Evaluation of the retinal morphological and functional findings in optic neuritis related to multiple sclerosis

Background/Aim. Unilateral optic neuritis (ON), and its pathological substrate retrobulbar neuritis (RBN), is a common presenting symptom of multiple sclerosis (MS). Retina is the most proximal part of the optic pathway, and due to its close structural and physiological similarity to the CNS, often referred to as the ?window into the brain?. Our aim was to establish the diagnostic and prognostic value of structural and functional examination using novel, SS-OCT and OCTA techniques, in patients with MS who experienced RBN. Methods. We used a novel technique, optical coherent tomography (OCT) and angiography (OCTA), to examine retinal structural and functional changes in both the affected and the non-affected eye of patients with MS, and compared the findings with the healthy controls. Results. Using OCT, we found a significant difference in the structural integrity of retinal layers between the eye in which RBN had been detected, and the contralateral, non-affected eye (83.73 ? 18.36 vs 98.67 ? 11.84; p = 0.013). On the other hand, the functional examination of macular vascular plexus did not show significant differences between the affected and the non-affected eye in these patients (41.86 ? 1.52 vs 42.52 ? 1.40; p= 0.228). Interestingly, comparing the non-affected eye of patients with RBN and healthy controls, OCT examination revealed highly significant thinning in the inner plexiform layer of the macular ganglion cell layer (mGCLinpl) (61.07 ? 5.04 vs 67.53 ? 4.57; p < 0.001), showing that this may be a particularly sensitive and reliable biomarker of pathological changes in MS, and perhaps other neurodegenerative diseases. Conclusion. Overall, our research showed that OCT and OCTA offer an unprecedented opportunity for a safe, reliable and repetitive assessment of structural and functional retinal changes, as invaluable diagnostic and prognostic tools, and paving way for better understanding of pathogenic mechanisms underlying inflammatory demyelinating and neurodegenerative diseases.