Abstract

In the article “Longitudinal optic neuritis-unrelated visual evoked potential changes in NMO spectrum disorders,” Drs. Ringelstein et al. observed progressive delays in visual evoked potential (VEP) latency, occurring independently of acute optic neuritis, in 167 patients with neuromyelitis optica spectrum disorders (NMOSD) using 548 longitudinally assessed full-field VEP studies over the course of ≥3 months. In response, Dr. Chen seeks clarification about the authors' finding of a reduction in VEP amplitude with ≥3 months of follow-up but not among those with ≥12 months of follow-up. Dr. Chen wonders whether there may be similar correlations between VEP amplitude and disease activity as seen with optical coherence tomography (OCT) measurements of the peripapillary retinal nerve fiber layer thickness—which seem to decrease in NMOSD patients with non-ocular relapses vs those with stable disease—and calls for prospective longitudinal studies with VEP, OCT, and MRI to further explore this topic. Responding to these comments, the authors note that whereas their more restricted analysis of patients with ≥12 months of follow-up was intended to address the potential amplification of measurement variability that may have occurred with their interpolation of shorter-interval data—i.e., for patients with <12 months follow-up—their sample size may have been insufficient to achieve significance for analyses of amplitude changes. Nonetheless, they note that latency findings showed consistent and reliable increases in both the main and sub-analyses. This exchange highlights the ongoing evolution of our understanding about progressive tissue damage in NMOSD, previously thought to occur only in the context of relapses. We agree with Dr. Chen that longitudinal correlation of visual tests of structure, physiology, and function will be necessary to understand how frequently subclinical progressive disease might occur in NMOSD. In the article “Longitudinal optic neuritis-unrelated visual evoked potential changes in NMO spectrum disorders,” Drs. Ringelstein et al. observed progressive delays in visual evoked potential (VEP) latency, occurring independently of acute optic neuritis, in 167 patients with neuromyelitis optica spectrum disorders (NMOSD) using 548 longitudinally assessed full-field VEP studies over the course of ≥3 months. In response, Dr. Chen seeks clarification about the authors' finding of a reduction in VEP amplitude with ≥3 months of follow-up but not among those with ≥12 months of follow-up. Dr. Chen wonders whether there may be similar correlations between VEP amplitude and disease activity as seen with optical coherence tomography (OCT) measurements of the peripapillary retinal nerve fiber layer thickness—which seem to decrease in NMOSD patients with non-ocular relapses vs those with stable disease—and calls for prospective longitudinal studies with VEP, OCT, and MRI to further explore this topic. Responding to these comments, the authors note that whereas their more restricted analysis of patients with ≥12 months of follow-up was intended to address the potential amplification of measurement variability that may have occurred with their interpolation of shorter-interval data—i.e., for patients with <12 months follow-up—their sample size may have been insufficient to achieve significance for analyses of amplitude changes. Nonetheless, they note that latency findings showed consistent and reliable increases in both the main and sub-analyses. This exchange highlights the ongoing evolution of our understanding about progressive tissue damage in NMOSD, previously thought to occur only in the context of relapses. We agree with Dr. Chen that longitudinal correlation of visual tests of structure, physiology, and function will be necessary to understand how frequently subclinical progressive disease might occur in NMOSD.

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