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  • Title: Vigabatrin associated visual field loss: a clinical audit to study prevalence, drug history and effects of drug withdrawal.
    Author: Newman WD, Tocher K, Acheson JF.
    Journal: Eye (Lond); 2002 Sep; 16(5):567-71. PubMed ID: 12194070.
    Abstract:
    PURPOSE: To survey clinical visual function including quantitative manual perimetry results in a group of patients taking vigabatrin; to assess the severity of any field defects; to tabulate cumulative and daily doses of medication and to assess possible changes in visual function over time. METHOD: A prevalence study of 100 out of 183 patients currently attending a tertiary referral epilepsy centre who were taking or had recently discontinued vigabatrin (duration 83-3570 days; mean 1885 days) as part of combination anticonvulsant therapy. Complete neuro-ophthalmic examination including Goldmann kinetic perimetry was performed and monocular mean radial degrees (MRD) to the I/4e isopter calculated. Patients were followed up at 6-monthly intervals for not less than 18 months. RESULTS: Acuity and colour vision remained stable in all patients regardless of changes in visual fields. Twenty per cent of patients had significant constriction of their visual field defined as a monocular MRD of 30 degrees or less. Males were significantly more likely to be severely affected than females (P < 0.01). Twenty one patients were followed after discontinuing vigabatrin treatment. Only three of these showed a change in MRD of 10 degrees or more with two deteriorating and one improving. No correlation between treatment duration or cumulative dosage/kg and the severity of defects could be demonstrated. CONCLUSIONS: Earlier reports of a high prevalence of both moderate and more serious field defects were confirmed in patients taking vigabatrin but not in epileptic patients taking other anti-convulsants. We found no evidence of progression or resolution of visual field defects on discontinuing the drug, and no relationship between dose history and visual deficit field loss. An idiosyncratic drug reaction within the neurosensory retina may underlie the pathogenesis of the visual field loss in some patients.
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