To analyze lesion dynamics within the same attack in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) versus multiple sclerosis (MS) and aquaporin-4-IgG-positive-neuromyelitis optica spectrum disorder (AQP4+NMOSD).

Retrospective observational multicenter study including patients from Mayo Clinic (USA) and Great Ormond Street Hospital for Children (UK). Inclusion criteria: (1)MOGAD diagnosis; (2)Availability of ≥2 brain MRIs (all within 30 days of attack onset) and (3)Brain involvement (i.e., ≥1 T2-lesion) on ≥1 brain MRI.  The initial and subsequent brain MRIs within the same MOGAD attack were evaluated for: new T2-lesions(s); resolved T2-lesion(s); both, or no change. This was compared to MS and AQP4+NMOSD attacks.

Our cohort included 55 MOGAD patients with 58 attacks, 38 MS, and 19 AQP4+NMOSD patients. In MOGAD, the initial brain MRI (median of 5 days from onset [IQR, 3-9]) was normal in 6/58 (10%) MOGAD attacks despite clinical symptoms (i.e., radiological lag). The commonest reason for repeat MRI was clinical worsening or no improvement (33/56[59%] attacks with details available). When compared to the 1^st MRI, the 2nd intra-attack MRI (median of 8-days from initial scan [IQR, 5-13]) showed: new T2-lesion(s) 27/58 (47%); stability 24/58 (41%); resolution of T2-lesion(s) 4/58 (7%); or both new and resolved T2-lesions 3/58 (5%). Findings were similar between children and adults. Steroid treatment was associated with resolution of >1 T2-lesion (6/28[21%] vs 1/30[3%], p=0.048) and a reduced the likelihood of new T2-lesions (9/28 vs 18/30, p=0.03). MRI changes favored MOGAD (34/58[59%]) over MS (10/38[26%], p=0.002) and AQP4+NMOSD (4/19[21%], p=0.007). Resolution of ≥1 T2-lesion was exclusive to MOGAD (7/58[12%]).

Radiologic lag is common within MOGAD attacks. Dynamic imaging suggests MOGAD over MS and AQP4+NMOSD. These findings have implications for clinical practice, clinical trial attack-adjudication and understanding of MOGAD pathogenesis.