Vigabatrin is effective in infantile spasms, particularly those associated with tuberous sclerosis. Its antiepileptic mechanism and its most serious limiting toxicity are respectively:

• A Blockade of GAT-1 GABA reuptake; hepatotoxicity
• B Irreversible inhibition of GABA transaminase; irreversible concentric visual field constriction ✓
• C Enhancement of GABA-A receptor opening frequency; Stevens-Johnson syndrome
• D Blockade of synaptic vesicle SV2A protein; retinal ganglion cell apoptosis with optic neuritis

Explanation

Vigabatrin is a structural analogue of GABA and acts as an irreversible, mechanism-based suicide inhibitor of GABA transaminase, raising cerebral GABA concentrations. Its major limitation is bilateral concentric visual field constriction, which is often asymptomatic and may be irreversible, mandating baseline and periodic visual field testing. Option A describes tiagabine, which inhibits GABA reuptake via GAT-1, and option D describes retinal toxicity wording closer to levetiracetam's target mixed with another drug's ocular profile.

Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.