Neurotoxic Effects of Organohosphorus Insecticides

TLDR

Organophosphorus insecticide poisoning causes acute cholinergic neurotoxicity and delayed neurotoxic effects that appear two to three weeks later. In 10 patients exposed to fenthion, monocrotophos, dimethoate, or methamidophos, paralysis of proximal limb, neck flexors, cranial nerves, and respiratory muscles developed 24–96 h after the cholinergic phase, lasting up to 18 days and sometimes requiring ventilatory support. One patient developed delayed polyneuropathy, three died, and electromyography revealed a postsynaptic neuromuscular junction defect underlying the intermediate syndrome that emerged after the acute cholinergic crisis but before delayed neuropathy.

Abstract

Acute neurotoxic effects during the cholinergic phase of organophosphorus insecticide poisoning and delayed neurotoxic effects appearing two to three weeks later are well recognized. We observed 10 patients who had paralysis of proximal limb muscles, neck flexors, motor cranial nerves, and respiratory muscles 24 to 96 hours after poisoning, after a well-defined cholinergic phase. The compounds involved were fenthion, monocrotophos, dimethoate, and methamidophos. Four patients urgently required ventilatory support. The paralytic symptoms lasted up to 18 days. A delayed polyneuropathy later developed in one patient. Three patients died. Electromyographic studies showed fade on tetanic stimulation, absence of fade on low-frequency stimulation, and absence of post-tetanic facilitation, suggestive of a postsynaptic defect. This neuromuscular junctional defect may have been the predominant cause of the paralytic symptoms, with neural and central components contributing to various degrees. Our patients appeared to have a distinct clinical entity (a so-called intermediate syndrome) that developed after the acute cholinergic crisis and before the expected onset of the delayed neuropathy.