Three weeks after recovery from an acute insecticide poisoning episode, a farmer develops symmetrical distal leg weakness with foot drop. Nerve conduction studies show a dying-back axonopathy. The pathogenesis of this delayed syndrome involves:
- A Inhibition of neuropathy target esterase (neurotoxic esterase) in axons ✓
- B Persistent inhibition of acetylcholinesterase at the neuromuscular junction
- C Immune-mediated demyelination triggered by the solvent carrier
- D Direct nicotinic receptor desensitisation
Explanation
Organophosphate-induced delayed polyneuropathy appears one to three weeks after exposure and results from phosphorylation and ageing of neuropathy target esterase, followed by a dying-back distal axonopathy. It is not caused by ongoing acetylcholinesterase inhibition, so it does not respond to atropine or oximes. The classic historical agent is tri-o-cresyl phosphate, responsible for the ginger jake paralysis epidemics.
Reference: Katzung's Basic and Clinical Pharmacology, 15th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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