Time to separate MOG-Ab-associated disease from AQP4-Ab-positive neuromyelitis optica spectrum disorder

Antibodies (Abs) against conformational myelin oligodendrocyte glycoprotein (MOG) are a recently well-recognized cause of acquired demyelination. MOG-Abs have been frequently reported in children presenting with acute disseminated encephalomyelitis and optic neuritis but also in adults with neuromyelitis optica spectrum disorder (NMOSD) and its limited forms.1 Although MOG-Abs were initially linked to a monophasic presentation,2 longer follow-up times have shown an increasing number of patients with positive MOG-Abs and relapses.3 The clinical phenotype of patients with MOG-Ab–associated relapsing disease is different from that of patients with multiple sclerosis (MS) but overlaps that of patients with aquaporin 4 (AQP4)–Ab NMOSD.2,4,5 The presence of MOG-Abs is usually associated with better visual and motor outcomes than AQP4-Ab and quicker response to first-line treatments,1 although a treatment-resistant group, who relapse on therapeutic doses of rituximab, has been reported.6