Myelin oligodendrocyte glycoprotein antibody‑associated disease (MOGAD) is a relatively recently characterized autoimmune disorder of the central nervous system (CNS) that presents with a range of clinical symptoms, often leading to misdiagnosis or delayed diagnosis [Banwell, 2023].
In this case‑based module, we will explore the distinctiveness of MOGAD compared to multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), discuss the unmet medical needs of patients with MOGAD, understand the burden of the disease and disability impact accruing at each attack, review diagnostic criteria and approaches, and delve into the pathophysiology and role of pathogenic antibodies in MOGAD.
Pre-test questionAmanda, aged 25 years, presents with myelitis. Her MOG antibody (MOG‑IgG) test results are low‑positive, and she is aquaporin‑4 IgG (AQP4‑IgG) seronegative. According to the recent International MOGAD Panel diagnostic criteria, are these findings sufficient to make a diagnosis of MOGAD?
Select an answer to continue
ANo. At least one supporting clinical or magnetic resonance image (MRI) feature is required to confirm a diagnosis in patients with low‑positive MOG‑IgG findings and who are AQP4‑IgG seronegative. A better diagnosis, including MS, needs to be excluded.Correct
BYes. MOG‑IgG testing is the gold standard, and positive findings definitively identify MOGAD.Incorrect
CYes. Since she is also demonstrating neurologic involvement, which would confirm a MOGAD diagnosis.Incorrect
DNo. A finding of deep gray matter involvement on a brain or brainstem MRI is required for MOGAD diagnosis.Incorrect
EI’m unsure.Incorrect
Correct answer · A
At least one supporting clinical or MRI feature is required to confirm a diagnosis in patients with low‑positive MOG‑IgG findings and who are AQP4‑IgG seronegative [Banwell, 2023]. A better diagnosis, including MS, also needs to be excluded before a diagnosis of MOGAD can be made.
A low‑positive MOG‑IgG test result can be inconclusive and may require further investigation in the context of the clinical picture. Other diseases can also present with similar symptoms to MOGAD, so a comprehensive workup is crucial for an accurate diagnosis [Bilodeau, 2019]; [Jarius, 2018]; [Jarius, 2016]; [Misu, 2023].
Case · Presentation
Both eyes. And then his bladder.
John, a 32‑year‑old Caucasian male, usually leads a healthy and active life as a software engineer, enjoying outdoor activities like hiking and cycling. However, he presented to the ophthalmology clinic with complaints of sudden‑onset decreased visual acuity in both eyes, accompanied by pain on eye movement. Despite an unremarkable past medical history, he had recently been experiencing headaches and fever. Upon examination, visual acuity was found to be reduced in both eyes (20/40 in the right eye and 20/70 in the left eye), with evidence of optic disc swelling noted during fundoscopy.
Following his initial presentation, a week later, John’s condition worsened, manifesting as constipation and urinary retention, prompting a referral to a neurologist.
Question 1Which of the following statements about MOGAD are true?
Select an answer to continue
AOptic neuritis (ON) is the most prevalent onset symptom in adults.Incorrect
BAcute disseminated encephalomyelitis (ADEM) is the most common clinical condition observed in children with MOGAD at the time of presentation.Incorrect
CMOGAD can manifest as either a monophasic illness or a relapsing condition.Incorrect
DAll of the above.Correct
Correct answer · D
ON is the most frequent initial symptom, especially in adults, while in children, ADEM is the usual first presentation either with or without involvement of the optic nerve, especially before the age of 11. Transverse myelitis is another frequently observed presentation feature [Banwell, 2023]. Unlike MS and NMOSD, where several clinical attacks are seen in relapsing forms of the disease, MOGAD can appear as either a monophasic or a relapsing condition [Banwell, 2023]. Studies have shown that 43 to 67% of MOGAD patients may experience a monophasic course, characterized by a single episode of demyelination with no further relapses [Epstein, 2021]; [Fan, 2022]; [Hor, 2023]; [Sechi, 2022]; [Yilmaz, 2024].
John’s clinical presentation of bilateral ON and bowel and bladder symptoms is suggestive that MOGAD may be a possible diagnosis. While MS and NMOSD may present with similar features, in MS, patients typically present with either ON or bowel and bladder symptoms. Additionally, in MS, unilateral decreased visual acuity is normally present, whereas in MOGAD, ON is frequently bilateral [Banwell, 2023]. Optic disc swelling on fundoscopy might be present in MS and NMOSD but is extremely frequent in MOGAD [Banwell, 2023].
