Vigabatrin‐Induced Retinal Toxicity: Unraveling the Gamma‐Aminobutyrate–Vitamin B 6 Axis and Metabolic Crosstalk

Abstract

ABSTRACT Vigabatrin (VGB) is an antiseizure medication used as an add‐on therapy for refractory focal seizures. Despite its clinical efficacy, VGB use is limited by retinal toxicity that may lead to permanent visual loss. This narrative literature review aims to elucidate the emerging molecular and metabolic mechanisms underlying VGB‐induced retinal toxicity, with particular emphasis on the interplay among gamma‐aminobutyrate (GABA) accumulation, taurine depletion, ornithine metabolism dysregulation, and vitamin B 6 ‐dependent pathways to identify potential therapeutic targets for preventing visual impairment. A comprehensive literature search was conducted using PubMed, ScienceDirect, and Google Scholar. Current evidence indicates that VGB‐induced retinal toxicity arises from a complex interplay among GABA accumulation, taurine depletion, taurine transporter modulation, dysregulated ornithine metabolism, and vitamin B 6 –pyridoxal 5′‐phosphate (PLP)‐dependent metabolic alterations. Understanding this complex interplay between GABA–vitamin B 6 axis and metabolic crosstalk offers opportunities for safer therapeutic approaches and potential protective strategies for patients undergoing long‐term VGB therapy. Future research should focus on mechanistic studies, pharmacokinetic profiling, genetic studies, and longitudinal clinical investigations to maximize both seizure control and retinal safety.