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Disease Information

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What is MOGAD?

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare inflammatory disease of the central nervous system (CNS). In MOGAD, the immune system attacks the protective coating around nerve fibers, called myelin, leading to damage in areas like the optic nerves, brain, and/or spinal cord1.

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How does MOGAD Develop?

While the exact cause of MOGAD is unknown, it is thought to be caused by autoantibodies known as myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG), which are antibodies in the immune system that mistakenly target healthy proteins in the body2. In MOGAD, these autoantibodies cause damage to healthy MOG proteins on the outer protective surface of nerve cells, leading to demyelination1,3. Demyelination can be compared to a power cord on a lamp short-circuiting when its protective plastic coating is stripped away. Without this insulation, the flow of electricity is disrupted, causing the lamp to flicker or fail to work. Similarly, in MOGAD, the loss of myelin impairs nerve signal transmission, leading to disruptions in nerve function4.

Recently, doctors have recognized that MOGAD is a distinct disease, separate from other neurological conditions like Neuromyelitis Optica Spectrum Disorder (NMOSD), Chronic Relapsing Inflammatory Optic Neuropathy (CRION) and Multiple Sclerosis (MS). Although these conditions can have similar symptoms, improved testing for MOG antibodies has made it easier to accurately diagnose MOGAD and tell it apart from other demyelinating diseases of the CNS5-6.

Who is affected by MOGAD?

Prevalence and incidence of MOGAD is still being studied, and the exact numbers can vary by region. However, research from different parts of the world shows that MOGAD is relatively rare. Estimates suggest that about 1.3 to 2.5 people per 100,000 have MOGAD, and each year, there are around 3.4-4.8 new cases per million people7.

Although MOGAD affects both men and women, and can happen at any age, it most commonly presents in those 28-30 years of age7. Around 30% of MOGAD cases occur in children, making it one of the more common causes of acquired central nervous system (CNS) demyelinating syndromes in young people8. Currently, unlike MS and NMOSD, MOGAD shows no clear racial preponderance or strong human leucocyte antigen associations, though further research is needed on how ethnicity may influence MOGAD expression8,9. As doctors become more familiar with MOGAD and testing becomes more widely available, it’s likely that more cases will be diagnosed in the future7.

Signs & Symptoms

MOGAD typically presents as a sudden onset of symptoms, referred to as an acute attack, which can vary in type and severity. It can also vary in how it presents over one’s lifetime, where it can be multiphasic (relapsing) or monophasic10,11,12.

  • Multiphasic: characterized by recurrent attacks following the initial episode
  • Monophasic: an individual experiences only a single attack throughout their lifetime13.

Monophasic classification represents approximately 50% of MOGAD cases. Emerging research suggests that young adults (below the age of 40) have a higher risk of relapse compared to those above the age of 408,14. However, the classification of MOGAD as monophasic has recently been challenged, and further research is needed. It is suggested that MOGAD may predominantly be a relapsing disease when observed over a longer follow-up period, with the monophasic nature of some individuals possibly being an artifact of insufficient observation time8.

Individuals with MOGAD may have varying levels of MOG-IgG over time, and higher titers are associated with a higher likelihood of an accurate diagnosis, as these elevated levels are more detectable in tests15,16. Increased MOG-IgG titers enhance diagnostic sensitivity, helping differentiate MOGAD from other demyelinating conditions15,16. Additionally, fluctuations in MOG-IgG levels can reflect disease progression and treatment response, providing valuable insights into disease activity and guiding therapeutic decisions15,16,17.

In children, ADEM is the most common clinical presentation, while ON and myelitis are more commonly observed in adults11;. In addition to these symptoms, fatigue is a significant and debilitating aspect of MOGAD31. Factors such as older age, bilateral optic neuritis (ON), other existing health conditions (comorbidities), and ongoing disease activity can worsen the severity of fatigue31. Furthermore, individuals living with MOGAD often show decreased visuomotor processing speed (such as difficulty reading or writing) and semantic fluency (such as difficulty with word retrieval), both of which correlate with the presence of cerebral lesions32. Uhthoff’s phenomenon is a temporary (less than 24 hours), worsening of neurological symptoms related to a demyelinating disorder such as MOGAD. This may occur when the bodies core temperature increases due to prolonged exposure to excessive heat (e.g., from hot weather, exercise, fever, saunas, or hot tubs)33.
Clinical Manifestations MOGAD typically presents with one or more of the following clinical manifestations. Optic neuritis (ON) is the most common symptom of MOGAD in adults. ON is inflammation of the optic nerve, often presenting as: • Blurry vision • Vision loss • Peripheral vision loss • Color vision loss • Optical disc edema • Impaired depth perception • Light sensitivity and glare/halos around lights at night ON can occur unilaterally, affecting one eye, or more commonly, bilaterally, affecting both eyes. Brainstem or cerebellar deficits result from lesions and inflammation in those areas. This may result in symptoms such as: • Double vision • Difficulty speaking • Difficulty swallowing • Difficulty with balance or coordination Myelitis, another common manifestation of MOGAD, is inflammation of the spinal cord which may cause: • Abnormal sensations such as numbness, tingling, burning, coldness, tickling, electrical shock or shooting pain • Loss of motor control • Bladder and bowel dysfunction • Stiff or weak muscles • Muscle spasms • Sexual dysfunction Cerebral monofocal or polyfocal deficits result from lesions in one or more areas of the brain which can lead to symptoms such as: • Difficulty speaking • Numbness • Vision problems • Loss of balance • Weakness in arms, face or legs Cerebral cortical encephalitis (CCE) is a rare and distinct form of MOGAD-related encephalitis. CCE is also termed “FLAMES”. The most common clinical symptoms of CCE or FLAMES include: • Seizures • Headaches • Fevers • Cortical symptoms related to the affected brain area o Aphasia o Encephalopathy o Hemiparesis Acute disseminated encephalomyelitis (ADEM) is a brief but widespread attack of inflammation in the brain and spinal cord, which can lead to the rapid onset of symptoms such as: • Confusion • Difficulty speaking • Loss of muscle coordination • Loss of balance • Headaches • Behavioral changes • Loss of consciousness • Seizures

