The Clinical and Radiologic Features of Patients with Myelin Oligodendrocyte Glycoprotein (MOG) Antibody-Associated Disease (MOGAD) in the City of Sakarya, Türkiye

Saadet Sayan; Esen Çiçekli; Onur Taydaş; Mohammadreza Yousefi; Tansu Doran; Dilcan Kotan

doi:10.12996/gmj.2025.4255

ABSTRACT

Objective

The study aims to share our knowledge on myelin oligodendrocyte glycoprotein antibody (anti-MOG) seropositivity in patients with demyelinating diseases, focusing on their clinical, serologic, and radiologic characteristics, as well as treatment options for MOG associated disease (MOGAD) cases.

Methods

This retrospective study included 332 of 450 demyelinating disease cases, aged 18 to 65 years, who were referred to our clinic from 2017 to 2023 with clinical and/or radiological signs of demyelination, followed by testing for the anti-MOG antibody. We applied the revised 2017 McDonald criteria and the 2023 MOGAD diagnostic criteria to those who tested positive for anti-MOG. Cases of anti-MOG seronegative multiple sclerosis (MS) and non-MOGAD were excluded. We detailed the clinical, serologic, and radiologic characteristics and treatment protocols of anti-MOG-positive/low-positive cases.

Results

Among the cases, 16 were clear/low anti-MOG seropositive; of these, 10 were diagnosed with MOGAD, three were MS associated with anti-MOG seropositivity, and three were considered possible MOGAD and followed up. Four MOGAD cases (40%) were double positive for anti-MOG and oligoclonal bands. Three MOGAD cases also had autoimmune diseases. Rare clinical presentations included sixth cranial nerve palsy, tetraparesis secondary to acute disseminated encephalomyelitis, wall-eyed bilateral internuclear ophthalmoplegia and progressive transverse myelitis in adulthood. A total of 300 cases were diagnosed with MS, and 1% of these cases were anti-MOG with low levels of seropositivity.

Conclusion

The pathogenesis, treatment, and prognosis of MOGAD differ from those of other demyelinating diseases. We aim to highlight the importance of recognizing MOGAD due to its potential association with autoimmune diseases, progressive nature, and dual seropositivity. Thus, it should be considered for its unique clinical and radiologic features.

Keywords:

Myelin oligodendrocyte glycoprotein, MOG, myelin oligodendrocyte glycoprotein antibody associated disease, atypical demyelinating diseasesi MOGAD.

INTRODUCTION

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) has been identified as a distinct immune-mediated demyelinating disease of the central nervous system, and recently published diagnostic criteria for MOGAD have facilitated its identification (1, 2). Although the global prevalence of the disease is still uncertain, studies suggest an incidence of 1.6-3.4 cases per million people per year in Europe, with a prevalence of 20 per million (3, 4). The median age of onset is between 20 and 30 years, with similar frequencies observed in both genders (2, 5).

Clinically, MOGAD is characterized by either monophasic or relapsing attacks that may include unilateral or bilateral optic neuritis (ON), acute disseminated encephalomyelitis (ADEM), cerebral monofocal or polyfocal deficits, brainstem or cerebellar deficits, and cerebral cortical encephalitis, often associated with epilepsy (2). The phenotype varies with age of onset, typically presenting as ON in adults and ADEM in children (6). The histopathologic mechanisms of MOGAD are distinct from other demyelinating diseases, such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), and this distinction extends to imaging features, treatment options, and responses. Standard immunomodulatory treatments for demyelinating diseases are often ineffective in MOGAD and may even worsen the disease (7, 8).

In this study, we investigated the presence and frequency of MOG antibodies in a cohort of patients with demyelinating diseases, along with the clinical, radiologic, and serologic features and treatment options for these cases based on the 2023 MOGAD diagnostic criteria in Sakarya, Türkiye.

