Purchase this article with an account.
T. Ban, S. Rahmani, J.R. Hetling; Changes In Spatial Erg Potentials Due To Local Retinal Dysfunction – Simulation And Experiment . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3090.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Eye diseases often result in localized dysfunction of the retina. Existing methods to evaluate local function include the multi–focal ERG and pattern ERG; both require specialized stimulus sources. Pilot work described here supports a third method utilizing standard full–field stimuli and a corneal electrode array. Spatial ERG data are correlated with the region and degree of retinal dysfunction (first proposed by Davey et al., 1988).
A 3–D finite–element model of a rat eye was constructed in AutoCAD and imported into ANSYS for simulation of electric fields. Major ocular structures, plus a tear film and extraocular adipose tissue, were defined by geometry and electrical conductivity. Model input was a 100 Hz sinusoidal change in charge distribution across the retina, of a magnitude chosen to result in a 100 µV amplitude field potential at the corneal pole (simulating net transretinal currents that contribute to the ERG). Retinal dysfunction of the inferior hemisphere was simulated by reducing the amplitude of charge distribution in that hemisphere. Simulated ERG potentials were evaluated at five points on the cornea. Simulation results were compared to experimental results obtained in rat using conventional full–field ERG techniques.
Simulated full–field retinal stimulation resulted in corneal potentials near the limbus that were 36 % reduced compared to potentials at the corneal pole; experimentally measured potentials were ∼55% reduced near the limbus. A 10% reduction in simulated transretinal current in the inferior hemisphere resulted in a 5 µV change in the ERG for at least one corneal position (approximate detection limit assuming typical noise levels and no signal averaging). The spatial variation of simulated corneal potentials was indicative of the location of the dysfunction.
Model validation is supported by comparison with experimental measurements. Large areas of slight retinal dysfunction result in significant, spatially distinct changes in potentials evaluated at the cornea. Resolution of the inverse problem (source localization) will be evaluated for more spatially–restricted areas of defect.
This PDF is available to Subscribers Only