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R. H. Kardon, D. Hood, J. Rouleau, S. Anderson, A. S. Wenick, P. Deng, L. Grover, Q. Ghadiali, M. M. Behrens, J. Odel; Structure Versus Function in Patients With Anterior Ischemic Optic Neuropathy (AION): A Test of a Linear Model. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2459.
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To test a linear model [1,2] relating the regional loss in retinal nerve fiber (RNFL) thickness measured with optical coherence tomography (OCT) to the corresponding regional loss in sensitivity measured with standard automated perimetry (SAP) from eyes with previous anterior ischemic optic neuropathy (ION).
24 individuals with anterior ischemic optic neuropathy (ION) (59.2Â±9.8 yrs) and 20 with normal vision (54.8Â±10.7 yrs) were tested. Time since acute ION ranged from 4.6 months to over 20.3 years (median of 2.8 years). All eyes had OCT RNFL thickness (fast circular scan, OCT3, Zeiss Meditech) and SAP (24-2 SITA standard, Zeiss Meditech) tested. Superior and inferior field regions, and corresponding disc sectors, were defined . The average RNFL thickness of inferior and superior disc sectors was plotted against the average total deviations (linear units) of the corresponding field regions and a model fitted to these data. According to the model, the RNFL thickness R = sT + b, where T is the relative SAP sensitivity loss (on a linear scale, e.g. for -3dB, T=0.5), s is the RNFL thickness attributable to axons in the healthy/normal state and b is the residual RNFL measured when all sensitivity and axons are lost.
The data for the ION patients were described by the same curve, previously fitted to the data from patients with glaucoma. For patients with arcuate losses greater than -15 dB, the RNFL thickness provides an estimate of b for the individual. This estimated value of b was essentially the same as the value for glaucoma . Further, it does not appear to change much, if any, during the atrophic, chronic stage (i.e. after 4.6 months) of ION.
The linear model, which fits data from glaucoma eyes [1,2], also provided a good fit of the RNFL loss vs. SAP field loss in ION. The residual RNFL thickness did not change after the acute stage of ischemic attack had subsided, suggesting a constant contribution from glial cells. The success of the model provides a framework for relating structural to functional damage in optic nerve diseases. 1. Hood JOSA (in press); 2. Hood, Anderson, Wall & Kardon (under review); 3. Garway-Heath et al, Ophthal (2000)
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