.png)
Neuroleptic malignant syndrome (NMS) is an uncommon but potentially fatal idiosyncratic reaction characterized by the development of altered consciousness, hyperthermia, autonomic dysfunction, and muscular rigidity on exposure to neuroleptic medications. NMS was previously associated with the use of high-potency neuroleptics, cases have begun to emerge as atypical. The mortality and morbidity associated with NMS can be decreased with early recognition, early discontinuation of the neuroleptics and aggressive treatment. This article presents a olanzapine-induced case in an adolescent, and treatment of NMS. The patient was a 15-year-old male adolescent with a history of mental retardation and epilepsy. The patient’s initial presentation to us on 28.04.2011 behavioral changes, irritability, numbness in hands and feet, talking to himself, cursing the people around him were in the emergency department with complaints. To our clinic for further evaluation and treatment of patients were being treated. As a result of consultation of pediatrics for the etiology of mental retardation, organic pathology was excluded and by pediatric neurology with a diagnosis of non-convulsive status epileticus 500 mg of valproic acid was started. Behavioral problems in patients who continued risperidone 1 mg and 5 mg biperiden was added and patients with a reduction of complaints had been externa. For 2 years he was treated with behavior therapy and using risperidone and biperiden was not needed. Patients with insomnia complaints in the outpatient clinic controls olanzapine 2.5 mg unrest began. In patient history we learned that he was brought to emergency department 5 consecutive days and the treatment was performed olanzapine 5 mg SC. He was brought to the emergency department because the family noted that the child had a tactile fever; was rigid, diaphoretic, tremulous, and difficult to arouse; and had persistent urinary incontinence. The patient was admitted to the pediatric intensive care unit, where he remained rigid and unresponsive except for incoherent speech. Biochemical tests were performed and elevated creatine kinase drew attention. He was treated for a presumptive diagnosis of NMS with IV benzodiazepine and hydration. To reduce the sequela of NMS; urinary alkalinization with sodium bicarbonate to maintain a urinary pH of 6.5 to 7.0; cardiac, pulse oximetry, and vital sign monitoring; and supportive care, including IV saline hydration were started. Additionally, we began physical therapy to prevent contractures. Observation of the patient revealed no side effects associated with the MNS, and he began to take food and medications orally and to co-operate partially. Insomnia was not evident. Decreased rigidity and tremor were observed. Vital signs were stable and the patient was discharged on the 34th day. Bambrick and Wilson reported that, MR has relative risk especially for recurrent NMS. NMS have been reported in the mortality rate of 4-30%. In this article, it has been reported that NMS induced by olanzapine in an adolescent on the basis of mental retardation. We want to emphasize the relationship between mental retardation, epilepsy and NMS associated with the use of atypical neuroleptics, and the importance of the monitoring as well as the follow-up.