of Bergman's glial cells (Eto et al, 2002).…”

Rescue of neuronal migration deficits in a mouse model of fetal Minamata disease by increasing neuronal Ca2+spike frequency

“…abnormal neuronal migration | congenital methylmercury poisoning D uring periods of fetal and early postnatal development, exposure to methylmercury (MeHg) induces congenital intoxication, leading to the development of characteristic neurological symptoms, including mental retardation, cerebellar ataxia, and cerebral palsy (1)(2)(3). This medical phenomenon is known as fetal Minamata disease (FMD).…”

Methylmercury Retards the Repair of Wounded Monolayer of Human Brain Microvascular Endothelial Cells by Inhibiting Their Proliferation without Nonspecific Cell Damage

“…& Fax: +81-76-229-6208; E-mail: t-kaji@ hokuriku-u.ac.jp MeHg in utero. 1,2) However, the mechanism for this difference remains unclear. In addition, the most typical problem appears to be the mechanism by which MeHg exhibits the toxicity, particularly in the neurons.…”