Neuroleptic Malignant Syndrome


Article Author:
Leslie Simon
Muhammad Hashmi


Article Editor:
Avery Callahan


Editors In Chief:
Mohamed Hegazy
Najib Murr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Kyle Blair
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
9/29/2019 7:55:11 PM

Introduction

Neuroleptic malignant syndrome (NMS) is a life-threatening syndrome associated with the use of dopamine-receptor antagonist medications or with rapid withdrawal of dopaminergic medications. NMS has been associated with virtually every neuroleptic agent but is more commonly reported with the typical antipsychotics like haloperidol and fluphenazine. Classic clinical characteristics include mental status changes, fever, muscle rigidity, and autonomic instability. While uncommon, NMS remains an important part of the differential diagnosis of fever and mental status changes because it requires early diagnosis and treatment to prevent significant mortality and death. Treatment involves immediately discontinuing the offending agent, aggressive supportive care to manage and prevent complications, and pharmacologic therapy in severe cases. The empiric medications most frequently used for refractory NMS include bromocriptine mesylate, a dopamine agonist, and dantrolene sodium, a muscle relaxant. If the syndrome is due to the rapid withdrawal of dopaminergic medication, rapid re-institution of the medication may improve symptoms.[1][2][3]

Etiology

The primary trigger for NMS is dopamine receptor blockade, most often due to an antipsychotic agent. NMS is usually associated with high-potency first-generation neuroleptic agents but also may be caused by low-potency and atypical antipsychotic agents, antiemetics, tricyclic antidepressants, and lithium. Rapid withdrawal of dopaminergic drugs, most often used to manage parkinsonian diseases, such as levodopa and amantadine, also may cause this syndrome. The rapid switching of one Parkinson medication to another also is associated with the development of NMS.[4][5][6]

Medications Associated with Neuroleptic Malignant Syndrome

Typical Neuroleptics

  • Haloperidol
  • Chlorpromazine
  • Fluphenazine
  • Thioridazine
  • Trifluordazine
  • Thiothixene
  • Loxapine
  • Bromperidol
  • Promazine
  • Clopenthixol

Atypical Neuroleptics

  • Olanzapine
  • Clozapine
  • Risperidone
  • Quetiapine
  • Ziprasidone
  • Arpiprazole
  • Zotepine
  • Amisulpride

Antiemetics

  • Droperidol
  • Dompridone
  • Metoclopramide
  • Promethazine
  • Proclorperazine

Others

  • Tetrabenazine
  • Reserpine
  • Amoxapine
  • Diatrizoate
  • Lithium
  • Phenelzine
  • Dosulepin
  • Trimipramine
  • Desipramine

Dopaminergic Agents (withdrawal)

  • Levodopa
  • Amantadine
  • Tolcapone
  • Dopamine agonists

Epidemiology

Incidence rates range from 0.01% to 3.2% of patients taking neuroleptic medications. The incidence is decreasing due to newer agents, which are less likely to cause NMS, and increased awareness of the condition. Most cases occur in young adults, but this is most likely because it is the age of first exposure to neuroleptic medications rather than an age-related risk. Men outnumber women 2:1, also related to the likelihood of exposure to the causative agent. Incidence due to the withdrawal of dopaminergic drugs is more likely in the geriatric population based on the likelihood of exposure to the inciting cause.

Pathophysiology

The pathophysiology of NMS is complex and incompletely understood.  Most symptoms are attributed to the sudden reduction in central dopaminergic activity due to a D2 receptor blockade or abrupt withdrawal of D2 receptor stimulation. This accounts for the characteristic muscle rigidity, hyperthermia, and mental status changes.  Other neurotransmitters are involved, and NMS has features suggestive of disruption of the sympathetic nervous system. Other theories suggest a calcium-mediated disruption of the musculoskeletal system, pathophysiologically similar to malignant hyperthermia. Familial clusters of patients with NMS and genetic testing suggest a predisposition to the development of NMS in certain individuals.[7][8][9]

History and Physical

The main risk factor for the developing NMS is the initiation or increase in dosage of a neuroleptic medication. High-potency and long-aging neuromuscular depot forms carry the greatest risk. The concurrent use of multiple neuroleptic agents or lithium also increases the risk. Abrupt withdrawal of dopaminergic agents is a less common but important cause of NMS. Symptoms of NMS develop over one to three days and include distinctive clinical features: fever, muscle rigidity, mental status changes, and autonomic rigidity.

