Dr. Lidiia PrakhovaNeurology • Neuroimmunology • Botulinum toxin therapy
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Neuroimmunology • Demyelinating Disorders of the Central Nervous System

MOGAD in Israel: Diagnosis and Treatment of MOG-IgG–Associated Disease

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a distinct immune-mediated disorder of the central nervous system that can cause optic neuritis, myelitis, ADEM and inflammatory brain syndromes. It is not a form of multiple sclerosis and is different from AQP4-positive neuromyelitis optica spectrum disorder (NMOSD).

Dr. Lidiia Prakhova is a neurologist and Doctor of Medical Sciences specializing in neuroimmunology and demyelinating disorders of the central nervous system. A consultation may include interpretation of a positive MOG-IgG result, reassessment of MRI findings and diagnosis, differentiation between MOGAD, NMOSD and multiple sclerosis, and discussion of whether long-term relapse-prevention therapy is needed.

Book a Consultation MOGAD Diagnosis
A positive MOG-IgG result does not always mean MOGAD. Low-positive results in particular require careful interpretation. The diagnosis should be based on a compatible clinical syndrome, appropriately performed antibody testing and supportive MRI findings, with exclusion of a better alternative diagnosis.
Practical Guidance

When a specialist consultation for MOGAD may be particularly useful

Your MOG-IgG test is positive, but it is unclear whether the result truly confirms MOGAD.
You have experienced severe, bilateral or recurrent optic neuritis.
You have had transverse myelitis, particularly with a long spinal cord lesion or involvement of the conus.
Different doctors or reports have suggested MOGAD, NMOSD or multiple sclerosis.
After a first attack, you need to decide whether long-term preventive treatment is necessary or whether observation may be appropriate.
A new relapse has occurred despite treatment and the long-term strategy needs to be reconsidered.
Important: rapidly worsening vision, new weakness in the arms or legs, urinary retention, rapidly progressive sensory loss, seizures or an acute change in consciousness require urgent medical assessment. A suspected acute MOGAD attack should not wait for a routine consultation.
About the Disease

What is MOGAD?

MOG antibody-associated disease (MOGAD) is an immune-mediated disorder associated with IgG antibodies against myelin oligodendrocyte glycoprotein (MOG), a protein located on the outer surface of CNS myelin and oligodendrocytes.

MOGAD is now recognized as a disease entity in its own right. Its immunological mechanisms, clinical patterns, MRI features and response to treatment differ from both multiple sclerosis and AQP4-IgG-positive NMOSD.

MOG-IgG

Antibodies against MOG are the key biomarker of the disease, but the laboratory result must always be interpreted together with the clinical syndrome and MRI findings.

One attack or recurrent disease

Some patients have a monophasic course with only one attack. Others experience recurrent inflammatory episodes. At the first event, future disease course cannot always be predicted reliably.

MOGAD ≠ MS

Conventional multiple sclerosis disease-modifying therapies are not standard treatment for MOGAD. Correct diagnosis therefore has direct consequences for treatment decisions.

One of the Most Common Questions

Positive MOG-IgG: does this mean I have MOGAD?

Not necessarily. MOG-IgG is not a general screening test that should be interpreted independently of the patient's symptoms.

When the result is convincing

The result is most informative when the patient has a typical inflammatory demyelinating attack — such as optic neuritis, myelitis or ADEM — and MOG-IgG is detected using a validated cell-based assay.

Low-positive MOG-IgG

Lower antibody levels have a higher risk of false-positive results. Clinical features, MRI findings and exclusion of multiple sclerosis or another diagnosis therefore become especially important.

Serum is the preferred sample for MOG-IgG testing. Cerebrospinal fluid testing may be useful in selected difficult cases, for example when the phenotype is strongly suggestive but serum testing is negative or equivocal. CSF testing does not replace correct interpretation of serum MOG-IgG.
Clinical Manifestations

What symptoms can MOGAD cause?

Optic neuritis

  • reduced vision in one or both eyes;
  • often significant pain with eye movement;
  • bilateral involvement is relatively common;
  • optic disc swelling may be prominent;
  • MRI may show a long optic nerve lesion and perineural enhancement.

Myelitis

  • weakness in the legs and/or arms;
  • numbness or other sensory changes;
  • difficulty walking;
  • bladder or bowel dysfunction;
  • the conus medullaris may be involved.

ADEM

Acute disseminated encephalomyelitis is particularly common in children. It may cause encephalopathy, drowsiness, behavioral changes, seizures and multifocal neurological symptoms.

