Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease or MOG Antibody Disease (MOGAD) is a condition that causes inflammation to the optic nerve(s), brain, and spinal cord.
Myelin oligodendrocyte glycoprotein (MOG) is found on the myelin sheath. The myelin sheath covers nerve cells and acts as an insulator. Myelin helps speed messages sent from the brain to the body through the central nervous system (CNS). 1
MOG is also believed to help maintain the structure of the myelin sheath by protecting and repairing it when it gets damaged. 1 MOG antibodies mistakenly attack MOG and the myelin sheath, causing inflammation to the optic nerve(s), spinal cord, and brain.
What are Antibodies?
White blood cells produce antibodies that attack viruses and bacteria in the bloodstream. They act as part of the immune system to destroy foreign viruses, bacteria, and other germs from causing infection. The immune system allows our bodies to defend themselves against infections previously encountered. 1
Usually, antibodies do not cause harm to the person. Still, sometimes they can misinterpret a friendly antibody for a foreign invader. The antibodies against MOG are responsible for the inflammation in the CNS. 1
What are MOG Antibodies?
In MOG Antibody Disease, the body generates antibodies that attack the MOG proteins and the myelin sheath, damaging the nerves beneath it. Nerve damage means the transmission of messages sent through the nerves is slowed down or stopped. 2
This is called demyelination, which tends to occur in the optic nerve (Optic Neuritis), the spinal cord (Transverse Myelitis), and the brain. In the past, MOG antibodies were thought to be a biomarker for Multiple Sclerosis (MS). But have now been recognised as a separate condition requiring different treatment. 3
Presentations and Symptoms
Symptoms of MOG Antibody disease can present differently from person to person. The most common presentation is Optic Neuritis (ON), followed by Transverse Myelitis (TM) and then Acute Disseminated Encephalomyelitis (ADEM). 3 4
Optic neuritis (ON) is when the eye's optical nerve(s) becomes inflamed due to damage to the myelin surrounding the nerves in one or both eyes simultaneously. 1 5
A common symptom of ON is eye pain, which can worsen when the eye moves. Other symptoms include vision loss which can be either temporary or permanent depending on the nerve damage. 1
Vision loss from optic neuritis can present as loss of central or peripheral vision, colour, or visual acuity. Some people also report seeing flickering, flashing, or sparkles when moving their eyes. 1 2 5 At the same time, vision loss is usually temporary, in some cases, it can be permanent and takes hours or days to happen and weeks to improve. 1 2 5
Optic neuritis is the most common MOGAD presentation among adult patients. It is recurrent or bilateral/simultaneous in approximately 50% of all cases. 6 Some patients complain of a headache around the eye or at the front of the head a few days before vision is affected. 7
Transverse Myelitis (TM):
Transverse Myelitis is when the spinal cord becomes inflamed, causing interruptions to nerve signals sent from the brain to the body, which can create a variety of symptoms.
The effects of TM on a person depend on which spinal cord segments are damaged.1 Symptoms tend to develop over a few hours or gradually over a few weeks. 1 2 The main symptoms of transverse Myelitis are pain, loss of/or abnormal body sensations, weakness of limbs, and bladder and bowel issues. 1 2
Transverse Myelitis in MOG Antibody Disease is often severe, with partial paralysis of lower limbs requiring a movement aid and/or bladder dysfunction requiring catheterisation at the patient's worst point. MRI scans of MOGAD spinal cord inflammation tend to be longitudinally extensive, spanning three contiguous vertebral body segments, although shorter lesions may coexist. 8
Acute Disseminated Encephalomyelitis (ADEM):
Acute Disseminated Encephalomyelitis (ADEM) is another presentation of MOG Antibody Disease. This MOGAD presentation displays symptoms such as headaches, fatigue, nausea, decreased consciousness, fever, and vomiting. In severe cases of ADEM, seizures and a coma can happen to a patient. 1 2 9 Severe ADEM attacks can require patients to be given ventilatory support in up to 3% of instances. 10
An ADEM or ADEM-like attack is the most common MOGAD presentation in children. Still, it can occur at any age.11 12 The brain's white matter is often targeted during an episode of ADEM, and symptoms tend to present quickly. ADEM is sometimes misdiagnosed as Multiple Sclerosis (MS) due to the similarity of symptoms and the appearance of brain inflammation on MRI scans. 1 2
Diagnosing MOG Antibody Disease tends to be done in three main ways. These are:
- MRI scans
- Lumbar punctures
- Blood Tests
If symptoms are also present in the eye, your healthcare professional may conduct an eye assessment. 3 DDue to MOGAD presenting similarly to other demyelinating conditions, these methods are often used in unison to arrive at the diagnosis.
