Visual field defects associated with vigabatrin therapy

Abstract

Objective-To estimate the prevalence of visual field defects in patients taking the anticonvulsant drug vigabatrin and to characterise the features of visual dysfunction found. Methods-Thirty three unselected patients attending neurology and epilepsy clinics were identified as taking vigabatrin and asked to attend for neuro-ophthalmic evaluation. A control group of 16 patients with epilepsy unexposed to vigabatrin was also evaluated. Visual fields were examined by static perimetry using a Humphrey field analyser. Patients underwent detailed ophthalmic examination, various blood tests, and brain MRI where necessary. Visual evoked responses (VERs), electro-oculograms (EOGs), and electroretinograms (ERGs) were recorded. Results-Of 31 assessable patients treated with vigabatrin, 16 (52%) had definitely abnormal visual fields, nine (29%) had fields that were inconclusive, four (13%) had normal fields, and two (6%) proved unable to cooperate with testing. In four patients some plausible cause was found for the field abnormality leaving 12 patients (39%) in whom a definite bilateral field defect was found, possibly caused by vigabatrin treatment. Of 16 control patients none had definitely abnormal fields, 12 (75%) had normal fields, and four (25%) had fields that were inconclusive. The field defects associated with vigabatrin treatment showed a characteristic pattern of concentric peripheral field loss with temporal and macular sparing. The VERs and ERGs were normal. The EOG Arden Index was reduced in patients taking vigabatrin, although this returned towards normal when vigabatrin was stopped, even in the presence of persistent field defects. Multifocal ERGs recorded in two patients were abnormal, showing marked reduction in amplitude of the peripheral focal ERG. Conclusions-Treatment with vigabatrin was associated with a high prevalence of peripheral visual field defects. This seemed to be the result of a toxic eVect of vigabatrin on the retina and seemed to persist if the drug was withdrawn. (J Neurol Neurosurg Psychiatry 1999;67:716-722)

Vigabatrin: longterm follow‐up of electrophysiology and visual field examinations

“…Arndt et al (1999) also found a permanent change in EOG after stopping VGB. Other researchers have claimed that the Arden ratio of the EOG is affected by current use of VGB (Bourcier Bareil et al 1999;Lawden et al 1999;Harding et al 2000;Johnson et al 2000;Coupland et al 2001;GraniewskiWijnands & van der Torren 2002).…”

Molecular Targets for Antiepileptic Drug Development

“…384 It is not clear whether the retinal pathology is a direct consequence of GABA-transaminase inhibition or is related to some other effect of vigabatrin, such as glutamic acid decarboxylase inhibition. Until it is shown that chronic inhibition of GABA-transaminase sufficient to suppress seizures can be achieved without risk of retinal damage, the utility of GABA-transaminase as an AED target will remain uncertain.…”

Retinal nerve fibre layer characteristics with vigabatrin-associated visual field loss—could scanning laser polarimetry aid diagnosis?

“…[5][6][7] The typical visual field loss is unusual in that it is one of the few causes of bilateral nasal field loss with temporal sparing. Screening for field defects with vigabatrin use is essential; however, a high proportion of patients taking this medication are unable to perform reliable field examinations due to their age or associated learning difficulties.…”