Vigabatrin raises brain GABA concentrations through a distinctive biochemical action. Its antiepileptic mechanism and its most feared adverse effect respectively are:

• A Irreversible inhibition of GABA transaminase and concentric visual field constriction ✓
• B Blockade of GABA reuptake transporter GAT-1 and retinal pigmentary degeneration
• C Allosteric potentiation of GABA-A receptors and optic neuritis
• D Irreversible inhibition of glutamate decarboxylase and colour vision loss

Explanation

Vigabatrin is a structural analogue of GABA that irreversibly inhibits GABA transaminase (GABA-T), the enzyme degrading GABA, thereby increasing synaptic GABA. Its use-limiting toxicity is bilateral concentric constriction of the visual field, occurring in up to a third of patients, requiring baseline and periodic perimetry. Option B describes tiagabine, which blocks the GAT-1 reuptake transporter. Vigabatrin does not act on GABA-A receptors or on glutamate synthesis.

Reference: Goodman and Gilman The Pharmacological Basis of Therapeutics, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.