Optic Neuritis (ON)

ON is the most common symptom of MOGAD in adults and is characterized by inflammation of the optic nerve, often presenting as severe
headaches or orbital pain. Additional symptoms associated with ON may include:

  • Blurry vision
  • Vision loss
  • Double vision
  • Peripheral vision loss
  • Color vision loss
  • Optical disc edema


ON can occur unilaterally, affecting one eye, or more commonly, bilaterally, affecting both eyes (Li et al., 2022; Rempe et al., 2021).

Transverse Myelitis (TM)

TM, another common manifestation of MOGAD, may occur alone or in conjunction with ON, and is characterized by inflammation of the spinal
cord which may cause:

  • Abnormal sensations such as numbness, tingling, burning, coldness, squeezing, electric shock, shooting pain, or itching
  • Muscle weakness
  • Loss of motor control
  • Bladder and bowel control issues
  • Stiff or weak muscles
  • Muscle spasms
  • Sexual dysfunction (Li et al., 2022)

Acute Disseminated Encephalomyelitis (ADEM)

ADEM involves a brief but widespread attack of inflammation in the brain and spinal cord, which can lead to the rapid onset of symptoms such as:

  • Confusion
  • Difficulty swallowing
  • Loss of coordination
  • Loss of balance
  • Headaches
  • Behavioral changes
  • Loss of consciousness
  • Seizures (Li et al., 2022)

Autoimmune Encephalitis (AE)

Autoimmune encephalitis (AE), or inflammation of the brain, is another manifestation of MOGAD. It can lead to symptoms such as:

  • Fever
  • Impairment or loss of consciousness
  • Seizures
  • Loss of coordination
  • Behavioral changes (Hegen et al., 2020)

Cerebral Cortical Encephalitis (CCE)

Until recently, encephalitis in MOGAD was believed to affect subcortical structures, similar to ADEM. However, a rare and distinct form of MOGAD-related encephalitis has recently been identified, known as cerebral cortical encephalitis (CCE), which is characterized by FLAIR (Fluid attenuate inversion recovery)-hyperintense Lesions in Anti-MOG-associated Encephalitis with Seizures (FLAMES). The most common clinical symptoms of FLAMES include:

  • Seizures
  • Headaches
  • Fevers
  • Cortical symptoms related to the affected brain area (Ogawa et al., 2017; Valencia-Sanchez et al., 2022; Maturu et al., 2023)

Diagnosis

Diagnosing MOGAD based on symptoms alone can be challenging due to the similarities with NMOSD, CRION and MS10. To establish a diagnosis, these other conditions must be excluded. Many individuals living with MOGAD may have previously been misdiagnosed with atypical MS or seronegative NMOSD or CRION, however are now considered to have MOGAD with a distinct clinical presentation8. This requires a careful differential diagnosis using clinical symptoms, laboratory results, and imaging findings. Prompt testing, especially in the acute phase of the disease, is critical for an accurate diagnosis and timely treatment, which can help improve outcomes for individuals living with MOGAD34.

 

For more information on the diagnostic criteria please visit the following page: https://mogproject.org/demystifying-the-diagnosis-of-mogad-take-home-points-for-patients-from-the-2023-international-mogad-panel-proposed-diagnostic-criteria/

MOG-IgG Testing

The most important criterion for MOGAD diagnosis is the presence of MOG-IgG antibodies. These antibodies can be detected in blood or cerebrospinal fluid (CSF), and their presence is a key marker for MOGAD. Below are key points related to the testing process for these antibodies:

  • Serum testing is the most common method
  • The live cell-based assay is the gold standard for testing MOG-IgG levels yet must be done prior to any treatment5.
  • MOG-IgG levels may decrease over time following an acute attack, which can result in false negative results.
    • For this reason, testing should be performed promptly after the onset of symptoms and repeated if necessary35.
  • CSF analysis may be useful when blood tests yield inconclusive results
    • MOG-IgG has been found in CSF of 12% of individuals who are seronegative yet present with symptoms of MOGAD, however this presence may be indicative of a more severe clinical presentation36,37,38.
 

However, the presence of MOG-IgG antibodies alone is not sufficient for a diagnosis, as antibody levels can fluctuate over time, and low levels may result in false-positives or negatives15.

A blood sample from a patient with MOG antibodies is added to target cells with MOG proteins on their surface. The MOG antibodies bind to the MOG proteins, and fluorescent antibodies bind to the MOG antibodies, causing fluorescence of the cells. The intensity of the fluorescence indicates that the patient is seropositive for MOGAD. In contrast, a blood sample from a patient without MOG antibodies is added to the same target cells. No binding occurs between MOG proteins and antibodies, so no fluorescence is produced, indicating the patient is Seronegative for MOGAD.

