The Neuroleptic Malignant Syndrome

Author(s):  
Edward Shorter ◽  
Max Fink

Reports of fatal febrile, hypertensive, tachycardic neurotoxic cases followed quickly on the introduction of potent new neuroleptic drugs in the 1970s. Patients became mute, rigid, posturing, and staring, showing the signs of catatonia. Labeled the neuroleptic malignant syndrome (NMS), attention was first given to neuroleptic blockade of dopamine receptors as the cause, but treatments with dopamine agonists (bromocriptine) and muscle relaxants (dantrolene) offered little benefit. When catatonia was recognized, treatments with benzodiazepines (lorazepam, diazepam) and induced seizures (electroshock, ECT) led to clinical relief and the saving of lives. The recognition of NMS as catatonia stimulated a revision of the century-long view of catatonia as a form of schizophrenia, with calls for catatonia to be considered independent of schizophrenia.

2019 ◽  
Author(s):  
Richard Sanders ◽  
Richard Krysiak

Serotonin syndrome (SS) and neuroleptic malignant syndrome (NMS) are iatrogenic life-threatening conditions with similar clinical symptoms. Altered mental status, rigidity, and autonomic instability are common in both serotonin overload and toxic dopamine antagonism. It is paramount that providers understand the key differences between these two pathologies, as pharmacologic treatments can exacerbate the condition if SS is mistaken for NMS or vice versa. Hyperreflexia, clonus, diarrhea, and vomiting suggest the excessive activity of serotonin circuits in SS, whereas prominent rigidity and hyporeflexia suggest the underactivity of dopamine circuits in NMS. Supportive care and discontinuing the offending agent(s) are keys to treating both syndromes, but serotonin antagonists (eg, cyproheptadine) could be helpful in SS, whereas NMS may sometimes benefit from muscle relaxants (eg, dantrolene) and dopamine agonists (eg, bromocriptine). Following recovery, decisions about further use of an inciting agent (or similar agents) require reconsideration of risks, benefits, and alternatives, based on newly realized hazards. It is usually important to wait at least 2 weeks before rechallenge with any drugs resembling the inciting agents. This review contains 1 figure, 5 tables, and 29 references. Key Words: bromocriptine, cyproheptadine, dantrolene, Hunter criteria, neuroleptic malignant syndrome, parkinsonism, serotonin syndrome


2013 ◽  
pp. 206-208 ◽  
Author(s):  
Albino Petrone ◽  
Michela Quartieri ◽  
Cinzia Falcone ◽  
Elina Suffredini ◽  
Marta Brandani ◽  
...  

Aripiprazole is a 2nd generation antipsychotic medication, atypical neuroleptic used for treatment of schizophrenia improving symptoms such as hallucinations, delusions, and disorganized thinking. A potentially fatal symptom complex sometimes referred to as neuroleptic malignant syndrome (NMS) has been reported in association with administration of antipsychotic drugs, including aripiprazole. Rare cases of NMS occurred during aripiprazole treatment in the worldwide clinical database. The disease is characterized by a distinctive clinical syndrome of mental status change, rigidity, fever, and dysautonomia. We report on a 63-year old woman with depression syndrome who developed neuroleptic malignant syndrome after twelve days of aripripazole 5 mg per day. Our case is added to the small number already described and suggests the need for caution when aripripazole is added to increase the effect of other antipsychotics.


2009 ◽  
Vol 43 (9) ◽  
pp. 1426-1432 ◽  
Author(s):  
Steven C Stoner ◽  
Megan M Dahmen ◽  
Mignon Makos ◽  
Jessica W Lea ◽  
Lora J Carver ◽  
...  

