Association between retinal layer thickness and cortical lesions at the onset of clinically isolated syndrome (P11-3.012)

Abstract

<h3>Objective:</h3> The aim of this study was to evaluate the relationship between retinal layer thickness, cortical lesions (CLs) and disability at the onset of the first demyelinating event (a clinically isolated syndrome (CIS), suggestive of multiple sclerosis (MS). <h3>Background:</h3> Neuroaxonal degeneration is considered the primary cause of permanent disability in patients with MS, thus new biomarkers to quantify neurodegeneration are needed. Reduced retinal layer thickness in MS exists irrespective of optic neuritis (ON) and has been correlated with disability and brain atrophy. In CLs, neuroaxonal degeneration is also present. The relationship between retinal atrophy, CLs and disability in CIS is not well established. <h3>Design/Methods:</h3> We performed a cross-sectional evaluation of thirty-nine patients with CIS known to have CLs as identified on 3T brain MRI, who also underwent Optical Coherence Tomography to quantify retinal layer thickness. We excluded affected eyes in ON patients and used the average values of both eyes in patients without ON. We performed linear regression analyses to evaluate the relationships between the retina measures and CLs characteristics as well as clinical outcomes. Significant results with p&lt;0.05 are reported. <h3>Results:</h3> We found that a thinner combined ganglion cell-inner plexiform layer (GCIPL) was associated with higher juxtacortical lesion numbers and volumes. A thinner peripapillary retinal nerve fiber was associated with higher leukocortical, juxtacortical and total cortical lesion volumes. A thinner GCIPL was correlated with greater disability as measured by the expanded disability status scale. A reduced thickness of GCIPL and inner nuclear layer were associated with MS diagnosis at presentation. <h3>Conclusions:</h3> This study provides support for a relationship between increased cortical damage and retinal layers thinning in CIS suggesting a common pathological process behind these alterations. The association between greater retinal damage and disability confirms the role of GCIPL as a possible biomarker of neurodegeneration even at this early stage of the disease. <b>Disclosure:</b> Dr. Varmpompiti has nothing to disclose. Dr. Chow has nothing to disclose. The institution of Dr. Foster has received research support from Medical Research Council. Dr. Kodali has nothing to disclose. Marios Yiannakas has nothing to disclose. Dr. Kanber has nothing to disclose. Ferran Padros, 8186 has nothing to disclose. Dr. Davagnanam has nothing to disclose. Prof. Ciccarelli has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Novartis. Prof. Ciccarelli has received personal compensation in the range of $0-$499 for serving on a Speakers Bureau for Merck. Prof. Ciccarelli has received personal compensation in the range of $10,000-$49,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for NEUROLOGY Journal. The institution of Ahmed Toosy has received research support from Rosetrees Trust. The institution of Sara Collorone has received research support from Rosetreest Trust. The institution of Sara Collorone has received research support from MAGNIMS/ECTRIMS.