What is myelin oligodendrocyte glycoprotein antibody disease?

Myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) are a spectrum of idiopathic, inflammatory, demyelinating diseases affecting the central nervous system (CNS). MOG is a glycoprotein uniquely expressed in oligodendrocyte membranes and myelin sheath in the CNS and although its exact function is not known it is thought to function in maintaining cell membrane stability and mediating the inflammatory cascade.1 Antibodies against this protein have long been known to cause inflammatory encephalomyelitis in animal models2 but more recently a subset of patients with this antibody and similar phenotype with CNS demyelinating and inflammatory disorders in humans have been identified.3 The exact pathogenesis of antibody induced injury is not confirmed yet but may possibly include complement activation.4

What are the demographics, incidence and prevalence of MOGAD?

The exact incidence and prevalence of MOGAD is not known due to lack of epidemiological studies and limitations in antibody testing although in one study its prevalence is estimated to be around 2.0 per 100,000 cases and its incidence around 3.4 per 1,000,000 person-years.5 Unlike other autoimmune inflammatory disorders there is less female predominance and has no clear ethnic bias.5–7 MOGAD typically affects children and young adults with the mean age of onset in adults being around early 30s.6,8,9  

What are the main clinical features and expected course of MOGAD?

Several distinct clinical phenotypes have been identified in MOGAD including optic neuritis, myelitis, brainstem syndrome, acute dissemination encephalomyelitis, and cortical encephalitis. MOGAD may have a monophasic or relapsing course and prognosis highly depends on the clinical phenotype and unlike MS progression is not typically seen.10 Acute disseminated encephalomyelitis (ADEM) presentation is most common in children whereas opticospinal presentation (optic neuritis, myelitis, and brainstem encephalitis) is more commonly seen in adults.

Optic neuritis

Optic neuritis is the most common presentation of MOGAD at disease onset6 occurring in approximately 60% of patients.11 MOGAD should be considered as an etiology in patients with undifferentiated optic neuritis as MOG antibodies can be detected in 2-5% of patients.12,13 Although optic neuritis in MOGAD can be either unilateral or bilateral, in comparison to multiple sclerosis (MS), in MOGAD the optic neuritis is more likely to be bilateral and associated with disc edema (papillitis) and sometimes peripapillary hemorrhage with recurrence seen in around 50% of patients.14 In majority of patients (89%) pain is preceded by vision loss by typically around 3 days.15

Optical coherence tomography (OCT) can be useful in evaluation of optic neuritis in MOGAD. Acutely, there is severe anterior optic nerve involvement marked by edema followed by recovery of edema and persistence of significant thinning of retinal nerve fiber layer for up to 12 months.16 This thinning is likely dependent on occurrence of optic neuritis and independent of optic neuritis thinning does not occur.16

In MOGAD in addition to visual acuity monitoring, visual field measurements could also be used to monitor functional impairment.17 Although the vision loss is severe at nadir of optic neuritis in MOGAD, the recovery after treatment is better than those with neuromyelitis optica spectrum disorders (NMOSD) optic neuritis.14 Some patients may improve without steroids, compared to patients treated after 2 days, those treated within 2 days of symptoms have a shorter time to recovery but final visual outcomes may not be affected.15


Myelitis is another common presentation in MOGAD which may occur alone or simultaneously as part of a multifocal attack, with optic neuritis occurring simultaneously in approximately 20-40% of patients.11

The typical presentation of myelitis in MOGAD patients is longitudinally extensive transverse myelitis (LETM) with involvement of greater than 3 vertebral segments and commonly involved areas include cervical and thoracic spinal cord.18 Conus involvement can also be seen in MOGAD and should also raise the possibility of MOGAD as the etiology of myelitis.19

Symptoms will vary based on the affected levels and include limb weakness and sensory changes, bowel or bladder dysfunction, and spasticity. Onset of attack involving myelitis has been shown to be a predictor of poor outcomes in MOGAD and permanent bladder and erectile dysfunction have been shown to be selectively more common than motor disability.6

Acute disseminated encephalomyelitis

In the pediatric population, ADEM is considered the most common presenting phenotype in MOGAD occurring in approximately 68% of patients.20 In children presenting with clinically isolated syndrome (CIS) or ADEM, around 40-57% can have MOGAD antibodies.21–23

The clinical presentation for ADEM is a multifocal CNS presentation associated with encephalopathy and is usually preceded by infectious or systemic illness symptoms. Typical presenting features include seizure, ataxia, weakness, and incoordination depending on the site of involvement.11

