The clinical neurophysiology of organophosphate poisoning

Abstract

Clinical nuerophysiological studies are presented of the effects of oral pyridostigmine bromide on normal neuromuscular transmission. This drug has recently been identified as providing an effective prophylaxis against accidental exposure to organophosphate anticholinesterases. In addition, it has also found use in clinical anaesthesia to reverse the effects of non - depolarizing muscle relaxants. Experiments are reported which investigate the action of pyridostigmine and low doses of the organophosphate sarin on single fibre electromyography (SFEMG) in man. Further studies examine the actions of pretreatment with pyridostigmine on muscle relaxation produced by the non - depolarizing relaxant alcuronium in the isolated human forearm. Pyridostigmine produces little change in SFEMG but jitter increases were detected after sarin exposure. In the isolated forearm pyridostigmine pretreatment did not affect degree of relaxation produced by alcuronium. The degree of fade produced on repetitive stimulation differed between onset and recovery of relaxation. This relationship may be affected by pyridostigmine. These results are discussed in relation to recent knowledge of the electrophysiological and structural actions of anticholinesterases at the skeletal neuromuscular junction and to hypotheses of the mechanism of neuromuscular fade.

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