Cortical involvement and leptomeningeal inflammation in myelin oligodendrocyte glycoprotein antibody disease: A three-dimensional fluid-attenuated inversion recovery MRI study

Background: Cortical demyelination and meningeal inflammation have been detected neuropathologically in multiple sclerosis (MS) and recently in myelin oligodendrocyte glycoprotein antibody disease (MOGAD). Objectives: To assess in vivo cortical and leptomeningeal involvement in MOGAD. Methods: We pr...

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Published in:Multiple sclerosis 2022-04, Vol.28 (5), p.718-729
Main Authors: Tzanetakos, Dimitrios, Tzartos, John S, Vakrakou, Aigli G, Breza, Marianthi, Velonakis, Georgios, Stathopoulos, Panos, Pantou, Eirini, Markakis, Ioannis, Papadimitriou, Dimitra, Karavasilis, Efstratios, Toulas, Panagiotis, Evangelopoulos, Μaria-Eleptheria, Koutsis, Georgios, Anagnostouli, Maria, Stefanis, Leonidas, Kilidireas, Costantinos
Format: Article
Language:English
Subjects:
Brain architecture
Demyelination
Gadolinium
Glycoproteins
Humans
Imaging, Three-Dimensional
Immunoglobulin G
Inflammation
Inflammation - pathology
Lesions
Magnetic resonance imaging
Magnetic Resonance Imaging - methods
Meninges
Meninges - diagnostic imaging
Meninges - pathology
Multiple sclerosis
Multiple Sclerosis - pathology
Myelin
Myelin-Oligodendrocyte Glycoprotein
Oligodendrocyte-myelin glycoprotein
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Summary:Background: Cortical demyelination and meningeal inflammation have been detected neuropathologically in multiple sclerosis (MS) and recently in myelin oligodendrocyte glycoprotein antibody disease (MOGAD). Objectives: To assess in vivo cortical and leptomeningeal involvement in MOGAD. Methods: We prospectively evaluated 11 MOGAD and 12 relapsing-remitting MS (RRMS) patients combining three-dimensional fluid-attenuated inversion recovery (3D-FLAIR) and 3D-T1-weighted (3D-T1w) sequences at 3-Tesla magnetic resonance imaging (MRI). Leptomeningeal contrast enhancement (LMCE) was assessed on 3D-FLAIR post-gadolinium (3D-FLAIRGd). Cerebral cortical lesions (CCLs) were classified as either intracortical–subpial (IC–SP) or leukocortical (LC). Results: CCLs were present in 8/11 MOGAD and 12/12 RRMS patients, with the number of CCLs being significantly lower in MOGAD (median (interquartile range (IQR)) 3 (0.5–4) vs 12 (4.75–19), p = 0.0032). In MOGAD, IC–SP lesions were slightly more prevalent than LC lesions (2 (0–2.5) vs 1 (0–2), p = 0.6579); whereas in RRMS, IC–SP lesions were less prevalent than LC lesions (3.5 (2.75–5.5) vs 9 (2–12.75), p = 0.27). LMCE was observed in 3/11 MOGAD and 1/12 RRMS patients; MOGAD with LMCE showed an increased median number of CCLs compared with MOGAD without LMCE (8 (4–9) vs 2.5 (0.75–3.25), p = 0.34). No correlation was observed between MOGAD MRI findings and (a) MOGAD duration, (b) serum MOG-immunoglobulin G1 titers, and (c) oligoclonal band presence. Conclusion: We described cortical lesion topography and detected for the first time LMCE using 3D-FLAIRGd sequences in MOGAD patients.
ISSN:1352-4585
1477-0970
DOI:10.1177/13524585211034362