Brainstem syndrome

Brainstem involvement is another frequent finding in MOGAD occurring in approximately 30% of MOGAD patients.24 In some cases this involvement can be asymptomatic, common presenting features in brainstem involvement include bulbar symptoms (e.g., dysphagia, dysarthria, diplopia, and nystagmus), hearing loss, vertigo, limb and trunk incoordination, central hypoventilation, and intractable nausea or vomiting.24 In contrast to NMOSD, area postrema syndrome occurs less frequently in MOGAD.25

Cortical encephalitis

Although rare, meningoencephalitis and encephalitic presentations of MOGAD can also occur.20,26 These entities have been referred to by various terms and acronyms including cerebral cortical encephalitis (CCE) or FLAIR-hyperintense lesions in anti-MOG antibody-associated cerebral cortical encephalitis with seizures (FLAMCES) described by steroid-responsive encephalitis, fever, headache, seizures, and cortical symptoms (e.g., aphasia, cognitive impairment, and weakness).27,28 

Aseptic meningitis

Another rare phenotype in MOGAD is steroid-responsive aseptic meningitis typically seen with or without leptomeningeal enhancement.29 Although imaging may show concurrent demyelination, in some cases leptomeningeal enhancement can be the sole presentation.29 

Peripheral nervous system

Several peripheral nervous system manifestations of MOGAD have been reported. These include myeloradiculitis with nerve root enhancement,30–32 combined central and peripheral demyelination (CCPD)32,33, and inflammatory neuropathies which may be responsive to immunotherapy and associated with concurrent antibodies targeting peripheral nervous system.33  

Generally, most patients are expected to have favorable outcome with expanded disability status scale (EDSS) <3 and more favorable compared to NMOSD.34 Typically children have a more favorable outcome compared to adult patients.35

Overall, prediction of risk of relapse in MOGAD remains challenging and there is conflicting data surrounding relationship between MOGAD seropositivity over time and risk of future relapses.36 Age of onset can be an indicator in predicting risk of relapse. Earlier and later age of onset (<18 years and > 50 years respectively) can both be associated with a more monophasic course compared to a relapsing course.10 Patients with optic neuritis have a higher risk of relapse as opposed to those with transverse myelitis or ADEM.36

What are the main MRI features of MOGAD?

Optic nerve

In MOGAD, magnetic resonance imaging (MRI) of optic neuritis can show an edematous, enlarged, and tortuous optic nerve with T2 hyperintensity and enhancement most commonly involving the anterior segments but sparing the retro chiasm structures.37 Roughly half the patients can also have optic nerve sheath and peribulbar structure enahncement.14 Most of the abnormality seen on MRI may resolve on subsequent imaging with treatment with the exception of residual T2 hyperintensity and optic atrophy.38

Spinal cord

Although in some cases of MOGAD myelitis, MRI can be normal,39 both scattered short segment involvement and longitudinally extensive transverse myelitis (LETM) are observed. Conus medullaris involvement is a key feature.18 The lesions are usually central affecting both gray and white matter involving more than 50% of the axial section of the cord.40 Several radiological biomarkers have been investigated in differentiating myelitis in MOGAD from other disorders including the pseudodilatation of the central canal (involvement of the gray matter producing a characteristic sagittal T2-hyperintense line surrounded) or the H-sign (central T2 hyperintensity confined to gray matter without gadolinium enhancement on axial images).41 Enhancement with relapses is less likely to be seen in MOGAD compared to other similar demyelinating disorders.41,42


Findings in ADEM usually include diffuse bilateral infra- and supra-tentorial signal abnormality in the cortical gray matter, subcortical white matter, deep white matter, and deep gray matter on fluid attenuated inversion recovery (FLAIR) imaging with scattered linear or nodular enhancement.18 Although there are no known unique radiographic patterns for MOGAD but presence of thalamic and pontine lesions may indicate MOGAD as the underlying etiology.18,43 Brain lesions in MOGAD are usually described as poorly demarcated and “fluffy” in appearance.44 Gadolinium enhancement can be seen in around 12% of lesions in MOGAD.45 Leptomeningeal and cranial nerve enhancement have also been described in MOGAD. Brain lesions in MOGAD typically display dramatic improvement on follow-up imaging.46 Neuroimaging in CCE associated with MOGAD can also have FLAIR signal abnormality involving the cortical and subcortical white matter as well as deep white and gray matter. These lesions are highly responsive to steroids and can show nodular or linear enhancement.7

