Is the devil we know the lesser of two evils?

Vigabatrin (γ-vinyl GABA), an irreversible inhibitor of GABA transaminase, was first licensed as an antiepileptic agent in Britain and the Republic of Ireland in 1989. Since then, it has been accepted into mainstream clinical practice in the care of adult and pediatric patients in over 40 countries.1 In 1998, the Food and Drug Administration (FDA) notified the manufacturer, Hoechst Marion Roussel (Kansas City, MO), that vigabatrin is “not approvable” based on the data submitted thus far, in light of some new concerns about this drug. These concerns include reports of severe, persistent, visual field defects noted in association with vigabatrin.2,3 Interestingly, the development of vigabatrin in the United States was delayed for several years owing to earlier concerns about white matter toxicity (intramyelinic edema) encountered in experimental animals, then resumed when such toxicity could not be demonstrated in humans.1 In this issue of Neurology, Cossette et al. compare vigabatrin with the traditional agent corticotropin (ACTH) in the treatment of infantile spasms (West syndrome).4 The report is based on a retrospective …