The majority of MOGAD patients presenting with ON exhibit a significant visual loss with initial ocular pain [Ambrosius, 2021]. It is recommended that adults or children with sudden‑onset painful or painless visual loss, or sudden‑onset squint, or sudden‑onset floaters, or severe lid edema need urgent referral for care [Cleveland Clinic, 2023].
Common bowel and bladder symptoms that occur in MOGAD include abdominal/pelvic pain, urinary urgency/incontinence, altered bowel habits, and urinary frequency [Banwell, 2023]. These symptoms suggest a sensory‑driven link between gastrointestinal and urological disorders in patients with MOGAD [Al‑Ani, 2023].
Case · Workup
Seronegative on the commercial test. Then they ran a live assay.
The neurologist performed a brain and spinal cord MRI on John which revealed bilateral optic nerve enhancement and conus involvement. These findings raised suspicions of a demyelinating disorder, leading the neurologist to order further investigations, i.e., infectious and autoimmune screening.
Infectious origins were excluded and a spinal tap revealed a slight increase of cells (25/µL) in the absence of oligoclonal bands. CSF pleocytosis, with white cell counts of more than 5 per µL, occurs in over 50% of patients with a first demyelinating attack and MOG‑IgG. Furthermore, although oligoclonal bands are detected in up to 20% of patients with MOG‑IgG, intrathecally restricted CSF oligoclonal bands strongly favor a diagnosis of MS [Banwell, 2023].
John was promptly started on intravenous (IV) corticosteroids for 5 days while awaiting the results of his autoimmune screening tests. A commercial test for AQP4‑IgG and MOG‑IgG was performed returning a seronegative result. Serum MOG‑IgG testing using a live cell‑based assay (CBA) was subsequently performed, revealing a low‑positive titer. The live CBA confirmed the presence of MOG antibodies in John’s serum.
Question 2What is the importance of a live CBA in diagnosing MOGAD, and how does it compare to other testing methods?
Select an answer to continue
AIt is less sensitive than fixed assays and is rarely used in clinical practice.Incorrect
BIt is more sensitive than fixed assays, particularly in detecting low titers of MOG‑IgG, which aids in the diagnosis of MOGAD.Correct
CIt provides no significant advantage over commercially available assays.Incorrect
DIt should only be used in cases where other tests are inconclusive.Incorrect
Correct answer · B
It is essential to demonstrate MOG‑IgG positivity using a dependable test to accurately diagnose MOGAD and lower the possibility of false‑positive or false‑negative results. The commercially available CBA that uses fixed transfected cells has a stated specificity of approximately 98%. However, the fixation process can disrupt the native spatial configuration of the MOG protein, lose some conformational epitopes, or generate cryptic epitopes, making it difficult to recognize MOG‑IgG accurately. The fixed CBA also has a lower level of sensitivity compared to the live CBA.
Nevertheless, a fixed competitive binding assay remains considerably more effective in accurately detecting MOG‑IgG than other non‑competitive binding assays, such as enzyme‑linked immunosorbent assay (ELISA) [Sechi, 2022]. ELISA is not recommended for MOG‑IgG measurement owing to low sensitivity and specificity [Banwell, 2023]. Thus, a panel of international experts strongly endorses serum testing for patients with suspected MOGAD using cell‑based assays that use full‑length human MOG to detect MOG‑IgG [Banwell, 2023].
Case · Diagnosis
A low titre alone is not enough. His was not alone.
Patients who exhibit one of the primary clinical attack types and have definitive positive results for MOG‑IgG in their serum, as determined by either a fixed or live CBA, can be diagnosed with MOGAD [Banwell, 2023]. Patients who have low‑positive serum MOG‑IgG titers detected through fixed or live CBAs, patients whose serum results are reported as positive without titers, or seronegative patients with positive CSF MOG‑IgG test results must also exhibit at least one of the supporting clinical or MRI features together with proven AQP4‑IgG seronegativity to be diagnosed with MOGAD. Patients should only be diagnosed with MOGAD after other potential diagnoses, including MS, that more effectively account for their symptoms have been ruled out [Banwell, 2023].
At this point, a diagnosis of MOGAD was made based on the proposed MOGAD diagnostic criteria. Criteria 1, 2, and 3 have all been fulfilled. John presented with a clinical demyelinating event of ON and myelitis (criterion 1). MOG‑IgG serum revealed a positive result (criterion 2). Although the titer was low, a seronegative AQP4‑IgG result was confirmed, and supporting clinical features were present in the form of bilateral simultaneous clinical involvement and conus involvement. Additionally, a comprehensive approach including clinical presentation, MRI imaging, CSF analysis, and antibody testing was used to exclude a better diagnosis such as NMOSD or MS (criterion 3).
