Electrophysiological studies of peripheral nerves in patients with organic mercury poisoning

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

“…Electrophysiological and histopathological results of MD patients were comparable to those of control people ( Table 1). The electrophysiological results gotten by Nagaki are consistent with those of MeHg poisoning studied in Iraq [19,30,43]. In addition, Tokuomi et al examined short-latency somatosensory evoked potentials (SSEP) in MD patients more than 10 years after the cessation of exposure to MeHg, and clarified that lesion of persistent sensory disorder in MD patients is in the somatosensory cortex, but neither the peripheral nerves nor the spinal cord nor the thalamus [39] (Fig.…”

Methylmercury poisoning, Clinical follow-up and sensory nerve conduction studies.

“…Touch, pain, temperature, and vibration sense were preserved with marked loss of position sense, two-point discrimination, and stereognosis. The relatively normal sensory and motor nerve conduction velocities in all our patients ( Table) and the preservation of deep tendon reflexes provide evidence suggesting that the late sensory symptomatology of methylmercury poisoning may not be on the basis of peripheral nerve lesions (LeQuesne et al, 1974;Rustam and Hamdi, 1974). The combination of findings on sensory examination is more compatible with a cortical aetiology.…”

“…Peripheral nerve abnormalities have not been demonstrated electrophysiologically in humans with methylmercury poisoning (LeQuesne et al, 1974;Pazderova et al, 1974;Von Berg and Rustam, 1974). A recent report has suggested that some patients may have abnormalities at the myoneural junction (Rustam et al, 1975).…”

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

“…In spite of overwhelming evidence in support of organic mercury inducing peripheral neuropathy in at least in some species, most importantly including humans, some skepticism has remained (12). Our attempt herein is to present an overview of the pathological ndings in the central and peripheral nervous system of Minamata disease patients through a case presentation, and to reemphasize the occurrence of peripheral neuropathy in human Minamata disease patients and in common marmosets, which show lesions very similar to those of human patients (6).…”