Serological and cerebrospinal fluid testing for MOGAD

Recently developed cell based assays (CBA) are the optimal method to test for the presence of immunoglobulin G (IgG) targeting MOG in serum. Previously used enzyme-linked immunosorbent assay (ELISA) or western blot assays are now known to be less specific and high risk for false positive results.47 Specifically a live cell-based methodology is preferred because it has shown to have a superior positive predictive value to the fixed cell assays and should be performed in all patients if possible.48 

The titer of antibodies appears to confer information regarding specificity as low titer live CBA positive results (i.e., when using a cutoff of 1:20) have been shown to be associated with a low positive predictive value of 72% and should be used with caution particularly in patients with atypical features.49 MOG antibodies are thought to be dynamic and may vary with time and treatment,24,50 and the titers are thought to be highest in temporal proximity of clinical attacks.51,52 There is conflicting data regarding increased risk of relapse with persistence of antibodies,53,54 although very high titers (>1:2560) have been shown to be associated with higher risk of relapsing course.51

Most (>50%) patients with MOGAD will have cerebrospinal fluid (CSF) lymphocytic pleocytosis (>5 white blood cells/mL) and marked pleocytosis (> 100 white blood cells/mL) is noted in approximately 13% of patients at the time of an attack.55 Patients will typically have mild protein elevation (< 100 mg/dL) and occasionally elevated IgG index may be seen.56 Oligoclonal bands can be seen transiently in about 15% of patients and its persistence should raise suspicion for other disorders.57 Testing for MOG antibodies should be performed if there is high index of suspicion for MOGAD as presence of MOG antibody in the CSF can further increase the sensitivity in the seronegative cases.58,59

Pleocytosis can be less frequently seen in MOGAD presentations with optic neuritis (19-34%) and highest in patients with transverse myelitis (83-85%).60

Several studies have also shown overlap positivity for N-methyl-D-aspartic acid (NMDA) receptor antibodies in patients with MOGAD61,62 however there is little overlap with AQP4-IgG antibodies in MOGAD.63–65 Systemic autoantibodies (ANA, dsDNA, SS-A, SS-B) are also not frequently observed to co-exist, in contrast to AQP4-IgG NMOSD.66

How is MOGAD different than NMOSD?

Both MOG-IgG and AQP4-IgG antibodies have been shown to be pathogenic in animal models.67–69 Although the role of complement activation as a downstream mechanism of injury has been well established in NMOSD, this is less clear in MOGAD.4,70 Pathologically NMOSD is classified as an astrocytopathy, while MOG IgG associated disorders are classified as oligodendrogliopathies and this difference is reflected in serum and CSF levels of glial fibrillary acidic protein (GFAP), a marker of astrocytic damage which is found less commonly in MOGAD patients compared to NMOSD.71

Although both MOGAD and NMOSD can occur at any age, typically the age of onset is earlier in MOGAD patients compared to NMOSD and the female predominance is less clear.43,72

Clinically MOGAD and NMOSD may have similar presentations. MOGAD has been reported to account for 40% of seronegative NMOSD73,74 and amongst patients with MOGAD, 20-30% fulfill the diagnostic criteria for seronegative NMOSD.75 Compared to NMOSD patients, MOGAD patients more frequently have a monophasic course, more often present with ADEM, and often have a favorable outcome.7,76 The optic nerve involvement in MOGAD is more likely to be bilateral.77 Seizures can be more frequently observed in MOGAD (14.7%) compared to AQP4 IgG NMOSD patients (1%).78 

Radiologically compared to NMOSD, presence of conus medullaris involvement and axial H-sign on spinal cord imaging are more likely to be seen in MOGAD.41,79–81 Furthermore, MOGAD spinal cord lesions are associated with less edema and enhancement compared to NMOSD.41,42 With optic neuritis, MOGAD is more likely to demonstrate tortuous and edematous optic nerves compared to NMOSD.37,82,83

Although both disorders can lead to residual long-term disability, overall visual and motor outcomes are better in MOGAD compared to NMOSD.44,84

How is MOGAD different than MS?

MOGAD patients are slightly younger and have less of a female predominance than MS.43

Clinically, both disorders can present similarly with TM, ON, or intracranial involvement.

