
MOGAD presents most commonly as ADEM, optic neuritis or transverse myelitis. 3,4 This number is likely to grow with increasing awareness of the disease.

Interestingly, MOGAD has a similar incidence as ADEM, with approximately 0.3 cases per 100,000 children recorded annually worldwide. The highest incidence of ADEM is recorded in winter and spring and the lowest in summer, likely reflecting seasonal variation in viral incidences. This discrepancy may be due to higher hospitalization rates from viral infections among these groups. 9 Black, Hispanic and children from other ethnic minority groups showed higher incidences than Caucasian children. 1,2,6,8,9 In a large retrospective USA study of over 3,000 paediatric ADEM hospitalizations between 20, the overall incidence of ADEM cases and costs were found to be increasing across all ages, except in the Northeastern USA. 5–8 The estimated worldwide incidence of ADEM is 0.2 –0.4 per 100,000 children annually, with up to 67 % presenting in those younger than 10 years.

The purpose of this review is, therefore, to clarify the differences between MOGAD and ADEM and provide practical updates based on real-world experience for the work-up and management of each.ĪDEM can have numerous causes, with over 70 % of cases preceded by infection. 4 However, here at the Cleveland Clinic Neurological Institute, it is our experience that many clinicians unfamiliar with neuroinflammatory disorders of childhood continue to diagnose, document and manage confirmed MOGAD cases exclusively as ADEM, which can result in suboptimal care. 3,4 Although MOGAD can present with ADEM, MOGAD is a specific disease with its own diagnostic criteria, prognostic implications and therapeutic requirements. 3 With increasing awareness and testing for MOGAD, many children who historically lacked a clear aetiology for ADEM are being diagnosed with MOGAD. 4 Both occur more frequently in children than adults.

2,3 Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease ( MOGAD), a specific neuronal antibody-mediated disease that can often present as ADEM, was discovered only in the last decade. Acute disseminated encephalomyelitis ( ADEM), first characterized in 1931, 1 is a non-specific clinical syndrome of polyfocal central nervous system (CNS) inflammatory demyelination it is characterized by encephalopathy and large, poorly demarcated cerebral white matter lesions.
