Which of the following is not used in the treatment of neuroleptic malignant syndrome?
Antipsychotics cause NMS.
Antipsychotics cause NMS.
Serotonin syndrome and neuroleptic malignant syndrome
Serotonin syndrome
Serotonin syndrome is a consequence of excess serotonergic activity in the CNS and can be conceptualised as serotonin toxicity. It is characterized by the triad of neuromuscular abnormalities (myoclonus, and clonus), altered mental state, and autonomic dysfunction.
The clinical picture ranges from mild agitation and tremor to extreme muscle rigidity with hyperthermia that demands immediate intervention. Analysis of a series of cases found neuromuscular abnormalities to be the most reliable diagnostic finding. Clonus (the involuntary muscular contraction following sudden stretching of the muscle), hyperreflexia, and muscular rigidity are nearly always present. The onset of symptoms is typically acute and rapidly progressive, following shortly after one or two doses of the offending medication.
The most frequent cause of severe reaction is the co-administration of an MAOI with an SSRI.
Treatment consists of withdrawing the cause, supportive care, control of agitation, and administration of a 5HT-2A antagonist such as cyproheptadine. Mild cases may only require benzodiazepines and fluids but more severe cases can require an intensive care environment.
Neuroleptic malignant syndrome (NMS)
NMS is not fully understood. There is some agreement however that it probably results from the result of dopamine blockade at the hypothalamus which messes up the thermo-regulatory system and hence results in hyperthermia (a core feature). It is also suggested that the use of antipsychotics (neuroleptics) causes calcium uptake into muscles resulting in muscle rigidity (another core feature, lead pipe rigidity) which results in rhabdomyolysis and so elevated levels of creatinine phosphokinase (CPK).
It is almost exclusively caused by antipsychotics (but is also associated with antidepressants and lithium). Rapid and large dose increases often trigger it, along with rapid dose reductions, and abrupt withdrawal of anticholinergics. It typically develops within 2 weeks of initial treatment but may occur at any time the drug is being taken. It can also be precipitated by agitation and/or dehydration.
Treatment is not always necessary. The first step is removal of the antipsychotic and the treatment of fever in addition to the use of a benzodiazepine. Other options which may be necessary include ECT, bromocriptine, and dantrolene.
The mortality rate is estimated to be up to 20%.
The following table lists the common risk factors for NMS.
| Risk factors for NMS |
|---|
| General Younger age Being male Physical exhaustion Dehydration or electrolyte imbalance Previous and family history of NMS Organic mental disorders Low serum iron levels Raised creatine kinase levels Comorbid substance misuse |
| Related to antipsychotic High loading dose Faster rate of loading High potency Sudden withdrawal |
Serotonin syndrome versus Neuroleptic malignant syndrome.
NMS and serotonin syndrome are easily confused. They are in fact very different and require different treatments. Common features include alteration in consciousness, sweating, autonomic instability, hyperthermia, and elevated CPK levels.
The history gives important clues about the diagnosis. Serotonin syndrome typically has an acute onset (within 24 hours of drug administration), whereas that of NMS is more insidious (typically taking up to 2 weeks to appear). Any recent change to the medication is also very important
