There is an emerging appreciation of autoimmune encephalitis33 that involves antibodies against epitopes in proteins that control neuronal excitability, such as the NMDA receptor,34 GAD65,35 and GABAB receptor subunits.36,37 Patients with antibody-mediated encephalitis often exhibit nonconvulsive seizures, in addition to memory loss, psychiatric symptoms, and other features. For some epitopes, preclinical data validate the immunoglobulin G fraction as causative for seizures. Treatment with immunotherapy can be effective, but additional therapeutic strategies are needed.36,38 The full extent of this clinical condition is just now becoming appreciated, and it remains almost certainly underdiagnosed at this point. Thus, future work should focus on earlier recognition of these presentations and early and robust diagnosis in order to achieve potentially effective treatment before the development of irreversible sequelae of neuroinflammation.