The diagnostic criteria for MOGAD underscore the importance of differentiation from other demyelinating disorders such as MS and NMOSD. Given the variability in disease course, treatment response, and long‑term outcomes, distinguishing MOGAD from other conditions is imperative [Misu, 2023]. Adherence to these established criteria ensures timely and suitable management, thereby minimizing the likelihood of misdiagnosis and enhancing patient care.
Question 3What distinguishes MOGAD from MS and NMOSD?
Select an answer to continue
AA core clinical demyelinating event and clear positive titers of MOG‑IgG.Correct
BLack of relapses.Incorrect
CNormal MRI findings.Incorrect
DExclusively affects older adults.Incorrect
Correct answer · A
High levels of MOG‑IgG are closely linked to the clinical symptoms suggested for MOGAD and differentiate these patients from those who exhibit clinical features and a disease course that is typical of AQP4‑IgG‑seropositive NMOSD or MS [Banwell, 2023]. Low titers of MOG‑IgG have limited discriminatory power and can be found in people with MS, other neurological disorders, and people in good health.
While the occurrence rate of MOG‑IgG seropositivity in patients diagnosed with clinically definite MS ranges from 0.3 to 2.5%, conducting universal testing for MOG‑IgG in individuals suspected to have MS would lead to a significant percentage of false‑positive results, making it highly discouraged. While it is uncommon to find clear positive MOG‑IgG titers in control subjects, a positive result may be observed in individuals who do not exhibit clinical characteristics of MOGAD, especially if MOG‑IgG is included in more comprehensive diagnostic panels. A low titer‑positive MOG antibody (MOG‑IgG) alone fails to meet the proposed criteria for MOGAD [Banwell, 2023].
Case · Imaging and CSF
The CSF was negative. That does not rule it out.
John’s CSF tested negative for MOG‑IgG antibodies, despite a low‑positive result in the serum. This scenario is not uncommon in MOGAD, where serum testing is generally more sensitive for detecting MOG‑IgG antibodies than CSF testing. While the presence of MOG‑IgG in the serum can indicate MOGAD, a negative result in the CSF does not rule out the disease. In fact, studies suggest that MOG‑IgG can be present in the serum without concurrent CSF positivity in a significant number of cases. Thus, John’s negative CSF result further underscores the necessity of integrating serum antibody findings with clinical presentation and MRI features to arrive at an accurate diagnosis of MOGAD [Carta, 2023]; [Sechi, 2022].
While serum is the preferred specimen type for MOG‑IgG testing, CSF testing is also useful. It is not unusual for both the serum and CSF to test positive at the same time. MOG‑IgG positive in the CSF without serum positivity occurs in 12 to 17% of cases [Carta, 2023]; [Redenbaugh, 2024]. Hence, it is advisable to perform CSF testing in patients exhibiting clinical and MRI characteristics that indicate MOGAD but have had negative results from blood testing [Sechi, 2022]. Nevertheless, like the occurrence of false‑positive serum MOG‑IgG results, there have been rare instances of false‑positive results in the CSF in other disorders such as MS, especially in the pediatric population [Armangue, 2020]. Therefore, it is crucial to interpret a positive result in the context of the patient’s clinical symptoms and MRI findings [Sechi, 2022].
Question 4What is a significant feature of MOGAD attacks compared to MS and NMOSD?
Select an answer to continue
AThe visual loss associated with MOGAD is more typically gradual onset rather than sudden.Incorrect
BResolution of T2 brain lesions over time.Correct
CAbsence of optic nerve involvement.Incorrect
DPoor response to corticosteroids.Incorrect
Correct answer · B
A notable feature of MOGAD attacks, compared to MS and NMOSD, is the complete resolution of T2 brain lesions over time. Research indicates that this resolution is most frequently observed in MOGAD when contrasted with AQP4‑IgG‑positve NMOSD and MS [Contentti, 2023]. This characteristic suggests that MOGAD may have a higher tendency for T2 lesion resolution on brain MRI, setting it apart from MS and NMOSD. This distinction highlights the significance of leveraging MRI findings, such as the resolution of T2 brain lesions, as a potential indicator to distinguish between these demyelinating disorders.
While a normal brain MRI can occur in up to 46% of patients with MOGAD with cerebral involvement, a significant proportion of individuals may exhibit abnormalities on brain imaging, highlighting the variability in radiological findings associated with this condition [Duan, 2021]; [Farkas, 2023].
Case · Timing
When you draw the blood changes what you find.
Serial testing raises a question the evidence has not yet settled — and the first test has a best moment.
