Acute ganglion cell loss during rapid visual recovery in optic neuritis.

ABSTRACT

PURPOSE: To report dynamic changes in the retinal ganglion cell layer (GCL) and visual function in acute and chronic optic neuritis (ON). METHODS: Sixteen eyes (15 patients) with acute ON were followed for 3.5 to 31 months (average, 10.2). The best-corrected visual acuity (BCVA) and thickness of the GCL plus the inner plexiform layer (GCL+IPL) were measured 4 to 13 times between baseline and the final visit using the ganglion cell analysis software in the Cirrus HD-OCT [high-definition optical coherence tomography] instrument. Goldmann perimetry was performed at baseline and at the final visit. RESULTS: The thickness of the GCL+IPL at baseline was within normal limits in the affected (80.4 ± 4.9 microns) and unaffected fellow eyes (80.5 ± 5.0 microns). Rapid thinning to 69 ± 7.3 microns occurred during month 1 in the affected eyes, slowing during month 2, and then reaching a minimum level (63.6 ± 8.7 microns). In contrast, BCVA was lowest (mean ± standard deviation logarithm of the minimum angle of resolution, -1.29 ± 0.96) in 11 eyes at baseline, increased markedly to -0.15 ± 0.37 during month 1, and reached a maximum level (-0.18 ± 0.19) during month 2 and (-0.02 ± 0.23) at the final visit. The BCVA in the other five eyes fluctuated during month 1, increased markedly during month 2, and then reached a maximum plateau (-0.07 ± 0.20). The patterns of visual field defects at baseline were varied, and were determinants of BCVA. The visual field largely recovered in 11 eyes, but small central scotomas in four eyes and an enlarged blind spot in one eye remained at the final visit. Eyes with the least GCL+IPL thinning at month 1 or 2 had the least depression in the final deviation map. CONCLUSIONS: In acute ON, the progression toward irreversible ganglion cell loss occurs rapidly during months 1 and 2. In contrast, visual function recovers rapidly during the same period. Remodeling of the neural network may occur between the photoreceptors and the reduced numbers of ganglion cells during the first months of ON. The small number of residual ganglion cells appears to compensate for the initial visual dysfunction.