Multiple sclerosis (MS) is an acquired chronic immune-mediated inflammatory condition of the central nervous system, affecting both the brain and spinal cord.¹

An autoimmune reaction targeting the myelin sheath around nerve fibres disrupts nerve messaging, with effects ranging from temporary slowdowns to complete blocks. Scarring (sclerosis) occurring with this demyelination can be partial or complete with lesions and plaques forming over time. There may also be damage to the nerve fibres themselves.²

Early in the disease, the body can often repair the myelin (remyelination) after an attack or relapse, and the brain may also be able to adapt by creating new neural pathways (plasticity). Symptoms can subside or resolve (remission) although the repaired myelin may be thinner meaning nerve message transmission can be slower.^2,3