An Investigation into the Stimulus Characteristics in Photosensitive Epilepsy with a Regard to Therapeutic Procedure

Abstract

The objectives of this investigation were to determine the effects of stimulus parameters on photosensitivity and that of therapeutic measures using sodium valproate (Epilim (R) ), thereby obtaining further insight into the characteristics and operation of photosensitive epilepsy. The most provocative stimulus in eliciting the photo convulsive response (PCR) was found to be a fine flashed-on grid pattern. The photosensitive visual evoked potential (VEP) was enhanced by optimal stimulation of the macula. Standard antiepileptic drugs had no beneficial effects on photosensitivity and, before sodium valproate treatment, some patients still exhibited photosensitivity even after 12 years from onset. Fifty photo convulsive patients, ranging in age from 6 - 25 years, were referred for investigation from hospitals in the Birmingham area. Recording was made of the basic and photically activated EEG and the VEP before and during sodium valproate treatment. Sixteen patients were similarly investigated after drug withdrawal. Sodium valproate was found to be particularly effective in the treatment of spontaneous and photically evoked generalised spike and wave abnormalities. Optimum dosage levels were found for each patient, which ranged from 600-1600 mg daily with a modal dosage of 1000 mg/day. The majority of patients (78%) showed a significant improvement in photosensitivity after a variable treatment period from 1 month to 2 years 9 months (mean 9 months). The basic EEG showed marked benefit, on average 4.5 months previous to the effect on photosensitivity. Sodium valproate reduced VEP amplitude to some extent but no effect occurred on occipital spikes. The general effect of sodium valproate withdrawal was either a reappearance or increase in spontaneous and photically evoked abnormalities. Clinical findings during treatment were favourable. Overall only 16% of patients showed definite side-effects as a result of sodium valproate therapy. The results are discussed in relation to the possible pathophysiological mechanisms of photosensitive epilepsy.