December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Vigabatrin Retinopathy
Author Affiliations & Notes
  • JM Wild
    Department of Optometry and Vision Sciences Cardiff University Cardiff United Kingdom
  • M Hope-Ross
    Birmingham and Midland Eye Centre
    City Hospital Birmingham United Kingdom
  • GF A Harding
    Neurosciences Research Institute Aston University Birmingham United Kingdom
  • AK Gupta
    Department of Neurophysiology
    City Hospital Birmingham United Kingdom
  • TA Betts
    Queen Elizabeth Psychiatric Hospital Birmingham United Kingdom
  • Footnotes
    Commercial Relationships    J.M. Wild, Aventis Pharma R; M. Hope-Ross, None; G.F.A. Harding, Aventis Pharma R; A.K. Gupta, None; T.A. Betts, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 238. doi:
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    • Get Citation

      JM Wild, M Hope-Ross, GF A Harding, AK Gupta, TA Betts; Vigabatrin Retinopathy . Invest. Ophthalmol. Vis. Sci. 2002;43(13):238.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: The anti-epileptic drug (AED) vigabatrin is associated with visual field loss. Although, clinical electrophysiology indicates a retinal origin for the defect, little information is available on the presence of fundal abnormality. We investigated, in a cross-sectional study, the prevalence of ophthalmic disorders in a cohort of patients exposed to vigabatrin. Methods: The first cohort comprised 27 consecutively presenting adult patients with epilepsy who had been exposed to vigabatrin (VE). The second cohort comprised 13 patients with epilepsy never exposed to vigabatrin (NE) or to any antiepileptic drug which elevated GABA levels. All patients firstly underwent ophthalmological examination by an experienced fellowship-trained retina specialist (MH-R). The visual field of each eye for 37 of the 40 patients was then examined using Program 30-2 and the Full Threshold strategy and, where necessary, Program 60-4 of the Humphrey Visual Field Analyzer 750. The remaining three patients, all in the VE cohort, underwent kinetic perimetry using the Goldmann perimeter. MH-R was masked to the AED history and to the results of the visual fields for each patient. The visual fields were examined, and evaluated, masked to the AED history and to the ophthalmic findings for each patient. Results: Eighteen of the 27 patients in the VE cohort exhibited vigabatrin attributed visual field loss (VA-VFL). No cases of field loss were found in the NE cohort. Of the 18 patients with VA-VFL, 14 exhibited optic atrophy (OA) (of whom 11 were bilateral) and 13 a retinal abnormality (vascular changes [VC], peripheral changes [PC], or fibrotic changes [FC]); 11 exhibited OA together with one or more retinal abnormalities. Of the 9 patients without VA-VFL, 4 exhibited retinal abnormality: one OA and VC, one FC, one PC and one drusen. The only retinal finding in the 13 controls were two cases of drusen; none exhibited OA. Conclusions: A characteristic spectrum of retinopathy is associated with VA-VFL.

Keywords: 390 drug toxicity/drug effects • 624 visual fields • 554 retina 

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