Noémie Hébert-Lalonde1, Lionel Carmant2, Philippe Major2, Marie-Sylvie Roy3, Maryse Lassonde1, Dave Saint-Amour4. 1. Department of Psychology, Université de Montréal, Montreal, Quebec, Canada; Research Center, CHU Sainte-Justine, Montreal, Quebec, Canada. 2. Research Center, CHU Sainte-Justine, Montreal, Quebec, Canada; Division of Neurology, Department of Pediatrics, Sainte-Justine Hospital, Université de Montréal, Montreal, Quebec, Canada. 3. Research Center, CHU Sainte-Justine, Montreal, Quebec, Canada. 4. Research Center, CHU Sainte-Justine, Montreal, Quebec, Canada; Department of Ophtalmology, Université de Montréal, Montreal, Quebec, Canada; Department of Psychology, Université du Québec à Montréal, Montreal, Quebec, Canada. Electronic address: saint-amour.dave@uqam.ca.
Abstract
BACKGROUND: We assessed central and peripheral visual field processing in children with epilepsy who were exposed to vigabatrin during infancy. METHODS: Steady-state visual evoked potentials and pattern electroretinograms to field-specific radial checkerboards flickering at two cycle frequencies (7.5 and 6 Hz for central and peripheral stimulations, respectively) were recorded from Oz and at the eye in seven school-age children (10.1 ± 3.5 years) exposed to vigabatrin early in life, compared with children early exposed to other antiepileptic drugs (n = 9) and healthy children (n = 8). The stimulation was made of two concentric circles (0 to 5 and 30 to 60 degrees of angle) and presented at four contrast levels (96%, 64%, 32%, and 16%). RESULTS: Ocular responses were similar in all groups for central but not for the peripheral stimulations, which were significantly lower in the vigabatrin-exposed group at high contrast level. This peripheral retinal response was negatively correlated to vigabatrin exposure duration. Cortical responses to central stimulations, including contrast response functions in the children with epilepsy in both groups, were lower than those in normally developing children. CONCLUSIONS: Alteration of ocular processing was found only in the vigabatrin-exposed children. Central cortical processing, however, was impaired in both epileptic groups, with more pronounced effects in vigabatrin-exposed children. Our study suggests that asymptomatic long-term visual toxicity may still be present at school age, even several years after discontinuation of drug therapy.
BACKGROUND: We assessed central and peripheral visual field processing in children with epilepsy who were exposed to vigabatrin during infancy. METHODS: Steady-state visual evoked potentials and pattern electroretinograms to field-specific radial checkerboards flickering at two cycle frequencies (7.5 and 6 Hz for central and peripheral stimulations, respectively) were recorded from Oz and at the eye in seven school-age children (10.1 ± 3.5 years) exposed to vigabatrin early in life, compared with children early exposed to other antiepileptic drugs (n = 9) and healthy children (n = 8). The stimulation was made of two concentric circles (0 to 5 and 30 to 60 degrees of angle) and presented at four contrast levels (96%, 64%, 32%, and 16%). RESULTS: Ocular responses were similar in all groups for central but not for the peripheral stimulations, which were significantly lower in the vigabatrin-exposed group at high contrast level. This peripheral retinal response was negatively correlated to vigabatrin exposure duration. Cortical responses to central stimulations, including contrast response functions in the children with epilepsy in both groups, were lower than those in normally developing children. CONCLUSIONS: Alteration of ocular processing was found only in the vigabatrin-exposed children. Central cortical processing, however, was impaired in both epileptic groups, with more pronounced effects in vigabatrin-exposed children. Our study suggests that asymptomatic long-term visual toxicity may still be present at school age, even several years after discontinuation of drug therapy.