Brighter Spotty Lesions Show Potential in Distinguishing AQP4-NMOSD From MOGAD

Disease Spotlight | <b>Disease Spotlight: NMOSD</b>

These findings have clinical implications for the diagnosis of AQP4-NMOSD and in helping clinicians differentiating it from other demyelinating diseases such as MOGAD.

By analyzing spinal MRI scans, investigators found a presence of brighter spotty lesions (BSLs) in patients with aquaporin-4 neuromyelitis optica spectrum disorder (AQP4-NMOSD) whereas this was not the case for those with myelin oligodendrocyte glycoprotein antibody disease (MOGAD).1

Senior author Ho Jin Kim, MD, PhD, consultant neurologist and principal scientist, National Cancer Center, Goyang, Korea, and colleagues concluded that BSL is a useful discriminator of myelitis in AQP4-NMOSD and MOGAD. They wrote that, "If this finding is reproduced by future investigation, BSL may emerge as a characteristic feature for revising the diagnostic criteria for AQP4-NMOSD."

Previous literature has shown that BSL is a helpful feature for discriminating AQP4-NMOSD from multiple sclerosis (MS) or other causes of myelopathy; however, there was no prior research explicitly comparing this marker in AQP4-NMOSD and MOGAD. A total of 133 spinal MRI scans, 65 from those with MOGAD and 68 from those with AQP4-NMOSD, were independently analyzed by a neuroradiologist and 2 neurologists.

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BSL was defined as a more hyperintense spotty lesion on axial T2 imaging than the usual T2-hyperintense lesion. The term "brighter" was used, in contrast to “bright” to describe these lesions, which reflected updates to the research lexicon. A total of 49 consecutive participants who had positive results for MOG antibodies and 61 age/attack severity-matched participants with positive results for AQP4 antibodies were included.

Using a 1.5-3T scanner, BSLs were found in 18 of 61 (30%) participants (19 of 28 [28%] of MRI scans) with AQP4-NMOSD, while none of the 49 participants (0 of 65 MRI scans) with MOGAD had BSLs (P <.0001). Between the 2 groups, T1 hypointense lesions and gadolinium enhancements were not significantly different. Although the difference was not significant (P = .0026), investigators did find that longitudinal extensive transverse myelitis (LETM) was common in patients with AQP4-NMOSD (54 of 61; 89%) and MOGAD (31 of 49; 63%). Notably, 2 of the 7 participants with AQP4-NMOSD who had LETM also had BSLs recorded.

There were a number of limitations to the study, including the fact that MRI protocols could not be completely unified due to their retrospective nature, although the exams reflected real-world clinical practice. This analysis also only included Asian populations, which the authors noted should prompt future prospective investigations, including pathological evaluations, in more diverse racial groups.

These findings were similar those recently conducted by Rabaste et al, which looked at the predictive value of axial-BSLs for AQP4-immunoglobulin seropositivity, and the radioclinical differences in patients with AQP4-NMOSD with and without axial BSLs. That retrospective study included 82 patients, 15 of which had AQP4-NMOSD and 67 others, considered as the other causes of myelopathy (OM) group.2

For patients with AQP4-NMOSD, the specificity and sensitivity of axial-BSLs was 94% (95% CI, 85.6-97.7) and 40% (95% CI, 19.8-64.3), respectively. Notably, investigators found that the presence of axial-BSLs was the only MRI characteristic associated with AQP4-IgG positivity (OR, 9.2 [95% CI, 1.2-72.9]; P = .022). Lastly, when comparing the 2 groups, median of cord expansion ratio was higher in those with axial-BSL (OR, 1.2; interquartile range [IQR], 1.1-1.3) than those without axial-BSL (OR, 1.1 [IQR, 1.0-1.2]; P = .046).

REFERENCES
1. Hyun JW, Lee HL, Park J. Brighter spotty lesions on spinal MRI help differentiate AQP4 antibody-positive NMOSD from MOGAD. Mult Scler J. Published online December 6, 2021. doi:10.1177/13524585211060326
2. Rabastéa, S, Cobo-Calvo, A, Nistiriuc-Muntean, V, et al. Diagnostic value of bright spotty lesions on MRI after a first episode of acute myelopathy. J Neuroradiol. 2021;48(1):28-36. doi:10.1016/j.neurad.2020.04.006