Imaging

  • Magnetic Resonance Imaging (MRI) is crucial in assessing inflammation and/or lesions in the optic nerves, spinal cord, and brain, which are commonly seen in MOGAD5.
    • However, in about 10% of cases, MRI findings may initially appear normal at the onset of symptoms, even when individuals living with MOGAD experience significant clinical disability and repeat MRI after days/weeks may be necessary39.
  • Optical coherence tomography (OCT) is often performed for evaluating optic nerve damage, which allows for direct visualization of the nerve’s condition.
  • Visual field testing can also be used to detect blind spots or other visual impairments caused by optic neuritis5,40.

Treatments: Acute and Preventative Care

Although there are currently no FDA-approved treatments specifically for MOGAD, various therapies can help manage symptoms, reduce relapses and control inflammation5. Treatment strategies vary depending on whether the individual is in the acute phase or needs long-term preventive care.

Acute Treatment

During the acute phase, the primary goal is to reduce inflammation and prevent further damage by targeting and lowering the levels of MOG-IgG antibodies. High-dose corticosteroids are typically the first-line treatment, administered either orally or intravenously. These steroids work by suppressing the immune system and reducing inflammation. However, prolonged use of corticosteroids can lead to steroid dependency and other side effects such as weight gain, elevated blood pressure, elevated blood sugar, cataracts, insomnia, osteoporosis, edema, heart rhythm abnormalities, muscle atrophy and more5,40. As such, after the initial acute attack, steroid tapering may be performed to gradually reduce the dosage of corticosteroids to minimize side effects while continuing to suppress inflammation. Steroid tapering must be done carefully to avoid a rebound increase in inflammation.

In some cases, additional treatments may be used in combination with or in place of steroids.  This may include:

  • Plasma exchange (PLEX/ plasmapheresis) can be performed to remove harmful MOG-IgG antibodies from the blood, offering additional immune modulation5,41. For risks/ side effects of PLEX, please see the following resources:
  • Corticosteroids help reduce inflammation and supress the immune response from the acute attack5,40. For the risks/ side effects of corticosteroids, please see the following resources:
  • Intravenous immunoglobulin (IVIG) involves infusing antibodies from healthy donors. The mechanism of action of IVIG is not fully understood but is thought to involve enhanced clearance and interference with MOG antibodies, as well as modulation of the immune response5,42. For the risks/ side effects of IVIG, please see the following resource:

Preventative Treatment

For individuals living with MOGAD who have a history of relapse, preventive treatments are typically recommended to avoid further relapses and minimize the risk of long-term disability.

After a first MOGAD attack, the decision to initiate long-term, preventive therapy depends on how the individual responds to acute treatment, the level of damage from the initial attack, and the risk for further relapses. In about 33% of individuals living with MOGAD, it is a one-time occurrence, with only one attack in their lifetime5,8,15. If the response to acute treatment after an initial attack is complete and MOG-IgG levels are undetectable, doctors may opt to delay long-term treatment until a second attack occurs. However, if the response to treatment is incomplete, and MOG-IgG levels remain elevated, immunomodulators may be recommended to prevent further relapses and minimize the risk of long-term disability. While there is no defined biomarker indicative of relapse in MOGAD, some physicians may recommend not to risk a second attack and initiate preventative treatment to avoid further damage. Risks of adverse effects from immunosuppressive therapies also need to be taken into consideration. These discussions should be individualized, and shared decision making between the physician and the patient is essential. Treatments to prevent MOGAD relapses may include:

  • Immunomodulators such as mycophenolate mofetil, rituximab43, tocilizumab and azathioprine40,44. These are used to reduce inflammation and prevent future attacks. For more information regarding the efficacy and side effects of immunomodulators, please see the following resources:
  • Intravenous immunoglobulin (IVIG) or subcutaneous immunoglobulin (SCIG), which involves regular infusions of antibodies from healthy donors45. These treatments help neutralize MOG antibodies and decrease the immune response that triggers relapses, proving highly effective when administered at the correct dosage and interval5,46,47.
  • Low-dose oral corticosteroids may be used for short periods following an attack and are sometimes taken in low doses long-term to prevent relapses in adults, though this treatment is not typically prescribed for children given the risks for adverse effects5,46.

Long-term management of MOGAD often involves a combination of these therapies to balance controlling inflammation and minimizing the side effects of chronic treatment5. Individuals living with MOGAD are unresponsive to conventional MS therapies like interferon beta and glatiramer, making accurate MOGAD diagnosis crucial for effective treatment44.

Ongoing Clinical Trials

Several promising treatments are currently being investigated in clinical trials. These treatments include:

 

  • Neonatal Fc receptor inhibitor (FcRn), rozanolixizumab. By blocking FcRn, which normally helps preserve MOG-IgG antibodies in the body, rozanolixizumab accelerates the degradation of MOG-IgG antibodies, thereby reducing the immune response48,49. Rozanolixizumab is currently in Phase 3 of clinical trials1.
    • Rozanolixizumab (cosMOG): This randomized, double-blind, placebo-controlled, multicenter study is designed to assess the efficacy and safety of rozanolixizumab in adult patients aged 18 to 89 with at least one relapse in the past 12 months. The study will include 104 participants worldwide and began on February 2, 2022, with an expected completion date of July 1, 2027.

