Forensic Medicine · Forensic Toxicology (General, Organophosphorus, Corrosives, Metals, Narcotics, Alcohol)

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
Correct answer: A. Inhibition of neuropathy target esterase (neurotoxic esterase) in axons

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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