Vigabatrin is an enzyme-activated, irreversible inhibitor of γ-aminobutyric acid (GABA) aminotransferase, which causes a marked increase in cerebral GABA concentration and a resulting anticonvulsant action. Recovery from its effects requires the synthesis of new enzyme, and this may take several days following a single dose. The pharmacokinetics of vigabatrin are not a good guide to its duration of action. It is cleared rapidly by renal elimination (giving a plasma half-life of approximately 7 to 9 hours), and therefore the effect of the drug long outlasts its presence in the body. Plasma drug level monitoring is therefore of little value in regulating vigabatrin therapy. The drug is not bound to plasma proteins. Interactions with other drugs would not be expected because of its predominant renal elimination and its lack of protein binding. Also, vigabatrin does not induce liver enzymes, as do many of the standard antiepileptic drugs. In several trials, however, a small but significant reduction in phenytoin levels has been seen following the addition of vigabatrin to the antiepileptic medication. The mechanism for this reduction in phenytoin levels has not yet been elucidated, though it does not appear to be of clinical significance. (J Child Neurol 1991;6(Suppl):2S7-2S10).