WH01
In Vivo Detection of Deep Retinal Neuronal Layer Changes Following Acute Optic Neuritis Utilizing Optical Coherence Tomography Derived Segmentation

Friday, May 30, 2014: 11:00 AM
Omar Al-Louzi, MD , Neurology, Johns Hopkins University, Baltimore, MD
Pavan Bhargava, MD , Neurology, Johns Hopkins University, Baltimore, MD
Scott D Newsome, D.O. , Department of Neurology, Johns Hopkins University, Baltimore, MD
Peter A Calabresi, MD, FAAN , Neurology, Johns Hopkins University, Baltimore, MD
Shiv Saidha, MD , Neurology, Johns Hopkins University, Baltimore, MD


PDF
Background:

Following acute optic neuritis (AON), retinal nerve fiber layer (RNFL) and ganglion cell layer (GCL) thinning are well-described. Inner (INL) and outer nuclear layer (ONL) abnormalities have recently been detected in multiple sclerosis (MS) and may be associated with increased accumulation of disability, underpinning their clinical importance. However, comprehensive assessment of INL and ONL changes following AON remains largely unexplored.

Objectives:

To determine whether objective changes in INL and ONL thicknesses occur following AON, and how these may be temporally related to thickness changes of the RNFL and GCIP (composite thickness of GCL + inner plexiform layer) following AON.

Methods: 34 patients (29 with relapsing-remitting MS and 5 with clinically isolated syndrome) underwent Cirrus-HD OCT imaging, including automated intra-retinal layer segmentation, as well as visual function testing within 4 weeks of AON onset  and serially thereafter (median: 25 months [range: 7-55]). Student's paired t-test was used to compare retinal layer thickness changes, relative to baseline, for each eye.

Results:

At the 4±1 month visit after AON, the mean decrease in GCIP thickness was 12.1% relative to baseline (n=29; p<0.001). During the same time period, there were concomitant increases in the average thicknesses of both the INL; mean 2.0% (p=0.003, 95% CI: 0.7, 3.3), and the ONL; mean 3.8% (p<0.001, 95% CI: 2.6, 5.1). The percentage increase in ONL thickness of the affected eyes at the 4±1 month visit was strongly correlated with the percentage decrease in GCIP thickness from baseline at the same visit (r=0.58, p=0.001). In patients with more than 2 years of follow up (n=16), INL and ONL thicknesses were significantly increased, relative to baseline, at 4±1 months (mean change: 2.6% and 2.9%; p=0.021 and 0.0008 respectively) but not after 24 months (mean change: 0.4% and -0.2%; p=0.64 and 0.67 respectively), despite persistent GCIP thinning (mean change: -13%; p<0.001).

Conclusions:

OCT segmentation demonstrates increases in INL and ONL thicknesses following AON in the absence of microcystic macular edema (MME). These increases may be proportional to the degree of GCIP loss in affected eyes which is a novel finding, raising the possibility that biological changes may occur in the deep retinal neuronal layers following AON. Exploring these changes could help further our understanding of the pathobiology of MS.