Purpose: In dogs, vigabatrin (VGB) has been associated with intramyelinic edema producing delayed central conduction in somatosensory and visual evoked potentials (SEP, VEP). No such effects have been reported in humans. We assessed whether abnormalities of central conduction could be detected prospectively in patients with epilepsy treated with VGB as long-term add-on medication.
Methods: Two hundred one patients with refractory partial epilepsy were enrolled and monitored for as long as 2 years. VGB was added to the treatment at an average dose of 2-3g/day. Conduction in somatosensory and visual pathways was assessed by median nerve SEP and pattern VEP recordings performed at inclusion and once every 6 months. The upper limit and test-retest variability of EP latencies were evaluated at time of enrollment in the patient group. Prolonged N13-N20 or P14-N20 SEP intervals and P100 VEP latency >2.5 SD above the baseline mean, observed on repeated runs in the same session and exceeding the test-retest variability at enrollment were considered to indicate central conduction slowing.
Results: One hundred nine patients completed the 2-year study period, and 92 discontinued VGB, of whom 37 were monitored with regard to EP until the end of the study. No consistent change in SEP or VEP was observed in the entire group during VGB treatment. The number of occasional EP values outside the baseline range in patients treated with VGB similar to that in patients whose VGB treatment had been discontinued.
Conclusions: We detected no evidence of changes in SEP and VEP attributable to altered neuronal conduction in the CNS during long-term VGB treatment.