2025 American Academy of Neurology Abstract Website

Objective:

To investigate the presence and topography of grey matter atrophy in patients with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and multiple sclerosis (MS).

Background:

Cortical and thalamic damage are established pathological features of multiple sclerosis (MS). In myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) deep grey matter and cortical lesions are commonly found, particularly during an acute attack. It is not yet known if such lesions later result in volume loss in these regions in MOGAD.

Design/Methods:

We enrolled 23 patients with MOGAD, 17 patients with MS, and 18 healthy volunteers. Each subject underwent a 7T brain MRI scan including high-resolution 3D acquired sequences: T1-weighted MP2RAGE (0.75 mm isotropic), T2-weighted SPACE (0.75 mm isotropic) and double inversion recovery (DIR)-SPACE (1 mm isotropic). T2-hyperintense lesions were segmented on DIR images, and FreeSurfer software (v7.3.2) was used to obtain deep gray matter volumes, in particular thalamus, as well as cortical volumes/thickness. Age- and sex-adjusted MANCOVA on ranked variables was used for between groups comparisons.

Results:

T2-hyperintense lesion count and volumes were higher in MS than MOGAD (p<0.001). Compared to healthy volunteers, participants with both MOGAD and MS displayed a global grey matter atrophy, involving the cortex, the thalami, and the other grey matter nuclei (p<0.001). White matter atrophy was only observed among MS patients (p=0.009). No significant volumetric differences emerged in the comparison between MOGAD and MS patients.

Conclusions:

Despite small sample size, this study shows evidence of grey matter atrophy in MOGAD in both the thalamus and cerebral cortex, despite a lower lesion burden compared to MS. Since the majority of lesions are known to resolve in MOGAD, further research is needed to understand whether grey matter atrophy is associated with prior demyelinating attacks.