A man presents with severe paraesthesiae (burning and tingling of lips, tongue, and extremities), profuse salivation, bradycardia, hypotension, and generalised weakness, progressing to ventricular arrhythmias. He consumed a herbal preparation. Post-mortem analysis identifies aconitine in the gastric contents. Aconitine causes toxicity primarily through which mechanism?

• A Irreversible sodium channel blockade preventing action potential generation
• B Persistent activation of voltage-gated sodium channels, preventing inactivation and causing maintained depolarisation ✓
• C Potassium channel activation causing hyperpolarisation and conduction block
• D Calcium channel blockade at L-type cardiac channels

Explanation

Aconitine (from Aconitum napellus and A. ferox —'Monkshood' or 'Bikh') binds to voltage-gated sodium channels in their open state and prevents their normal inactivation (closing). This causes persistent depolarisation of excitable membranes (nerve and cardiac). In the heart, prolonged depolarisation leads to ventricular fibrillation and bradyarrhythmias. Neurologically it produces paraesthesiae, motor weakness, and respiratory paralysis. The sensation of tingling starting at the lips and spreading centripetally is the classical prodrome. There is no antidote; treatment is supportive with anti-arrhythmics.

Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.