Antibody-mediated encephalitides: distinct diseases with transdisciplinary implications

The discovery of antibody-mediated glial and neuronal disorders has transformed the diagnosis and treatment of neurological diseases previously considered idiopathic or not recognised as immune-mediated. Antibody-mediated disorders targeting glial aquaporin-4 and myelin oligodendrocyte glycoprotein are distinct nosological entities, defined by specific targets, mechanisms, syndromes, and therapeutic implications. By contrast, antibody-mediated disorders targeting neuronal antigens (ie, autoimmune encephalitides) are still frequently analysed collectively, with data from different disorders pooled as if they represent a single disease rather than distinct entities. Evidence from anti-NMDA receptor encephalitis, anti-LGI1 encephalitis, and anti-IgLON5 disease (used here as exemplars of autoimmune encephalitides) indicates that individual autoimmune encephalitides differ in demographics, triggers, mechanisms, clinical manifestations, post-acute trajectories, and treatment requirements. The broad, heterogeneous presentations of autoimmune encephalitides require coordinated multidisciplinary care within and beyond neurology, involving specialists in paediatrics, infectious diseases, epilepsy, movement disorders, sleep medicine, intensive care, cognitive rehabilitation, and other relevant disciplines. Such interdisciplinary collaboration facilitates the recognition of new diseases and elucidation of the causes of previously unclassified disorders. Improving patient care requires not only aetiological and mechanistic insight to enable development of targeted therapies but also strengthened cross-specialty expertise to optimise diagnosis and management.