Cortical involvement and leptomeningeal inflammation in myelin oligodendrocyte glycoprotein antibody disease: A three-dimensional fluid-attenuated inversion recovery MRI study. (April 2022)

• Record Type: Journal Article
• 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
• Is Part Of: Multiple sclerosis. Volume 28:Number 5(2022)
• Page Start: 718
• Page End: 729
• Publication Date: 2022-04
• Subjects: Cortical demyelination -- leptomeningeal inflammation -- multiple sclerosis -- MOGAD -- 3D-FLAIR MRI; Central nervous system -- Diseases -- Periodicals; Myelin sheath -- Diseases -- Periodicals; Inflammation -- Periodicals; Multiple sclerosis -- Periodicals; Central Nervous System Diseases -- Periodicals; Demyelinating Diseases -- Periodicals; Inflammation -- Periodicals; Multiple Sclerosis -- Periodicals; Système nerveux central -- Maladies -- Périodiques; Gaine de myéline -- Maladies -- Périodiques; Inflammation (Pathologie) -- Périodiques; Sclérose en plaques -- Périodiques; Electronic journals; 616.834005
• DOI: 10.1177/13524585211034362
• Languages: English
• ISSNs: 1352-4585

Abstract

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.