Knowledge about the diagnosis of autoimmune encephalitis (AE) is rapidly expanding. In the last 15 years, multiple new antibodies have been described. Anti-N-methyl-D-aspartate receptor (NMDAR)–antibody-mediated encephalitis, in particular, has been found to be common among teenagers and young adults and accounts for up to 86% of AE in patients aged <18 years. Other antibodies associated with AE (leucine-rich glioma-inactivated 1, contactin-associated protein-like 2, glutamic acid decarboxylase 65-kilodalton isoform, γ-aminobutyric acid A, and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) are reported in children as case reports or series and with less clear typical clinical syndromes.3–9 

The presentation and clinical course of anti-NMDAR encephalitis has been extensively described in the literature.10,11  The NMDAR is located on neuronal cell surfaces with high concentration in the limbic system, hypothalamus, and forebrain. When pathogenic antibodies to the ionotropic glutamate receptors subunit of the receptor are present in the cerebrospinal fluid (CSF),...

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