Anti-N-Methyl-D-Aspartate (NMDA) receptor encephalitis is a severe form of autoimmune encephalitis associated with antibodies against subunits of the NMDA receptor. Most patients with anti-NMDA receptor encephalitis are admitted to hospital with symptoms progressing from psychiatric symptoms to memory disturbance, seizures, dyskinesia, and catatonia. Motor changes, autonomic dysfunction and impaired consciousness may occur. Between 20-57% of female patients with NMDA receptor antibody are thought to have underlying tumor, which is mostly ovarian teratoma. The cases may take place during pregnancy or postpartum during, when a differential diagnosis must be made from the other perinatal psychiatric cases. We present a postpartum patient with anti-NMDA receptor encephalitis who is misdiagnosed as neuroleptic malignant syndrome by neurologists. A 23-year-old female, postpartum 4 months, with no psychiatric history was admitted to psychiatric unit after two weeks of progressive slurred speech, behavioral changes and psychotic features. There was waxy flexibility in extremities. WBC: 11200, AST: 165, ALT: 165 and was CK: 7936. Temperature was37.3°C. EEG showed non-specific slowing. Catatonia, Neuroleptic Malignant Syndrome(NMS) and NMDA receptor encephalitis were thought in differential diagnosis. Consultations did not show any pathology. Diagnosis made as catatonia and ECT was started. On the next day, she had a generalized tonic-clonic seizure. Diazepam 1mg was given and was referred to neurology. At that time, WBC count was 17000, temperature was 37.5°C. There was no infection sign on blood culture, urine examination and lumbar puncture material.After ten hours follow up, she was re-admitted to psychiatry unit. Temperature was 37.9-38.1°C, confusion was apparent and general condition was poor. No specific reason was diagnosed. Haloperidol and biperidene were started. Because of increased CRP, infectious disease consultant started cephalosporin. Delirium symptoms were observed so NMDA Receptor encephalitis was reconsidered. On second day, patient was referred again to neurology. Diagnosis was made as NMS by neurologists and bromocriptine 5 mg/d and lorazepam 1–2 mg/d were given for 13 days. When she was moved back to psychiatry unit, delusions with disorientation were apparent. Aripiprazole 5mg/d was added to same treatment and awaited up to antibody results, which came out positive. The patient was diagnosed as NMDA Receptor Antibody Encephalitis by psychiatrists and re-transferred to neurology for specific treatment. It is claimed that as the encephalitis start, 10 to 20 days later, patients develop a movement disorder, variations in blood pressure, heart rate and temperature and may become less conscious, which fits our case. Recovery is not always to the premorbid level; severe deficits may persist. Besides, improvement is often slowly. That is why some patients are now being treated after recognition of the clinical symptoms and signs, while the antibody result is awaited, to try to improve recovery. Psychiatrists should exclude autoimmune causes for acute psychosis in patients especially in the perinatal group.