A 14 year old female presented with 3 weeks of progressive lower extremity sensory loss followed by disabling motor weakness, incontinence, and blurry vision. MRI spine showed spinal cord edema from the level of T1-T11 confirming the suspicion of transverse myelitis. Lumbar puncture showed leukocytosis (WBC 402) and CSF positive for oligoclonal bands. Serology was positive for AQP4R antibodies confirming the presence of NMOSD. Patient was treated with intravenous methylprednisolone and rituximab, regained some strength in lower extremities, and was transferred to inpatient rehabiliation.
Upon arrival to inpatient rehab, the family reported the patient had been experiencing two weeks of progressive changes in sleeping patterns and personality attributed to adjustment and acute hospitalization. Over the first week of rehab admission, the patient had progressive decline characterized by development of echolalia, hallucinations, delusions, catatonia, blunt affect, and tachycardia. It was found on record review that the patient was positive for NMDA receptor antibodies on initial workup. This combined with her clinical decompensation was consistent with an overlapping anti-NMDAR encephalitis. She was re-pulsed with methylprednisolone and 2g/kg IVIG for treatment of NMDAR encephalitis and ultrasound and PET scans obtained to investigate for underlying ovarian teratoma were negative. She is currently undergoing rituximab treatments outpatient with mild improvement in motor and mental status.