Frequency of New or Enlarging Lesions on MRI Outside of Clinical Attacks in Patients With MOG-Antibody-Associated Disease

Abstract

Background and objective: To determine the frequency of new or enlarging T2-hyperintense or enhancing lesions outside of clinical attacks in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) vs multiple sclerosis (MS) and aquaporin-4 antibody positive neuromyelitis optica spectrum disorder (AQP4+NMOSD).

Methods: We retrospectively included Mayo Clinic patients with MOGAD with: (1) MOG-Immunoglobulin-G positivity by live cell-based assay, (2) fulfilling proposed MOGAD diagnostic criteria, and (3) baseline and follow-up paired MRIs without interval attacks. A neurologist and neuroradiologist reviewed MRIs (T2-fluid attenuated inversion recovery brain, T2 spine, and T1-postgadolinium brain and spine) to identify new or enlarging lesions. A MOGAD subset was then compared to patients with MS and AQP4+NMOSD, based on broadly similar interscan intervals.

Results: We included 105 patients with MOGAD (median age, 31 years [range, 2-80]; 60% female) with 373 paired MRIs. In total, 10/105 (9.5%) patients and 13/373 (3%) scans had one or more new T2 lesions (brain, 12/213 [6%]; spine, 1/160 [0.6%]); and 8/367 (2%) had enhancing lesions. New brain lesions were less in MOGAD (1/25 [4%]) than MS (14/26 [54%], p < 0.0001) but did not differ from AQP4+NMOSD (1/13 [8%], p = 1.0) in subgroup analysis. New spinal lesions were rare across groups (0%-4%).

Discussion: New or enlarging MRI lesions rarely develop outside of clinical attacks in MOGAD differing from MS. Surveillance MRIs in MOGAD have limited utility with implications for clinical practice and trial design.

Figure 1. Examples of New or Enlarging Lesions Occurring Between Attacks in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease

(A) The reference coronal MRI (T2-FLAIR) image reveals bilateral internal capsule and a left hemispheric T2-hyperintense lesion (A1, arrowheads) that on follow-up showed enlargement of the right internal capsule and left subcortical white matter T2-hyperintense lesions (A.b, arrows) in the absence of a new attack. (B) The reference axial MRI T2-FLAIR image (B.a) reveals normal brainstem and cerebellum signal while the follow-up image shows a new T2-hyperintensity in the left middle cerebellar peduncle (B.b, arrow) in the absence of a new clinical attack. The T2-lesion resolved completely and was no longer visible on a subsequent MRI FLAIR image (B.c) highly consistent with the expected evolution of a MOGAD lesion. (C) The reference axial MRI T2-FLAIR image (C.a) and axial T1 postgadolinium image (C.b) of the supratentorial region reveals no abnormalities but on follow-up show a new T2-hyperintensity had developed in the right frontal region (C.c, arrow) that enhanced after gadolinium (C.d, arrow) in the absence of a new attack. The lesion had resolved completely and was no longer visible on FLAIR (C.e) or T1 postgadolinium (C.f) images on a subsequent MRI highly consistent with the expected evolution of a MOGAD lesion. (D) The reference sagittal MRI cervical spine T1-weighted images postgadolinium revealed some subtle gadolinium enhancement (D.a, arrowhead) that increased in size in the follow-up (D.b, arrow) in the absence of a new attack despite no change in the T2-hyperintense cord lesion (not shown). The enhancement had resolved completely and was no longer visible on subsequent T1 postgadolinium image (D.c) highly consistent with the expected evolution of a MOGAD lesion. Abbreviations: FLAIR = fluid attenuated inversion recovery; MOGAD = myelin oligodendrocyte glycoprotein antibody-associated disease.