Abstract

Background Demyelination and axonal loss following acute optic neuritis (AON) can be respectively measured as delayed visual evoked potentials (VEPs) and as reduced thickness of retinal nerve fiber (RNFL) and ganglion cell-inner plexiform layer (GCL-IPL) at optical coherence tomography (OCT). Traditionally, atrophy of GCL and IPL, which contains cell bodies and dendrites of the ganglion cells, is measured at the macula, but can be also measured with faster peripapillary scans at the optic nerve head. We explored if, in addition to the GCL measured at the macula, GCL-IPL atrophy could be detected with peripapillary scans and its association with VEPs evolution after AON. Methods Twenty subjects with unilateral AON underwent OCT and full-field VEP at baseline in the acute phase (8 ± 6 days after onset) and after 1 month (33 ± 5 days) and 4 months (128 ± 11 days). RNFL and GCIPL were segmented from peripapillary scans, GCL from macular scans. We explored the time evolution of RNFL, GCIPL, and GCL thickness over time and their correlation with VEP latency. Results Macular GCL was significantly reduced at 1 month (34.49 ± 4.42 μ m) compared to baseline (36.31 ± 3.67 μ m; p = 0.008). Peripapillary RNFL and GCIPL reduction was instead significant only at 4 months (RNFL: 97.32 ± 16.07 μ m at baseline and 96.65 ± 16.73 μ m at 1 month vs 92.11 ± 16.98 μ m at 4 month, p = 0.023; GCIPL: 47.94 ± 3.22 μ m at baseline and 46.61 ± 4.63 μ m at 1 month vs 43.96 ± 6.65 μ m at 4 month, p = 0.005). Baseline VEP latency correlated with OCT measures both at 1 month (RNFL: r = −0.648, p = 0.001; GCIPL: r = −0.495, p = 0.019; GCL: r = −0.742, p r = −0.616, p = 0.004; GCIPL: r = −0.564, p = 0.010; GCL: r = −0.748, p Discussion After AON, macular changes seem to precede detectable atrophy at peripapillary level, even within ganglion cell layers, suggesting this region as the most suitable to track early neurodegeneration. Demyelination in the acute phase, as measured by early VEPs, is associated with subsequent neuroretinal neurodegeneration and suggests the usefulness of VEPs as early predictor of ON outcome for individualized treatment and for patients’ selection for clinical trials assessing remyelination and neuroprotective strategies.

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