Purpose. To determine the natural history of visual field defects in a group of patients known to haveVigabatrin-associated changes who elected to continue themedication because of good seizure control. Methods. All p...Purpose. To determine the natural history of visual field defects in a group of patients known to haveVigabatrin-associated changes who elected to continue themedication because of good seizure control. Methods. All patients taking Vigabatrin alone or in combination with other antiepileptic drugs for at least 5 years (range 5- 12 years) were entered into a visual surveillance programme. Patients were followed up at 6- monthly intervals for not less than 18 months (range 18- 43 months). In all, 16 patients with unequivocal defects continued the medication. Following already published methodology (Eye 2002; 16;567- 571) monocular mean radial degrees (MRDs) to the I/4e isopter on Goldmann perimetry was calculated for the right eye at the time of discovery of a visual field defect and again after not less than 18 months follow-up. Results. Mean right eye MRD at presentation was 36.98° (range 22.25- 51.0), compared to 38.40° (range 22.5- 49.75) after follow-up; P=0.338 unpaired t-test. Only one patient demonstrated a deterioration in visual field during the study period and discontinued treatment. Conclusion. Established visual field defects presumed to be due to Vigabatrin therapy did not usually progress in spite of continuing use of the medication. These data give support to the hypothesis that the pathogenesis of Vigabatrin-associated visual field defects may be an idiosyncratic adverse drug reaction rather than dose-dependent toxicity.展开更多
文摘Purpose. To determine the natural history of visual field defects in a group of patients known to haveVigabatrin-associated changes who elected to continue themedication because of good seizure control. Methods. All patients taking Vigabatrin alone or in combination with other antiepileptic drugs for at least 5 years (range 5- 12 years) were entered into a visual surveillance programme. Patients were followed up at 6- monthly intervals for not less than 18 months (range 18- 43 months). In all, 16 patients with unequivocal defects continued the medication. Following already published methodology (Eye 2002; 16;567- 571) monocular mean radial degrees (MRDs) to the I/4e isopter on Goldmann perimetry was calculated for the right eye at the time of discovery of a visual field defect and again after not less than 18 months follow-up. Results. Mean right eye MRD at presentation was 36.98° (range 22.25- 51.0), compared to 38.40° (range 22.5- 49.75) after follow-up; P=0.338 unpaired t-test. Only one patient demonstrated a deterioration in visual field during the study period and discontinued treatment. Conclusion. Established visual field defects presumed to be due to Vigabatrin therapy did not usually progress in spite of continuing use of the medication. These data give support to the hypothesis that the pathogenesis of Vigabatrin-associated visual field defects may be an idiosyncratic adverse drug reaction rather than dose-dependent toxicity.
