Early effects of methylmercury on the visual evoked response of the dog.

A disturbing characteristic of methylmercury (MeHg) intoxication is the preclinical "silent" stage. This stage is followed by the sometimes rapid onset of clinical signs such as peripheral sensory loss, motor difficulties, and visual and auditory impairment. The objective of this study was to search for "preclinical" changes in the electrophysiological activity of the central nervous system of dogs exposed to methylmercury chloride. Because of the prominence of the visual system in the MeHg literature, the visual evoked response (VER) was selected for evaluation. A dose rate of 500 microgram/kg/day po was expected to cause clinically apparent toxicosis in about 2 mon. After 1 week of exposure, a subtle distortion of the VER occurred. In a parallel group of dogs, blood mercury was 0.74 microgram/ml at this time, and brain mercury content was 1.28 microgram/g at the occipital cortex. Although the dogs continued to receive MeHg, VERs remained remarkably stable for the next 5 to 8 weeks, and then rapidly degraded during the nest few days as the dogs exhibited visual and motor disabilities. In many species, when brain Hg is about 15 microgram/g, clinical and histopathologic changes are usually present, and may even be detected at 8 microgram/g. Distortion of the VER at 1.28 microgram/g Hg at the visual cortex demonstrates that CNS changes exist during the "silent" stage of toxicosis, and at a brain Hg content suggesting physiologic dysfunction of neurons rather than neuronal death.