Case Report: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder Masquerading as Multiple Sclerosis: An Under-Recognized Entity?

Yang Zheng,Yin-Xi Zhang,Er-Chuang Li,Chun-Hong Shen,Meng-Ting Cai,Wei Fang

doi:10.3389/fimmu.2021.671425

Abstract

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) covers a wide spectrum of manifestations and is defined by the presence of MOG seropositivity. However, in a proportion of patients, there may be an overlap in some of the clinical and radiological manifestations between MOGAD and multiple sclerosis (MS). Being wary of this entity is critical to ensure appropriate therapy. Herein, we present a case with recurrent episodes of short-segment myelitis typical for multiple sclerosis, but later diagnosed as MOGAD by MOG antibody seropositivity. This case, along with previous reports, highlights an increasingly recognized subgroup in MOGAD with initial clinical phenotypes suggestive of MS, but later showing a disease course and therapeutic response compatible with MOGAD. Given the potential overlap of some clinical phenotypes in patients with MS and those with MOGAD, we recommend MOG antibody testing in all patients with recurrent short-segment myelitis, conus medullaris involvement, and those who demonstrated steroid dependence.

Highlights

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is increasingly recognized as a distinct disease entity, yet with a wide spectrum of presentations [1]
We report a case with findings initially concerning for multiple sclerosis (MS) yet subsequently diagnosed with MOGAD (Figure 1)
It is recognized that patients with MOGAD could have typical MS attacks at onset [2,3,4]

Summary

INTRODUCTION

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is increasingly recognized as a distinct disease entity, yet with a wide spectrum of presentations [1]. The patient returned to the clinic when on 10 mg/d prednisolone and reported aggravation of numbness and FIGURE 2 | Spinal MRI of the first and third attack. (A–C) Cervical (T2-weighted imaging) and thoracic (fat-saturated T2-weighted imaging) spinal MRI of the initial attack revealed multiple T2-hyperintense lesions throughout the spinal cord. The patient reached both the temporal and spatial dissemination criteria of clinically definite MS Another course of intravenous methylprednisolone (500 mg/d) was initiated with a complete remission of symptoms. Repeat spinal MRI revealed co-existence of both new lesions and old lesions along the cervical and thoracic cords (Figures 2D–F). Given the constellation of recurrent short-segment myelitis, serum MOG antibody positivity and prominent therapeutic response to and dependence on steroid, the diagnosis of MOGAD was made. The patient declined repeat brain or spinal imaging due to an absence of clinical signs or symptoms

DISCUSSION

18 Myelitis

Findings

ETHICS STATEMENT