An Autopsy Case of Minamata Disease (Methylmercury Poisoning)—Pathological Viewpoints of Peripheral Nerves

Abstract

The outbreak of methylmercury poisoning in the geographi c areas around Minamata Bay, Kumamoto, Japan in the 1950s has become known as Minamata disease. Based on earlier reports and extensive pathological studies on autopsied cases at the Kumamoto University School of Medicine, destructive lesions in the anterior portion of the calcarine cortex and depletion predominantl y of granular cells in the cerebellar cortex came to be recognized as the hallmark and diagnostic yardstick of methylmercury poisoning in humans. As the number of autopsy cases of Minamata disease increased, it became apparent that the cerebral lesion was not restricted to the calcarine cortex but was relatively widespread. Less severe lesions, believed to be responsible for the motor symptoms of Minamata patients, were often found in the precentral, postcentral, and lateral temporal cortices. These patients also frequently presented with signs of sensory neuropathy affecting the distal extremities. Because of few suf ciently comprehensive studies, peripheral nerve degeneration has not been universally accepted as a cause of the sensory disturbances in Minamata patients. The present paper describes both biopsy and autopsy ndings of the peripheral nerves in a male sherman who died at the age of 64 years and showed the characteristic central nervous system lesions of Minamata disease at autopsy. A sural nerve biopsy with electron microscopy performed 1 month prior to his death showed endoneurial brosis and regenerated myelin sheaths. At autopsy the dorsal roots and sural nerve showed endoneuria l brosis, loss of nerve bers, and presence of Büngner's bands. The spinal cord showed Wallerian degeneration of the fasciculus gracilis (Goll's tract) with relative preservation of neurons in sensory ganglia. These ndings support the contention that there is peripheral nerve degeneratio n in Minamata patients due to toxic injury from methylmercury.

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

“…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). We tested whether MeHg exposure had an effect on AQP11 expressions in the brain.…”

“…It was hypothesized that the most vulnerable sites in experimental MeHg intoxication are in the cortices along deep sulci and fissures, and cerebral edema in the early stages might cause ischemia followed by acceleration of the neuronal injury around deep sulci (Shaw et al, 1979;Eto et al, 2001). MeHg-treated common marmosets showed lesions in the cerebrum, cerebellum, and peripheral nerves (Eto et al, 2001(Eto et al, , 2002. The common marmoset is an appropriate model for brain edema caused by MeHg, because this species has deep sulci in the form of the calcarine and Sylvian fissures.…”

Heavy metal poisoning: management of intoxication and antidotes

“…Granule cells in the cerebellum are lost, while neighboring Purkinje cells are preserved. Sensory fibers of the peripheral nerves may also be damaged [101,102].…”

Chemodosimeters for mercury(II) and methylmercury(I) based on 2,1,3-benzothiadiazole

“…Inorganic mercury species can damage the brain, heart, kidney, stomach, and intestines [3]. Because of lipid solubility and easy absorptivity, in the family of mercury species which take part in the biogeochemical cycle of mercury, methylmercury species (CH 3 HgX) are the most toxic species which can cause neurological damages [4], including fetal brain damage, DNA damage, cognitive and motion disorders, vision and hearing impairment and minamata disease [5]. Therefore, the detection of mercury species has received increasing attention in recent years.…”