Bilateral visual field constriction has been recently reported in patients
treated with vigabatrin. It has been considered that vigabatrin, a GABA ago
nist antiepileptic drug, was specifically responsible for this visual field
defect. We present four observations sharing the same characteristics of c
hronic tunnel vision. Three patients had had vigabatrin but the fourth one
received other antiepileptic drugs, progabide, an agonist of post-synaptic
GABA receptors, and phenobarbital which interferes with GABA-A receptors. I
t is thus possible to hypothesize a retinal toxicity triggered by chronical
ly increased GABA transmission. If this is confirmed, an accurate incidence
of symptomatic and asymptomatic visual field constriction with GABA-mimeti
c drugs should be established, as well as the patients' profiles which are
more at risk. Patients currently under this type of treatment should be che
cked by both manual and automatic perimetry every six months to one year.