A Magnetic Resonance Imaging (MRI) scan can look at the brain, spine, and optical nerve to see where inflammation has occurred. An MRI uses a strong magnetic field and radio waves to generate the image.
The scan can detect inflammatory lesions, indicating areas where MOGAD has attacked the myelin. Lesions can show whether a patient has a relapsing attack of MOG Antibody Disease.
During an MRI scan, you must lay still in a long machine that makes much noise. The scan is painless, and its duration depends on how much the body is being examined.
A lumbar puncture (also called a spinal tap) can look at the cerebrospinal fluid surrounding the brain and spinal cord. Spinal fluid is extracted by inserting a needle between the spine's bones. Anti-MOG antibodies can be found within the fluid and confirm a diagnosis of MOGAD.
The lower back will be numbed with anaesthetic in this procedure, although some people still find it uncomfortable. Drinking water and lying down for an hour after a lumbar puncture can reduce the chance of a headache.
A specialist blood test can detect anti-MOG antibodies in a patient's blood. If the blood tests positive for MOG antibodies, a healthcare professional could diagnose MOG Antibody Disease depending on the other methods. 3
Those with persistent detection of anti-MOG antibodies may be more likely to have a relapsing rather than monophasic disease. However, antibodies may decrease over time and may not be detectable early in the disease process or during remission.
Suppose eye pain or loss of vision affects the eye. In that case, a healthcare professional may perform an eye assessment to check the optic nerve. However, a diagnosis of MOG Antibody Disease is unlikely to be given from an eye assessment alone.
There are two different types of MOG Antibody Disease treatments. Acute treatments are given at the onset of an attack/relapse, and preventative therapies help stop future relapses from happening.
There are no official treatment guidelines for MOG Antibody Disease, so treatments are prescribed 'off-label.'
IV & Oral Steroids:
A healthcare professional will likely treat an initial attack or relapse of MOG Antibody Disease with IV corticosteroids. IV steroids reduce inflammation that has already occurred. These steroids are given via a cannula/IV into your bloodstream, generally for 3-5 days. 1 3
IV followed by oral steroids such as Prednisone/Prednisolone for 3-12 months. If you take oral steroids for several months, your healthcare provider may prescribe additional medication to stop side effects. 1
You should stop oral steroids gradually, and your healthcare provider should gradually reduce the dosage before stopping completely. When taking oral steroids, your body stops producing its natural form of steroids. Your body needs time to start making its steroids again, and suddenly stopping may increase the risk of another attack. 1
Plasma Exchange (PLEX):
If the IV steroids are unsuccessful, your healthcare provider may administer Plasma Exchange (PLEX) alongside the steroids. PLEX is used when a patient shows severe symptoms of demyelination. 3
PLEX works by replacing the plasma of the individual's blood with new plasma or an artificial substitute. Any inflammatory antibodies or proteins, such as anti-MOG antibodies in the plasma, are removed from the patient. The PLEX procedure takes several hours to complete and could take several sessions over a few days. 5
While clinical trials have not yet proven PLEX's effectiveness in MOG Antibody Disease, beneficial outcomes have been shown for other autoimmune conditions such as Transverse Myelitis. 5
While some people may only have one attack from MOG Antibody Disease (monophasic), some may have multiple attacks. Multiple episodes are known as multiphasic, and often these people are put on preventative treatments to prevent further attacks from happening.
Most of these preventative treatments focus on suppressing the immune system, so anti-MOG antibodies are not produced.
