🩺Neuroleptic Malignant Syndrome #NMS
🌟The biologic basis of #NMS is not known, but neuroleptic antipsychotic agents block dopamine D2 receptors, a family of G protein–coupled receptors that bind extracellular dopamine, and this blockade is inferentially implicated in the disorder.
🌟The typical presentation of #NMS is:
🔸#Dysautonomia, particularly tachycardia and rapidly fluctuating hypertensive or hypotensive blood pressure.
🔸 #Hyperthermia to 40°C or higher.
🔸 #Delirium that in the severe form is catatonia.
🔸 #Rigidity.
🌟 The medications that are associated with #NMS include high-potency, first-generation (typical) #antipsychotic agents such as haloperidol, fluphenazine, and pimozide. The syndrome is less common and less severe with second-generation agents than with first-generation agents. Other drugs that block dopamine, such as metoclopramide, droperidol, prochlorperazine, and dopamine-depleting agents such as tetrabenazine.
🌟 Differential diagnosis includes other states of rigidity and hyperthermia, most importantly, #Acute_serotonin_syndrome which may cause acute dysautonomia, although hyperreflexia, clonus, myoclonus, and shivering, which characterize serotonin syndrome, are not components of #NMS. The muscular salience in serotonin syndrome is closer to spasticity than to the lead-pipe rigidity of neuroleptic malignant syndrome, and hyperreflexia is characteristic of serotonin syndrome, in contrast to the diminished or normal tendon reflexes in #NMS.
🌟Management of #NMS requires a tiered approach to the main features of the syndrome: blood-pressure instability, hyperthermia and rhabdomyolysis from severe rigidity, and the potential for respiratory compromise. Recovery times vary but generally range from 7 to 11 days and may be roughly predicted from the half-life of the implicated neuroleptic drug.
#synapse #NeuroCritical