The DSM-V Criteria for diagnosing NMS are as follows:

Major Criteria (all required)

  • Exposure to dopamine-blocking agent
  • Severe muscle rigidity
  • Fever

Other Criteria (at least two required)

  • Diaphoresis
  • Dysphagia
  • Tremor
  • Incontinence
  • Altered level of consciousness
  • Mutism
  • Tachycardia
  • Elevated or labile blood pressure
  • Leukocytosis
  • Elevated creatine phosphokinase

Evaluation

Evaluation should include a comprehensive metabolic panel including electrolytes and serum creatinine, creatine phosphokinase level, urinalysis for myoglobinuria, and arterial or venous blood gas to screen for metabolic acidosis. Diagnosis can be made clinically, but supporting lab work is usually consistent with rhabdomyolysis with an elevated CK and acutely declining renal function. The elevated CK can be profound and typically correlates with disease severity. Leukocytosis is common with white blood cell counts ranging from 10,00 to 40,000 mm3 with a left shift. Transaminases may also be mildly elevated. In patients where the diagnosis is less clear, neuroimaging and lumbar puncture may be necessary to exclude structural and infectious diagnosis from the differential. Other laboratory testing such a lithium levels and screening for drugs of abuse may be helpful in selected cases.

Treatment / Management

NMS is a neurologic emergency, and delays in diagnosis and treatment can lead to significant morbidity or death. Discontinuing the offending agent is paramount, followed by supportive therapy. [10][11]This includes aggressive cooling and correction of volume deficits and any electrolyte imbalances. Patients are prone to cardiac dysrhythmias and respiratory failure due to chest wall rigidity. Treat with antiarrhythmic agents and mechanical ventilation as needed. More severe cases are managed with empiric pharmacologic therapy. Meta-analyses and case reports suggest that these may shorten the course and reduce morbidity and mortality. Bromocriptine, a dopamine agonist, given orally or via gastric tube, is used to reverse the hypodopaminergic state. Dantrolene, a muscle relaxant may be administered intravenously or orally in less severe cases.  Benzodiazepines also may be useful in controlling agitation. If the syndrome is due to a rapid withdrawal of dopaminergic agents, restarting the drug may reduce symptoms. Electroconvulsive therapy also has been reportedly effective in refractory cases. Patients should be admitted for close monitoring in an intensive care unit setting.[12]

Differential Diagnosis

NMS is one of a group of drug-related acute dysautonomias with common features of fever, rigidity and autonomic dysfunction. Serotonin syndrome has similar features to NMS and is most easily distinguished by causative agent, most frequently the serotonin-specific reuptake inhibitors. The hyperthermia and muscle rigidity is usually less severe with serotonin syndrome than with NMS, and serotonin syndrome is more commonly associated with gastrointestinal symptoms, hyperreflexia, and myoclonus. Malignant hyperthermia is almost clinically indistinguishable from NMS, but the history of exposure to depolarizing muscle relaxants, most commonly succinylcholine, or inhaled anesthetic agents make the distinction clear in most cases. Malignant catatonia may present with fever, rigidity, akinesia and altered mental status. It is important to distinguish from NMS because lethal catatonia is often treated with neuroleptics. Treatment with antipsychotics is risky because many reviewers cannot distinguish between lethal catatonia and NMS. Distinguishing features of malignant catatonic include increased positive symptoms as compared to NMS and a behavioral prodrome of automatisms, agitation, or psychosis.

Multiple other medical conditions can mimic NMS, and NMS may be easily misdiagnosed and attributed to another condition. The most common mimics are central nervous system (CNS) infections such as meningitis or encephalitis, heat stroke, agitated delirium, toxic encephalopathies, withdrawal syndromes, metabolic emergencies, and nonconvulsive status epilepticus.