Currently, there are no approved medications for MOG Antibody Disease. Still, some of the following treatments do have some success in preventing relapses:
Intravenous Immunoglobulin (IVIG):
Intravenous immunoglobulin (IVIG) is a treatment where antibodies from healthy donors are injected into the patient. The antibodies are made by the donor's immune system and help regulate the patient's immune responses.
IVIG is reported to have some success in preventing relapses, and some studies from the United Kingdom support this.13
Mycophenolate Mofetil (CellCept):
Mycophenolate Mofetil (also known as Cellcept) is an oral medication often taken twice daily to suppress the immune system. This medication was initially approved to prevent patients' bodies from rejecting transplanted organs.
Blood draws are required upfront and when taking Cellcept to monitor liver toxicity and confirm that the immunosuppression is working correctly. Cellcept is also reportedly medically unadvised during pregnancy due to increased chances of miscarriage and potential defects. Due to this, Cellcept may not be the most suitable preventative treatment for some patients.13
Azathioprine (Imuran) is an oral treatment often taken twice daily to suppress the immune system. Similarly to Cellcept, Imuran requires blood draws before and during treatment to monitor the effects of the medication on the body.
Imuran has also been used to treat organ transplant rejection, rheumatoid arthritis, and other autoimmune disorders. Steroids may also need to be used in combination with Imuran to prevent attacks that bring additional complications. Use of Imuran during pregnancy is also not advised due to an increased risk of miscarriage and defects.13
Rituximab, also known as Rituxan, is a treatment given by IV that suppresses the immune system by depleting a type of white blood cell known as B-cells. This treatment is given four times yearly at an outpatient medical centre.
Monthly blood draws are also required for this treatment to monitor B-cells to ensure the treatment is working as intended. Rituximab may be a safer treatment in pregnancy compared to Cellcept and Imuran. However, planned pregnancy is still advised.
Compared to other autoimmune conditions such as AQP4 NMO, MOGAD patients tend to have a quicker recovery and cause less severe disability in most people. A patient may require rehabilitation therapy depending on the disability caused by a MOG Antibody Disease attack.
A patient may also require therapies depending on which symptoms of a MOGAD attack are the most severe. For example, those with symptoms relating to inflammation of the spine may need physical therapy to regain strength in their arms or legs.
In some cases, individuals may have to learn different ways of performing activities to overcome the disability. The therapy aims to increase the individual's independence to create the greatest quality of life.
Physical therapy focuses on increasing/retaining strength, coordination, and ability to use muscles affected by demyelination. This therapy could include techniques to control the bladder and bowels and how to use compensating devices such as canes and wheelchairs.
An individual suffering from physical deficits may benefit from seeing a physiotherapist. Physiotherapy is likely to come in the form of movements and exercises to be repeated often to regain muscle flexibility and strength. In doing so, therapy may improve the effects of muscle spasticity, weakness, and spasms.
Occupational therapy focuses on increasing or maintaining an individual's independence after a MOGAD attack, such as improving a patient's ability to perform everyday tasks.
Some examples are being able to dress and clean themselves, make meals, and complete tasks around the house. Improvements to the home could also improve the quality of living and safety of the individual.
Therapists may advise on strategies involving personal care and leaving home to fit the patient's functional ability.
Vocational therapy involves helping individuals find or retain their positions of employment. Vocational therapy can also include improving an individual's skills, searching for potential employers, and helping with job searches.
Another role of a vocational therapist may be to communicate with an employer on your behalf to suggest changes in the workplace to accommodate your condition better after your MOGAD attack.
Psychotherapy involves managing the mental effects of being diagnosed and living with MOG Antibody Disease. Psychotherapy could include stress, anxiety, depression, sexual dysfunction, and other emotions and behaviours.
Being diagnosed and living with a rare condition such as MOG Antibody Disease can significantly affect your mental health. If you believe it has affected your mental health significantly, then looking into psychotherapy may be beneficial.
Finding others diagnosed with MOGAD to connect with may lighten the mental load of living with this condition. You may want to check out our list of MOG Antibody Disease Support Groups to find others also diagnosed with the condition.
