17 workers in a thermometer factory exposed to mercury for periods ranging from 1 to 40 years all had high urine and blood mercury levels on undergoing electromyographic examination. All were clinically free from central and peripheral nervous symptoms. 88% had subclinical neuropathy, mainly distal and axonal. There was no correlation between severity of the neuropathy and blood and urine mercury levels or between severity of neuropathy and duration of exposure to mercury. The presence of a subclinical neuropathy in symptomless workers exposed to mercury is perhaps the most reliable index for the detection of the early toxic effects of mercury on the peripheral nerve fiber when it is probably still reversible.
Two cases of clinically and electromyographically proven ethylene oxide neuropathy occurred among 12 workers at the Lecco Hospital Sterilization Center. Cessation of exposure to the gas, which had lasted for two years, was followed by swift remission of the symptoms and complete normalisation of the EMG record at follow-up six months later. The paucity of published data on the subject may well mean that the real risk of ethylene oxide toxicity is being underrated.
The aim of this study was to investigate the possible influence of arteriovenous fistula (AVF) on nerve conduction velocity in patients on intermittent hemodialysis and its relevance to the pathogenesis of carpal tunnel syndrome (CTS). The data on 22 patients showed no statistically significant differences in the electrographic parameters considered. This suggests that AVF by the end-to-end method plays no significant part in the alteration of nerve conduction. Possibly radial steal phenomena, which occur with other types of AVF, are at least partly responsible for the reported cases of CTS.
Although amitriptyline is not usually regarded as toxic to the peripheral nervous system (PNS) and is even prescribed by some for neuropathic pain, there are sporadic reports of peripheral neuropathy following overdose or prolonged use of the drug. The scarcity of data leads us to report a case we have followed for 3 years clinically and electromyographically. A 54 year old man on oral amitriptyline 150 mg uninterruptedly for 2 years consulted us for lower limb paresthesias and was found on clinical examination to have reduced ankle jerks and mild distal global hypoesthesia. EMG yielded a pattern of sensorimotor neuropathy compatible with axonal disease in all four limbs. The history was unremarkable and the laboratory data were within normal limits. After discontinuation of amitriptyline therapy both the clinical and EMG pattern gradually normalized. We draw attention to the possible risk, infrequent though it is, of PNS neurotoxicity of a widely used drug reputedly harmless from this point of view.
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