Temporal Evolution of MRI Lesions Identified in Different CNS Demyelinating Disorders

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Complete resolution of the index T2-lesion and resolution of all T2 lesions occurred most often in patients with MOGAD rather than AQP4-IgG-NMOSD or MS.

Research recently published in Neurology by investigators at Mayo Clinic showed that complete resolution of T2-lesion occurs more frequently in patients with myelin-oligodendrocyte-glycoprotein-IgG-associated disorder (MOGAD) compared with other demyelinating diseases such as aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD) or multiple sclerosis (MS).

Senior author Eoin P. Flanagan, MBBCh, neurologist, Mayo Clinic Rochester, and colleagues concluded that, "this has implications for diagnosis, monitoring disease activity, and clinical trial design, while also providing insight into pathogenesis of central nervous system demyelinating diseases.”

In this descriptive study, investigators identified 156 patients (MOGAD, n = 38; AQP4-IgG-NMOSD, n = 51; MS, n = 67) who had brain or myelitis attack, available attack MRI within 6 weeks, and follow-up MRI beyond 6 months without interval relapses in that region to better understand lesion evolution. Neuroradiologists were blinded to diagnosis and reviewed MRIs independently to determine resolution of T2-lesions by consensus.

A total of 172 attacks (brain, n = 81; myelitis, n = 91) were identified in the study. Complete resolution of the myelitis index lesion, with or without normalization of the entire spine MRI, was observed in 72% of MOGAD, 17% of MS, and 14% of patients with AQP4-IgG-NMOSD (P <.001). All index lesions in the APQ4-IgG-NMOSD and MS groups that resolved completely were infra-tentorial while in the MOGAD group they were both supra-tentorial (n = 6) and infra-tentorial (n = 7).

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A complete resolution of all the specific T2 abnormalities at MRI follow-up was more common with MOGAD for both brain (MOGAD, 39%; AQP4-IgG-NMOSD, 10%; MS, 5%) and spinal cord (MOGAD, 79%; AQP4-IgG-NMOSD, 0%; MS, 0%) attacks. The median time from acute to first available normal brain MRI in those in whom T2-lesions resolved were 19 months in the NMOSD group (range, 1-96), 26 months in APQ4-IgG-NMOSD (range, 18-95), and 11 months in the MS group (range, 10-13). In patients with MOGAD with a myelitis attack, the median time to first normal follow-up MRI was 9 months (range, 1-96).

When predicting T2-lesion resolution in patients with MOGAD, no significant associated was found with time interval between acute and follow-up MRI, gender, acute lesion area, abnormal gadolinium enhancement on acute MRI, interval disease relapses in other CNS regions, cervical versus thoracic spinal cord location, MOGAD phenotype, monophasic versus relapsing course of the disease, administration of acute treatment and its type, or commencement of long-term immunosuppressive therapy and its types.

Acute immunotherapy was more commonly a monotherapy of intravenous and/or oral corticosteroids in the MS cohort (43 of 46; 93%), compared to the MOGAD (23 of 38; 61%) and AQP4-IgG-NMOSD (29 of 46; 63%) groups (P <.001). Notably, single-agent treatments with intravenous immunoglobulins (IVIG; 2 patients with MOGAD) or plasma exchange (PLEX; 1 patient with AQP4-IgG-NMOSD).

In patients with brain attacks, the median axial area reduction for the index lesions was higher in MOGAD (213 mm2 [range, 55-873]) compared to AQP4-IgG-NMOSD (104 mm2 [range, 0.7-597]) and MS (36 mm2 [range, 0-506]) (all, P <.001). Investigators noted there was no significant difference between patients with AQP4-IgG-NMOSD and MS in the median relative percent reduction from acute MRI.

In the spinal cord, the median index lesion area reduction was similar in patients MOGAD and AQP4-IgG-NMOSD both on sagittal (262 mm2 [range, 0-888] versus 309 mm2 [range, 0-1885]; P = .4) and axial (34 mm2 [range, 4-100] versus 23 mm2 [range, 1-118]; P = .3) images, although the median relative percent reduction in size compared to the acute MRI was higher in the MOGAD group.

Flanagan et al noted that the study is limited by the retrospective nature and lack of standardized MRI assessment of CNS lesions at a regular time interval on the same MRI scanner. Despite the need for such studies, they are often difficult to execute.

REFERENCE
Sechi E, Krecke KN, Messina SA, et al. Comparison of MRI lesion evolution in different central nervous system demyelinating disorders. Neurology. Published online July 14, 2021. doi: 10.1212/WNL.0000000000012467