Recognising a Relapse
A MOGAD attack occurs when there is inflammation within the central nervous system. Inflammation in the central nervous system could be in the optic nerve, spinal cord, or brain. 1
During a relapse, the inflammation may present where you experience a recurrence of previous symptoms. However, an attack could also cause you to experience new symptoms of the prior episode. MOG antibody titres are reported to be higher in number when relapsing than in remission, so blood tests may be used to confirm relapse. 1
If you believe you are having a relapse, you need to seek medical advice quickly.
Recovery from MOG Antibody Disease
Recovery from a MOG Antibody Disease attack is often more favourable than other autoimmune conditions such as AQP4 NMO due to better recovery and less disability. Compared to AQP4-positive conditions, further attacks are also less likely. 4
The impact of attacks on disability seems to vary, with studies reporting no differences between one and multiple attacks. However, other studies report worsening disability when more attacks occur. 3
According to case-based studies, those presenting with Transverse Myelitis are most likely to be left with long-term disability. Some cases also report residual disability developing in 50-80% of MOGAD patients. 3
Depending on how badly the disabilities and symptoms affect a person, some lifestyle complications may arise. Difficulties can involve residual disability, depending on how the MOG Antibody Disease attack presents itself.
Those with optic neuritis may experience residual vision loss due to the MOGAD attack. Visual defects could include blurred or loss of colour vision, depth perception, and issues when looking at light, such as glares. Patients who fully recover their vision after optic nerve inflammation may experience temporary returns of vision loss in times of stress, heat exposure, or physical exertion.
People who suffer from visual defects may need visual aids to compensate for these issues. We recommend that you speak to an ophthalmologist or optician who can help.14
Spasticity is the stiffness or spasms in our muscles often caused by a spinal cord attack. This complication can be caused or worsened by your environment, including temperature and humidity and changes in your body's position. 14
Spasticity can be a complex issue to manage. Still, flexibility can be gained with exercise or stretching regularly and equipment such as splints if needed. Patients can also use medication to treat spasticity and treatments such as Botox injections. 14
Treating spasticity mainly aims to regain and improve daily living function. Working with an occupational therapist may be needed to compensate for the spasticity, and reducing pain could also be addressed to improve the person's standard of living. 14
If untreated, spasticity could cause further issues impacting mobility and independence. We recommend finding therapists involved in spinal cord injuries. 14
Neuropathic pain can be described in many ways, including burning, stabbing, tingling, or constricting. This pain occurs when nerve signals are being sent through the body but in an incorrect way. 14
While neuropathic pain from MOGAD can recover quickly, patients can use various medications to treat it. Findings suggest that no drug works for everyone, so some trial and error will need to be used to find one that works best. Other treatments, such as hypnosis, acupuncture, and meditation, may be somewhat successful in treating neuropathic pain. 14
Neuropathic pain could also be worsened by internal and external factors such as body or external temperature, stress, infections, menstrual cycle, or humidity. Because of this, pain is not always a good indicator of relapse or worsening of the MOGAD condition. 14
Bladder and Bowel Complications:
Another complication of spinal cord inflammation caused by MOG Antibody Disease is bladder and bowel issues. 14
Bladder issues could include incontinence, frequency, and retention of urine. Working with a urologist who ideally understands spinal cord conditions may help address this issue. Equipment such as semi-permanent catheters and intermittent self-catheterisation could also help with MOGAD bladder complications. 14
The main bowel issue associated with demyelination is constipation. A high-fibre diet and regular and adequate fluid intake are recommended to prevent this, and frequent exercise can help. Patients can also use medications to help regulate bowel movements when necessary. 14
Fatigue is when you lack physical or mental energy and can be an issue when dealing with/recovering from MOG Antibody Disease. Fatigue in MOGAD is more often a result of the indirect problems of the condition, such as medication, lack of sleep, stress, or depression. 14
If a healthcare professional can identify the underlying cause of fatigue, it should be addressed where possible. Examples of this could include reducing pain which improves sleep, or addressing depression to feel less fatigued. 14
Additionally, exercise can build stamina and reduce fatigue in the long run. Patients can also use exercise to reduce stress which also contributes to fatigue. Finding something enjoyable is recommended so that you stick with it and remember not to push yourself too hard initially. 14
Resting and saving energy for planned activities could be helpful when dealing with fatigue. Additionally, the home and working environment could be adapted so that less energy is used when navigating them. 14
Many people find that being diagnosed with MOG Antibody Disease has a damaging effect on their and their family's mental health. Being saddened or demoralised is normal and some time may be spent grieving. But if, after a while, it begins impacting your relationships and living, it should be acknowledged and treated. 14
Depression is treatable, and talking to a psychiatrist/psychologist could be beneficial. Psychotherapy previously mentioned on this page could also be helpful alongside joining some of the MOG Antibody Disease support groups.14