For more details: https://mogproject.org/clinical-trials/#cosmog

  • IL-6 receptor targeted drugs, satralizumab and tocilizumab, which work to suppress the immune response involved in MOGAD attacks. These are in Phase 3 and Phase 2/3 of clinical trials, respectively50,51,52,53.
    • Satralizumab (METEOROID): This randomized, double-blind, placebo-controlled, multicenter study aims to evaluate the efficacy, safety, pharmacokinetics, and pharmacodynamics of satralizumab in patients aged 12 years or older with a confirmed diagnosis of MOGAD. Eligible participants must have experienced at least one relapse in the past 12 months or at least 2 attacks in the past 24 months. The trial, involving 152 participants worldwide, began on August 30, 2022, and is set to conclude on December 31, 2028.

For more details: https://mogproject.org/clinical-trials/#meteoroid

    • Tocilizumab (TOMATO): This randomized, controlled multicenter study aims to evaluate the safety and efficacy of tocilizumab in patients aged 12 years or older with a confirmed diagnosis of MOGAD. Eligible participants must have experienced at least one relapse in the past 12 months or at least 2 attacks in the past 24 months. The trial, involving 102 participants in China, began on July 9, 2024, and is set to conclude on July 1, 2026.

For more details: https://clinicaltrials.gov/study/NCT06452537?intr=tocilizumab&cond=MOGAD&rank=1

Prognosis and Understanding Relapsing Disease

The prognosis for individuals with MOGAD can vary significantly, making it difficult to predict the likelihood of relapses, their severity, and the extent of recovery following subsequent attacks11. While it’s suggested that approximately 67% of individuals experience relapses, it is uncertain who will relapse or when these relapses might happen8. Understanding relapse patterns is crucial for managing the long-term course of the disease and improving patient outcomes.

Risk Factors for Relapse

 

Tracking relapse patterns over time is crucial for assessing the progression of MOGAD, as accumulated disability is believed to result from relapses rather than continuous progression8. Certain factors have been associated with an increased risk of relapse in individuals living with MOGAD:

  • Age: Older children17.
  • Gender: Female54.
  • Ethnicity: Hispanic/Latino54.
  • Initial symptoms: Individuals presenting with ON as an initial symptom17.
    • Presence of the non-p42 epitope in patients particularly with an ON phenotype is the first serological marker that may be indicative of relapse55.
  • Seropositivity: Persistent seropositivity (the presence of MOG-IgG antibodies) in blood tests after an acute attack may indicate a higher risk of relapse in some individuals15,17. However, patients who become seronegative can return to seropositive and experience an attack, and some patients who remain seropositive do not have relapses56.

Importance of Early Diagnosis and Relapse Management

Getting an early diagnosis of MOGAD and prompt treatment following the first attack is crucial for preparing individuals living with MOGAD for the possibility of future relapses57,58. MOGAD attacks, especially those involving the spinal cord (myelitis and ADEM), can cause significant neurological damage that may be permanent, leading to long-term disability12. Individuals living with MOGAD who experience myelitis during their initial attack are at higher risk of enduring long-term functional impairments12.

 

For individuals at high risk of relapse, ongoing preventive treatment, such as those described above, have been shown to reduce the likelihood of future relapses54. Interestingly, ON is the most common symptom observed during relapse, regardless of the symptoms during the initial attack40.

 

Early intervention and prompt treatment during relapses can help prevent new and permanent damage to the nervous system, which in turn may minimize long-term disability and improve the overall prognosis for individuals living with MOGAD. In some instances, this swift treatment allows patients to recover partially or entirely back to their pre-attack baseline57.

 

A pseudo-relapse in MOGAD refers to the temporary recurrence or worsening of neurological symptoms, often triggered by external factors such as heat, stress, infections, or other physical or emotional stressors. Unlike true relapses, pseudo-relapses are characterized by their transient nature, with symptoms fluctuating in severity and typically improving within 24-48 hours. Clinically, pseudo-relapses can be distinguished from genuine relapses by the absence of new or worsening lesions on MRI, indicating that they do not reflect disease progression. However, physicians must exercise caution in making this distinction if there is an exam change, as relapses can occasionally occur despite negative MRI findings59. Pseudo-relapses are thought to result from factors that exacerbate existing symptoms without triggering active inflammation or demyelination in the central nervous system (CNS).

Impact on Quality of Life​

Being diagnosed with MOGAD can affect an individual’s quality of life (QoL). The physical symptoms of an attack, such as vision impairment, mobility issues and weakness can interfere with daily activities and limit a person’s independence. These limitations may affect an individual living with MOGAD’s ability to:

  • Maintain employment
  • Manage personal care
  • Engage in social or recreational activities

In addition to the physical impact, mental health challenges are common among individuals living with MOGAD. Studies have found that these individuals may experience heightened:

  • Anxiety60
  • Depression60
  • Fatigue31
  • Cognitive difficulties60
  • Social isolation60 
 

These psychological and emotional burdens often compound the physical challenges of the disease, making effective management of MOGAD essential not just for preventing relapses, but also for improving overall well-being.

