Eye movements and ocular biomarkers in mild traumatic brain injury: from oculomotor pathophysiology to diagnosis and prognosis.

Anti-N-methyl-D-aspartate (anti-NMDA) receptor encephalitis, first described in 2007, is now recognized as the most common subtype of autoimmune encephalitis (AE) []. This disease is characterized by antibodies against the NMDA receptor (NR1) subunit of the NMDA receptor and typically presents with acute or subacute psychiatric symptoms, seizures, cognitive decline, abnormal movements, or autonomic dysfunction []. While the association of anti-NMDA receptor encephalitis with paraneoplastic tumors, particularly ovarian teratomas, is well established, gliomas are rarely implicated []. Moreover, glioma patients may themselves exhibit seizures, cognitive impairment, or behavioral changes, which are also clinical manifestations of anti-NMDA receptor encephalitis, thereby complicating differential diagnosis []. The pathophysiological link between glioma and anti-NMDA receptor encephalitis remains unclear, but aberrant expression of neuronal proteins such as NMDA receptor on glioma cells has been proposed, potentially leading to immune sensitization []. Here, we report an exceptionally rare case of anti-NMDA receptor encephalitis that developed after surgical resection of a right insular astrocytoma []. This case highlights the diagnostic challenges in distinguishing glioma-related neurological symptoms from anti-NMDA receptor encephalitis and underscores the importance of considering autoimmune etiologies in postoperative patients with unexplained neurological deterioration.