Papers of the Week

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.