(668) Something Old, for Something New, Something Borrowed to Treat the Blues

Introduction: Anti-NMDA receptor encephalitis (ANMDARE) can develop when antibodies triggered by an ovarian teratoma, cross link and internalize NMDA receptors (NDMARs). NMDAR loss leads to hyperactivity of motor, oculomotor, cognitive and limbic basal ganglia circuits which manifests as neuropsychiatric (NP) symptoms. Tramadol is a non-competitive NMDAR antagonist that binds to GluN2B NMDAR subunits, preventing NMDAR internalization. Tramadol can be considered in the management of refractory NP symptoms in ANMDARE.

Description: A 13-year-old female with new headaches and a 7-day history of limbic, cognitive, and motor dysfunction was admitted with repetitive lip smacking, tooth grinding, tongue protrusion/retraction, intermittent animal-like vocalizations, and extreme aggression. Anti-NMDAR antibody titer (CSF) was elevated at 1:256. Immunotherapies included, IVIG, high dose steroids, plasmapheresis, and rituximab. Clonazepam, clonidine, baclofen, and gabapentin were titrated for control of whole body dyskinesias (AIMS score 36 to 3). Refractory cognitive and limbic dysfunction improved with tramadol administration. Worsening of agitation was noted when tramadol had to be stopped when patient developed intestinal infection, with improvement upon restarting. A resurgence of severe psychosis and extreme aggression again occurred during rehab care when tramadol was discontinued prompting readmission for acute care.

Discussion: Efficacy of tramadol for control of refractory dystonia and dyskinesias secondary to anti-NMDA receptor encephalitis has been reported. This case report is the first to document a potential role for tramadol in the management of dysfunction within multiple cortico-basal ganglia-thalamic circuits in the setting of ANMDARE