The use of vigabatrin seems to increase the risk of a unique and specific pattern of bilateral, mainly asymptomatic visual field constriction. This risk should be considered when using vigabatrin. Visual field testing should also be performed before treatment and during routine follow-up for patients on vigabatrin.

Summary:Purpose: To study the prevalence and features of visual field constrictions (VFCs) associated with vigabatrin (VGB) in children.Methods: A systematic collection of all children with any history of VGB treatment in fifteen Finnish neuropediatric units was performed, and children were included after being able to cooperate reliably in repeated visual field tests by Goldmann kinetic perimetry. This inclusion criterion yielded 91 children (45 boys; 46 girls) between ages 5.6 and 17.9 years. Visual field extent <70 degrees in the temporal meridian was considered abnormal VFC.Results: There was a notable variation in visual field extents between successive test sessions and between different individuals. VFCs <70 degrees were found in repeated test sessions in 17 (18.7%) of 91 children. There was no difference in the ages at the study, the ages at the beginning of treatment, the total duration of the treatment, general cognitive performance, or neuroradiologic findings between the patients with normal visual fields and those with VFC, but the patients with VFC had received a higher total dose of VGB. In linear regression analysis, there were statistically significant inverse correlations between the temporal extent of the visual fields and the total dose and the duration of VGB treatment. The shortest duration of VGB treatment associated with VFC was 15 months, and the lowest total dose 914 g.Conclusions. Because of a wide variation in normal visual-field test results in children, the prevalence figures of VFCs are highly dependent on the definition of normality. Although our results confirm the previous findings that VFC may occur in children treated with VGB, our study points out the need to reevaluate critically any suspected VFC to avoid misdiagnosis. Nevertheless, our study suggests that the prevalence of VFC may be lower in children than in adults, and that the cumulative dose of VGB or length of VGB therapy may add to the personal predisposition for developing VFC.

Sixty adult patients with partial epilepsy who have been treated with vigabatrin for 7 months to 14 years as mono- or add-on therapy were examined with repeated kinetic Goldmann perimetries to evaluate the prevalence, risk factors, and long-term outcome of vigabatrin-associated visual field defects. A follow-up examination was performed after 4 to 38 months (mean, 15 +/- 7) in 55 patients, 29 of whom had discontinued vigabatrin therapy. Neither reversion nor progression in visual field constriction was observed.

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Background/aim-Many antiepileptic drugs have influence on visual functions. The aim of this study was to investigate possible changes in contrast sensitivity, macular photostress, and brightness acuity (glare) tests in patients with epilepsy undergoing vigabatrin (VGB) or carbamazepine (CBZ) monotherapy compared with healthy volunteers. Methods-32 patients undergoing VGB therapy, 18 patients undergoing CBZ therapy, and 35 healthy volunteers were asked to participate in an ophthalmological examination. In the previous study, visual field constrictions were reported in 40% of the patients treated with VGB monotherapy. In the present study, these VGB and CBZ monotherapy patients were examined for photopic contrast sensitivity with the Pelli-Robson letter chart and brightness acuity and macular photostress with the Mentor BAT brightness acuity tester. Results-Contrast sensitivity with the Pelli-Robson letter chart showed no difference between these groups and normal subjects (ANOVA: p= 0.534 in the right eye, p= 0.692 in the left eye) but the VGB therapy patients showed a positive correlation between the contrast sensitivity values and the extents of the visual fields in linear regression (R = 0.498, p = 0.05 in the right eye, R = 0.476, p = 0.06 in the left eye). Macular photostress and glare tests were equal in both groups and did not differ from normal values. Conclusion-The results of this study indicate that carbamazepine therapy has no eVect on contrast sensitivity. Vigabatrin seems to impair contrast sensitivity in those patients who have concentrically constricted in their visual fields. Neither GBZ nor VGB aVect glare sensitivity. (Br J Ophthalmol 2000;84:622-625) Carbamazepine (CBZ) is a standard antiepileptic drug for partial and generalised tonicclonic seizures. Its mechanism of action is to inhibit high frequency neuronal firing by blocking the voltage gated sodium channel. Visual disturbances such as nystagmus, diplopia, and blurred vision are well known adverse eVects of CBZ.1 Abnormal contrast sensitivity and enhanced glare sensitivity have been reported earlier in patients undergoing CBZ therapy.2-4 -Aminobutyric acid (GABA) is an inhibitory neurotransmitter in the central nervous system (CNS) as well as in horizontal, amacrine, bipolar, and ganglion cells of the retina.5-7 Vigabatrin ( -vinyl-GABA, VGB) is a selective irreversible inhibitor of GABA transaminase. Inhibition of GABA transaminase produces greater available pools of presynaptic GABA for release in CNS synapses. Vigabatrin has both antiseizure and antiepileptogenic properties with few adverse eVects. Currently, VGB is approved in over 60 countries for the adjunctive management of partial epilepsy not satisfactorily controlled by conventional therapy and for initial monotherapy in the management of infantile spasms.Spontaneous cases of bilateral concentric constriction of visual fields have recently been described in connection with VGB therapy. 10-14In a case report on three VGB therapy patients, Krauss et al 15 described cha...