N-methyl-d-aspartate receptor encephalitis (NMDARE) is becoming a well-recognised cause of symptomatic seizures in the context of an encephalitic illness. Directly pathogenic anti-NMDA receptor antibodies bind to the glutamate subunit of the NMDA receptor, leading to receptor capping and internalisation [1–3]. Neuronal dysfunction in fronto-striatal connections and prefrontal networks, leads to the clinical symptom clusters including psychiatric features, movement disorders, autonomic disturbances and seizures.
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