Acute encephalitis, meningitis, or brain abscess must be excluded in patients presenting with fever and mental status changes to avoid delay in treatment of CNS infection. This involves lumbar puncture for cerebrospinal fluid analysis and neuroimaging in certain cases. Patients on antipsychotic drugs are predisposed heat-related illness, which may mimic NMS. Acute intoxication with many recreational drugs such as cocaine, MDMA, amphetamines, methamphetamines, and phencyclidine may have similar features. Abuse of recreational drugs may occur in the setting of medical therapy with antipsychotics making the clinical picture unclear. Several withdrawal syndromes may present with features similar to NMS, especially Baclofen withdrawal which is best managed by the reinstitution of baclofen therapy or with benzodiazepines. Alcohol and benzodiazepine withdrawal also may share features with NMS as do the withdrawal syndromes of other sedatives and hypnotics. Thyrotoxicosis and pheochromocytoma may both have features similar to NMS.

Prognosis

Early mortality reports were greater than 30% for NMS; however, increased awareness, earlier detection, and better supportive care has reduced mortality to less than 10%. With early recognition and aggressive treatment, most patients will fully recover in 2 to 14 days. Delayed treatment may result in significant morbidity such as residual catatonia, parkinsonism, renal, or cardiopulmonary complications. When fatal, deaths are usually due to cardiac arrhythmias, disseminated intravascular coagulation, respiratory failure, or renal failure. Many patients may be successfully restarted on neuroleptic medications, but some will develop recurrent symptoms. Guidelines for re-initiation of neuroleptic therapy recommend waiting at least two weeks after resolution of symptoms, using lower-potency agents, starting with low doses and slowly titrating to effect, and avoiding lithium in conjunction with neuroleptics. Patients should be instructed to avoid dehydration and should be carefully monitored for any symptoms of recurrent NMS.

Enhancing Healthcare Team Outcomes

NMS is a medical emergency that is best managed by a multidisciplinary team. These patients are ideally managed in the ICU with very close monitoring. The key is hydration and supportive therapy. There is no specific drug to reverse this disorder. Anecdotal reports on dantrolene continue to appear but a few case studies indicate that the drug may neither be effective or safe.[13]

For most patients in whom the offending drug is discontinued, the prognosis is good.


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Neuroleptic Malignant Syndrome - Questions

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Which symptom is not associated with neuroleptic malignant syndrome?



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Neuroleptic malignant syndrome is most common with:



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Which of the following drugs is most likely to cause a fever?



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A patient is placed on therapy with an antipsychotic drug. Four weeks later, he presents with fever, catatonia, stupor, and Parkinsonian features suggestive of neuroleptic malignant syndrome. Which of the following medications is most appropriate?



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After taking haloperidol, a patient develops muscle rigidity, fever, and sweating. What is the best treatment for this patient?



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A patient with head trauma is extremely agitated in the emergency room. He is administered a medication to sedate him and he develops neuroleptic malignant syndrome (NMS). Which is not a feature of neuroleptic malignant syndrome?



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What is the drug of choice in the management of neuroleptic malignant syndrome?



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Which of the following is not characteristic of neuroleptic malignant syndrome?



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Which of the following is NOT seen in neuroleptic malignant syndrome?



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Which is NOT a symptom of neuroleptic malignant syndrome?



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Which of the following is not a characteristic of neuroleptic malignant syndrome?



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Which of the following is not a feature of neuroleptic malignant syndrome in a patient receiving haloperidol?



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In a patient with neuroleptic malignant syndrome, what is the treatment of choice?



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What should be the first action when neuroleptic malignant syndrome is suspected?



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Which of the following drugs is the first-line treatment choice for neuroleptic malignant syndrome?



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What is the cause of neuroleptic malignant syndrome?



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A 17-year-old patient starts a new drug and now presents with fever, muscle rigidity, altered mental status, and signs of autonomic instability. Treatment is started with antipyretics, intravenous hydration, and dantrolene. What is the most likely drug involved in this adverse reaction?



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Which of the following is not commonly seen in neuroleptic malignant syndrome?



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Which is true regarding neuroleptic malignant syndrome (NMS)?



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What neurotransmitter is implicated in neuroleptic malignant syndrome?



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Which of the following symptoms is seen less in neuroleptic malignant syndrome than in serotonin syndrome?



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Which of the following is not used to treat neuroleptic malignant syndrome?



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Which is not a clinical sign of neuroleptic malignant syndrome?



