Case Presentation: A 42 year-old man with a past medical history of alcohol use disorder, depression and prior suicide attempt who was admitted to psychiatry after a gabapentin overdose while intoxicated. His home medications included sertraline, naltrexone, and gabapentin. Ethanol level on admission was 204 mg/dL. Sertraline was continued and he was started on trazodone due to insomnia. Due to persistent insomnia, trazodone dose was gradually uptitrated and hydroxyzine was also given during his psychiatric hospitalization. Three weeks into the hospitalization, the patient exhibited diaphoresis, tremors, and an unsteady gait. Physical examination revealed rigidity in all extremities, but no signs of hyperreflexia or clonus. He reported taking four anti-anxiety pills brought in by his mother, but this was unwitnessed by hospital staff. The things brought in by the patient’s mother were unclear. Differential diagnosis included toxic ingestion, alcohol withdrawal, benzodiazepine withdrawal, catatonia, and serotonin syndrome, with NMS considered less likely. He received lorazepam and phenobarbital, and was later started on a dexmedetomidine drip for suspected alcohol withdrawal. Lab results revealed WBC: 10.81, creatinine phosphokinase level (CPK): 934, creatinine level: 1.48, ethanol level: less than 10 mg/dL and a negative urine toxicology screen. Due to respiratory depression, he required intubation and all psychotropic medications were discontinued. The patient became intermittently febrile and agitated, displaying rigidity during episodes of agitation despite receiving high doses of ketamine and propofol. Bromocriptine was initiated empirically, leading to improvement in rigidity. Sedation was gradually weaned. The patient had no further episodes of agitation. He was successfully extubated six days after intubation and discharged on a prolonged bromocriptine taper.
Discussion: NMS results from dopamine receptor blockade by typical antipsychotics or withdrawal from antiparkinsonian drugs. NMS is characterized by fever, muscle rigidity, altered mental status, diaphoresis, tremors, tachycardia, hypertension, leukocytosis, and elevated CPK levels. All of the symptoms do not need to be present for diagnosis and there may be an overlap of altered mental status, autonomic dysfunction, and elevated CPK in both NMS and alcohol withdrawal can lead to misdiagnosis. Our patient’s history of multiple alcohol withdrawal admissions and the unknown medications provided by his mother complicated the diagnosis. Additionally, SSRIs like sertraline along with dopamine antagonists may increase the risk of NMS by exacerbating dopaminergic deficits. Our patient had been on sertraline, trazodone, and hydroxyzine for three weeks during hospitalization. Trazodone and hydroxyzine can negatively impact dopamine levels and have been associated with cases of NMS. Given the potential exacerbating effects of SSRIs on dopaminergic function, clinicians should have a high index of suspicion for NMS in similar cases, ensuring timely intervention to optimize patient outcomes.
Conclusions: NMS can mimic other disorders, such as alcohol withdrawal, serotonin syndrome, catatonia, and malignant hyperthermia. Therefore, clinicians should maintain a higher suspicion for NMS in patients taking an SSRI along with medications that reduce the dopaminergic action.