Adult onset RE differs from childhood onset with a median age of onset of 19, a prolonged prodrome, and less severe hemiparesis and hemispheric atrophy. Both adult and childhood histopathology is characterized by cortical inflammation, neuronal loss, and gliosis confined to one hemisphere. Common pathological features include microglial and lymphocytic nodules, perivascular cuffing, and neuronal demise. IL-6 induces autoimmunity and B-Cell differentiation, and facilitates the differentiation of IL-17 producing T-helper cells. Additionally, IL-6 stimulates the differentiation of CD8+ cytotoxic T cells, which promotes excitotoxicity-induced neuronal damage in RE. Tocilizumab is a humanized anti-interleukin (IL)-6 receptor monoclonal antibody which blocks IL-6-mediated signal transduction, making it a potential therapy for RE. 

A now 27 year old woman presented with seizures following a febrile illness in 2014. No specific etiology or antibodies were identified. Serial brain MRIs demonstrated progressive asymmetric atrophy of the left cerebral hemisphere, more pronounced over the frontotemporal region and basal ganglia. Initial EEG showed seizure foci in left motor and speech areas, with increased seizure frequency over time with the development of epilepsia partialis continua.   She also developed right hemiparesis, and had recurrent hospitalizations for status epilepticus. She was treated with anticonvulsant polytherapy, VNS, and immunomodulatory therapies including methylprednisolone, IVIG, plasmapheresis, mycophenolate mofetil, and rituximab without improvement. She had ongoing infections, innumerable daily seizures, and recurrent status epilepticus. Monthly tocilizumab was started, and seizure frequency decreased to 1-3 seizures daily with continued improvement.