Question 5When is the optimal timing for initial MOG‑IgG testing in suspected MOGAD cases?
Select an answer to continue
ADuring routine annual check‑ups.Incorrect
BOnly during relapse episodes.Incorrect
CDuring acute attacks before treatment.Correct
DExclusively at the time of initial diagnosis.Incorrect
Correct answer · C
Unfortunately, there is a lack of data to guide the best timing for conducting serial MOG‑IgG testing and how to interpret the results. There is a need for a universally accepted definition of persistence of MOG‑IgG, and it is necessary to conduct further studies to determine the predictive importance of persistent seropositivity [Banwell, 2023].
However, according to some research, the optimal timing for initial MOG‑IgG testing in suspected MOGAD cases is during acute attacks before treatment. Testing during this period increases the likelihood of detecting MOG‑IgG, therefore, aiding in the prompt diagnosis and appropriate management of MOGAD [Ambrosius, 2020].
Case · Treatment
He got better. Not all the way better.
There are currently no approved treatments specifically for MOGAD [Hiya, 2023].
Question 6Which of the following is commonly used for primary management of acute MOGAD attacks?
Select an answer to continue
AMaintenance IV immunoglobulin (IVIG).Incorrect
BRituximab.Incorrect
CHigh‑dose corticosteroids.Correct
DEculizumab.Incorrect
Correct answer · C
There are currently no approved treatments specifically for MOGAD [Hiya, 2023]. Expert opinion recommends the use of high‑dose IV corticosteroids as a first‑line treatment for patients presenting with acute MOGAD attacks due to their high responsiveness [Al‑Ani, 2023].
While IV steroids led to an improvement in John’s visual acuity, his recovery was only partial, as his bowel and bladder symptoms persisted. This partial response is common among MOGAD patients, who often experience residual disability even after treatment with high‑dose corticosteroids [Al‑Ani, 2023]. Studies have shown that while corticosteroids can be effective in reducing acute inflammation, many patients do not fully return to their pre‑attack baseline, leading to lasting deficits in neurological function [Deschamps, 2021]. This underscores the chronic burden of disease experienced by MOGAD patients, where each clinical attack can lead to cumulative disability, significantly impacting quality of life [Luo, 2021]. The heterogeneity of symptom presentation and recovery further complicates management, as there are currently no approved therapies specifically targeting MOGAD, and treatment decisions often rely on data extrapolated from similar demyelinating diseases [Barreras, 2022].
This highlights a significant unmet need for targeted therapies that may provide more consistent and comprehensive disease control, prevent relapses, and improve long‑term outcomes for patients living with MOGAD [Al‑Ani, 2023].
The optimal treatment approach for MOGAD remains controversial, especially considering that MOGAD may have a monophasic course in some patients [Barreras, 2022]. While some patients with MOGAD may benefit from immunotherapy, there is a lack of evidence‑based guidelines for the treatment of MOGAD [Tisavipat, 2023]. Preventive treatment is generally recommended for patients with relapsing MOGAD [Barreras, 2022], although a recent study reported that initiating maintenance therapy from the first attack substantially reduced the relapse risk for the patients [Deschamps, 2024]. Ongoing research is focusing on evaluating various treatment options for MOGAD through randomized controlled trials to establish effective and safe therapeutic strategies for this rare autoimmune disorder of the CNS.
Case · Takeaways
Test the antibody. Then read it in context.
John’s case underscores the diagnostic challenges associated with
MOGAD and highlights the importance of conducting antibody testing for MOG‑IgG in
addition to clinical history and examination findings and MRI, to achieve accurate
diagnosis. Moreover, it emphasizes the heterogeneous nature of MOGAD presentation, wherein
clinical manifestations may vary widely and require a comprehensive approach to
management.
In conclusion, MOGAD represents a distinct entity from MS and NMOSD,
characterized by the presence of MOG antibodies and compatible clinical features. Patients
with MOGAD can experience a relapsing course and significant disability impact,
highlighting the unmet medical needs in this population. Early recognition and diagnosis
of MOGAD, through comprehensive clinical/paraclinical evaluation and antibody testing, are
essential for appropriate management and improved patient outcomes.
01Consider MOGAD in patients presenting with clinical
features suggestive of demyelinating disorders, particularly if there are suggestive
features.
02Utilize comprehensive diagnostic work‑up,
including MRI and MOG‑IgG testing, to differentiate MOGAD from other demyelinating
disorders.
03Early initiation of appropriate treatment and close
monitoring are crucial for minimizing residual or accrual disability in patients with
MOGAD.
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