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Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
Published on: April 14, 2014
Recurrence-Independent Progressive Inner-Retinal Thinning After Optic Neuritis: A Longitudinal Study
Yeji Moon1, Yujin Gim, Kyung-Ah Park
1Department of Ophthalmology (YM), Asan Medical Center and University of Ulsan College of Medicine, Seoul, Korea; Department of Ophthalmology (YG), Ewha Womans University Seoul Hospital, Seoul, Korea; Department of Ophthalmology (K-AP), Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; Department of Ophthalmology (HKY), Seoul National University College of Medicine and Bundang Hospital, Seongnam, Korea; Department of Ophthalmology (S-JK, JHJ), Seoul National University College of Medicine and Hospital, Seoul, Korea; and Department of Neurology (S-MK), Seoul National University College of Medicine and Hospital, Seoul, Korea.
Background:
Longitudinal changes in the inner retina in patients with optic neuritis (ON) may be helpful in monitoring patients and determining maintenance treatment. The aim of this study was to investigate longitudinal changes in the inner retina after subsiding of acute demyelinating ON and to identify the factors associated with such changes.
Methods:
In this multicenter retrospective observational study, we reviewed the medical records of 77 patients with ON, including 23 with neuromyelitis optica spectrum disorder with aquaporin 4 (AQP4)-immunoglobulin G (IgG) (AQP4 group), 23 with myelin oligodendrocyte glycoprotein (MOG)-antibody-associated disease (MOG group), 18 with multiple sclerosis (MS group), and 13 with idiopathic ON (iON group). We measured the thickness of the peripapillary retinal nerve fiber layer (pRNFL) and the macular ganglion cell-inner plexiform layer (mGCIPL) using optical coherence tomography (OCT) at baseline and at follow-up examinations (mean follow-up duration, 29.6 ± 8.6 months; mean number of OCT, 4.2 ± 1.2) in the absence of ON recurrence.
Results:
The estimated rate of pRNFL thinning in the AQP4, MOG, MS, and iON groups was 0.66 (95% confidence interval, 0.35-0.97), 0.35 (0.04-0.66), 0.53 (0.16-0.90), and 0.25 (-0.18 to 0.68) μm/year, respectively, indicating that, in the iON group in contrast to the other groups, there was no significant decrease of pRNFL thickness. Among the AQP4, MOG, and MS groups, there was no significant difference in the rate of pRNFL thinning ( P = 0.560). The rate of mGCIPL thinning in the AQP4 and MOG groups was 0.25 (0.04-0.46) μm/year and 0.38 (0.23-0.53) μm/year, respectively. Meanwhile, the rate of mGCIPL change in the MS and iON groups was 0.04 (-0.12 to 0.19) and 0.00 (-0.17 to 0.16) μm/year, respectively, which indicates that there was no significant mGCIPL thinning in the latter 2 groups. Between the AQP4 and MOG groups, meanwhile, the rate of mGCIPL change did not significantly differ ( P = 0.295). Age older than 40 years was associated with significant progression of mGCIPL thinning ( P = 0.005).
Conclusions:
We noted inner retina thinning progression independent of relapse activity in AQP4-ON, MOG-ON, and MS-ON. Because subclinical neuroaxonal damage continues to be incurred after an acute attack of ON subsides despite suppression of new attacks, long-term follow-up and neuroprotection should be considered to be integral to the treatment of patients with ON.
