Abstract
The management of neuroleptic malignant syndrome (NMS) remains a topic of debate. It has been recommended to stop neuroleptics completely for 2 weeks [1], which in very acute patients is problematic, as evidenced by the following case:
A 41-year-old Caucasian man was admitted to hospital with a mixed bipolar schizo-affective episode (ICD-10) and mild mental retardation. Upon admission, he was highly agitated, dysphoric and showed delusions of persecution. During a 14 year history of bipolar schizoaffective disorder he had received various antipsychotics without any history of NMS. Upon admission, haloperidol (20 mg/day), diazepam (20 mg/day) and valproate (900 mg/day) were administered, with little therapeutic effect. At the end of the second week, levomepromazine (200 mg/day) was added. As the patient developed parkinsonism, a decision was made to change to risperidone, while haloperidol and diazepam were slowly reduced. On day 18 of hospital treatment, the patient suddenly developed a temperature of 39.2 ° C with no indication of an infection. Parkinsonism had worsened, diaphoresis was observed and there were periods of clouded consciousness. Creatine kinase was 58.3 ∝ mol/L/s (reference: < 2.8; no history of intramuscular injection), and there was a leukocytosis of 15 800/mL. Antipsychotics were immediately discontinued and lorazepam (4 mg/day) was commenced. Three days later the patient was highly agitated, dysphoric and delusional, so that antipsychotic treatment seemed necessary. As he became normothermic, and as CK and extrapyramidal side-effects decreased, a challenge with quetiapine was attempted (initially 50 mg/day, slowly increased to 400 mg/day). Under close monitoring of CK and temperature, acute psychopathology remitted, with no signs of recurrence of NMS.
This case fulfils strict criteria for NMS [2]. While certain risk factors for developing NMS have been described [2], it is still impossible to predict what antipsychotics will cause NMS in which patients. This patient suffered from mental retardation, which is a known risk factor for NMS, as is possibly schizo-affective disorder [3]. Furthermore, polypharmacy increases the risk of NMS. Although there are now various reports that quetiapine may cause NMS (for example [4]), its favourable clinical profile was the reason we chose to use it, albeit cautiously, in this case. Clearly, this must not be generalized, as there is at least one report of a failed challenge with quetiapine after NMS [5].