To describe the clinical, radiologic, laboratory and treatment features of MOG antibody-associated disease (MOGAD).

MOGAD identified an autoimmune disorder that presents as CNS demyelination, defined by autoantibodies to myelin oligodendrocyte glycoprotein (MOG). The development of specific cell-based assays (CBA) allowed the description of a variety of clinical manifestations.

The objective of this study is to describe a series of MOGAD cases from a single center in Argentina.

We performed a retrospective observational study at the Neuroimmunology Unit of Ramos Mejia Hospital, a Public Hospital of Buenos Aires City, Argentina, of patients with MOAGD.

Ten patients were included. The male / female ratio was 1: 1. The median age at the onset of symptoms was 30 years (range 8-60), two were pediatric. The initial clinical presentation was optic neuritis (ON) 80%, transverse myelitis (MT) 10% and NO + MT 10%. Seven patients (70%) presented a monophasic course. The relapses were ON (66.6%), 2(13.3%) MT, 1 (6.66%) NO + MT, 1 (6.66%) ADEM. The pediatric patients presented NMOSD phenotype. At the beginning, three patients (30%) presented normal brain MRI, five patients had gadolinium enhancement in one or both optic nerves, one presented a brainstem lesion and one unspecific lesion. 4/7 (57%) presented pathological findings on spinal cord MRI: 3 with involvement greater than three spinal segments, 1 of them affecting also the conus and the last one only the conus. All had negative oligoclonal bands in cerebrospinal fluid. Relapses were treated with intravenous methylprednisolone and 1 patient required add-on plasmapheresis. 8 patients received prolonged immunosuppression.

The most frequent clinical presentation was optic nerve involvement. Pediatric-onset patients had a different onset phenotype  from adults. Most of the patients showed a good response to corticosteroid therapy for the treatment of relapses and some needed chronic immunosuppression.