Search

The existence of antibodies to myelin oligodendrocyte glycoprotein (MOG) in some patients with CNS demyelinating disease has been recognised for 30 years, but their clinical utility as biomarkers, and potential pathogenicity in humans has only become apparent in the past 15 years. The advent of more precise live cell-based assays for antibody detection in serum and cerebrospinal fluid (CSF) has greatly refined the clinical phenotype of demyelinating diseases associated with MOG antibodies. Distinct patterns of MOG antibody associated disorder (MOGAD) include acute disseminated encephalomyelitis (ADEM) in children; and overlap with neuromyelitis optica spectrum disorders (including classical Devic’s presentations), optic neuritis, transverse myelitis, and focal encephalitis in both children and adults. A number of other rare presentations have also been described. Here we summarise what is currently known of the pathophysiology, clinical presentation and management of MOGAD.