Although neuroleptic malignant syndrome (NMS) was initially thought to be a rare, idiosyncratic complication, the incidence estimates have been rising over the years. A part of this increase can be explained on the basis of an over-inclusive definition of NMS. The unitary concept of NMS has been challenged recently and a spectrum concept has been enunciated on the basis of findings of retrospective chart-reviews which have used too broad a definition of NMS. The authors describe three cases of neuroleptic-related toxicity with different clinical presentations which appeared in a manner apparently supporting the spectrum concept. They discuss this controversial concept critically, however, and caution against its overzealous use in routine clinical practice owing to its far-reaching clinical implications.
The neuroleptic malignant syndrome is a rare but potentially fatal complication of neuroleptic administration. Many clinicians may not be familiar with this complication. This case report highlights the clinical features of neuroleptic malignant syndrome and its management.
Creatine kinase (CK) is an enzyme that is found widely in muscle tissues. Raised levels would occur when there is muscle damage. Raised levels are used as one of the diagnostic criteria for Neuroleptic Malignant Syndrome (NMS). This study looks at CK levels in 30 psychotic inpatients without NMS and compares them with 10 patients with NMS. It was found that 67% of the patients without NMS had raised CK levels, 20% of whom had levels in excess of 1000 IU/L. The rest had a two to five-fold increase over normal limits. Raised levels were associated with the use of intramuscular injections and physical restraints, situations which are well known to result in muscle injury. All the NMS patients had raised CK levels but 40% had levels below 1000 IU/L. Our findings support the idea that CK levels, though helpful, should be interpreted with care as raised levels are nonspecific.
A 38-year-old man with an underlying psychiatric illness presented with altered sensorium and abnormal behaviour. He was febrile at 38°C and weak looking; otherwise no other abnormalities were detected. A blood film conducted for malarial parasite (BFMP) revealed Plasmodium falciparum; hence a diagnosis of cerebral malaria was made. He was treated with antimalarial drugs for 2 days prior to being transferred out to the ward following clinical improvement. He subsequently developed episodes of stupor and refusal of feeding. Following an evaluation by the psychiatrist, a diagnosis of catatonic schizophrenia was made and he was started on oral sulpiride and benhexol. Unfortunately, he developed high-grade fever at 40°C with muscle rigidity and fasciculation. The diagnosis of neuroleptic malignant syndrome (NMS) was clinched and the antipsychotics were discontinued. However he succumbed to NMS several days later due to multiorgan failure.