Cacciaguerra, Laura; Abdel-Mannan, Omar; Champsas, Dimitrios; Mankad, Kshitij; Krecke, Karl N; Chen, John J; Syc-Mazurek, Stephanie B; ... Flanagan, Eoin P; + view all Cacciaguerra, Laura; Abdel-Mannan, Omar; Champsas, Dimitrios; Mankad, Kshitij; Krecke, Karl N; Chen, John J; Syc-Mazurek, Stephanie B; Redenbaugh, Vyanka; Lopez-Chiriboga, Alfonso S; Valencia-Sanchez, Cristina; Hemingway, Cheryl; Tillema, Jan-Mendelt; Ciccarelli, Olga; Pittock, Sean J; Hacohen, Yael; Flanagan, Eoin P; - view fewer (2024) Radiologic Lag and Brain MRI Lesion Dynamics During Attacks in MOG Antibody–Associated Disease. Neurology , 102 (10) , Article e209303. 10.1212/WNL.0000000000209303.

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Abstract

Background and Objectives: Knowledge of the evolution of CNS demyelinating lesions within attacks could assist diagnosis. We evaluated intra-attack lesion dynamics in patients with myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) vs multiple sclerosis (MS) and aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorder (AQP4+NMOSD). // Methods: This retrospective observational multicenter study included consecutive patients from Mayo Clinic (USA) and Great Ormond Street Hospital for Children (UK). Inclusion criteria were as follows: (1) MOGAD, MS, or AQP4+NMOSD diagnosis; (2) availability of ≥2 brain MRIs (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 a single attack were evaluated for the following: new T2 lesions(s); resolved T2 lesion(s); both; or no change. This was compared between MOGAD, MS, and AQP4+NMOSD attacks. We used the Mann-Whitney U test and χ2/Fisher exact test for statistical analysis. // Results: Our cohort included 55 patients with MOGAD (median age, 14 years; interquartile range [IQR] 5–34; female sex, 29 [53%]) for a total of 58 attacks. The comparison groups included 38 patients with MS, and 19 with AQP4+NMOSD. In MOGAD, the initial brain MRI (median of 5 days from onset [IQR 3–9]) was normal in 6/58 (10%) attacks despite cerebral symptoms (i.e., radiologic lag). The commonest reason for repeat MRI was clinical worsening or no improvement (33/56 [59%] attacks with details available). When compared with the first MRI, the second intra-attack MRI (median of 8 days from initial scan [IQR 5–13]) showed the following: 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 reduced the likelihood of new T2 lesions (9/28 vs 18/30, p = 0.03). Intra-attack 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 lesions was exclusive to MOGAD (7/58 [12%]). // Discussion: Radiologic lag is common within MOGAD attacks. Dynamic imaging with frequent appearance and occasional disappearance of lesions within a single attack suggest MOGAD diagnosis over MS and AQP4+NMOSD. These findings have implications for clinical practice, clinical trial attack adjudication, and understanding of MOGAD pathogenesis.

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