Vigabatrin; its effect on the electrophysiology of vision

Vigabatrin is known to induce visual field defects in approximately one third of patients treated with the drug. It is apparent from electrophysiological studies that the cause of this defect is at retinal level probably as a result of the build up of GABA. Studies of electrophysiological retinal parameters such as the EOG and photopic, scotopic and 30-Hz flicker ERG have revealed changes in Arden Index, photopic a and b wave latency and amplitude, changes in oscillatory potentials, and changes in latency and amplitude of the 30Hz response. However, many of these changes such as the Arden Index, oscillatory potentials, latency and amplitude of photopic b wave appear to be related to current anti-epileptic drug treatment rather than visual field defects. Certain parameters, particularly the amplitude of the 30-Hz flicker response, do appear to correlate with the severity of the field defect. Paediatric patients treated with the drug at age 9 years or below cannot reliably perform visual field perimetry. To identify these patients a special VEP H-Stimulus has been developed to produce separate responses from central and peripheral field stimulation by alternating at slightly separate rates. Forty-five healthy children between ages 3 and 10 years have been used to develop a normal database. This technique has a sensitivity of 75% and a specificity of 87.5% in identifying the field defect and may be used in children with epilepsy from age 3 upwards.