MOGAD

Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease (MOGAD) is an autoimmune disease affecting the Central Nervous System. This disease leads to flare-ups of inflammation in areas such as the optic nerves, brain, and spinal cord. Symptoms often develop over a few hours to days.  

MOGAD can present in three ways, depending on the site of inflammation:

• Optic Neuritis, which refers to the inflammation of the nerves of the eyes. This causes loss or blurring of vision, problems with seeing colours and blind spots in vision. Patients may also experience pain around the eye.
• Transverse Myelitis, which refers to inflammation of the spinal cord. Symptoms include weakness in the legs and/or arms, altered sensation (numbness, pins and needles), as well as bladder and bowel dysfunction.
• Acute Disseminated Encephalomyelitis, the inflammation of the brain and spinal cord. This causes confusion, behavioural changes, and nervous system damage. This condition is more common in children and rare in adults.  

What is the cause of MOGAD?

This autoimmune condition is caused by an autoantibody called Myelin Oligodendrocyte Glycoprotein Immunoglobulin G (MOG IgG).

What are the risk factors of MOGAD?

• MOGAD can affect anyone of any age, but children and young adults are slightly more likely to develop this condition. 
• Recent infections are a risk factor as well.

How is MOGAD diagnosed?

A key part of the diagnosis is a blood test that checks for MOG antibodies, which are the proteins responsible for causing this disease.

Magnetic Resonance Imaging (MRI) scans of the brain, optic nerves and spinal cord are also performed to pinpoint and assess the extent of inflammation. 

Many patients also undergo lumbar puncture, or spinal tap, to test for infections and other abnormalities. 

There is currently no cure for MOGAD but there are management options for acute attacks, to prevent a relapse or to provide relief for symptoms.

Acute Treatment

Early intervention after an attack is essential to minimise the risk of permanent damage. Options include acute immunotherapy, such as steroids and plasma exchange.  

Steroids are injected through the vein (intravenously) over the course of three to five days. Following this, oral steroids are administered for one to three months, in a gradual dose reduction.

Plasma exchange is done by drawing blood out through the veins using a specialised machine, which separates out the plasma containing harmful antibodies. A replacement fluid is mixed in, and blood is cycled back into the body. Each session takes around two to four hours.

Long-Term Relapse Prevention

Patients are often kept on oral steroids for a period of several months and up to a year to reduce the risk of relapses.  

Some patients are given other long-term medications to prevent relapse of MOGAD. These treatments include: 

• Mycophenolate mofetil 

This medicine suppresses a specific white blood cell (lymphocytes), preventing it from attacking new cells or a new organ in the body.

Mycophenolate mofetil is taken orally thirty minutes to one hour before food.

• Azathioprine 

This medication stops lymphocytes from making new DNA and multiplying, suppressing the body’s immune system.

Azathioprine is an oral medication to be taken with or after food, to reduce stomach upset.

• Rituximab 

In certain types of autoimmune diseases, the body’s B cells (a type of immune cell) may be producing harmful antibodies that attack the body’s tissue. Rituximab is a medicine that destroys these B cells.

It is given via a drip into the vein (intravenously) every six months. There is a slight risk of infection, which can be reduced by blood monitoring.

• Tocilizumab

This medicine blocks the effect of a specific protein (Interleukin-6), which may be causing harmful inflammation.

Tocilizumab is injected into the vein via infusion (intravenous infusion), every 4 weeks. This has to be done in the hospital or clinic for typically one hour.

• Intravenous immunoglobulin infusions 

This treatment uses pooled donor antibodies to neutralise MOG antibodies, suppressing inflammation in the central nervous system. It helps stop acute attacks or acts as a long-term maintenance therapy to prevent future relapses in MOGAD patients.

This is administered via a drip into the vein (intravenously) over consecutive days at the hospital.

Depending on the type of attack and severity of symptoms, patients may experience:

• Changes to their vision
• Changes to mobility
• Changes to bladder control
• Pain

Medications can be prescribed to address these symptoms. Additionally, physiotherapy and occupational therapy are often required to help improve mobility and daily functioning.

Long term steroids or immunosuppressive treatment may also lead to side effects such as infections, bone thinning, skin thinning and slightly increased risk of certain cancers. Our specialists will discuss the risks and benefits of the different treatment options with you.

Most patients respond well to early treatment and studies are ongoing to learn more about the long-term outlook for MOGAD. Patients with MOGAD and other autoimmune neurological diseases are often followed up in the long term by a multidisciplinary team.