When MOGAD mimics MS: diagnostic and therapeutic insights from a unique CNS demyelinating case

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) lacks specificity in clinical and neuroimaging characterization. Expanding clinical and MRI findings is important for understanding MOGAD; however, the role of oligoclonal bands (OCBs) remains unclear.

A previously healthy man presented with slowed responses, slurred speech, and an unsteady gait for one week. Brain MRI-enhanced scans revealed nodular, circular, perivascular Line-like, and pepper-like enhancements. Anti-MOG antibody titer was 1:100, and OCBs were present in both serum and cerebrospinal fluid (CSF), with higher number of bands in the CSF. The patient received intravenous methylprednisolone pulse therapy and showed remarkable clinical and radiological improvements. Oral prednisone tapering and mycophenolate mofetil were used to prevent relapse. MRI demonstrated MS-like lesion activity during the 2-year follow-up period, though no clinical relapse occurred.Anti-MOG antibody titer was 1:32 in both CSF and serum, and OCBs were present only in the CSF (≥ 2 discrete bands).We used the cell-based assay (CBA) to detect the antibody status of MOG and NMDAR-Abs in both serum and cerebrospinal fluid (CSF) samples. The detection of MOG-IgG antibodies in the case used the fixed Cell-Based Assay. The specific secondary antibody was the FITC-conjugated goat anti-human IgG antibody.

This case reveals that varied MRI features in MOGAD underscore the complexity of the disease. Although OCB positivity is associated with a higher risk of relapse in MOGAD patients [1-3]continuous MRI remains the primary method for detecting subclinical disease activity. Due to its invasive nature and limited value in assessing disease progression, repeated CSF analysis for routine OCB monitoring is not recommended.