Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease known as MOG Antibody Disease (MOGAD) is a neuro-inflammatory condition that can cause inflammation to the optic nerve(s), the brain, and the spinal cord.
MOG is found on the surface of oligodendrocytes of the myelin sheath of the nerves in the Central Nervous System (CNS). It is thought that MOG repairs the myelin sheath when they're damaged. MOG antibodies mistakenly attack the myelin sheath causing inflammation to the optic nerve(s), spinal cord, and/or brain.
What are Antibodies?
Antibodies are produced by white blood cells and 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. This allows our bodies to defend themselves against infections previously encountered. 1
Usually, antibodies do not cause harm to the person, but sometimes they can misinterpret a friendly antibody for a foreign invader. The antibodies against MOG are responsible for the inflammation in the CNS and a diagnosis of MOGAD or Anti-MOG disease is made. 1
What are MOG Antibodies?
Myelin oligodendrocyte glycoprotein (MOG) is found on the surface of the myelin sheath. The myelin sheath covers nerve cells and acts as an insulator. MOG helps the speed of 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. This is done by protecting and repairing it when it gets damaged. 1
In MOG Antibody Disease, the body generates antibodies that attack the MOG proteins. When this occurs the myelin sheath is also attacked, damaging the nerves beneath it. This means that the transmission of messages sent through the nerves is slowed down or stopped. 2
This is called demyelination and this tends to occur in the optic nerve (Optic Neuritis), the spinal cord (Transverse Myelitis), and the brain. In the past, MOG antibodies were once thought to be a biomarker for Multiple Sclerosis (MS). But have now been recognised as a separate condition requiring different treatment to MS. 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 optical nerve(s) in the eye becomes inflamed due to the myelin surrounding the nerves being damaged. This can occur in one or both eyes at the same time. 1 5
A common symptom of ON is pain in, around, or behind the eye which can get worse 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 and/or peripheral vision, colour, or visual acuity and some people also report seeing flickering, flashing, or sparkles when moving their eyes. 1 2 5 Whilst vision loss is usually temporary, in some cases, it can be permanent and tends to take hours or days to happen and weeks to improve. 1 2 5
Optic neuritis is the most common MOGAD presentation amongst adult patients and is reported to be recurrent or bilateral/simultaneous in approximately 50% of all cases. 6 Additionally, up to 50% of patients complain of a headache either 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 TM has on a person depend on which segments of the spinal cord have been 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 sensations of the body, 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 spinal cord inflammation caused by MOGAD tend to be longitudinally extensive spanning 3 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 tends to display 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 but can occur at any age.11 12 The white matter of the brain is often targeted during an episode of ADEM and symptoms tend to present quickly. ADEM can be often misdiagnosed with 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, then an eye assessment may also be conducted. 3 Due 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 be used to look at the brain, spine and optical nerve to see where inflammation has occurred. This is done by using a strong magnetic field and radio waves to generate the image.
Inflammatory lesions can be spotted in the scan, indicating areas where the myelin has been attacked by MOGAD. These lesions can be used to see whether a patient is having a relapsing attack of MOG Antibody Disease.
To have an MRI scan you must lay still in a long machine which makes a lot of noise when in use. The scan itself is painless and its duration is dependent on how much of the body is being scanned.
A lumbar puncture (also called a spinal tap) can be used to look at the cerebrospinal fluid that surrounds the brain and spinal cord. This is performed by inserting a needle between the bones of the spine. Anti-MOG antibodies can be found within the fluid and confirm a diagnosis of MOGAD.
In this procedure, the lower back will be numbed with anaesthetic, although some people still find it uncomfortable. It is reported that drinking water and lying down for an hour after a lumbar puncture reduces the chance of a headache.
A specialist blood test can be used to detect anti-MOG antibodies in the blood of a patient. If antibodies for MOG are found then a diagnosis of MOG Antibody Disease is likely to be the cause of demyelination. 3
It is reported that 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.
If symptoms are affecting the eye such as eye pain or loss of vision then an eye assessment may be done to check the optic nerve. However, a diagnosis of MOG Antibody Disease is unlikely to be given from an eye assessment alone.
Treatment of MOG Antibody Disease can be broken down into two different types. Acute treatments are given at the onset of an attack/relapse whereas preventative treatments are given to stop future relapses from happening.
Currently, treatment guidelines for MOG Antibody Disease have not yet been established and treatments are being prescribed ‘off label’.
