May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Multifocal Electroretinogram Evidence Reveals That the Degree of Vigabatrin Toxicity Is Dependent on Retinal Layer
Author Affiliations & Notes
  • M. L. Conway
    Optometry, Aston University, Birmingham, United Kingdom
    Department of Optometry and Visual Science, City University, London, United Kingdom
  • S. L. Hosking
    Optometry, Aston University, Birmingham, United Kingdom
    Department of Optometry and Visual Science, City University, London, United Kingdom
  • R. P. Cubbidge
    Optometry, Aston University, Birmingham, United Kingdom
  • P. L. Furlong
    Optometry, Aston University, Birmingham, United Kingdom
  • Footnotes
    Commercial Relationships M.L. Conway, None; S.L. Hosking, None; R.P. Cubbidge, None; P.L. Furlong, None.
  • Footnotes
    Support None.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 5974. doi:
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      M. L. Conway, S. L. Hosking, R. P. Cubbidge, P. L. Furlong; Multifocal Electroretinogram Evidence Reveals That the Degree of Vigabatrin Toxicity Is Dependent on Retinal Layer. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5974.

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

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Abstract

Purpose:: To establish the site of retinal toxicity associated with the anti-epileptic drug Vigabatrin (VGB).

Methods:: The sample comprised 13 patients (mean age 40.2 +/- 14.2y) diagnosed with epilepsy and exposed to VGB therapy. Each participant underwent standard white-white automated perimetry on one randomly selected eye, using Program 30-2 Full Threshold algorithm on the Humphrey Field Analyser. Multifocal electroretinogram (mfERG) examination was conducted using the Visual Evoked Response Imaging System (VERIS) on the same eye of each patient. A participant’s response was identified as defective if the averaged waveform in any ring was reduced by more than two standard deviations (SD) from a database consisting of 17 clinically normal individuals (mean age 36.7 +/- 17.7y). Scalar product field abnormality maps were also constructed by plotting reductions in waveforms that exceeded two and three standard deviations in scalar product (nV/deg sq) from normal.

Results:: Visual field defects (VFDs) were evident in 5 patients (38%) exposed to VGB treatment; these patients also demonstrated abnormal first- and second-order scalar product densities. A further 4 patients (31%) with normal visual fields demonstrated abnormal second-order scalar product densities. No patients exhibited VFDs without mfERG defects. The spatial locations of VFDs did not correspond to the defective scalar product maps. Abnormal mfERG responses were evident in both current and previously treated VGB recipients.

Conclusions:: mfERG investigations demonstrate that 69% of patients exposed to VGB demonstrate functional loss at the retinal photoreceptors, Muller, amacrine and ganglion cells; this is almost twice the number detected using conventional visual field testing and suggests that earlier reports might have significantly underestimated the true prevalence of retinal toxicity related to the drug. Findings also indicate that second order responses relating to the inner retinal layers (ganglion, amacrine, and Muller cells) are primarily affected in the milder (earlier) cases of retinal pathology attributed to VGB while the first order responses relating to the outer retinal layers (photo receptors) are primarily affected in the later more severe cases.

Keywords: electroretinography: non-clinical • drug toxicity/drug effects • visual fields 
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