MATERIALS AND METHODS

Patient Selection

This study has a single-center, retrospective, observational research design. Following our inclusion criteria, we included patients aged 18 to 65 years with one or more demyelinating diseases, such as ON, myelitis; cerebral monofocal or polyfocal deficits; brainstem or cerebellar deficits; or cerebral cortical encephalitis often associated with epilepsy, along with typical or atypical demyelinating lesions on cranial and spinal magnetic resonance imaging (MRI). A total of 450 cases were referred to our outpatient demyelinating disease clinic between 2017 and 2023. Patients who were not tested for MOG antibodies were excluded (n=96). We collected demographic, clinical, radiologic, and serologic data for the included cases. We systematically applied the revised 2017 McDonald criteria to 332 cases evaluated for anti-MOG antibodies, and the 2023 MOGAD diagnostic criteria to those that were anti-MOG seropositive (2, 9). Cases that were anti-MOG seronegative and diagnosed with MS according to the 2017 revised McDonald criteria, as well as those with anti-MOG seronegative demyelinating features that did not meet MS diagnostic criteria, were excluded from the study. Anti-MOG seropositive cases were evaluated in subgroups as part of our research (Figure 1 and Figure 2).

Radiologic Methods

MRI scans were performed using a 1.5 Tesla scanner (Voyager, GE Medical Systems, USA). Routine imaging included axial pre- and post-contrast T1-weighted, axial and sagittal T2-weighted, and axial fluid-attenuated inversion recovery images of the brain. In addition, cervical spine imaging included sagittal T1-weighted, sagittal T2-weighted, and post-contrast sagittal T1-weighted fat-saturated images. A radiologist with a decade of experience retrospectively reviewed these images.

Laboratory Methods

Serologic tests related to demyelinating diseases, including anti-MOG, anti-neuromyelitis optica aquaporin-4 (AQP4), and oligoclonal band (OCB), were performed before intravenous steroid administration (10). Isoelectric focusing followed by immunoblotting was used to detect OCBs in serum and cerebrospinal fluid (CSF) in the neuroimmunology laboratory. A cell-based indirect immunofluorescence assay was used to detect AQP4 antibodies in serum (11). Detection of MOG antibodies in serum was performed using a live cell-based assay method at Koç University Research Center for Translational Medicine (12).

Statistical Analysis

Data analysis was performed using SPSS 23.0 (IBM) software. Normality and homogeneity of the data were assessed by the Kolmogorov-Smirnov test and the Levene’s test, respectively. Data distributions were presented as mean ± standard deviation or median (minimum-maximum) based on normality and homogeneity. All tests were two-tailed, and p<0.05 was considered statistically significant.

Ethical approval was obtained from the Ethics Committee of Sakarya University Faculty of Medicine on June 30, 2022 (approval number: 146336, date: 30.06.2022).

RESULTS

We evaluated 332 cases with one or more clinical core demyelinating events according to the MOGAD diagnostic criteria 2023, and known serologic status for anti-AQP4, anti-MOG, and OCB. Among these, 16 cases with clear or low-positive anti-MOG serology were investigated for MOGAD (Figure 2) and categorized based on clinical, radiologic, and serologic features. Detailed data are shown in Tables 1-5.

Group 1: Cases diagnosed with MS based on clinical, radiological, and laboratory characteristics according to the 2017 revised McDonald criteria with low anti-MOG seropositivity.

There were three cases in this group: one male and two females. The median disease duration was 3 years (range 3-33), and the median age at onset was 52 years (range 42-54). Detailed clinical, radiologic, and serologic features, as well as treatment options, are summarized in Table 1 and Table 2.

These cases exhibited core clinical features (Figure 2) but lacked additional supportive clinical or MRI features according to the 2023 MOGAD criteria. Despite being diagnosed with MS according to the 2017 McDonald criteria, they also had anti-MOG seropositivity. In our study, the rate of low anti-MOG seropositivity in MS cases was 1%.

