Bilateral retinal pathology following a first-ever clinical episode of autoimmune optic neuritis.

Neurol Neuroimmunol Neuroinflamm

From the Department of Health Sciences and Technology (C.A.W.), Swiss Federal Institute of Technology; Neuroimmunology and Multiple Sclerosis Research (C.A.W., P.M., T.S., J.V.M.H., S.S.), Department of Neurology, University Hospital Zurich and University of Zurich; Department of Information Technology and Electrical Engineering (P.M.), Swiss Federal Institute of Technology; and Department of Ophthalmology (J.V.M.H.), University Hospital Zurich and University of Zurich.

Published: March 2020

Objective: This longitudinal study aimed to assess changes in retinal structure and visual function following a first-ever episode of acute optic neuritis (ON).

Methods: Clinical and optical coherence tomography (OCT) data obtained over a period of 12 months were retrospectively analyzed in 41 patients with a first-ever clinical episode of acute ON. OCT scans, high-contrast visual acuity (HCVA), and low-contrast visual acuity (LCVA) were acquired at baseline and at 1, 3, 6, and 12 months thereafter. Macular ganglion cell and inner plexiform layer (GCIP), peripapillary retinal nerve fiber layer (pRNFL), and macular inner nuclear layer (INL) thicknesses were assessed by OCT. Linear mixed-effects models were used to analyze OCT variables of ipsilateral ON and contralateral non-ON (NON) eyes over time.

Results: The mean change of GCIP thickness in ON eyes was significant at all follow-up time points, with nearly 75% of the total reduction having occurred by month 1. In ON eyes, thinner GCIP thickness at month 1 correlated with lower LCVA at month 3. Mean pRNFL thickness in ON eyes differed significantly from NON eyes at all postbaseline time points. INL thickness was significantly increased in ON eyes (month 1) but also in contralateral NON eyes (month 12).

Conclusions: Retinal structural damage develops rapidly following acute ON and is associated with subsequent functional visual deficits. Our results also suggest bilateral retinal pathology following unilateral ON, possibly caused by subclinical involvement of the contralateral NON eyes. Moreover, our data may assist in clinical trial planning in studies targeting tissue damage in acute ON.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7051214PMC
http://dx.doi.org/10.1212/NXI.0000000000000671DOI Listing

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