Vigabatrin is an antiepileptic used for infantile spasms (West syndrome) and as adjunctive therapy for focal seizures. Its mechanism of action is:

• A Blocks voltage-gated sodium channels in use-dependent manner reducing repetitive firing
• B Enhances chloride conductance at GABA-A receptors by prolonging channel opening frequency
• C Irreversibly inhibits GABA transaminase (GABA-T), increasing synaptic GABA concentrations ✓
• D Blocks glutamate AMPA receptors reducing excitatory neurotransmission

Explanation

Vigabatrin (gamma-vinyl GABA) is a structural analogue of GABA that acts as an irreversible mechanism-based inhibitor (suicide inhibitor) of GABA transaminase (GABA-T), the enzyme that degrades GABA in GABAergic nerve terminals. By permanently inactivating GABA-T, vigabatrin causes accumulation of GABA at synaptic terminals, enhancing inhibitory tone. The irreversible mechanism means new enzyme must be synthesised for GABA levels to normalise after discontinuation. Vigabatrin's major adverse effect is peripheral visual field loss (retinal toxicity), requiring regular visual field monitoring.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.