Post-infectious N-methyl-D-aspartate Receptor Encephalitis Antibody Associated with Coxsackie Virus Infection
Elise Johnson1, Ahmed Obeidat1, Danish Pardhan1, Mohamed Osman1, Mohamed Hommeida1, Sam Hooshmand1
1Medical College of Wisconsin
Objective:
To describe the first case of N-methyl-D-aspartate receptor antibody encephalitis (NMDARE) associated with Coxsackie meningoencephalitis.
Background:
NMDARE is the most common cause of autoimmune encephalitis. Often, no trigger for antibody production is identified. Etiologies commonly reported are oncogenic and post-infectious. The identification of the trigger impacts both treatment and prognosis.
Design/Methods:
Case report and Literature review. The authors searched PubMed for articles using the keywords: “N-methyl-D-aspartate", "encephalitis”, and “Coxsackie virus”.
Results:
A 22-year-old immunocompetent female presented with headache, agitation, and altered mental status. CSF analysis in the emergency room revealed lymphocytic pleocytosis, WBC of 43 with 78% lymphocytes. Testing revealed a positive Coxsackie A/B virus with a high serum titer. Serum autoimmune encephalitis panel, including NMDA-R antibody, was negative. This panel was not obtained in CSF. She was discharged home with supportive care. Over the following week, her mental status declined with further agitation, hyperphagia, and hypersexuality. A repeat lumbar puncture revealed normalized WBC of 2 and positive NMDA-R antibody. Continuous EEG showed non-convulsive status epilepticus. A CT of the abdomen and pelvis without evidence of teratoma. She received intravenous methylprednisolone and plasmapheresis with minor improvement. Subsequently intravenous immunoglobulin and rituximab infusion with improvement in mental status and resolution of seizure activity on EEG. She was discharged on psychiatric medications: sertraline, trazodone, and Ativan. These medications were successful without recurrence of mood disturbance but with residual memory difficulties.
Conclusions:
Prolonged or worsening post-infectious encephalitis should prompt consideration of secondary autoimmune encephalitis, a treatable condition. NMDARE is increasingly recognized following HSV encephalitis. To date, no case has been documented secondary to the Coxsackie virus. Our case adds to the growing list of triggers for NMDARE and highlights the need for antibody testing for those with refractory encephalitis despite having an identified cause.