Myelin is the protective coating that wraps around nerve fibres in the brain, spinal cord, and optic nerves. Loss of myelin, known as a demyelinating event, can lead to physical symptoms, for example loss of vision, or weakness in a limb. These events can occur in diseases other than MS and it is important to determine if a person has MS or another disease as the treatment approach can be very different.
One component of myelin is called myelin oligodendrocyte glycoprotein (MOG). Recently, an MS Research Australia-supported scientist, Dr Fabienne Brilot-Turville from The University of Sydney and the Children’s Hospital, and her team have described the symptoms in people that have antibodies to MOG in the blood.
Antibodies are normally produced by the body to help fight off infections, for example, the flu. But the body can also mistakenly produce antibodies that target the tissues and cells in your own body and this can cause autoimmune diseases.
The collaborative group led by Dr Brilot-Turville and her clinical research scholar, Dr Sudarshini Ramanathan from the University of Sydney and Westmead Hospital, investigated demyelinating conditions in people that had MOG antibodies and what characteristics they have. They have published their findings in the Journal of Neurology, Neurosurgery, and Psychiatry.
Dr Brilot-Turville and her team have previously investigated the role that the MOG antibody plays in demyelinating diseases in children, but in this study they looked at the nature of demyelinating disease in both adults and children with MOG antibodies in their blood.
They looked at the physical symptoms, the number of relapses, and change in disability and other characteristics in 33 paediatric and 26 adult patients. They found that demyelinating events happened more frequently in females than males, and more often in Caucasians than other races. Interestingly, almost half of the people investigated had had an infection in the month prior to the event. This infection may have increased the activity of their immune system, making it more likely to attack the body’s own myelin.
People with MOG antibodies presented with a range of symptoms. The most common symptom was optic neuritis (partial or complete blindness in one or both eyes) in adults and acute disseminated encephalomyelitis (ADEM) in children. ADEM is inflammation in the brain and can present as a range of symptoms, similar to MS.
The team also looked at the many brain scans (MRIs) that were performed in the patients in the study. They found that 44% of these scans did not show any brain lesions, which are often present on MS brain scans. The authours said that this may be useful when trying to diagnose someone with MS or another disease.
These people with MOG antibodies in this study responded well to steroid medications, and other immunotherapies including rituximab. For many, their disability improved after treatment, with 42% completely recovering from an episode. Incomplete recovery was seen more often in people that suffered from an episode of transverse myelitis (inflammation in the spinal cord). Recovery was also reduced when people had multiple relapses.
This research shows that diseases with similar causes and symptoms can have different outcomes in terms of number of relapses, change in disability, and response to medications. Their research shows that MS-like diseases in which MOG antibodies are present may need to be classified and treated differently than MS. In practice, the research will ultimately make it easier for clinicians to quickly identify individuals who have a form of demyelinating disease that is not MS and therefore swiftly determine the most appropriate treatment options to deliver the best outcomes for that individual.