We report two cases of autoimmune-encephalitis that presented as eating disorders.
Case 1: An 18-year-old female with ANA-positive JIA, idiopathic scoliosis, OCD and GAD with a history of anorexia-nervosa, at ten-years of age, presented with reduced oral intake, altered mental status, and catatonia. Serum NMDAR antibody was indeterminate. She received methylprednisolone. She had a relapse of symptoms with steroid taper and she also developed urinary incontinence. EEG showed three focal-seizures originating in the right frontocentral region with left side spread. She received steroids, plasmapheresis, and IVIG. Her refractory catatonia and worsening dysphagia-food refusal were treated with Ativan and NGT feeds. She was started on Rituximab. Her Ativan was weaned with improvement in her catatonia, oral intake, and functional abilities.
Case 2: A 13-year-old female with PMH of ADHD in early childhood presented with reduced oral intake, weight loss - seen at the eating disorder clinic; sudden onset behavioral changes–irritability, reduced concentration, and increased emotional lability. She subsequently developed tonic-clonic-seizures. The exam showed deficits in executive functioning and psychosis. EEG showed left temporal spikes and right-sided paroxysmal seizure activity. She was treated with Lamictal and Trileptal. She received IVIG, steroids, and Rituximab. CSF studies were positive for anti NMDAR antibody. She had relapse of symptoms with the steroid taper. She was admitted for additional plasmapheresis/PLEX and steroid therapy. She is presently on monthly cycles of Dexamethasone, IVIG and is functional, doing well in school.
Recent animal studies indicate the direct association between Somatostatin(SST) neurons in the Nucleus Tuberalis-Lateralis (NTL/TN) and appetite, weight gain, and food intake. This could be due to possible inhibition of TN-SST neurons causing appetite suppression, and with use of benzodiazepines, these pathways get activated to promote food intake. This needs further investigation.