中枢神経炎症性脱髄性疾患の最近の進歩

抄録

Recently, the treatment strategy for central nerve system inflammatory demyelinating disease has been remarkably progressing. In multiple sclerosis (MS), eight disease modifying drugs (DMD) became available and made it possible to suppress not only relapses but also disease progression. Now it is a consensus that early DMD initiation will lead to better long–term outcome. In neuromyelitis optica spectrum disorders (NMOSD), aquaporin 4 (AQP4) protein, which is expressed on the foot process of astrocyte, is the key target of the disease–specific autoantibody, especially in those with AQP4 antibody–positive NMOSD. Recently, multiple biological products got covered by health insurance, which contributed to achieve prevention of clinical relapses. Each product has distinct mode of action and possible adverse events. So those biological products should be safely utilized with accurate understanding of possible adverse events and enough explanation to patients. Finally, a novel disease entity of which characteristics is the positivity of autoantibody against myelin oligodendrocyte glycoprotein (MOG) protein. MOG antibody–associated disease (MOGAD) demonstrates acute disseminated encephalomyelitis, optic neuritis, or multiple other phenotypes. Novel and the first international diagnostic criteria for MOGAD has been published. So far it is not recommended to measure MOG antibody for all the patients with MS even though it is important to differentiate MOGAD from MS.