Author Of 1 Presentation
P0704 - Cortical involvement in MOG IgG–positive patients : a multicenter MRI study (ID 1853)
Abstract
Background
Cortical involvement in neuropathological studies has been identified in Multiple Sclerosis (MS) and recently in myelin oligodendrocyte glycoprotein antibody disease (MOGAD) patients. Neuroimaging findings also seem to confirm cortical involvement as cerebral cortical lesions (CCLs) and leptomeningeal contrast enhancement (LMCE) have been shown in 3D-FLAIR sequences in MS patients.We described recently LMCE in MOGAD-patients with 3D-FLAIR post-gadolinium (3D-FLAIRED) sequences.
Objectives
To assess the presence and type of CCLs and the possible relation between CCLs and LMCE in MOGAD-patients using a 3 Tesla-MRI-scanner.
Methods
We conducted a brain MRI study including 11 MOGAD patients (MOG-IgG1 serum detection with cell-based-assay) with CNS demyelination and 12 Relapsing-Remitting MS (RRMS) patients as a control-group. In these groups, 8/11 and 6/12 were females, with a mean age at MRI acquisition 45.2 years and 38.25years in MOGAD and RRMS groups respectively. Exclusion criteria of this study were a clinical relapse or administration of intravenous corticosteroids within one month preceding MRI acquisition. LMCE foci were identified as hyperintensities on 3D-FLAIRED and not on 3D-T1-weighted-post-gadolinium sequences. For the detection of CCLs both high signal on 3D-FLAIR and low in 3D-T1-weighted sequences were required. Due to limitations of 3Tesla, CCLs were classified in two subgroups: a) intracortical/subpial or b) leukocortical lesions.
Results
CCLs were detected in 8 out of 11 patients in the MOGAD-group with mean-number-of-lesions (MNLs) 4.375 and in all of the RRMS-group with MNLs 12.25. In MOGAD, leukocortical-MNLs (2.143) was similar to intracortical/subpial-MNLs (2.714), whereas a predomidance of leukocortical (MNLs 9.82) versus intracortical/subpial (MNLs 4.82) lesions was observed in RRMS. LMCE was observed in 3 out of 11 in the MOGAD-group and in 1 out of 12 in the RRMS–group. In the MOGAD-group, LMCE presence was related to a higher lesion number in both lesion subtypes when compared to the MOGAD patients without LMCE.
Conclusions
Our study showed the ability of 3D-FLAIR joint with 3D-T1-weighted sequences in disclosing and classifying CCLs in MOGAD. An association between LMCE and the extent of cortical demyelination in MOGAD was evident, suggesting that meningeal inflammation may contribute in cortical lesion development. Moreover, cerebral cortical lesion number was higher in RRMS compared to MOGAD.