IV & Oral Steroids:
An initial attack or relapse of MOG Antibody Disease is likely to be treated with IV corticosteroids. IV steroids are used to reduce inflammation that has already occurred. These steroids are given via a cannula/IV into your bloodstream, generally for 3-5 days. 1 3
This may be followed by oral steroids such as Prednisone/Prednisolone for 3-12 months. If you are taking oral steroids for several months, additional medication may also be prescribed to stop side effects. 1
Oral steroids should not be stopped suddenly and the dosage should be gradually reduced before stopping completely. When taking oral steroids, your body stops producing its natural form of steroids. Your body needs to be given time to start producing its steroids again and stopping suddenly may also increase the risk of another attack. 1
Plasma Exchange (PLEX):
If the IV steroids are unsuccessful, Plasma Exchange (PLEX) may also be administered alongside the steroids. PLEX is often considered 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 to complete. 5
Whilst 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
Whilst some people may only have one attack from MOG Antibody Disease, (known as monophasic), some may have multiple attacks. This is 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 but some of the following treatments do have some success in preventing relapses:
Intravenous Immunoglobulin (IVIG):
Intravenous immunoglobulin (IVIG) is a treatment where antibodies taken 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 this is supported by some studies from the UK. 13
Mycophenolate Mofetil (CellCept):
Mycophenolate Mofetil, (also known as Cellcept), is an oral medication often taken twice daily which suppresses the immune system. This medication was originally approved to prevent patients' bodies from rejecting transplanted organs.
Blood draws are required both upfront and when taking Cellcept to monitor for liver toxicity and to 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 that is to be generally 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 in 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 which is also known as Rituxan is a treatment given by IV which suppresses the immune system by depleting a type of white blood cell known as B-cells. This treatment is generally given four times per year 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 is also reported to be safer in pregnancy compared to Cellcept and Imuran, however, planned pregnancy is still advised.
Compared to other autoimmune conditions such as AQP4 NMO, MOGAD patients are reported to have a quicker recovery and cause less severe disability in most people. Rehabilitation therapy may be required depending on the level of disability caused by a MOG Antibody Disease attack.
Therapies may also be required depending on which symptoms of a MOGAD attack are the most severe. For example, those with symptoms relating to inflammation of the spine may require physical therapy to regain strength in their arms and/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 independence of the individual to great the greatest quality of life.
Physical therapy is focused on increasing/retaining strength, coordination, and ability to use muscles affected by demyelination. This also includes techniques to control 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. This is likely to come in the form of movements and exercises to be repeated often to regain flexibility and strength in muscles. In doing so, the effects of muscle spasticity, weakness, and spasms may be improved.
Occupational therapy is focused on increasing or maintaining an individual's independence after a MOGAD attack. This will likely be focused around 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. Depending on the deficit, improvements to the home may be suggested to improve the quality of living and safety of the individual.
Therapists may also be able to advise on strategies involving personal care and leaving the home to fit the functional ability of the patient.
Vocational therapy involves helping individuals find or retain their positions of employment. This can also involve 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. This could be to suggest changes in the workplace to better accommodate your condition. This could be useful if you are left with significant deficits from your MOGAD attack.
Psychotherapy involves managing the mental effects of being diagnosed and living with MOG Antibody Disease. This 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 have a significant effect on 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 is occurring 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, a relapse could also cause you to experience new symptoms from the previous attack. MOG antibody titres are reported to be higher in number when having a relapse than they were 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 reported to be more favourable than other autoimmune conditions such as AQP4 NMO due to better recovery and less disability. Further attacks are also less likely when compared to AQP4 positive conditions. 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. These are caused by residual disability and many of these are dependent on the way the MOG Antibody Disease attack presented itself.
Those who had optic neuritis may experience residual vision loss as a result of the MOGAD attack. This could include blurred or loss of colour vision, loss of 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 you speak to an ophthalmologist or optician who may be able to help. 14
Spasticity refers to the stiffness or spasms in our muscles which can range from minor stiffness to painful muscle spasms. Generally, this would be expected with those who suffered from spinal cord demyelination as a result of a MOGAD attack. This complication can be caused or worsened by your environment such as temperature and humidity as well as changes in your body’s position. 14
This can be a difficult issue to manage but flexibility can be gained with exercise or stretching regularly and equipment such as splints if needed. Medication can also be used to treat spasticity as well as treatments such as Botox injections. 14
The main aim of treating spasticity is to regain and improve the function of daily living and working with an occupational therapist may be needed. Ways of compensating 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 would recommend finding therapists who are experienced in dealing with spinal cord injuries if possible. 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
Whilst neuropathic pain from MOGAD can recover in time, various medications can be used to treat it. Findings suggest that no medication that 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 also 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 as a result 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 be useful in addressing 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. To address this a high-fibre diet is recommended alongside regular and adequate fluid intake and frequent exercise can help. Medications can also be used to help regulate bowel movements when necessary. 14
Fatigue is when you have a lack of physical and/or mental energy and can be an issue when dealing with/recovering from MOG Antibody Disease. It is thought that fatigue in MOGAD is more often a result of indirect issues of the condition such as medication, lack of sleep, stress, or depression. 14
If the underlying cause of fatigue can be identified 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 be used to build stamina and reduce fatigue in the long run. Exercise can also be used 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, to begin with. 14
Resting and saving energy for planned activities could be a useful strategy 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 useful 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.