[Pathophysiology and Prognostic Factors of Autoimmune Encephalitis].
More and more forms of autoimmune encephalitis are being identified with the clinical spectrum ranging from epilepsy over movement disorders to psychosis. The increasing appreciation of clinical symptoms raises questions about the underlying pathophysiological mechanisms and prognostic factors. Numerous novel findings on the aetiology demonstrate that diverse tumours, but also infections of the central nervous system such as Herpes encephalitis can trigger autoimmune encephalitis. Antibodies against neuronal surface epitopes are directly pathogenic in the majority of cases. They act via binding and internalization of target proteins, receptor blockage, or activation of complement. Most relevant for the patients' prognosis are the type and titer of antibodies (e. g. against NMDA, GABA, AMPA receptors or voltage-gated potassium channel complexes), associated tumours, sufficiently aggressive immunotherapies, and imaging as well as cerebrospinal fluid biomarkers.
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D001323:Autoantibodies / Q000097:blood*; D001932:Brain Neoplasms / Q000150:complications / Q000175:diagnosis / Q000276:immunology; D003167:Complement Activation / Q000276:immunology; D004660:Encephalitis / Q000175:diagnosis* / Q000276:immunology* / Q000628:therapy; D020803:Encephalitis, Herpes Simplex / Q000150:complications / Q000175:diagnosis / Q000276:immunology; D050031:Hashimoto Disease / Q000175:diagnosis* / Q000276:immunology* / Q000628:therapy; D006801:Humans; D007167:Immunotherapy; D009474:Neurons / Q000276:immunology; D011379:Prognosis; D016194:Receptors, N-Methyl-D-Aspartate / Q000276:immunology; D012307:Risk Factors
D001323:Autoantibodies; D016194:Receptors, N-Methyl-D-Aspartate