Abstract

In 1987, 10 patients were reported to have developed facial, proximal limb, and respiratory muscle weakness. Because this symptom complex occurs in the interval between the acute cholinergic crisis and the possible development of a delayed motor neuropathy called organophosphate-induced delayed neuropathy, this new entity was termed the intermediate syndrome (IMS). The acute cholinergic crisis is because of the inhibition of acetylcholinesterase (AChE), which is clinically most important, and the delayed neuropathy has been linked to inhibition of a separate esterase termed the neuropathy target esterase or neurotoxic esterase. The pathogenesis of IMS was unclear and the question arose whether IMS bore a separate structure-activity relationship. Treatment was mainly symptomatic. Atropine did not seem to influence the course of IMS. No definite mechanism of IMS was identified, but the authors wondered whether the necrotizing myopathy was induced by acute organophosphate poisoning in patients. A definite therapeutic regimen that successfully treats or ideally prevents IMS is not available. In fact, a high index of suspicion allowing early diagnosis and intensive care facilities for respiratory monitoring, tracheal intubation, and artificial ventilation, when necessary, are the best guarantees for a favorable outcome. The clinical recognition of IMS is no longer problematic for most medical workers in the field, and considerable progress toward the elucidation of the underlying mechanisms has been made in the 10 years following the initial description.

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