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Vigabatrin Associated Visual Field Loss: a Clinical Audit to Study

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Vigabatrin Associated Visual Field Loss: a Clinical Audit to Study Eye (2002) 16, 567–571 2002 Nature Publishing Group All rights reserved 0950-222X/02 $25.00 www.nature.com/eye WD Newman, K Tocher and JF Acheson Vigabatrin associated CLINICAL STUDY visual field loss: a clinical audit to study prevalence, drug history and effects of drug withdrawal Abstract convulsants. We found no evidence of progression or resolution of visual field Purpose To survey clinical visual function defects on discontinuing the drug, and no including quantitative manual perimetry relationship between dose history and visual results in a group of patients taking deficit field loss. An idiosyncratic drug vigabatrin; to assess the severity of any field reaction within the neurosensory retina may defects; to tabulate cumulative and daily underlie the pathogenesis of the visual field doses of medication and to assess possible loss in some patients changes in visual function over time. Eye (2002) 16, 567–571. doi:10.1038/ Method A prevalence study of 100 out of sj.eye.6700168 183 patients currently attending a tertiary referral epilepsy centre who were taking or had recently discontinued vigabatrin Keywords: vigabatrin; visual failure; visual (duration 83–3570 days; mean 1885 days) as fields part of combination anticonvulsant therapy. Complete neuro-ophthalmic examination Introduction including Goldmann kinetic perimetry was performed and monocular mean radial Vigabatrin (Sabril, Hoechst Marion degrees (MRD) to the I/4e isopter calculated. Roussel/Aventis Ltd) was introduced into UK Patients were followed up at 6-monthly clinical practice on a trial basis in the mid- intervals for not less than 18 months. 1980s and granted a licence in 1989. Since Results Acuity and colour vision remained 1997 numerous reports have appeared stable in all patients regardless of changes in describing an association between use of the visual fields. Twenty per cent of patients had anticonvulsant and bilateral symmetrical loss 1–8 significant constriction of their visual field of visual field. It is hypothesised that in Dept of Neuro- defined as a monocular MRD of 30 degrees addition to effects on cerebral function, ophthalmology, or less. Males were significantly more likely irreversible inhibition of GABA National Hospital for to be severely affected than females aminotransferase with consequent elevation of Neurology & Neurosurgery Ͻ Queen Square (P 0.01). Twenty one patients were GABA levels in the inner retina is the London WC1N 3BG, UK followed after discontinuing vigabatrin priniciple cause of the depressed visual treatment. Only three of these showed a function and this is supported by Correspondence: change in MRD of 10 degrees or more with electrophysiological data.9–15 Outer retinal and JF Acheson MRCP two deteriorating and one improving. No possibly also cortical effects may play a role.12 FRCOphth Dept of Neuro- 11 correlation between treatment duration or Males may be more susceptible than females ophthalmology, cumulative dosage/kg and the severity of but the role of other risk factors such as National Hospital for defects could be demonstrated. cumulative dosage is less clear. There are Neurology & Neurosurgery Conclusions Earlier reports of a high reports of visual recovery after drug Queen Square prevalence of both moderate and more withdrawal16,17 but in a larger study of 13 London WC1N 3BG, UK Tel: +44 (0)20 7837 3611 serious field defects were confirmed in patients, Johnson et al found no association ext 3388 patients taking vigabatrin but not in between the recovery of visual function and Fax: +44 (0)20 7676 2041 epileptic patients taking other anti- either treatment duration or cumulative dosage.18 E-mail: jachesonȰuclh.org Vigabatrin associated visual field defects: a systematic audit WD Newman et al 568 As part of an on-going surveillance and audit screening programmes. Analysis of the kinetic visual exercise on visual field loss associated with vigabatrin field data was done by measuring the radial distance in a population of 183 patients attending a tertiary in degrees at each of 12 points, 30 degrees apart, of the referral epilepsy clinic conducted since 1998, we have I/4e isoptre of the visual field. The mean peripheral collected data on drug history and visual performance field diameter was then determined and the results on kinetic perimetry. We report our observations on expressed as mean radial degrees (MRD) averaged for the relationship between total dosage of vigabatrin and each eye of each patient and compared to those the presence of field defects, and the consequences of obtained from controls. This method follows the discontinuing the drug. techniques described in the NIH-sponsored Diabetic Retinopathy Trial in 198119 and latterly used in the study of vigabatrin-associated visual field loss by Patients and methods Krauss, Johnson and co-workers.11,18,20 The study commenced in March 1999. All patients who All patients were then examined by an were currently, or had in the past, taken