Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Practical recommendations for diagnosis and management

Abstract

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a distinct antibody-mediated disease characterized by heterogeneous manifestations. Despite some overlap with other demyelinating CNS disorders, specific clinical-MRI features of MOGAD have been identified that facilitate early diagnosis. Paediatric and adult populations can be similarly affected but differ in the predominant clinical phenotypes, which include optic neuritis, myelitis, acute disseminated encephalomyelitis, brainstem/cerebellar syndromes, and cerebral cortical encephalitis.

Based on the recently international MOGAD panel proposed diagnostic criteria, a correct diagnosis of MOGAD relies on the detection of serum or CSF MOG antibodies (Abs) using cell-based assays in patients with compatible clinical-MRI phenotypes. Relapses occur in 40–80 % of cases with no single factor being able to reliably predict the disease course after onset, although monitoring antibody titers may offer some guidance. Intravenous steroids with subsequent tapering and rapid escalation to plasma exchange in case of incomplete recovery are usually administered in the acute stage, with intravenous immunoglobulins considered as a possible alternative. Chronic treatment should be administered in relapsing patients or in case of incomplete recovery from the presenting attack. In this review, we summarise the main features of MOGAD, with a focus on the clinical/imaging characteristics, diagnosis and treatment approach and propose practical recommendations for clinicians.