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Limiting Retinal Toxicity of Vigabatrin in Children with Infantile Spasms

Commentary Infantile spasms (West syndrome) is a catastrophic epilepsy affecting infants. Prompt recognition and treatment of infantile spasms (within 3–4 weeks after onset) using effective therapy are essential for good seizure and developmental outcome. Effective treatments include hormonal agents (ACTH or prednisolone) and vigabatrin (1). Vigabatrin (VGB) is particularly effective in children with infantile spasms (IS) due to tuberous sclerosis and preferred over hormonal treatments in this setting (2). Vigabatrin use is associated with risk of developing visual field loss, which first begins as a bilateral nasal wedgeshaped field defect, progressing eventually to bilateral concentric loss of vision. Typically, the affected individual is unaware of the field defect until it becomes severe. Ophthalmologic monitoring is recommended at baseline, every 3 months during treatment, and 3 to 6 months after completing therapy. In adults, the interval should be at least every 6 months (3, 4). It is uncommon for a patient to develop a visual field defect on VGB in less than 3 months; therefore, VGB should be discontinued if there has not been meaningful seizure reduction after 3 months of treatment (3). Willmore et al. reviewed data from Vigabatrin clinical trials for the treatment of infantile spasms and refractory complex partial seizures in adults. Confirmed visual field defects were noted in 25%-50% of adults and in 15% of children following 9-11 months of treatment (3). Maguire et al. examined the prevalence of visual field defects in 1,678 vigabatrin-treated patients from 32 published studies (included adults and older children) using perimetry. Visual field loss occurred in 44% of adults, 34% of children, and 7% of control subjects. The relative risk for visual field loss was 4.0; larger mean cumulative dose of VGB and increasing age were associated with a higher proportion of visual field loss (4). In a retrospective study of 93 adult patients taking VGB for ≥6 months, visual field constriction occurred in 52.7% of patients and as early as 1.1 years. There was no correlation of visual field defects with either the maximum or cumulative VGB dosage or duration of exposure. The authors suggested that the retinopathy was an idiosyncratic drug response due to a genetic predisposition (5). Visual field defects also occur in patients with refractory epilepsy not on VGB, especially those taking gabaergic AEDs such as phenobarbital or tiagabine (6). Visual field testing in young children is often difficult. White Sphere Kinetic Perimetry has been done successfully in developmentally delayed children using a larger object (6 vs 1.7 for Goldman Kinetic Perimetry); 8/28 children or 29% were found to have visual field defects in this study (7). However, 20 Vigabatrin Retinal Toxicity in Children With Infantile Spasms: An Observational Cohort Study.