ABSTRACT
INTRODUCTION: The diagnosis of optic neuritis (ON), or inflammation of the optic nerve, is based on clinical findings: first marked by rapidly progressive visual decline associated with eye pain accentuated by eye movements; abnormalities of color perception and/or contrast sensitivity may also be reported. In this case, inflammatory neuropathies are associated with anti-MOG antibodies. MOGs, oligodendrocytic glycoproteins involved in the production of myelin, were identified nearly three decades ago in association with demyelinating ON. The first series were reported in children following demyelinating neurological manifestations, particularly in ADEM (acute demyelinating encephalomyelitis) or multiple sclerosis (MS) [1]. Anti-MOGs are associated with neuropathies in the phenotypic setting of the neuromyelitis optica (NO) spectrum, and anti-Aquaporin 4 antibodies (AQP4) are negative by definition. Thus, anti-MOG could explain up to 30 % of cases of seronegative optic neuritis; their presence thus represents a significant diagnostic aid for the clinician, especially during a first neurological episode [1]. The first short published series in AQP4-/MOG+populations revealed primarily ophthalmological involvement with a good prognosis for recovery [1]. Knowledge of these antigens is important; it may permit not only an understanding of the physiopathology but also the stratification of patients in terms of prognosis and response to treatment [2]. Thus, the early diagnosis of anti-MOG positive ON must prompt aggressive initial treatment and a more or less maintenance therapy to prevent recurrence. The role of the ophthalmologist remains paramount, since most cases present with purely ocular involvement. MATERIALS AND METHODS: We report herein the clinical, ophthalmological, laboratory and radiological data for 25 patients (45 eyes) managed between February 2011 and January 2017. All of our patients had optic neuritis associated with anti-MOG antibodies. All patients underwent the following testing: - Visual acuity; - Humphrey and/or Goldmann visual field; - Non-mydriatic fundus photography; - Optic disc OCT; - 3 Tesla orbital-cerebral MRI with and without contrast; - Standard and immunological laboratory testing for anti-MOG and anti AQP4 antibodies by Western Blot and ELISA. RESULTS: The male: female ratio of the population was 0.92 (13 women and 12 men). The average age at onset was 35.68 years (15 to 60 years); 40 % of the subjects were between 31 and 40 years old. The initial symptoms leading to consultation were mostly visual acuity (80 %) and pain (88 %). Involvement was bilateral in 80 % of cases (5 unilateral). Initial visual acuity was poor; 52 % of eyes were less than or equal to count fingers. The course was favorable however, with visual acuity returning to 10-12/10 after 6 months of follow-up (84 % of eyes). Orbital/cerebral MRI with attention to the visual pathways revealed involvement of the anterior visual pathways with gadolinium uptake in 92 % of cases. Of the 35 eyes initially considered affected, the main initial diagnoses were: - 36 % retro-bulbar optic neuritis (RBON); - 40 % anterior optic neuritis (AON); - 24 % other; of which 16 % were initially diagnosed as acute anterior ischemic optic neuropathy (AAION). 96 % of patients received corticosteroid treatment in the acute phase. 16 % required plasma exchange sessions. Maintenance therapy was proposed for only 36 % of the population. CONCLUSION: Optic neuritis is a pathology frequently encountered in ophthalmology; a good knowledge of symptoms and clinical signs is essential for early diagnosis and optimal management. The identification of autoantibodies, including anti-MOG antibodies, is important for patient management and is part of the required testing for all cases of optic neuritis, in order to adapt the treatment of the acute episode and to provide maintenance therapy to avoid recurrence.
