To analyze myelin content within lesions and in the normal-appearing (NA) brain tissue in patients with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) versus multiple sclerosis (MS) and healthy controls (HC).

The phenomenon of T2-lesion resolution in patients with MOGAD has led to questioning of if such T2-lesions in attacks are due to true demyelination or transient myelin edema.

This cross-sectional observational study included patients with MOGAD (n=14) and age- and sex-matched patients with MS (n=6) and HC (n=15). All participants underwent a standardized brain MRI research protocol at 7T field strength including a quantitative T1 sequence (i.e., MP2RAGE). Patients were scanned during disease remission, and prior clinical MRI scans were analyzed for the presence of acute T2-lesions resolved. The longitudinal relaxation rate (R1=1/T1 relaxation time) was calculated from MP2RAGE and was used as proxy of myelin content (i.e., the higher the R1 the greater the myelin content).

MOGAD patients showed a trend towards reduced R1 in the NA deep grey matter compared to HC (0.651 vs 0.674, p=0.05), and overall similar to MS. When MOGAD patients were divided by history of cerebral MRI lesions, those with prior T2-lesions displayed significant reduction of R1 indicative of reduced myelin content in the NA deep grey matter (0.608 vs 0.674) and white matter (0.716 vs 0.765) compared to HC (p<0.01 for both), despite resolution of most acute T2-lesions. We found a total of 126 chronic T2-lesions in patients with MOGAD and 142 in patients with MS. The R1 was significantly reduced in MS lesions (0.528) compared to MOGAD’s (0.572, p=0.001).

Our data suggest that demyelination underlies T2-lesions in MOGAD but that myelin loss may be less than in MS. The reduction of the R1 may indicate either incomplete remyelination or a change in the magnetic tissue properties of the new myelin.