Recurrent Optic Neuritis (rON) is characterised by Anti-MOG Antibodies: A follow-up study (P5.274)

Abstract

Objective: To investigate patients with recurrent optic neuritis (rON) for anti-MOG antibodies. Background: Autoantibodies to myelin oligodendrocyte glycoprotein (MOG) have been identified in some patients with inflammatory demyelinating diseases including pediatric multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM) and AQP4-seronegative NMO spectrum disorders (NMOSD). rON refers to a clinically distinct subset of patients, thought to fall within the rubric of NMODS. These patients characteristically exhibit several steroid-sensitive episodes of optic neuritis (ON) and do not develop spinal cord symptomatology. Methods: We examined sera from 111 AQP4-negative patients with clinical features of either multiple sclerosis or NMOSD using a cell-based assay, which detects structural and extracellular anti-MOG epitopes. Screening was performed with human embryonic kidney cells, transiently transfected with MOG C-terminally fused to EGFP. Results: Anti-MOG antibodies were detected in 8 patients with ON; 5 of them were diagnosed as definite rON because they had 蠅3 episodes of ON without any other clinical symptomatology. Brain/orbital MRI or CSF analyses (when available) were normal except for optic nerve enhancement in two of them. Spinal cord MRI depicted a small subclinical chronic lesion in the cervical spine in one of 8 patients who never developed clinical symptoms of myelitis during our follow-up period. All anti-MOG-positive patients were steroid responsive but two of them, required other immunosuppressants, plasmapheresis or IVIG to suppress or prevent relapses. Conclusion: Patients with the clinically distinct entity of rON (AQP4-negative) are characterized by antibodies against MOG. Because anti-MOG antibodies have been also detected in typical NMOSD (either AQP4-negative or AQP4-positive), different MOG epitopes may distinguish rON from NMOSD. Whether in rON patients the anti-MOG antibodies are causally connected to conduction block in the optic nerve or demyelination is unclear. The pathogenicity of these antibodies is currently explored on optic nerve ex vivo preparations in our laboratory.

Disclosure: Dr. Chalmoukou has nothing to disclose. Dr. Stathopoulos has nothing to disclose. Dr. Alexopoulos has nothing to disclose. Dr. Akrivou has nothing to disclose. Dr. Dalakas has received personal compensation for activities with Baxter, Novartis, Grifols, CSL, Octapharma, Dysimmune Diseases Foundation, and Therapath. Dr. Dalakas has received personal compensation in an editorial capacity for Therapeutic Advances i