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Autoimmune encephalitis can be defined as central nervous system inflammation, secondary to multiple causes, where we can possibly identify the formation of auto-antibody against neurotransmitter receptors or neuronal surface proteins. Approximately 50% of patients are seropositive; the auto-antibody against N-methyl-D-aspartate receptor (NMDAR) are the most common. In the pediatric population, the clinical presentation is characterized by movement disorders and seizures, psychiatric manifestations are more commonly found in young adults. An early intervention is associated with a better prognosis in these patients. In contrast to the seropositive group, seronegative autoimmune encephalitis is linked with less movement alterations and is related with a worse cognitive outcome. Much remains to be discovered about possible etiologies, molecular processes, detection, and interaction of yet undescribed antibodies,as well as increasing our knowledge about clinical manifestations in early disease and new diagnostic techniques that could improve the diagnosis of autoimmune encephalitis. The main goal of this document is to review the updates of the molecular field about the antibody against GluK2 and its clinical presentation in pediatric population; COVID-19 as a possible cause of autoimmune encephalitis; recognize the importance of psychiatric manifestation in early disease, especially catatonia as a marker of severity; additionally consider new imaging diagnostic method such as positron emission tomography (PET), which has shown to be more sensible than MRI (goal standard).