MOGAD (MOG antibody disease): symptoms, causes and treatment

MOGAD stands for myelin oligodendrocyte glycoprotein antibody-associated disease. The Oxford University Hospitals leaflet explains that MOG is found on the myelin sheath of nerve cells, the layer that insulates and protects nerves. In MOG antibody demyelination, MOG antibodies attack this protein and damage the myelin sheath.

A UK case series from a district general hospital in south-east England describes MOGAD as an autoimmune inflammatory disorder of the central nervous system that is distinct from multiple sclerosis and from aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4 NMOSD). The Oxford leaflet says MOG antibodies are believed to cause similar attacks to AQP4 antibodies, but the disease develops differently and needs to be treated differently.

The same case series says MOGAD appears relatively more frequent among demyelinating conditions in children than in adults, although any age can be affected.

The Oxford leaflet says MOG antibodies have been found in people with optic neuritis (inflammation of the optic nerve), transverse myelitis (inflammation of the spinal cord) and ADEM (acute disseminated encephalomyelitis), an inflammatory brain condition often following an infection and more common in children.

For optic neuritis, it says MOG optic neuritis usually affects one eye but sometimes both at the same time. It causes visual disturbances such as blurred vision, problems seeing colours and areas of missing central or side vision, and can sometimes cause complete loss of vision. It often causes pain in or behind the eye, particularly when the eye is moved.

For transverse myelitis, the leaflet lists muscle weakness in the legs and/or arms, altered sensations such as pins and needles or numbness, bladder and bowel problems and pain. Symptoms may develop quickly over a few hours or gradually over weeks, and severity depends on how far the inflammation has spread and how much damage has occurred.

• Blurred or lost vision in one or both eyes, with pain on eye movement.

• Changes in colour vision or patches of missing vision.

• Weakness in the arms or legs.

• Numbness, pins and needles or pain.

• Bladder or bowel problems.

Sudden loss of vision, a rapid change in vision with eye pain, new weakness in the limbs or new bladder or bowel problems need urgent medical assessment, through NHS 111, an eye casualty or A&E depending on how severe they are. Call 999 for sudden severe weakness, loss of consciousness or a seizure.

If you already have a diagnosis, the Oxford leaflet says that if you think you are having a relapse you should seek medical advice promptly from your GP and your NMO specialist nurse. If symptoms last more than 24 hours, contact the nurse; out of hours, your GP can contact the on-call neurologist.

The Oxford leaflet says MOG antibodies are believed to be the cause of the disease, rather than just a marker of it. It explains that some antibodies simply help identify a disease, while others cause it, and MOG antibodies are believed to fall into the second group.

The leaflet does not say what triggers the antibodies to form, and it notes that the antibody test has only recently become reliable, so there is much still to learn. ADEM, one of the patterns, often follows an infection, according to the same leaflet.

Diagnosis combines symptoms, scans and a blood test for MOG antibodies. The UK case series says diagnosis combines clinical, radiological and serological evaluation, with MOG-IgG detection by a live cell-based assay currently regarded as the gold standard, and describes typical MRI findings such as optic neuritis with sheath enhancement, spinal cord inflammation over a long segment, ADEM-type lesions and brainstem or cerebellar lesions.

The Oxford leaflet says the earlier antibody test was unreliable and that MOG antibodies are now detected using a more reliable technique. In some UK cases a lumbar puncture, to sample the fluid around the brain and spinal cord, is also performed to look for other causes.

The Oxford leaflet says the first attack is likely to be treated with intravenous corticosteroids such as methylprednisolone, given through a drip, which may be followed by prednisolone tablets for 3 to 12 months. It says the specialists currently recommend staying on prednisolone for up to a year, although treatment may stop earlier if MOG antibodies become undetectable by six months.

If prednisolone continues for more than 2 to 3 months, medicines to protect the stomach lining and vitamin supplements to protect the bones are needed. Steroids should not be stopped suddenly, because the body needs time to restart its own steroid production, and stopping suddenly could raise the risk of another attack.

The leaflet says another option is not to use regular prednisolone and instead to treat attacks if they occur, because relapses often recover well. It says the Oxford team does not currently recommend longer-term prednisolone beyond one year unless there are multiple or severe attacks. If a further attack happens, it recommends quick treatment with high-dose corticosteroids, and it may discuss longer-term immune-suppressant medicine to prevent further attacks.

The UK case series describes patients treated with intravenous methylprednisolone, tapering oral prednisolone, plasma exchange and, in one case, mycophenolate as a steroid-sparing treatment. These were individual cases at specialist centres.

The Oxford leaflet says most people recover well from relapses and many have a full recovery, but not all. After optic neuritis you may be left with some level of visual impairment, and after transverse myelitis you may be left with bladder, bowel or sexual function problems. Management of these is discussed with your neurology team and GP.

It adds that some people do have further attacks, and that the risk may be reduced by taking prednisolone for 3 to 12 months after the first episode. After recovery, a follow-up MRI may be offered as a baseline to compare against if new symptoms develop, and changes on MRI usually get better.

The leaflet itself was published in 2019, so check with your specialist team for the latest approach.

The UK case series says MOGAD appears relatively more frequent among demyelinating conditions in children than in adults, but any age can be affected. The Oxford leaflet says ADEM is more common in children.

The sources used for this page do not give specific advice on pregnancy or breastfeeding. If you have MOGAD and are planning a pregnancy, discuss it with your neurologist before stopping or starting any medicine.

On the NHS, MOGAD is usually diagnosed after an eye or neurology emergency assessment, and managed by neurology with support from specialist services. The Oxford leaflet says the National Highly Specialised Service for Neuromyelitis Optica is based at the John Radcliffe Hospital in Oxford and the Walton Centre in Liverpool, with specialist nurses who offer advice to patients.

Private neurology and eye appointments are also available, but acute attacks should be assessed urgently through the NHS. Antibody tests are best interpreted by a neurology team experienced in demyelinating disease.