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Scott D. Walter, Hiroshi Ishikawa, Kristin Galetta, James Wilson, Steven Galetta, Elliot Frohman, Peter Calabresi, Joel S. Schuman, Laura J. Balcer; Relation of Ganglion Cell Layer Thinning to Axonal Loss, Visual Function, and Quality of Life in Multiple Sclerosis. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6658.
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We used high-resolution spectral-domain optical coherence tomography (OCT) with retinal segmentation to determine how ganglion cell loss relates to history of acute optic neuritis (ON), retinal nerve fiber layer (RNFL) thinning, visual function, and quality of life (QOL) in an MS cohort.
Cirrus OCT (Carl Zeiss-Meditec, Dublin, CA) images were captured in 133 MS patients and 40 disease-free controls. Retinal layer segmentation was performed using algorithms published for studies of glaucoma. Thicknesses of the ganglion cell layer/inner plexiform layer (GCL+IPL), RNFL, outer plexiform/inner nuclear layer (OPL+INL), and outer nuclear/photoreceptor layer (ONL+PRL) were measured. Participants completed low-contrast letter acuity, high-contrast visual acuity (VA) testing, and the NEI-VFQ-25 questionnaire as a measure of visual QOL. Logistic regressions were performed accounting for age and within-patient, inter-eye correlations.
GCL+IPL and RNFL thicknesses were reduced in MS eyes vs. controls (p=0.01, p=0.001 respectively), but there were no significant differences in OPL+INL and ONL+PRL thickness. Among 264 MS eyes (94 eyes with history of ON, 170 eyes without), thinner GCL+IPL and RNFL were associated with a prior history of ON (GCL+IPL 61.5±9.5 vs. 67.4±10.2µm, p<0.001; macular RNFL 38.5±11.6 vs. 44.5±11.0µm, p<0.001). Lower GCL+IPL thickness was associated with thinner RNFL (p<0.001), and with worse visual function and QOL, even accounting for RNFL thickness (low-contrast acuity, 2.5%, p<0.001; 1.25%, p<0.001; VA, p=0.03; NEI-VFQ-25 composite, p=0.005). OPL+INL and ONL+PRL did not correlate with history of ON, RNFL thickness, visual function, or QOL.
Thinning of the GCL+IPL is strongly related to visual function and vision-related QOL in MS, even after controlling for the effects of RNFL thinning. Our findings parallel those of brain MRI studies suggesting that neuronal degeneration occurs somewhat independently of axonal loss and is more closely tied to disability. Retinal segmentation will allow us to study temporal associations between axonal and neuronal loss in MS, ON, and other optic neuropathies.
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