Olanzapine-associated neuroleptic malignant syndrome

Kontaxakis, V.P.; Havaki-Kontaxaki, B.J.; Christodoulou, Nikos; Paplos, K.G.

doi:10.1016/s0278-5846(02)00202-6

Cited by 25 publications

(18 citation statements)

References 38 publications

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“…This patient received repeated daily doses of olanzapine. The role of olanzapine and its combination with levomepromazine in the development of NMS has been previously described [5, 8]. The plasma level of olanzapine should not have exceed therapeutic levels as it is mainly metabolized by CYP1A2 and to a lesser extent by CYP2D6.…”

Section: Discussionmentioning

confidence: 99%

Neuroleptic malignant syndrome in an adolescent with CYP2D6 deficiency

et al. 2013

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We describe a patient with dystonia and psychotic symptoms treated with standard doses of antipsychotics, who developed neuroleptic malignant syndrome (NMS). A 16-year-old male with a history of misuse of dextromethorphan and pseudoephedrine for recreational purpose presented with dystonia and a psychotic episode. Following continuous treatment with olanzapine (10 mg/day), repeated injections of levomepromazine (37.5 mg/day), and a single injection of haloperidol (2.5 mg), the patient developed NMS. Muscular rigidity, fever (up to 41 °C), hypotension (100/70 mmHg), tachycardia (120 beats per minute), tachypnea (26 breaths per minute), elevated leukocyte count (up to 16.6 × 103/μL), and elevated serum creatinine phosphokinase (CPK) (up to 15,255 U/L) were observed. A diagnosis of NMS was made according to the DSM-IV TR criteria. Genotyping revealed that he was homozygous for a non-functional CYP2D6*4 allele. The case highlights the importance of therapeutic drug monitoring in identification and differentiation of drug-induced effects in psychiatric disorder to prevent NMS and its complications. In addition, genotyping of CYP2D6 might be considered in patients with symptoms suggestive of drug toxicity who are treated with neuroleptics metabolized via the CYP2D6 pathway, as carriage of one or more non-functional alleles may increase the risk for adverse reactions, such as NMS.

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Section: Discussionmentioning

confidence: 99%

Neuroleptic malignant syndrome in an adolescent with CYP2D6 deficiency

et al. 2013

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“…These cases were associated with either a recent increase in the therapeutic dose of olanzapine or the addition of or a change from another antipsychotic agent [4,11]. Features of NMS in cases following therapeutic treatment with olanzapine and other atypical antipsychotics commonly follow a typical pattern with autonomic instability, hypertonia and lead-pipe rigidity, and mental status changes [12,13].…”

Section: Discussionmentioning

confidence: 99%

“…Olanzapine has been used increasingly in the treatment of psychosis due to purported lower incidence of side effects than seen with classical neuroleptics. However, numerous case reports describing NMS have been reported with therapeutic use of this agent [1][2][3][4][5]. In previous cases, NMS has been observed in patients on therapeutic doses of other antipsychotic agents, when olanzapine subsequently had been added, or when it had been started as a new single therapeutic agent.…”

Section: Introductionmentioning

confidence: 99%

Neuroleptic malignant syndrome developing after acute overdose with olanzapine and chlorpromazine

2009

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Neuroleptic malignant syndrome (NMS) is a relatively uncommon side effect that may develop after a recent increase in the therapeutic dose of an antipsychotic medication or the addition of a new agent in therapeutic doses.Case Report: We report a case of NMS developing in a 36-year-old female patient 2 days following deliberate self-poisoning with 30 ϫ10-mg olanzapine tablets, 7 ϫ100-mg chlorpromazine tablets and an unknown amount of escitalopram. These were the patient's own medications. She had not been taking these for several weeks. The patient initially presented with sedation from her overdose which resolved over the next 24 hours. Following this, over the subsequent 24 hours, she became progressively confused, ataxic, hypertonic, ferbrile and tachycardic, with marked lead pipe rigidity of the limbs. Head CT, lumbar puncture and septic screen were all negative. She was treated with intravenous midazolam infusion, nasogastrically administered bromocriptine, external cooling and was mechanically ventilated. She gradually improved over a period of 10 days, with residual confusion lasting another week, and was discharged well with no deterioration from her premorbid neurologic state.Conclusion: To our knowledge, although there are numerous cases reported with therapeutic use, NMS has not been reported to develop following acute olanzapine overdose. Clinicians should be aware that this may be an uncommon side effect of antipsychotic medication.

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“…However, a review of NMS cases with atypical antipsychotics [9] reveals contradictory findings. The clinical presentation of NMS due to clozapine differs from that due to conventional antipsychotics in that there are fewer extrapyramidal symptoms.…”

Section: Discussionmentioning

confidence: 99%