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Neuroleptic malignant syndrome (NMS) is a potentially fatal adverse reaction to neuroleptic or antipsychotic drugs. As differential diagnosis of NMS from some certain organic and other psychiatric disorders (like delirium) is usually not easy, sometimes NMS and sometimes other etiologic organic disorders may not be noticed. Therefore, diagnostic findings must be analyzed regarding all possible disorders. In this case report we aimed to emphasize the importance of differential diagnose through a case; an adolescent with mental retardation using antipsychotic treatment for behavioral problems and hospitalized with a pre-diagnosis of NMS. The case is 15 years old male with severe mental retardation. For the last 10 months insomnia, irritability and self-destructive behavior has showed up and a startup dose of 1 mg/day risperidone treatment was given. However, because of exacerbation of irritability and self-destructive behaviors other antipsychotic options are given consecutively (quetiapine up to 600 mg/day, olanzapine up to 10 mg/day). Even though with high doses of antipsychotics, self-destructive behaviors could not be contained and reached to life threatening level. While he was taking 10 mg/day olanzapine, he was referred to child psychiatry clinic due to oculogyric crisis, clouding of consciousness, lack of food and şuid intake and hyperthermia. He was hospitalized in the intensive care unit of department of pediatrics with a pre-diagnosis of NMS. Physical examination results; the patient’s conscious level was confusing, fever (38.4°C), hypotension (90/60 mmHg), tachycardia (144 beats per minute), and tachypnea were present but there was no muscular rigidity and no extrapyramidal symptoms except oculogyric crisis. Laboratory data showed elevated white blood cell count (16/ mm3), elevated creatinine phosphokinase (3431 U/l), detectable liver function test results (aspartate aminotransferase, 106 IU/L; alanine aminotransferase, 191 IU/L). Myoglobinuria, blood urea nitrogen and creatinine levels were normal. Chest X-ray, EEG and brain computed tomography revealed no abnormalities. Antipsychotic treatment had been stopped and the patient was monitored. Midazolam treatment was given for agitation and biperiden treatment (4 mg/day) was given for oculogyric crisis. As the etiologic factor of the reason the effect of high dose antipsychotic treatment was still unclear, additional investigation had been made and pericardial effusion was found. Empiric antibiotherapy had been started. After two weeks, CK and liver function test results regressed to normal levels, and impairment of consciousness and pericardial effusion got better. Beside these improvements, interestingly his agitation decreased and self-destructive behaviors disappeared. NMS may show up in any period of the antipsychotic treatment. But mostly shows tendency to be seen during early periods of the treatment. In this case the patient was taking antipsychotic treatment for years. Beside there was no muscle rigidity, which is one of the criteria of the tetrad of NMS. Nevertheless, pericardial effusion was explaining the hyperthermia, elevation of CK levels, and self-destructive behavior and the agitation of the patient with severe mental retardation due to pain. In conclusion, before making diagnosis of NMS an attentive and elaborated differential diagnosis considering all medical conditions without being limited with only neuropsychiatric disorders is suggested.