vigabatrin as ophthalmologist (JFA or WDN) who were masked to part of combination anticonvulsant therapy and were the findings of the visual field examination. Each attending the epilepsy clinic at the National Hospital patient underwent a full neuro-ophthalmic examination for Neurology and Neurosurgery, London or the to assess any possible visual or ocular comorbidity National Society for Epilepsy at Chalfont, Bucks, UK including pupillary responses, anterior segment were identified and referred for ophthalmological biomicroscopy at the slit lamp and both direct and assessment. indirect fundus examination following pupillary Each patient was interviewed using a standardised dilatation with tropicamide 1%. proforma designed to reveal both symptomatic and Patients were then given rolling 6-month follow-up asymptomatic ocular disease. This included details of appointments. At subsequent visits changes to past ocular history including family history of ocular medication were noted and any new visual symptoms disease; refractive history; neurological and were enquired of. A repeat examination of best neurosurgical history and a drug history. The patients corrected visual acuity for near and distance, colour were asked if they had any visual problems, and then vision, and pupillary responses was carried out prior graded questions were asked in order to elicit any to performing a visual field test as described at their visual disturbance that might be related to vigabatrin, first attendance. The visual fields were undertaken by which included general questions about recent onset of the same perimetrist (KT). Control data were obtained any visual problems, to more direct questions of from a group of 10 patients with epilepsy taking other blurred vision; tunnel vision/restricted peripheral anticonvulsants who had never taken vigabatrin and a vision/ flickering lights. All the patients had been group of 10 healthy volunteers. informed by the referring neurologists that the reason The visual field data were analysed as a continuous for referral was a suspected link between reduced variable using a commercially available statistically peripheral vision and vigabatrin. package (SPSS). Only values from the right eye were Best corrected distance (Snellen) and near acuity used in the analysis. In addition, the visual fields were were recorded. Colour vision was assessed using the also arbritrarily assigned into those who had 17 number plate version of the Ishihara significant visual field defects (visual field of 30 or less pseudoisochromatic test. Goldmann kinetic field testing mean radial degrees) and those who did not (with a to the I/4e and V/4e isoptres only was performed, visual field of more than 30 MRD). This level of field with all the tests performed on the same regularly loss was believed likely to reflect clinically significant calibrated machine (Haag–Streit, with background loss of function although we were unable to test this luminance of 31.5 apostilbs, and using appropriate full assumption more fully. aperture spectacle correction for the central field) by the same experienced perimetrist (KT). Fixation was Results carefully monitored by direct visualisation of the fixating eye and by rechecking points both outside and The patients inside the area of the apparent seeing field at specific meridians. Automated static perimetry was not used One hundred and eighty-three patients were invited because of unacceptably high poor reliability indices in for examination; 14 failed to attend. One hundred and both our own patient population and others,17 using sixty-nine patients were examined, 94 male and 79 full-threshold stategies and the lack of validated female with a mean age of 37 years (range: 17–79, scoring systems for analysis of suprathreshold median 37 years). The following patients were Eye Vigabatrin associated visual field defects: a systematic audit WD Newman et al 569 excluded from the data analysis: 17 patients who were whom six were female and 14 were male. They had on unable to complete visual field assessment due to average been taking vigabatrin for 1943 days (median cognitive impairment; six patients with pre-existing 1668 days) and had taken a mean estimated total of ocular pathology which could affect visual field results 5380 g. This compares with the group with visual fields (either glaucoma or age-related macular degeneration); of 31 MRD or greater who had a mean age of 37 years 26 patients who had visual field defects arising from (median 35.5 years, SD 10.5) of whom 40 were female previous intra-cranial surgery for epilepsy; and 14 who and 40 male. These patients had taken a mean had pre-existing intra-cranial tumours. estimated total of 4574 g and had been on the drug for The data from the remaining 100 patients (54 male a mean time of 2758 days. Analysis of variance and 46 female) were used for analysis. The patients’ revealed no significant difference between the total ages ranged from 18 to 68 years with an average age amount of drug consumed by the two groups (F = 0.5, of 38 years (median 37 years), the mean treatment P = 0.48), or the period of treatment (F = 0.4, P = 0.5).
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