Vigabatrin is an antiepileptic drug for the treatment of partial seizures.
The anticonvulsant effect is achieved by irreversible inhibition of the enz
yme GABA-transaminase which catalyses the inactivation of GABA. Vigabatrin
has been associated with visual field loss and electrophysiological abnorma
lities. The purpose of the study was to determine any alterations in normal
volunteers of the visual field and the visual electrophysiology resulting
from a short exposure to vigabatrin. A three-way, double-blind study of pla
cebo, carbamazepine and vigabatrin was undertaken at baseline and on days t
wo, four and nine. Seven subjects completed all three cycles and 14 subject
s (six females and eight males; mean age 27.3 years SD 6.7) completed at le
ast one cycle. Static threshold automated perimetry comprised Humphrey Visu
al Field Analyzer Programs 30-2 and 30/60-2. Electro-oculography and electr
oretinograms were performed with undilated pupils using the Medelec Ganzfel
d stimulator GS2000. The visual field was unaffected by placebo, carbamazep
ine or vigabatrin. The group mean amplitudes and latencies for the scotopic
ERG, 30Hz flicker ERG and the oscillatory potentials remained unchanged fo
r any cycle. The group mean photopic ERG b-wave latency increased from base
line (p<0.05); no significant change occurred with carbamazepine or placebo
. The group mean Arden Index for vigabatrin decreased from baseline to day
9 (p<0.01); no significant differences were present for carbamazepine or pl
acebo. Vigabatrin has a rapid effect on both the photopic ERG and the EGG;
however, the changes merely reflect alterations in retinal GABA levels seco
ndary to concomitant blocking of GABA transaminase by existing vigabatrin t
herapy.