Cortical encephalitis

Seizures, headache and focal cortical symptoms may occur, together with characteristic cortical MRI abnormalities. One recognized phenotype is known as FLAMES.

MOGAD Diagnosis

How is MOGAD diagnosed?

Current diagnosis follows international MOGAD criteria. A positive antibody test alone is not sufficient: a compatible clinical demyelinating event is required, and a better alternative diagnosis must be excluded.

Identify a compatible clinical syndrome Typical presentations include optic neuritis, myelitis, ADEM, brainstem or cerebellar syndromes, and cerebral cortical encephalitis.
Test for MOG-IgG Serum testing with a validated cell-based assay is preferred. The laboratory method and antibody level or titer are important when interpreting the result.
Review MRI The optic nerves, brain and spinal cord may need to be evaluated. In complex cases, reviewing the actual MRI images can be considerably more informative than relying only on the radiology report.
Test for AQP4-IgG when appropriate This is important in a compatible clinical setting to exclude AQP4-positive NMOSD.
Exclude an alternative diagnosis Particular attention is paid to multiple sclerosis, NMOSD, infectious disease, systemic autoimmunity and other inflammatory disorders of the CNS.

What to bring to your consultation

Bring your MOG-IgG result including the laboratory and testing method, AQP4-IgG results, the actual MRI scans of the brain, spinal cord and/or orbits, cerebrospinal fluid results, ophthalmological reports and discharge summaries from previous attacks.

Book a Consultation
Differential Diagnosis

MOGAD, NMOSD and multiple sclerosis: key differences

MOGAD AQP4-NMOSD Multiple sclerosis
Main antibody MOG-IgG AQP4-IgG No disease-specific serum antibody
Optic neuritis Often bilateral; anterior optic nerve involvement, optic disc swelling and perineural enhancement are relatively characteristic Often severe; posterior optic nerve involvement and optic chiasm involvement may occur More commonly unilateral
Myelitis Long or short spinal cord lesions may occur; conus involvement is characteristic Longitudinally extensive central myelitis is common Spinal cord lesions are more often short and peripheral
ADEM Characteristic, particularly in children Not typical Not typical
CSF oligoclonal bands Usually absent or transient Usually absent Frequently present
Long-term treatment Individualized relapse prevention; IVIG and other immune therapies may be used Targeted long-term immunotherapy MS-specific disease-modifying therapies

These are typical patterns rather than absolute rules. Diagnosis in an individual patient depends on the combination of clinical presentation, antibody results, MRI findings and additional investigations.

Acute Attack Treatment

Why timely treatment of a MOGAD attack matters

Contemporary observational data suggest that earlier treatment of the first MOGAD attack may be associated with a lower subsequent relapse risk. Rapid control of inflammation is also important for protecting vision and spinal cord function.

High-dose corticosteroids

Acute attacks are commonly treated with high-dose intravenous methylprednisolone. MOGAD is often highly corticosteroid responsive.

Plasma exchange

In a severe attack or when recovery after corticosteroids is inadequate, plasma exchange may be considered as an early escalation strategy.

IVIG

Intravenous immunoglobulin may be used as an alternative or additional acute treatment in selected situations, including in pediatric MOGAD.

After the acute phase, some patients receive a gradual oral corticosteroid taper over several weeks. The appropriate duration is individualized because very rapid corticosteroid withdrawal has been associated with early return of inflammatory disease activity in some patients.
Long-Term Strategy

Does everyone need long-term treatment after the first MOGAD attack?

No. Long-term immunotherapy is not automatically required after every first MOGAD event. This is an important difference from AQP4-positive NMOSD.

Some patients remain monophasic and never experience another attack. Others develop relapsing disease, and repeated attacks can cause cumulative injury to the optic nerves, spinal cord or brain.

After a first attack, treatment decisions may take into account the severity of the initial event, completeness of recovery, clinical phenotype, MOG-IgG evolution, age, estimated relapse risk and the potential consequences of another attack.

When long-term relapse-prevention therapy is particularly considered

  • after a confirmed recurrent MOGAD attack;
  • after a severe first attack with incomplete recovery;
  • with recurrent or severe optic neuritis;
  • when another attack could have major functional consequences;
  • in selected high-risk patients even after the first event.
Intravenous immunoglobulin
IVIG

Maintenance IVIG has some of the strongest observational evidence among therapies historically used off-label for relapse prevention in MOGAD.

In a large cohort of relapsing MOGAD, annualized relapse rates were lower with IVIG than with B-cell-depleting therapy or mycophenolate. These data, however, were not derived from a direct randomized comparison.

