2022 年 39 巻 3 号 p. 322-326
1. History of autoimmune–mediated encephalitis
Clinical research of autoimmune–mediated encephalitis originated from the report of paraneoplastic limbic encephalitis in 1960. In 2001, antibodies to voltage–gated potassium channel (VGKC) were reported in patients with acute non–paraneoplastic encephalitis. Thereafter, autoantibodies to cell surface proteins in acute non–paraneoplastic encephalitis began to draw attention. In 2002, antibodies to GluN2B were reported in patients with acute encephalitis, and antibodies to the complex of n–methyl–D–aspartate (NMDA)–type GluR subunits (NMDAR) were reported in 2007.
2. Anti–NMDAR encephalitis and non–herpetic acute limbic encephalitis (NHALE)
NHALE has been defined as an acute encephalitis characterized by onset of limbic symptoms, and patients with NHALE usually have antibodies to NMDAR, but rarely have antibodies to VGKC or to n–terminal α–enolase.
3. Diversity of anti–NMDAR encephalitis and anti–NMDAR antibodies
Recently, test for anti–NMDAR antibodies has become available in general hospitals. This has led to the recognition of the diversity of clinical characteristics of anti–NMDAR encephalitis and diseases with anti–NMDAR antibodies.
4. Outlook of autoimmune–mediated encephalitis
Passive transfer of anti–NMDAR antibodies has not fully explained all the clinical characteristics of anti–NMDAR encephalitis. Further research is required.
