Dynamic MRI Lesion Evolution in Pediatric Myelin-Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD)
Omar Abdel-Mannan1, Dimitrios Champsas2, Sharmila Manivannan3, Kshitij Mankad4, Rachel Kneen5, Manali Chitre3, Sukhvir Wright6, Evangeline Wassmer6, Cheryl Hemingway4, Thomas Rossor7, Ming Lim7, Olga Ciccarelli8, Yael Hacohen2
1Queens Square MS Centre, UCL Queen Square Institute of Neurology, 2UCL Queen Square Institute of Neurology, 3Addenbrooke’s Hospital, 4Great Ormond Street Hospital for Children, 5Alder Hey Children’s Hospital, 6Birmingham Children’s Hospital, 7Evelina London Children's Hospital, 8UCL Institute of Neurology
Objective:

To evaluate MRI lesion evolution over time and correlate with patients’ clinical state.

Background:
In Myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD), both radiological lag with worsening of the MRI during clinical recovery and dramatic lesion resolutions have been reported. There are few studies studying lesion evolution in pediatric MOGAD.
Design/Methods:

Clinical and paraclinical features were reviewed in children (<18yr) with MOGAD from five UK tertiary paediatric neurosciences centres between 2014-2022.

Results:
 558 MRI scans from 152 patients and 295 attacks were available for analysis. Median age at presentation was 6.1yrs (IQR 4.0-10.6), 64 (42.1%) were male and 41 (26.9%) were of non-White ethnicities. At final follow-up (median period 4.42 years, IQR: 2.28-7.74) 57/152 (37.5%) had a relapsing disease course. Median number of relapses were 3, IQR (2-4). At onset, brain lesions were seen in 84/152 (55.2%), spine in 31/152 (20.3%), optic nerve in 48/152 (31.5%) and gadolinium-enhancing lesions in 34/42 (80.9%). MRI was normal in 8/152(5.2%) at first scan, of which 4/8 had new asymptomatic lesions within 1 month. New asymptomatic lesions (> 1 month) following first clinical event were seen in 17/152 (11.1%) with persistent contrast enhancement in 8/49 (16.3%). Of 89 patients who had follow-up imaging following first attack, 16 relapsed within 6 months, complete lesion resolution was reported in 26/89 (17.5%) (22 monophasic, 4 relapsing) following 1st acute attack, 7/35(20%) after 2nd acute attack, and 1/16 (6.2%) following 3rd acute attack and none following further relapses. Partial resolution of MRI lesions was seen in 19/51 (37.2%) monophasic patients and 9/39(23%) relapsing patients after the first follow-up scan (p>0.5).
Conclusions:

Lesions in paediatric MOGAD are dynamic and timing of MRI scanning may reveal different regional involvement. Unlike in MS, a significant number of MOGAD patients will have complete lesion resolution at first follow-up, although this repair ability is reduced in relapsing patients.

10.1212/WNL.0000000000203960