Please see these helpful resources to support living with MOGAD:

Our YouTube Channel: https://www.youtube.com/@themogproject

Rehabilitative & Long-Term Care​

Rehabilitation therapy can assist in restoring function, improving QoL, and promoting independence for those living with MOGAD. Starting rehabilitation early following an attack can prevent the complications associated with disuse and addresses functional impairments resulting from neurological damage. Rehabilitation strategies are individualized to the specific symptoms and challenges an individual living with MOGAD is experiencing after an acute attack. These specialists make up the multidisciplinary team focused on ensuring holistic health for individuals living with MOGAD61.

Physical Therapists

Physical therapists play a vital role in addressing mobility issues such as spasticity, muscle weakness, and pain that result from damage to the central nervous system (CNS)62. This damage can lead to muscle tightness, involuntary contractions, and limited movement63. To help manage these challenges, physical therapists develop personalized exercise programs that focus on stretching and strengthening muscles to improve range of motion and restore functional mobility64,65. They may also recommend assistive devices, like splints, to support weakened muscles and joints65. Pain in MOGAD can stem from neuropathic causes, such as nerve damage that results in burning, stabbing, or shooting pain, or from musculoskeletal issues like spasticity and joint pain caused by immobility63. Physical therapists help manage pain by improving muscle strength and flexibility through targeted exercises64,65. They also use techniques such as massage, stretching, and TENS therapy (Transcutaneous Electrical Nerve Stimulation) to alleviate discomfort and improve overall function64.

Speech and Language Pathologists

Speech and language pathologists are integral in addressing swallowing difficulties and speech impairments that arise when muscles involved in speech and swallowing are weakened or damaged by MOGAD67. Swallowing therapy is provided to help individuals maintain safe swallowing and reduce the risk of choking, often through techniques like thickened liquids or swallowing exercises69. For individuals experiencing speech impairments, speech pathologists offer exercises aimed at improving articulation, breathing, and language skills to enhance clarity and communication69,70.

Urologists

Urologists are directly involved in managing bladder dysfunction, bowel dysfunction, and sexual dysfunction, which are common challenges for individuals living with MOGAD78,79. Bladder dysfunction can occur when nerve pathways that control the bladder are impaired, resulting in incontinence or urinary retention78,79. Urologists help by recommending bladder training, medications such as anticholinergics, and in some cases, catheterization to improve bladder control80. Similarly, bowel dysfunction caused by neurological impairment can lead to constipation or fecal incontinence79. Urologists recommend dietary modifications, stool softeners, and regular bowel training to manage these symptoms effectively79. Sexual dysfunction, often resulting from nerve damage, can affect sexual arousal and function79,80. Urologists work with individuals to address this through sexual health counseling, medications, and adaptive devices to improve sexual function and quality of life79,80.

Occupational Therapists

Occupational therapy helps individuals with MOGAD regain independence in daily activities while addressing specific symptoms such as pain, balance issues, and fatigue65,66. For individuals experiencing musculoskeletal pain or joint stiffness, occupational therapists recommend adaptive tools like reachers or button hooks to reduce strain during tasks such as dressing and eating65,67. They also provide ergonomic strategies to improve comfort and joint mobility67. To address balance problems and mobility challenges, occupational therapists evaluate posture and recommend assistive devices like canes or walkers to improve stability65. They teach safe mobility techniques to reduce the risk of falls and enhance independence68. For those affected by fatigue, occupational therapists guide individuals in energy conservation techniques, helping them prioritize tasks and manage their stamina throughout the day67,68.

Neuropsychologists

Neuropsychologists provide valuable support in managing depression, anxiety, and behavioral issues that can result from neurological changes or the emotional burden of living with MOGAD32,65. These professionals may help patients cope with mood swings, anxiety, and other emotional challenges, promoting better emotional well-being32. Cognitive impairments, such as memory loss and difficulty concentrating, often occur as a result of brain lesions caused by MOGAD71,72. Neuropsychologists assess these cognitive challenges and develop personalized rehabilitation programs, incorporating techniques to improve attention, memory, and problem-solving skills32. Additionally, behavioral issues such as impulsivity, irritability, or mood swings occur due to damage in the frontal lobes of the brain73. Neuropsychologists use behavioral therapy to address emotional regulation, helping individuals manage and cope with behavioral changes74,75.

Neuro-Ophthalmologists and low vision rehabilitation specialists

Neuro-ophthalmologists and low vision rehabilitation specialists are vital members of the healthcare team when it comes to addressing low vision caused by optic nerve damage76,77. These specialists assess the degree of visual impairment using tools like Optical Coherence Tomography (OCT) scans and visual field tests to monitor recovery and detect early signs of relapse77. In addition to medical treatment, they recommend assistive devices such as magnifiers, screen readers, and modified lighting to assist with daily tasks like reading and using a computer76. Low vision rehabilitation also involves training individuals in adaptive techniques for safe navigation and performing daily activities despite visual impairments76.

Chronic Fatigue Specialists

Chronic fatigue specialists are crucial in managing chronic fatigue, a pervasive issue caused by neurological stress and the burden of living with a chronic illness. These specialists teach individuals how to manage their energy effectively through pacing techniques, improving sleep hygiene, and incorporating stress management strategies to help individuals optimize their daily functioning without overexerting themselves81,82,83. In some cases, medication may also be used to support individuals in managing symptoms and improving their quality of life84.

