In 1961, Russell proposed a mechanism of neurological injury in paraneoplastic syndromes to the formation of autoantibodies triggered by exposure of the immune system to certain types of cancer. Later in 1968, Corsellis and colleagues described a few patients with lung cancer who also developed neurologic symptoms - memory loss, neuropsychiatric disturbances, and seizures - without evidence of brain metastases. At autopsy, the investigators found significant inflammatory involvement of limbic areas and termed this new entity ‘limbic encephalitis’. In 1981, John Newsom-Davis was the first to establish an autoimmune mechanism for paraneoplastic neurological disorder by successfully treating three cases of Lambert-Eaton myasthenic syndrome with plasma exchange and immunosuppression with steroids. In 1990, Posner compared serum and CSF profiles of 18 patients before and after plasmapheresis, concluding that autoantibodies in paraneoplastic syndrome may be synthesized in the CSF. In 2001, Ligouri et al. and Buckley et al. separately presented case reports of two individuals with reversible limbic encephalitis associated with voltage-gated potassium channels (VGKC) antibodies. In 2005 Dalmau and colleagues described encephalitis associated with NMDA receptor autoantibodies in 12 patients with NMDA encephalitis.