Group 2: Cases with one or more clinical findings of motor, sensory, and optical deficits, along with radiologically demyelinating lesions that are atypically located or not spatially and temporally disseminated according to 2017 revised McDonald criteria, and with clear or low anti-MOG seropositivity.

This group included 13 cases evaluated according to the 2023 MOGAD diagnostic criteria (Figure 1). All cases met the core clinical features of MOGAD and were further divided into three subgroups according to their clinical, radiologic, and serologic characteristics.

Group 2a: Cases with core clinical features according to the 2023 MOGAD diagnostic criteria and clear anti-MOG seropositivity.

This group included nine cases, three males, and six females. The median disease duration was 3.5 years (1-22 years) and the median age at onset was 39.5 years (21-58 years). One case (case 4) had a late onset (≥50 years), while the others developed the disease in adulthood (18-49 years). Detailed clinical, radiologic, and serologic features, as well as treatment options, are presented in Tables 1-5. Three cases had accompanying autoimmune diseases.
Rare clinical presentations included sixth cranial nerve involvement in case 9; adult-onset ADEM and recurrent myelitis in case 10; wall-eyed bilateral internuclear ophthalmoplegia (WEBINO), in case 12; and tetraparesis secondary to transverse myelitis (TM) with a relapsing-progressive course in case 7. Indeed, case 7 was refractory to intravenous methylprednisolone (IVMP) and plasmapheresis, requiring ongoing treatment with rituximab and intravenous immunoglobulin (IVIG). The clinical courses of the cases were as follows: five were relapsing, three were monophasic, and one had a relapsing-progressive course. OCB seropositivity was detected in four cases. The dual positivity rate, defined as the OCB seropositivity alongside clear anti-MOG seropositivity, was 40% among the MOGAD cases in our study. Treatment options varied, with four cases receiving azathioprine, three receiving rituximab, and one receiving a combination of IVIG and rituximab. Demographic, clinical, radiologic, and serologic characteristics and treatment options are summarized in Tables 1-5.

Group 2b: Cases with supportive clinical and MRI features according to the 2023 MOGAD diagnostic criteria with low anti-MOG seropositivity.

Case 13, a female, had a disease duration of 3 years. Her clinical, radiologic, and serologic features and treatment options are detailed in Table 1 and Table 5.

Group 2c: Cases with supportive clinical features but only supportive MOGAD radiologic features on MRI according to the 2023 MOGAD diagnostic criteria and with low anti-MOG seropositivity.

There were three cases in this group: one male and two females. The median disease duration was 3 years (2-9 years) and the median age was 22 years (21-29 years). Clinical presentations included isolated ON and brainstem attacks in case 15 and cerebral cortical deficit findings in cases 14 and 16. OCB was negative in all cases (Table 1). Despite low anti-MOG seropositivity, these cases were considered suspicious for MOGAD, and were followed closely, as their clinical and radiologic features did not meet the revised 2017 McDonald criteria or the additional supporting clinical and MRI criteria for 2023 MOGAD. Detailed demographic, clinical, radiologic, and serologic data are presented in Tables 1-5.

DISCUSSION

MOGAD differs from other central neuroinflammatory diseases because of its unique clinical, radiologic, and immunologic features (13) and specific diagnostic criteria (2). In our study, 10 cases were diagnosed with MOGAD. It is noteworthy that MOG serology in the same patient can fluctuate from seropositivity to low seropositivity or even seronegativity within six months of symptom onset (14). In our study, three cases with low anti-MOG seropositivity were closely followed clinically, radiologically, and serologically because they did not fully meet the diagnostic criteria. We believe that the monophasic nature of the disease and the timing of anti-MOG serologic testing (>6 months after symptom onset) may contribute to the diagnostic challenges.