CONCLUSION

While MOGAD is a serious and complex medical condition, ongoing research and clinical trials are making excellent progress toward improved treatment outcomes. With appropriate support, individuals living with MOGAD can maintain or even improve their quality of life (QoL), maximize functional independence, and manage the condition’s complexities. By prioritizing early intervention, personalized treatment plans, and continuous care, individuals with MOGAD can lead fulfilling lives despite the challenges posed by the disease.

References

  1. cosMOG – About MOGAD. Available from: https://www.cosmogstudy.com/about-mog-ad/. Accessed on September 30, 2024.
  2. Elkon and Casali. Nat Clin Pract Rheumtol. 2009; 4: 491-498. Nature and functions of autoantibodies – PMC
  3. Jeyakumar et al. Eye. 2024;38:2289-2301. springernature_eye_3108 2289..2301
  4. Harry and Toews. Handbook of Developmental Neurotoxicity. 2007; 87-115. Myelination, Dysmyelination, and Demyelination – PMC
  5. Hegen and Reindl. Ther Adv Neurol Disord. 2020;13:1-20. Recent developments in MOG-IgG associated neurological disorders – PubMed
  6. Gastaldi et al. J Neurol. 2020;267(23):3555-3564. Cell-based assays for the detection of MOG antibodies: a comparative study – PubMed
  7. Hor and Fujihara. Front Neurol. 2023;14:1260358. Epidemiology of myelin oligodendrocyte glycoprotein antibody-associated disease: a review of prevalence and incidence worldwide – PubMed
  8. Trewin et al. Autoimmun Rev. 2025: 24: 103693 MOGAD: A comprehensive review of clinicoradiological features, therapy and outcomes in 4699 patients globally – PubMed
  9. Grant-Peters et.al Ann Clin Transl Neurol. 2021: 8: 1502-1507 No strong HLA association with MOG antibody disease in the UK population – PMC
  10. Ambrosius et al. Int J Mol Sci. 2020;22:100. Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Management – PMC
  11. Li et al. Front Aging Neurosci. 2022;14:850743. Clinical Features and Imaging Findings of Myelin Oligodendrocyte Glycoprotein-IgG-Associated Disorder (MOGAD) – PubMed
  12. Jurynczyk et al. Brain. 2017;140:3128-138. Clinical presentation and prognosis in MOG-antibody disease: a UK study – PubMed
  13. Santoro et al., Ann Clin Transl Neurol. 2023: 10: 672-685. Attack phenotypes and disease course in pediatric MOGAD – PMC
  14. Satukijchai et al. JAMA Netw Open. 2022; 5: e2142780 Factors Associated With Relapse and Treatment of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease in the United Kingdom – PubMed
  15. Lopez-Chiriboga et al. JAMA neurol. 2018;75:1355-1363. Association of MOG-IgG Serostatus With Relapse After Acute Disseminated Encephalomyelitis and Proposed Diagnostic Criteria for MOG-IgG-Associated Disorders – PubMed
  16. Wendel et al. Neurol Neuroimmunol Neuroinflamm. 2022: 9: e200035 Temporal Dynamics of MOG Antibodies in Children With Acquired Demyelinating Syndrome – PubMed
  17. Waters et al. Jama Neurol. 2020;77:82-93.dendrocyte Glycoprotein Antibody Analyses and Outcomes in Children With DemyelinSerial Anti-Myelin Oligoating Syndromes – PubMed 
  18. Asseyer et al. Mult Scler Relat Disord. 2020; 40: 101965. Prodromal headache in MOG-antibody positive optic neuritis – ScienceDirect
  19. Rempe et al. Mult Scler Relat Disord. 2021; 48:102718. Anti-MOG associated disorder-Clinical and radiological characteristics compared to AQP4-IgG+ NMOSD-A single-center experience – PubMed
  20. Transverse Myelitis. Available from: https://www.ninds.nih.gov/health-information/disorders/transverse-myelitis  Accessed on February 2, 2025.
  21. Filippi and Rocca. White Matter Diseases. 2020: 12: 109-125. Acute Disseminated Encephalomyelitis – PMC
  22. Shilo et al. Eur J Paediatr Neurol. 2016: 20: 361-367. Long-term motor, cognitive and behavioral outcome of acute disseminated encephalomyelitis – ScienceDirect
  23. Valencia-Sanchez et al. Ann Neurol. 2022;92:297-302. Cerebral Cortical Encephalitis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease – PubMed
  24. Pace et al. Eur J Neurol. 2024: 32: e16550.Cerebral cortical encephalitis in adults with myelin oligodendrocyte glycoprotein antibody‐associated disease: A national case series – PMC
  25. Jain et al. Mult Scler Relat Disord. 2021: 49: 102759.  “FLAMES: A novel burning entity in MOG IgG associated disease” – PubMed
  26. Ogawa et al., Neurol Neruoimmunol Neuroinflamm. 2017: 4: e322 MOG antibody-positive, benign, unilateral, cerebral cortical encephalitis with epilepsy – PubMed
  27. Maturu et al., 2023. Cureus. 2023;15(2): e34994. Unilateral Autoimmune Encephalitis: A Case Report on a Rare Manifestation of Myelin Oligodendrocyte Glycoprotein Antibody Disease – PMC
  28. Banwell et al. Lancet Neurol. 2023: 22:268-282. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria – PubMed
