Six weeks after surviving a severe poisoning by a specific insecticide, a farmer develops progressive weakness of distal limb muscles with foot drop, absent ankle jerks, and glove-and-stocking sensory loss. Nerve biopsy shows a central-peripheral distal axonopathy. The responsible mechanism is irreversible inhibition of:

• A Acetylcholinesterase at neuromuscular junctions
• B Butyrylcholinesterase in plasma
• C Neuropathy target esterase (neurotoxic esterase) ✓
• D Cytochrome oxidase in mitochondria

Explanation

Organophosphate-induced delayed polyneuropathy appears 2 to 4 weeks after exposure to certain OP compounds such as tricresyl phosphate, triorthocresyl phosphate (ginger jake paralysis) and some others. It results from phosphorylation and ageing of neuropathy target esterase (NTE), producing a dying-back distal axonopathy affecting long motor and sensory axons. It is independent of acetylcholinesterase inhibition and does not respond to oximes or atropine.

Reference: Katzung's Basic and Clinical Pharmacology, 15th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.