Swelling of the Outer Retinal Layers in Acute Optic Neuritis (P4.042)

Background: Previous studies have demonstrated retinal nerve fiber layer swelling(RNFL) in acute optic neuritis(AON). In this cohort of patients, within 2 weeks of visual loss,we confirm and extend these findings, showing novel early changes in the outer retinal layers. Objectives: To examine the effect of AON on the retinal layers in the macular and papillo-macular bundle(PMB). Methods: 46 AON patients(33 men, 13 women, mean age 35) were recruited within 14 days of visual loss. Peripapillary RNFL thickness, macular volume and PMB scans were obtained. Retinal segmentation analysis was carried out. Average thickness measures for RNFL, ganglion cell and inner plexiform layer(GC/IPL), inner nuclear +outer plexiform layer(IN/OPL). In addition composite measures of ganglion cell complex(GCC= GC/IPL +NFL), outer retinal complex(ORC=outer nuclear layer + photoreceptor layer) and total retinal thickness were obtained. Results: Total macular retinal thickness was significantly greater in the affected compared with the fellow eye(p=0.008). Average macular ORC thickness was also significantly greater in the affected eye(p=0.001) with visible fluid in this layer in 2 patients. ORC thickness in both the nasal and temporal macular was increased uniformly when compared to the fellow eye. Total PMB thickness was significantly greater in the affected compared to the fellow eye(p=0.093). Average PMB GCC and ORC layers were significantly thicker in the affected eye(p=0.043, p=0.033 respectively). Peripapillary RNFL swelling was not significantly correlated with ORC thickness in the macula or PMB but was correlated with PMB GCC thickness(p= 0.0003). Conclusions: We found significant swelling in the ORC(macula & PMB) and GCC layers(PMB). Swelling of the ORC has not been reported previously in acute optic neuritis. The uniform nasal and temporal swelling and lack of correlation with RNFL thickness suggests a mechanism for ORC swelling other than spread of oedema from an inflamed optic nerve. A possible mechanism would be intrinsic cytotoxic oedema. Disclosure: Dr. Raftopoulos has nothing to disclose. Dr. Chen has nothing to disclose. Dr. Hickman has nothing to disclose. Dr. Toosy has nothing to disclose. Dr. Wheeler-Kingshott has received personal compensation for activities with Biogen Idec as an advisory board member. Dr. Altmann has received personal compensation for activities with Merck & Co., Inc. Dr. Mallik has nothing to disclose. Dr. Paling has nothing to disclose. Dr. Yiannakas has nothing to disclose. Dr. Schmierer has received personal compensation for activities with Sanofi-Aventis Pharmaceuticals Inc., Novartis, and Merck Serono as a speaker. Dr. Sheridan has nothing to disclose. Dr. Sharrack has nothing to disclose. Dr. Giovannoni has received personal compensation for activities with AbbVie, Biogen Idec, Canbex Therapeutics, Genzyme Sanofi, Ironwood Pharmaceuticals Inc., Novartis, Merck, Merck Serono, Roche, Synthon, Teva, Vertex, and Bayer Schering Pharma as a scie Dr Balcer received personal compensation from Biogen Idec and consulting for Biogen Idec, Vaccinex and Genzyme. She is on a clinical trial advisory board for Biogen-Idec., Prof. Miller has received honoraria through payments to his employer, UCL Institute of Neurology, for Advisory Committee and/or Consultancy advice in multiple sclerosis studies from Biogen Idec,;, Dr. Ishikawa has nothing to disclose. Dr. Kapoor received personal compensation for activities with Biogen Idec, Novartis, Genzyme, and Teva.