“…Autoimmune encephalitis, such as anti-NMDA-receptor encephalitis, is typically associated with a subacute onset of neuropsychiatric symptoms, and can often be identified by the presence of antineuronal autoantibodies or inflammatory changes in the cerebrospinal fluid (CSF), electroencephalography (EEG) pathologies, and evidence of encephalitis in magnetic resonance imaging (MRI) or [18F]fluorodeoxyglucose positron emission tomography (FDG PET; [1][2][3][4][5]. Until now, a series of antineuronal autoantibodies against surface (e.g., NMDA-R, LGI1, CASPR2, AMPA1/2-R, GABA-B-R, DPPX) or intracellular antigens (e.g., Yo, Hu, CV2/CRMP5, Ri, Ma1/2, SOX1, GAD65, amphiphysin), or "potentially antineuronal" systemic antibodies (e.g., antinuclear antibodies [ANAs] against double-stranded [ds]-DNA or gliadin autoantibodies) (3)(4)(5) are known. The associated neuropsychiatric syndromes are classically characterized by a combination of neurological (e.g., seizures, movement disorders, focalneurological deficits, or reduced consciousness) and psychiatric (e.g., psychosis, mania, or catatonia) symptoms (3,6,7).…”