Radiologically, optic neuritis in MS is less likely to be bilateral or affect a long segment of optic nerve.37,85 Although MOGAD patients often will have abnormalities on brain MRI these lesions have a distinct appearance that is different from MS lesions.76 Intracranial lesions in MOGAD are less likely to involve inferior temporal lobe and ovoid lesions perpendicular to lateral ventricle are less frequently observed. MOGAD intracranial lesions are likely to present as fluffy thalamic and pontine lesions.43 Central vein sign is less commonly seen in MOGAD compared to MS.86 Spinal cord lesions in MS are likely short segment and peripheral as opposed to LETM seen in MOGAD which affects the central cord.43 Conus medullaris involvement is more likely to be seen in MOGAD.41,79 OCBs can be a differentiating feature in CSF since they are seen very commonly (up to 95%) in MS as opposed less common and transient presence in MOGAD (5-15%).43

How is MOGAD diagnosed?

Recently proposed diagnostic criteria for MOG-IgG is based on the following core clinical events and exclusion of alternate etiologies including multiple sclerosis:87

  1. ADEM
  2. Optic neuritis
  3. Myelitis
  4. Brainstem or cerebellar deficits
  5. Cerebral monofocal or polyfocal deficits
  6. Cerebral cortical encephalitis with or without seizures

The diagnosis requires one of the above if serum MOG-IgG antibody testing is clearly positive (live cell-based assay with a clear positive cutoff or a fixed cell-based assay result with a titer ≥1:100).

If serum MOG-IgG results are positive without a reported titer, low positive titer, or negative in the serum but positive in CSF (fixed or live cell-based assay) then the diagnosis requires additionally establishing negative serum AQP4-IgG antibody and presence of at least one of the following supporting features:

  1. Optic neuritis
    1. Bilateral simultaneous clinical involvement
    2. Longitudinal optic nerve involvement (> 50% length of the optic nerve)
    3. Perineural optic sheath enhancement
    4. Optic disc edema
  2. Myelitis
    1. Longitudinally extensive myelitis
    2. Central cord lesion or H-sign
    3. Conus lesion
  3. Brain, brainstem, or cerebral syndrome
    1. Multiple ill-defined T2 hyperintense lesions in supratentorial and often infratentorial white matter
    2. Deep grey matter involvement
    3. Ill-defined T2-hyperintensity involving pons, middle cerebellar peduncle, or medulla
    4. Cortical lesion with or without lesional and overlying meningeal enhancement

Who should be tested for MOGAD?

In general, MOGAD testing should be considered in patients without a clear alternative diagnosis as false positive results can occur. In the absence of established alternate diagnoses, MOGAD testing should be highly considered in patients presenting with ADEM, optic neuritis (unilateral or bilateral), myelitis (with or without spinal cord lesions), brainstem or cerebellar syndromes, myeloradiculitis, or those with undifferentiated intracranial lesions with supportive features as listed in the diagnostic criteria above.

What is the general approach to a MOGAD relapse?

Intravenous corticosteroids are our initial acute treatment. Similar to other expert opinion,36 the typical Mellen Center regimen is methylprednisolone 1000mg IV as a single daily dose on 3-5 consecutive days followed by a prolonged steroid taper. Depending on availability, bioequivalent high dose oral steroids, prednisone 1250 mg daily, can also be used as substitute for intravenous steroids. Concurrent H2 blockers should be used while using prolonged steroid courses to reduce the risk of ulcers.

We use varying slow taper regimens anywhere from 2-6 months depending on the severity of presentation and planned long term regimen and if applicable should be continued for approximately 1-2 months after initiation of long-term immunotherapy. We consider plasmapheresis or IVIG as a second line treatment for patients not responsive to the initial steroid regimen and hospitalization should be considered in patients with severe brainstem syndrome or myelitis.

How do we prevent relapses in MOGAD?

There is limited data on long term management of risk of recurrence in MOGAD with randomized controlled trials lacking in this area. As with acute treatment our approach is similar to NMOSD maintenance therapy.

Several studies have supported evidence for maintenance IVIG as an effective therapy to prevent relapses.88,89 Other small observational data support the use of azathioprine, mycophenolate, methotrexate, and rituximab in reduction of relapse rate in MOGAD.36,89,90 Given the hypothetical role of IL-6 in MOGAD tocilizumab has also been successfully used in a few cases to treat rituximab-refractory MOGAD.36,91,92 There are ongoing trials including evaluation of satralizumab (NCT05271409) and azathioprine (NCT05349006) in treatment of MOGAD. In addition, there has been interest in evaluating the role of Fc receptor antibody (rozanolixizumab) in treatment of MOGAD and will be subject of future research.

At the Mellen center, we recommend long term immunotherapy with one of the above agents for all patients diagnosed with MOGAD although this decision should be individualized, depending on severity and recovery.


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