Anti-MOG seropositivity is found in 0-2.5% of MS cases (15). The coexistence of anti-MOG and OCB seropositivity may complicate the diagnosis of demyelinating diseases. In our study, three out of 300 MS cases had low anti-MOG seropositivity, but none had additional data supporting a core clinical event of MOGAD. Our results indicate a 1% rate of anti-MOG seropositivity in MS, which is consistent with the existing literature. Dual seropositivity for anti-MOG and OCB occurs in 15-50% of MOGAD cases (16, 17). Although the clinical significance of this dual serology is not fully understood, it is associated with a higher incidence of polyfocal clinical presentations, greater lesion burden on MRI, more brain lesions, lesser optic nerve enhancement, and a higher relapse rate compared with anti-MOG monoseropositivity (17, 18). In our study, 40% of the 10 MOGAD cases were dual seropositive. These cases, in line with the literature, showed a greater lesion burden on MRI, multifocal clinical presentation, and minimal contrast enhancement of the optic nerve.

The incidence of MOGAD is approximately 1.6-2.39 per million people per year, with a similar gender distribution (2, 19). However, our study found a female predominance (70%), which differs from the literature. We attribute this discrepancy to the small size of our disease cohort.

In adults, ON is the most common clinical manifestation of MOGAD (20). Consistent with the literature, ON was the most common phenotype in our study (n=5), while there was only one case that presented with ADEM, which is rare in adults. MOGAD-ON typically presents bilaterally, either synchronously or sequentially (20), and often follows a relapsing course (6). In our study, the clinical courses of the three MOGAD-ON cases were different: one had bilateral ON occurring sequentially, one had monophasic ON, and one had relapsing unilateral ON. We believe that the sequela of optic atrophy in the contralateral eye prevented bilateral ON presentation, in case 4. According to the literature, the radiologic phenotype of MOGAD-ON includes an edematous, swollen, and tortuous optic nerve with T2 hyperintensity along the prechiasmatic pathwayff and typical peripheral enhancement of the optic nerve and orbital fat on orbital MRI (21). In our study, radiologic imaging appeared normal for MOGAD-ON. We believe that the delay between clinical onset and imaging, along with the subsequent resolution of symptoms, may have influenced our radiologic findings. Although MOGAD-ON may improve without treatment, corticosteroids are highly effective in the acute phase (21, 22). All of our ON cases showed clinical recovery, supporting these findings.

TM is the second most common clinical manifestation of MOGAD, occurring in 26% of cases (20). TM may occur as an isolated disease, in association with ON, or as part of ADEM (23). Longitudinal involvement of three or more vertebral segments is a common radiologic feature, although shorter, fragmented, or multifocal spinal cord lesions are also seen. The clinical course of our three MOGAD-TM cases varied: one presented with isolated monophasic myelitis, another with myelitis associated with a history of ON, and the third with ADEM and relapsing myelitis. Radiologic features included a two-segment long T2 hyperintense lesion in the anterior segment of the spinal cord at the C6-7 level in case 7, a two-segment long contrast-enhanced lesion on thoracic MRI in case 8, and a vertebra-long focal T2 hyperintense lesion in the left anterior horn of the spinal cord in case 10. Although MOGAD-TM generally has a good prognosis (2), case 7 had a progressive course and was refractory to treatment, contrary to typical expectations.

MOGAD brain lesions are predominantly located in the supratentorial region and typically present as a few (≤3) bilateral, hyperenhancing, ill-defined T2 hyperintense lesions (24). These lesions often appear in the deep gray matter (5) and middle cerebellar peduncles (25), with diffuse involvement of the pons and areas adjacent to the fourth ventricle more common than in seropositive NMOSD (25). Most MOGAD brain lesions resolve on follow-up MRI (60-79%), although some persist (2, 8). In our study, radiological findings were resolved completely in three cases, partially in one case, and persisted in two cases.