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A 17-year-old patient presents 10 days after he was started on a neuroleptic drug. His mother states that he has had a high fever and his mental status is altered. He appears to be very stiff and is not verbally responsive. On physical exam, he has a fever of 39.8 C, is extremely diaphoretic, tachycardic, and tachypneic. He appears rigid and has a shuffling gait. He has no idea what is happening and appears very ill. Which of the following is not associated with the patient's ongoing condition?



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A nurse is rounding on a client with new onset schizophrenia admitted 5 days ago, who is being treated with haloperidol. After entering the room to perform an assessment and administer morning medications, the nurse notices an entirely different client than she encountered a few days ago. The client is sweating profusely, confused, feels hot, has labored respirations, and is lying in a bed full of urine. The client's temperature is 103.2 F (39.6 C), respiratory rate 32, blood pressure 192/106 mmHg, heart rate 132 beats/min, and severe muscle rigidity is evident. How should the nurse proceed in providing care for this client? Select all that apply.



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A client with schizophrenia is admitted to the behavioral health unit because he has stopped taking his medications. Over the last few weeks, his behavior has been out of control, and he has had episodes of extreme paranoia and hallucinations. He agrees to take the drug risperidone. Twenty-four hours later, the nurse on rounds assesses the client and sounds an emergency alarm indicating that the client has developed neuroleptic malignant syndrome. What clinical features will you note in the client? Select all that apply.



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Neuroleptic Malignant Syndrome - References

References

Duma SR,Fung VS, Drug-induced movement disorders. Australian prescriber. 2019 Apr;     [PubMed]
González-Romero MF,Avina-Galindo AM,Elbe D,Friedlander R,Vila-Rodriguez F, Lifesaving Electroconvulsive Therapy for a Child With Autism Spectrum Disorder, Severe Self-Injurious Behavior, and Neuroleptic Malignant Syndrome. The journal of ECT. 2019 Apr 22;     [PubMed]
Morcos N,Rosinski A,Maixner DF, Electroconvulsive Therapy for Neuroleptic Malignant Syndrome: A Case Series. The journal of ECT. 2019 Apr 22;     [PubMed]
Ott M,Werneke U, A Mixed Presentation of Serotonin Syndrome Versus Neuroleptic Malignant Syndrome in a 12-Year-Old Boy. Pediatric emergency care. 2019 May;     [PubMed]
van Rensburg R,Decloedt EH, An Approach to the Pharmacotherapy of Neuroleptic Malignant Syndrome. Psychopharmacology bulletin. 2019 Feb 15;     [PubMed]
Salik I,Marwaha R, Electroconvulsive Therapy 2019 Jan;     [PubMed]
Manabe S,Yanagi H,Ozawa H,Takagi A, Neuroleptic malignant syndrome as part of an akinetic crisis associated with sepsis in a patient with Lewy body disease. BMJ case reports. 2019 Feb 28;     [PubMed]
Jamshidi N,Dawson A, The hot patient: acute drug-induced hyperthermia. Australian prescriber. 2019 Feb;     [PubMed]
Kane JM,Correll CU,Delva N,Gopal S,Savitz A,Mathews M, Low Incidence of Neuroleptic Malignant Syndrome Associated With Paliperidone Palmitate Long-Acting Injectable: A Database Report and Case Study. Journal of clinical psychopharmacology. 2019 Mar/Apr;     [PubMed]
Grover S,Sathpathy A,Reddy SC,Mehta S,Sharma N, Parkinsonism-hyperpyrexia syndrome: A case report and review of literature. Indian journal of psychiatry. 2018 Oct-Dec;     [PubMed]
Ratto D,Joyner RW, Dantrolene 2019 Jan;     [PubMed]
Kaliora SC,Zervas IM,Papadimitriou GN, [Electroconvulsive therapy: 80 years of use in psychiatry]. Psychiatrike = Psychiatriki. 2018 Oct-Dec;     [PubMed]
Litman RS,Smith VI,Larach MG,Mayes L,Shukry M,Theroux MC,Watt S,Wong CA, Consensus Statement of the Malignant Hyperthermia Association of the United States on Unresolved Clinical Questions Concerning the Management of Patients With Malignant Hyperthermia. Anesthesia and analgesia. 2019 Apr;     [PubMed]

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