Mycophenolate mofetil
MMF

Mycophenolate mofetil is used as an oral steroid-sparing maintenance treatment and may reduce relapse frequency. It has been used in both adult and pediatric MOGAD.

Rituximab
anti-CD20

Rituximab can reduce relapse risk in some patients, but its effect in MOGAD is less predictable than in AQP4-positive NMOSD. Breakthrough attacks may occur despite effective peripheral B-cell depletion.

Other approaches

Azathioprine, prolonged low-dose corticosteroids and other immunosuppressive or immunomodulatory approaches may be considered in selected situations. Treatment choice depends on age, disease phenotype, comorbidities, pregnancy planning, tolerability and treatment availability.

Multiple sclerosis therapies should not automatically be used for MOGAD. MOGAD has a different disease mechanism, and conventional MS disease-modifying therapies are not appropriate relapse-prevention treatment for MOGAD.
Major 2026 Update

The first positive Phase III randomized trial in MOGAD

Satralizumab — METEOROID

−68%

In 2026, results of the randomized, double-blind, placebo-controlled Phase III METEOROID trial were presented in patients with relapsing MOGAD.

Satralizumab, a monoclonal antibody targeting the interleukin-6 receptor, reduced the risk of a new MOGAD relapse by 68% compared with placebo.

At 48 weeks, 87.3% of patients receiving satralizumab remained relapse-free compared with 66.5% receiving placebo.

This is the first positive pivotal randomized trial specifically in MOGAD. As of September 2026, satralizumab has not yet been specifically approved for the treatment of MOGAD, and regulatory submissions are expected based on these results.

Rozanolixizumab and FcRn

Another therapeutic strategy aims to reduce circulating IgG through inhibition of the neonatal Fc receptor (FcRn). Rozanolixizumab is being studied in the international Phase III cosMOG program. Definitive efficacy results in MOGAD are not yet available.

MOGAD treatment is therefore beginning to move from therapies borrowed from other autoimmune diseases toward treatments investigated specifically for MOGAD.

Prognosis

What is the long-term outlook for MOGAD?

Many patients recover well from the initial attack. Visual recovery following MOGAD-associated optic neuritis, for example, is often better than after optic neuritis associated with AQP4-positive NMOSD.

MOGAD should nevertheless not be considered a harmless disease. A severe initial event or repeated relapses may leave persistent visual loss, motor disability, bladder dysfunction, chronic pain, epilepsy or other neurological consequences.

Monophasic MOGAD

Some patients never experience another attack. This is one reason why preventive treatment after the first event is individualized.

Relapsing MOGAD

When attacks recur, effective relapse prevention becomes the main therapeutic goal because repeated attacks can lead to cumulative neurological injury.

Expert Consultation

What can be addressed during a MOGAD consultation?

Interpret a positive MOG-IgG result

Review the testing method, antibody level, clinical syndrome and MRI findings to determine how strongly the result supports MOGAD.

Reassess the diagnosis

Differentiate MOGAD from NMOSD, multiple sclerosis and other inflammatory disorders of the central nervous system.

Expert MRI review

Review the actual optic nerve, brain and spinal cord MRI studies for imaging patterns that support or argue against MOGAD.

Define a long-term strategy

Decide whether observation after the first attack is reasonable or whether relapse-prevention treatment should be considered; in recurrent MOGAD, review or select maintenance therapy.

Consultation with Dr. Lidiia Prakhova

A consultation may be particularly useful after a positive MOG-IgG test, recurrent optic neuritis, myelitis, uncertainty between MOGAD, NMOSD and multiple sclerosis, or when a decision is needed about starting or changing long-term relapse-prevention therapy.

