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.