Sixty epileptic patients chronically receiving GVG underwent to automatic perimetry and to flash electroretinogram (ERG) and visual evoked potentials (VEPs). All patients suffered from partial epilepsy. The mean GVG dose was 2887±871 mg/die (ranging from 1000 to 4000). The mean treatment duration was 56.6±43.5 months (ranging from 2 to 182). In 50 patients GVG was associated with other antiepileptic drugs (carbamazepine in 46 of them). One of them complained of visual symptoms. ERG was normal in all the subjects. The VF evaluation was normal in 13 and not reliable in 10 subjects. Thirty-seven subjects showed different kind of VF defects, which were explainable by a retinal/prechiasmatic lesion in 22 of them (17 subjects showed a binasal defect, 5 a concentric costriction). In these patients VEPs were normal in 17 subjects and showed a delayed latency in 4, a reduced amplitude in 1. The VF alterations occurred more frequently in the patients with a treatment duration longer than 18 months. Our data show that asymptomatic VF defects occur frequently in patients with partial epilepsy chronically receiving GVG. The relationship between the occurrence of VF defect and treatment duration suggest that GVG plays a pathophysiological role.

Automatic perimetry abnormalities in Vigabatrin chronically treated epileptic patients

Versino M.;
1999-01-01

Abstract

Sixty epileptic patients chronically receiving GVG underwent to automatic perimetry and to flash electroretinogram (ERG) and visual evoked potentials (VEPs). All patients suffered from partial epilepsy. The mean GVG dose was 2887±871 mg/die (ranging from 1000 to 4000). The mean treatment duration was 56.6±43.5 months (ranging from 2 to 182). In 50 patients GVG was associated with other antiepileptic drugs (carbamazepine in 46 of them). One of them complained of visual symptoms. ERG was normal in all the subjects. The VF evaluation was normal in 13 and not reliable in 10 subjects. Thirty-seven subjects showed different kind of VF defects, which were explainable by a retinal/prechiasmatic lesion in 22 of them (17 subjects showed a binasal defect, 5 a concentric costriction). In these patients VEPs were normal in 17 subjects and showed a delayed latency in 4, a reduced amplitude in 1. The VF alterations occurred more frequently in the patients with a treatment duration longer than 18 months. Our data show that asymptomatic VF defects occur frequently in patients with partial epilepsy chronically receiving GVG. The relationship between the occurrence of VF defect and treatment duration suggest that GVG plays a pathophysiological role.
1999
Epilepsy; Vigabatrin; Visual field defects
Tartara, A.; Galimberti, C. A.; Sartori, I.; Versino, M.; Politini, L.; Manni, R.; Perucca, E.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11383/2153213
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