Book a Consultation
FAQ

Frequently asked questions about MOGAD

Does a positive MOG-IgG result automatically mean I have MOGAD?
No. Particularly with a low-positive result, the clinical syndrome, MRI findings, testing method and alternative diagnoses must be considered. A positive antibody result without a compatible inflammatory demyelinating event should not automatically lead to a diagnosis of MOGAD.
Is MOGAD a type of multiple sclerosis?
No. MOGAD is a separate immune-mediated demyelinating disease with a different biomarker, clinical spectrum, MRI pattern and treatment strategy.
Are MOGAD and NMOSD the same disease?
No. Classical AQP4-positive NMOSD is associated with AQP4-IgG, whereas MOGAD is associated with MOG-IgG. They differ in pathophysiology, clinical manifestations, MRI features, prognosis and treatment.
Can MOGAD occur only once?
Yes. Some patients have a monophasic disease course and never experience another attack. Other patients develop recurrent disease, and future course cannot always be predicted accurately after the first event.
Does everyone need maintenance treatment after the first attack?
No. The decision depends on the severity of the first attack, degree of recovery, disease phenotype, estimated relapse risk and the potential consequences of another attack.
Why is IVIG often discussed for relapsing MOGAD?
Maintenance intravenous immunoglobulin has shown favorable outcomes in several observational studies of relapsing MOGAD and remains an important relapse-prevention option. The best treatment still depends on the individual patient.
What changed in MOGAD treatment in 2026?
In the Phase III METEOROID trial, satralizumab significantly reduced the risk of relapse in patients with relapsing MOGAD. This was the first positive pivotal randomized study specifically in MOGAD.
Can vision recover after MOGAD optic neuritis?
Visual recovery is often good, particularly when treatment is started promptly. Severe or repeated attacks can nevertheless cause permanent visual impairment.
Can pregnancy be planned with MOGAD?
In many cases, yes. Pregnancy should ideally be discussed in advance with the treating neurologist, particularly in relapsing disease or when maintenance immunotherapy is being used.
Can I get a second opinion if MOGAD has already been diagnosed?
Yes. A second opinion may be particularly useful for a low-positive MOG-IgG result, atypical MRI findings, uncertainty between MOGAD, NMOSD and multiple sclerosis, or before committing to long-term immunotherapy.
Related Topics

More about neuroimmunological disorders

Neuromyelitis Optica Spectrum Disorder (NMOSD) AQP4-IgG testing, differential diagnosis from MOGAD and current approaches to relapse prevention. Multiple Sclerosis Diagnosis, treatment selection and management of multiple sclerosis.
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Author

Dr. Lidiia Prakhova

Neurologist, Doctor of Medical Sciences. Main clinical areas of expertise include neuroimmunology, multiple sclerosis, NMOSD and MOGAD.

The information on this page is intended for educational purposes and does not replace an individual medical consultation.

Key Scientific References

  1. Banwell B, Bennett JL, Marignier R, et al. Diagnosis of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: International MOGAD Panel Proposed Criteria. Lancet Neurol. 2023;22(3):268–282. doi:10.1016/S1474-4422(22)00431-8.
  2. Sechi E, Gastaldi M, Cortese R, et al. Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Practical recommendations for diagnosis and management. J Neuroimmunol. 2026;410:578781. doi:10.1016/j.jneuroim.2025.578781.
  3. Budhram A, Flanagan EP. Testing for myelin oligodendrocyte glycoprotein antibodies: Who, what, where, when, why, and how. Mult Scler. 2025;31(5):505–511. doi:10.1177/13524585251313744.
  4. Kwon YN, Kim B, Kim JS, et al. Time to Treat First Acute Attack of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease. JAMA Neurol. 2024;81(10):1073–1084. doi:10.1001/jamaneurol.2024.2811.
  5. Deschamps R, Guillaume J, Ciron J, et al. Early Maintenance Treatment Initiation and Relapse Risk Mitigation After a First Event of MOGAD in Adults: The MOGADOR2 Study. Neurology. 2024;103(3):e209624. doi:10.1212/WNL.0000000000209624.
  6. Tisavipat N, Wilf-Yarkoni A, Al-Ani A, et al. Relapse and disability outcomes in incident MOGAD patients undergoing watchful waiting after onset. Mult Scler Relat Disord. 2025;102:106631. doi:10.1016/j.msard.2025.106631.
  7. Chen JJ, Huda S, Hacohen Y, et al. Association of Maintenance Intravenous Immunoglobulin With Prevention of Relapse in Adult MOGAD. JAMA Neurol. 2022;79(5):518–525. doi:10.1001/jamaneurol.2022.0489.
  8. Bilodeau PA, Vishnevetsky A, Molazadeh N, et al. Effectiveness of immunotherapies in relapsing myelin oligodendrocyte glycoprotein antibody-associated disease. Mult Scler. 2024;30(3):357–368. doi:10.1177/13524585241226830.
  9. Levy M, Flanagan E, Kümpfel T, et al. Safety and Efficacy of Satralizumab in Patients with Relapsing Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease (MOGAD): Results from the Phase 3 METEOROID Trial. Neurology. 2026. doi:10.1212/WNL.0000000000217915.
  10. Andersen J, Brilot F. Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Insights Into Pathogenesis and Biomarkers of Prognosis. Semin Immunol. 2025;78:101944. doi:10.1016/j.smim.2025.101944.
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