1. Palace J, Everett R. MOG Antibody Demylination Information for Patients.; 2019.
2. MOG antibody demyelination. Great Ormond Street Hospital for Children NHS Foundation Trust. https://www.gosh.nhs.uk/conditions-and-treatments/conditions-we-treat/mog-antibody-demyelination. Published 2018. Accessed November 26, 2020.
3. Wynford-Thomas R, Jacob A, Tomassini V. Neurological update: MOG antibody disease. J Neurol. 2019;266(5):1280-1286. doi:10.1007/s00415-018-9122-2
4. Myelin Oligodendrocyte Glycoprotein Antibody Disorders. Cleveland Clinic. https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/mog-antibody-disease. Accessed November 19, 2020.
5. MOG Antibody Disease Acute Treatments. Siegel Rare Neuroimmune Association. https://wearesrna.org/living-with-myelitis/disease-information/mog-antibody-disease/acute-treatments/. Accessed December 20, 2020.
6. Chen JJ, Flanagan EP, Jitprapaikulsan J, et al. Myelin Oligodendrocyte Glycoprotein Antibody–Positive Optic Neuritis: Clinical Characteristics, Radiologic Clues, and Outcome. Am J Ophthalmol. 2018;195:8-15. doi:10.1016/j.ajo.2018.07.020
7. Asseyer S, Hamblin J, Messina S, et al. Prodromal headache in MOG-antibody positive optic neuritis. Mult Scler Relat Disord. 2020;40:101965. doi:10.1016/j.msard.2020.101965
8. Sechi E, Cacciaguerra L, Chen JJ, et al. Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management. Front Neurol. 2022;13. doi:10.3389/fneur.2022.885218
9. Acute Disseminated Encephalomyelitis Information Page. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/Disorders/All-Disorders/Acute-Disseminated-Encephalomyelitis-Information-Page. Published 2019. Accessed November 29, 2020.
10. Zhao-Fleming HH, Valencia Sanchez C, Sechi E, et al. CNS Demyelinating Attacks Requiring Ventilatory Support With Myelin Oligodendrocyte Glycoprotein or Aquaporin-4 Antibodies. Neurology. 2021;97(13):e1351-e1358. doi:10.1212/WNL.0000000000012599
11. Cobo-Calvo A, Ruiz A, Rollot F, et al. Clinical Features and Risk of Relapse in Children and Adults with Myelin Oligodendrocyte Gly-coprotein Antibody-Associated Disease. Ann Neurol. 2021;89:30-41. doi:10.1002/ana.25909ï
12. Mariotto S, Monaco S, Peschl P, et al. MOG antibody seropositivity in a patient with encephalitis: Beyond the classical syndrome. BMC Neurol. 2017;17(1). doi:10.1186/s12883-017-0971-6
13. MOG Antibody Disease Prognosis & Management. Siegel Rare Neuroimmune Association. https://wearesrna.org/living-with-myelitis/disease-information/mog-antibody-disease/prognosis-management/. Accessed December 20, 2020.
14. MOG Antibody Disease Long-Term Care. Siegel Rare Neuroimmune Association. https://wearesrna.org/living-with-myelitis/disease-information/mog-antibody-disease/long-term-care/. Accessed December 28, 2020.