An infant with West syndrome is treated with vigabatrin with good seizure control. At follow-up the ophthalmologist documents concentric constriction of visual fields bilaterally. The mechanism of vigabatrin that underlies both its efficacy and this adverse effect is:

• A Blockade of T-type calcium channels in thalamic neurons
• B Irreversible inhibition of GABA transaminase, raising brain GABA levels ✓
• C Enhancement of slow inactivation of voltage-gated sodium channels
• D Positive allosteric modulation of synaptic GABA-A receptors

Explanation

Vigabatrin irreversibly inhibits GABA transaminase (GABA-T), the enzyme that degrades GABA, thereby increasing CNS GABA concentrations. This makes it effective against infantile spasms, where it remains a first-line agent, but retinal GABA accumulation causes progressive, often irreversible visual field constriction, mandating periodic perimetry. T-type channel blockade defines ethosuximide, and slow sodium inactivation defines lacosamide.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.