Two cases presented with rare neuro-ophthalmologic manifestations: one with WEBINO and the other with sixth nerve palsy. Only one case of WEBINO and two cases of sixth nerve palsy have been reported in MOGAD (26, 27). Our understanding of MOGAD-related optic nerve involvement beyond ON is expanding, with new phenotypic findings such as WEBINO and sixth nerve palsy being documented.

Recent studies suggest that the late onset of inflammatory demyelinating disease may be associated with more severe clinical findings and higher levels of disability (28). Our seventh MOGAD case is consistent with this hypothesis, as it involved an age of onset over 50 years, a progressive course of paraplegia, and an inadequate response to treatment. In the literature, MOGAD has been associated with comorbid rheumatologic diseases such as SLE and Sjögren’s syndrome (29, 30). In our study, three cases had concomitant autoimmune diseases: ankylosing spondylitis (AS), Familial Mediterranean Fever (FMF), and Hashimoto’s thyroiditis. Only one AS+MOGAD case has been documented, suggesting that TNF-alpha inhibitors may exacerbate MOGAD symptoms (31). Our AS + MOGAD case did not receive any immunosuppressive or TNF-alpha inhibitor treatment at diagnosis. Therefore, we believe that our case may be the first in the literature. While MS is often associated with FMF, the association between FMF and MOGAD is poorly documented in the literature (32). Thus, our case of FMF + MOGAD is considered rare. Hashimoto’s thyroiditis is known to coexist with both MS and MOGAD (33, 34). Our case of MOGAD + Hashimoto’s thyroiditis supports these findings.

The acute treatment regimen for MOGAD typically involves high-dose IV corticosteroids for 3-5 days, similar to other demyelinating diseases, although there is no consensus on tapering steroids after acute treatment (35, 36). IVIG or plasma exchange is often used when standard treatment fails to produce adequate improvement (38, 39). In our study, two cases underwent plasma exchange after 5 days of IVMP, one case received IVIG after IVMP, and another was treated with IVMP for 5 days followed by gradual tapering of long-term oral steroids, which were reduced gradually over the following months. Long-term treatment includes various immunosuppressive agents based on the experience of individual centers, mycophenolate mofetil, azathioprine, rituximab, and IVIG, administered either intravenously or subcutaneously (37). In our study, azathioprine, rituximab, and repeated IVIG were used for maintenance therapy.

Study Limitations

The limitations of our study can be divided into three main categories. First, the small number of cases diagnosed with MOGAD. Secondly, a lack of access to CSF and complete radiological data for all cases. Finally, a delay in performing serologic tests was observed in three cases. Our study emphasizes the need for more extensive research to better understand the diagnosis, clinical presentation, effective treatment, and course of MOGAD.

CONCLUSION

We aimed to highlight the importance of recognizing MOGAD due to its potential association with autoimmune diseases, progressive nature, and dual seropositivity. Thus, it should be considered for its unique clinical and radiologic features. Despite the limited size of our series, our findings contribute to the literature supporting the generally mild clinical course of MOGAD.

Ethics

Ethics Committee Approval: Ethical approval was obtained from the Ethics Committee of Sakarya University Faculty of Medicine on June 30, 2022 (approval number: 146336, date: 30.06.2022).

Informed Consent: Retrospective study.

Acknowledgment

The authors declare no competing interests. The anti-MOG assays in this study were performed at Koç University Research Center for Translational Medicine (KUTTAM). This project was supported by TUBITAK (project number: 118S397). We thank Dr. Atay Vural for supervising the MOG-IgG assays.

Authorship Contributions

Surgical and Medical Practices: S.S., O.T., M.Y., T.D., D.K., Concept: S.S., E.Ç., O.T., D.K., Design: S.S., D.K., Data Collection or Processing: S.S., D.K., Analysis or Interpretation: S.S., D.K., Literature Search: S.S., D.K., Writing: S.S., E.Ç., O.T., M.Y., D.K.

Conflict of Interest: No conflict of interest was declared by the authors

Financial Disclosure: This project was funded by TUBITAK (project number: 118S397).

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