Prognostic Factors Associated with Axonal Loss after Optic Neuritis (P4.175)

Objective We investigated possible associations between baseline clinical, electrophysiological and imaging measurements of acute optic neuritis (AON), and the extent of axonal loss after 6 months. Background AON is a common manifestation of multiple sclerosis in which neuroaxonal degeneration can lead to persistent visual impairment. The clinical and pathological factors which determine prognosis at onset have not been fully characterized. Design/Methods 86 participants in a phase II trial of neuroprotection with phenytoin in AON were investigated a mean of 8 days after symptom onset. Visual function (logMAR, low contrast acuity, Farnsworth-Munsell 100 hue measured color perception), optical coherence tomography (retinal nerve fiber layer [RNFL] thickness, macular volume), electrophysiology (VEP latency, amplitude), and optic nerve MRI (optic nerve lesional length, cross-sectional area) were obtained at baseline, and after 6 months. Pearson correlation coefficients and multiple linear regression were used to identify associations between baseline measurements and RNFL thickness at 6 months. Results In the placebo group, greater baseline affected RNFL thickness, when adjusted for baseline unaffected RNFL thickness (ie degree of affected RNFL swelling), was associated with final RNFL thinning (r=-0.34, p=0.03); this was not observed in the active group (r=-0.08, p=0.639). Also in the placebo group, baseline VEP latency was negatively associated (r=-0.39, p=0.010), and baseline VEP amplitude positively associated (r=0.37, p=0.017), with final RNFL thinning; results were similar in the active group. There were also significant negative associations in both placebo and active groups between baseline logMAR acuity, Farnsworth-Munsell 100 hue error score, and final RNFL thinning. There were no significant associations between baseline low contrast acuity or MRI lesion characteristics, and RNFL thinning. Conclusions The results in this cohort studied shortly after onset of AON confirm and extend previous findings, and suggest that measurements reflecting the intensity of acute inflammation, and possibly demyelination, are associated with axonal degeneration. Disclosure: Dr. Raftopoulos has nothing to disclose. Dr. Hickman has nothing to disclose. Dr. Toosy has received personal compensation for activities with Biogen Idec. Dr. Sharrack has nothing to disclose. Dr. Mallik has nothing to disclose. Dr. Paling has received personal compensation for activities with Teva Pharmaceuticals. Dr. Altmann has nothing to disclose. Dr. Yiannakas has nothing to disclose. Dr. Malladi has nothing to disclose. Dr. Sheridan has nothing to disclose. Dr. Sarrigiannis has nothing to disclose. Dr. Hoggard has nothing to disclose. Dr. Koltzenburg has received personal compensation from Pfizer, GlaxoSmithKline, Inc., and Merck Pharma. Dr. Koltzenburg has received research support from Pfizer. Dr. Wheeler-Kingshott has received personal compensation for activities with Biogen Idec as a consultant. Dr. Wheeler-Kingshott has received research support from the UK MS Society, UCL/UCLH, NIHR, BRC, EPSRC, ISRT, Wings for Life, and New Zealand Brain R Dr. Schmierer has received personal compensation for activities with Roche, Biogen, Teva, and, Novartis. Dr. Giovannoni has received personal compensation for activities with AbbVie Biotherapeutics Inc., Biogen, Bayer HealthCare, Genzyme, Merck Serono, Sanofi-Aventis, Teva, Ironwood, and Novartis. Dr. Miller has nothing to disclose. Dr. Kapoor has received personal compensation for activities with National Multiple Sclerosis Society, Multiple Sclerosis Society of GB&NI, and Novartis.