  29. Demyelinating Disease. Available from: Demyelinating Disease: What It Is, Symptoms & Treatment Accessed February 2, 2025.
  30. Banks et al. J Neurol Neurosurg Psychiatry. 2022: 92: 384-390. Brainstem and Cerebellar Involvement in MOG-IgG Associated Disorder versus Aquaporin-4-IgG and MS – PMC
  31. Ladakis et al. Mult Scler J Exp Transl Clin. 2022; 8: 10.1177/20552173221131235. Fatigue is a common symptom in myelin oligodendrocyte glycoprotein antibody disease – Dimitrios C Ladakis, Jennifer Gould, Jenny M Khazen, Julia M Lefelar, Scott Tarpey, Charles J Bies, Rebecca Salky, Kathryn C Fitzgerald, Pavan Bhargava, Bardia Nourbakhsh, Elias S Sotirchos, 2022
  32. Passoke et al. J Neurol Neurosurg Psychiatry. 2024; 333994. Cognition in patients with myelin oligodendrocyte glycoprotein antibody-associated disease: a prospective, longitudinal, multicentre study of 113 patients (CogniMOG-Study) – PubMed
  33. Panginikkod et al., Uhthoff Phenomenon. 2022 Oct 24. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing Uhthoff Phenomenon – PubMed
  34. Forcadela et al. Neurol Neuroimmunol Neuroinflamm. 2023: 11: e200183. Timing of MOG-IgG Testing Is Key to 2023 MOGAD Diagnostic Criteria – PubMed
  35. Nguyen et al. Mult Scler J Exp Transl Clin. 2024; 10: 2055217241274610. The positive predictive value of MOG-IgG testing based on the 2023 diagnostic criteria for MOGAD – PubMed
  36. Carta et al. Neurology. 2023: 100: e1095-e1108. Significance of Myelin Oligodendrocyte Glycoprotein Antibodies in CSF: A Retrospective Multicenter Study – PMC
  37. Redenbaugh et al. Ann. Neurol. 2024: 96: 34-45. Diagnostic Utility of MOG Antibody Testing in Cerebrospinal Fluid – Redenbaugh – 2024 – Annals of Neurology – Wiley Online Library
  38. Greco et al. J Neurol Neurosurg Psychiatry. 2024: 333554. Clinical, prognostic and pathophysiological implications of MOG-IgG detection in the CSF: the importance of intrathecal MOG-IgG synthesis | Journal of Neurology, Neurosurgery & Psychiatry
  39. Sechi et al. Mult Scler. 2021; 27: 303-308.  Frequency and characteristics of MRI-negative myelitis associated with MOG autoantibodies – PubMed
  40. Jarius et al. J Neuroinflammation. 2016;13:230. MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome – PubMed
  41. Tonev and Momchilova. Biomedicines. 2023;11:328. Therapeutic Plasma Exchange in Certain Immune-Mediated Neurological Disorders: Focus on a Novel Nanomembrane-Based Technology – PubMed
  42. American College of Rheumatology – Intravenous Immunoglobulin. Available from: Intravenous Immunoglobulin (IVIG) Accessed on September 30, 2024.
  43. Spagni et al. J Neuro Neruosurg Psychiatry. 2023; 94:62-69. Efficacy and safety of rituximab in myelin oligodendrocyte glycoprotein antibody-associated disorders compared with neuromyelitis optica spectrum disorder: a systematic review and meta-analysis – PubMed
  44. Hacohen et al. Jama Neruol. 2018; 75:478-487. Disease Course and Treatment Responses in Children With Relapsing Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease – PubMed
  45. Sotirchos et al. Multi Scler Relat Disord. 2022;57:103462 Treatment of myelin oligodendrocyte glycoprotein antibody associated disease with subcutaneous immune globulin – PubMed
  46. Bruijsten et al. Eur J Paediatr Neurol. 2020;29:41-53. E.U. paediatric MOG consortium consensus: Part 5 – Treatment of paediatric myelin oligodendrocyte glycoprotein antibody-associated disorders – PubMed
  47. Chen et al. Mult Scler Relat Disord. 2022;68:104237. Details and outcomes of a large cohort of MOG-IgG associated optic neuritis – ScienceDirect
  48. Kiessling. Sci Transl Med. 2017;9: 1208. The FcRn inhibitor rozanolixizumab reduces human serum IgG concentration: A randomized phase 1 study – PubMed
  49. Sechi et al. Front Neurol. 2022;13:885218. Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management – PubMed
  50. Yamamura et al. N Engl J Med. 2019;22:2114-22124. Trial of Satralizumab in Neuromyelitis Optica Spectrum Disorder | New England Journal of Medicine
  51. Sheppard et al. Hum Vaccin Immunother. 2017;13:1972-1988. Tocilizumab (Actemra) – PubMed
  52. METEOROID-A clinical trial to compare satralizumab with placebo, with or without background therapy, in people with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Available from: https://forpatients.roche.com/en/trials/autoimmune-disorder/mog-antibody-disease/a-study-to-evaluate-the-efficacy–safety–pharmacokinet-94806.html Accessed on September 30, 2024.
  53. TOMATO- Safety and Efficacy of Tocilizumab in Patients With Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease.Accessed on September 30, 2024.
  54. Virupakshaiah et al. J Neurol Neurosurg Psychiatry. 2024;333464. Predictors of a relapsing course in myelin oligodendrocyte glycoprotein antibody-associated disease – PubMed
