Botulinum toxin type A produces its therapeutic effect in benign essential blepharospasm by which mechanism?
- A Blocking sodium channels in motor axons
- B Competitive antagonism of nicotinic receptors on the muscle fiber
- C Cleaving SNAP-25 and preventing acetylcholine release at the neuromuscular junction ✓
- D Inhibiting acetylcholinesterase in the synaptic cleft
Explanation
Botulinum toxin A is internalized by motor nerve terminals and cleaves SNAP-25, a protein of the SNARE complex, thereby preventing fusion of acetylcholine vesicles with the presynaptic membrane. Chemodenervation weakens orbicularis oculi spasm for roughly 3 months, after which sprouting restores transmission and injection is repeated. Competitive receptor blockade is the action of curare-like agents, and anticholinesterases such as pyridostigmine increase acetylcholine and would worsen spasm.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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