Vigabatrin is a
GABA (
gamma-aminobutyric acid)
transaminase inhibitor that elicits an
antiepileptic effect by enhancing inhibitory neurotransmission in the brain.
Vigabatrin has been previously associated with concentric peripheral visual field loss and visual electrophysiological abnormalities. Recently, visual function deficits of the central retina have been identified in a proportion of patients receiving
vigabatrin; these include disturbances in colour perception, contrast sensitivity and short-wavelength automated perimetry. Consequently, it is suggested that
vigabatrin-associated
retinal toxicity is diffuse inducing subtle central visual dysfunction and more severe peripheral visual defects. Reductions in cerebral blood flow and cerebral metabolic rate for
glucose occur in
epilepsy patients receiving
antiepileptic drug therapy. Despite the known cerebral haemodynamic alterations in
epilepsy and the visual consequences of
vigabatrin therapy, ocular blood flow has only recently been investigated in this group. We present findings from a series of novel investigations that identify compromised
retinal microvascular perfusion and pulsatile ocular blood flow (POBF) in
epilepsy patients. The reduction in POBF was exacerbated in
epilepsy patients treated with
vigabatrin compared to conventionally treated
epilepsy patients. A number of theories are presented to explain compromised ocular blood flow in
vigabatrin treated
epilepsy patients, and the possibility of a GABAergic mechanism of toxicity is discussed.