Pathology of human organic mercury poisoning: Lessons from an autopsy case.

We had an opportunity to perform a general autopsy of a case with chronic organic mercury toxicosis in 2017. He had been engaged in synthesizing a variety of organic mercury compounds throughout the four years from 1966 and developed chronic organic mercury poisoning in 1969. Almost forty years on, he still remained to complain of persistent paresthesia at finger tips and tongue, and of narrowed visual field. Neurological examinations clarified a rise of two-point discrimination thresholds, a systemic increase of touch thresholds, constriction of the visual field caused by general visual depression, and sensorineural hearing loss while primary modalities of his somatic, visual, and auditory sensations were preserved. These symptoms and signs are characteristic of human organic mercury poisoning. Furthermore, he had difficulty in processing a lot of visual and auditory information at a time. His two-point discrimination thresholds and systemic elevation of touch thresholds were comparable to those of mild organic mercury poisoning cases. He had slight sensory ataxia, but not cerebellar ataxia. Brain [18F]-2-fluorodeoxyglucose positron emission tomography analysis exhibited marked hypometabolism at bilateral postcentral gyrus, striate cortex, and superior temporal gyrus, but not the cerebellum. Histopathological studies revealed considerable decrease of granular neurons and neuronal networks in bilateral primary somatosensory, visual, and auditory cortices. Those characteristic brain lesions fairly explain increase of thresholds of somatic, visual, and auditory sensations, and degradation of integrating sensory information. It is noted that damages to the peripheral nervous system and the cerebellum were not detected and that his intellectual faculties were preserved.

Minamata disease revisited: an update on the acute and chronic manifestations of methyl mercury poisoning.

The first well-documented outbreak of acute methyl mercury (MeHg) poisoning by consumption of contaminated fish occurred in Minamata, Japan, in 1953. The clinical picture was officially recognized and called Minamata disease (MD) in 1956. However, 50 years later there are still arguments about the definition of MD in terms of clinical symptoms and extent of lesions. We provide a historical review of this epidemic and an update of the problem of MeHg toxicity. Since MeHg dispersed from Minamata to the Shiranui Sea, residents living around the sea were exposed to low-dose MeHg through fish consumption for about 20 years (at least from 1950 to 1968). These patients with chronic MeHg poisoning continue to complain of distal paresthesias of the extremities and the lips even 30 years after cessation of exposure to MeHg. Based on findings in these patients the symptoms and lesions in MeHg poisoning are reappraised. The persisting somatosensory disorders after discontinuation of exposure to MeHg were induced by diffuse damage to the somatosensory cortex, but not by damage to the peripheral nervous system, as previously believed.

[Methylmercury causes diffuse damage to the somatosensory cortex: how to diagnose Minamata disease].

The first acute case of methylmercury (MeHg) poisoning by the consumption of fish arose in Minamata, Japan, in 1953. It was officially recognized and called Minamata disease (MD) in 1956. There are still arguments about the definition of MD in terms of its associated clinical symptoms and lesions even 50 years after the initial recognition of MD. Studies on this MD epidemic are reviewed along with its historical background. Since MeHg dispersed from Minamata to the Shiranui Sea, residents living around the sea had been exposed to low-dose MeHg through fish consumption for about 20 years (at least from 1950 to 1968). These chronic MeHg poisoning patients complained of paresthesia at the distal parts of their extremities and around the lips even 30 years after the cessation of exposure to MeHg of anthropogenic origin. The persisting somatosensory disorders after the discontinuation of exposure to MeHg were induced by diffuse damage to the somatosensory cortex, but not by damage to the peripheral nervous system, as previously believed. Based on these findings, symptoms and lesions in MeHg poisoning are reappraised.

Reappraisal of somatosensory disorders in methylmercury poisoning.

The first well-documented methylmercury (MeHg) poisoning by consumption of fish arose in Minamata, Japan in 1953. MeHg had dispersed from Minamata to the Shiranui Sea. The temporal changes in MeHg in the umbilical cords indicate that residents living around that Sea had been exposed to low-dose MeHg through fish consumption for about 20 years (at least from 1950 to 1968). They have complained of paresthesia at the distal parts of the extremities and around the lip even 30 years after the cessation of exposure to anthropogenic MeHg. The thresholds of touch and two-point discrimination of those residents and Minamata disease (MD) patients were examined using the quantifiable instruments. They could perceive the stimulation of touch although their touch thresholds significantly increased in comparison to those of the control people. Their touch thresholds increased at the proximal extremities and the trunks as well as at the distal extremities. The evenly distributed increases at both distal and proximal parts revealed that the persistent somatosensory disturbances were not caused by the injuries to their peripheral nerves. The thresholds of two-point discrimination, which are associated with the function of the somatosensory cortex, increased at both forefingers and the lip in both groups. Taking into consideration that, the apraxia limb kinetics, astereognosis and disorder of active sensation, which are all associated with damage to the somatosensory cortex, were detected, it is proposed that the persisting somatosensory disorders after discontinuation of exposure to MeHg were induced by diffuse damage to the somatosensory cortex.