  55. Liyanage et al. J Neurol Neurosurg Psychiatry. 2024 95: 544-553. The MOG antibody non-P42 epitope is predictive of a relapsing course in MOG antibody-associated disease – PubMed
  56. Hyun et al. J Neurol Neurosurg Psychiatry. 2017: 88: 811-817 Longitudinal analysis of myelin oligodendrocyte glycoprotein antibodies in CNS inflammatory diseases | Journal of Neurology, Neurosurgery & Psychiatry
  57. Whittam et al. J Neurol. 2020;267:3565-577.  Treatment of MOG antibody associated disorders: results of an international survey – PubMed
  58. Kwon et al. JAMA Neurol. 2024; 2811. Time to Treat First Acute Attack of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease – PubMed
  59. Levy et al. Mult Scler Relat Disord. 2023;72: 104613 Multiple types of relapses in MOG antibody disease – PubMed
  60. Said et al. Mult Scler J Exp Transl Clin. 2024;10: 20552173241274605. Quality of life is impaired in myelin oligodendrocyte glycoprotein antibody associated disease – PubMed
  61. MOGAD Clinic – Overview – Mayo Clinic Accessed on February 2 2025.
  62. Rosenthal et al. JIM 2020:68: 321-330. CNS Inflammatory Demyelinating Disorders: MS, NMOSD and MOG Antibody Associated Disease – Jacqueline F Rosenthal, Benjamin M Hoffman, William R Tyor, 2020
  63. Asseyer et al. Front Neurol. 2020: 11: 778. Pain in NMOSD and MOGAD: A Systematic Literature Review of Pathophysiology, Symptoms, and Current Treatment Strategies – PubMed
  64. Kubsik-Gidlewska et al. Adv Clin Exp med. 2017: 26: 709-715. Rehabilitation in multiple sclerosis – PubMed
  65. MOG Antibody Disease Information. Available from: MOG Antibody Disease Information – MyMyelitis Accessed on February 2 2025.
  66. Park et al. Brain Neurorehabil. 2021: 15:e9. Multidisciplinary Rehabilitation for Relapsing Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease: A Case Report – PMC
  67. Occupational Therapy in Neuro Rehab: Restoring Function and Independence. Available from: Occupational Therapy in Neuro Rehab: Restoring Function and Independence. Accessed February 2 2025.
  68. De-Bernardi-Ojuel et al. Int J Environ Res Public health. 2021: 18:1432. Occupational Therapy Interventions in Adults with Multiple Sclerosis or Amyotrophic Lateral Sclerosis: A Scoping Review – PMC
  69. Speech therapy: How it helps in multiple sclerosis. Available from: Speech therapy for multiple sclerosis (MS): An overview Accessed February 3 2025.
  70. Tang. J Clin Exp Neuroimmunol. 2024: 9:4. Understanding Aphasia: A Speech Therapist’s Approach to Neurological Disorders
  71. Risi et al. J. Neurol. Sci. 2025: 470: 123413 Longitudinal assessment of cognitive function in patients with non-relapsing MOG-IgG associated disease – Journal of the Neurological Sciences
  72. Unmet Needs and Challenges Across Pediatric and Adult MOGAD Populations. Available from: Unmet Needs and Challenges Across Pediatric and Adult MOGAD Populations. Accessed February 3 2025.
  73. Understanding and Managing Multiple Sclerosis Mood Swings. Available from: Multiple Sclerosis Mood Swings Explained. Accessed February 5 2025.
  74. Neurobehavioral Therapy: Transforming Lives Through Brain-Based Interventions. Available from: Neurobehavioral Therapy: Brain-Based Interventions for Mental Health Accessed February 5 2025.
  75. Turner and Knowles. Fed Pract. 2020: 37:S31-S35. Behavioral Interventions in Multiple Sclerosis – PMC
  76. Optic Neuritis: How Long for recovery? Available from: Optic Neuritis: How Long for Recovery? – Eye Surgery Guide Accessed February 5 2025.
  77. What is a Neuro-Ophthalmologist? Available from: What Are the Diseases Treated by Neuro-Ophthalmologists? Accessed February 5 2025.
  78. Li et al. Neurology. 2020: 95: e2924-e2934. A clinico-neurophysiological study of urogenital dysfunction in MOG-antibody transverse myelitis – PubMed
  79. DasGupta and Fowler. Therapy in Practice. 2003: 63: 153-166. Bladder, Bowel and Sexual Dysfunction in Multiple Sclerosis | Drugs
  80. Bientinesi et al. Int neuronal J. 2020: 24: 118-126. Managing Urological Disorders in Multiple Sclerosis Patients: A Review of Available and Emerging Therapies – PMC
  81. Pacing: Mastering your energy to manage chronic illness. Available from: Pacing: Mastering your energy to manage chronic illness better – Carenity Accessed February 5 2025.
  82. Gupta et al. BMJ Open. 2023: 13:e060401. Sleep hygiene strategies for individuals with chronic pain: a scoping review – PMC
  83. Fatigue in the Context of MS. Available from: MS and Fatigue Fact Sheet | Cleveland Clinic. Accessed February 6 2025.
  84. Multiple Sclerosis (MS) and Sleep. Available from: MS and Sleep Disturbances: Insomnia, Nocturia, & Coping | Sleep Foundation. Accessed February 6 2025