Background: Traditional treatment approaches for the management of restless legs syndrome (RLS) and Parkinson's disease (PD) include the use of medications that either directly or indirectly increase dopamine levels. In turn, a potential adverse event that could be expected is the development or exacerbation of psychiatric-related symptoms. Objective: To evaluate and describe the incidence of psychosis and associated behavioral features in patients taking ropinirole for RLS or PD. Methods: Patients were identified from a computerized database search of outpatients being treated with ropinirole for 1 of 2 medical conditions: PD or RLS. Data were collected in a retrospective manner from 95 patients who were tracked over the course of their therapy to determine whether psychosis or associated behavioral symptoms developed as a result and whether an intervention was needed to adjust ropinirole dosing or if additional medications had to be added to control features associated with psychosis. Results: A total of 284 patients being treated for RLS or PD were identified; of this group, 95 patients were identified as being treated for PD or RLS with ropinirole. Of the 95 patients being treated with ropinirole, 13 developed psychotic features that required therapeutic intervention with either the use of an antipsychotic or dose adjustment of ropinirole. PD patients included in this study were numerically more likely to develop psychotic features compared with RLS patients; however, the difference was not statistically significant (p = 0.122). The results do suggest that this risk is increased when ropinirole is used as part of a dual therapy approach with dopamine agonists in the treatment of either PD or RLS (p = 0.003). Discussion: Dopamine agonists have long been used as preferred treatment in the management of PD and RLS. When treating either PD or RLS in the psychiatric population, the concern arises that increased activity at dopamine receptors may induce or exacerbate psychiatric features. A potential clinical concern with the use of ropinirole is the potential for patients to develop psychiatric features, although there are few data available to demonstrate whether stimulation of targeted individual dopamine receptors is linked to the development or exacerbation of psychotic features. It is also undetermined whether concurrent antipsychotic treatment provides any protective benefit against psychosis, especially in patients already being treated for psychotic symptoms. Conclusions: Our findings suggest that ropinirole may play a role in inducing or exacerbating psychosis and its associated features, although a number of confounding variables prevent the determination of a clear association and suggest that further investigation is warranted in controlled clinical trials.


1997 ◽  
Vol 37 (1) ◽  
pp. 79-81 ◽  
Author(s):  
J W Lowe Td Mb Bs Mrcp (Uk) Frc Path

The technique of immunocytochemistry was used to identify myoglobin in kidney, confirming a diagnosis of neuroleptic malignant syndrome following an otherwise obscure autopsy in a decomposed body. The features of neuroleptic malignant syndrome are reviewed with a differential diagnosis of myoglobin renal casts. The report emphasizes a thorough and detailed assessment of deaths which occur during treatment with neuroleptic drugs.


2003 ◽  
Vol 121 (3) ◽  
pp. 121-124 ◽  
Author(s):  
Francisco Garcia Soriano ◽  
Elcio dos Santos Oliveira Vianna ◽  
Irineu Tadeu Velasco

CONTEXT: A case of neuroleptic malignant syndrome and acute respiratory distress syndrome is presented and discussed with emphasis on the role of muscle relaxation, creatine kinase, and respiratory function tests. CASE REPORT: A 41-year-old man presented right otalgia and peripheral facial paralysis. A computed tomography scan of the skull showed a hyperdense area, 2 cm in diameter, in the pathway of the anterior intercommunicating cerebral artery. Preoperative examination revealed: pH 7.4, PaCO2 40 torr, PaO2 80 torr (room air), Hb 13.8 g/dl, blood urea nitrogen 3.2 mmol/l, and creatinine 90 mmol/l. The chest x-ray was normal. The patient had not eaten during the 12-hour period prior to anesthesia induction. Intravenous halothane, fentanyl 0.5 mg and droperidol 25 mg were used for anesthesia. After the first six hours, the PaO2 was 65 torr (normal PaCO2) with FiO2 50% (PaO2/FiO2 130), and remained at this level until the end of the operation 4 hours later, maintaining PaCO2 at 35 torr. A thrombosed aneurysm was detected and resected, and the ends of the artery were closed with clips. No vasospasm was present. This case illustrates that neuroleptic drugs can cause neuroleptic malignant syndrome associated with acute respiratory distress syndrome. Neuroleptic malignant syndrome is a disease that is difficult to diagnose. Acute respiratory distress syndrome is another manifestation of neuroleptic malignant syndrome that has not been recognized in previous reports: it may be produced by neuroleptic drugs independent of the manifestation of neuroleptic malignant syndrome. Some considerations regarding the cause and effect relationship between acute respiratory distress syndrome and neuroleptic drugs are discussed. Intensive care unit physicians should consider the possibility that patients receiving neuroleptic drugs could develop respiratory failure in the absence of other factors that might explain the syndrome.


Cephalalgia ◽  
1998 ◽  
Vol 18 (4) ◽  
pp. 174-182 ◽  
Author(s):  
A Mascia ◽  
J Qqaacute;fra ◽  
J Schoenen

The dopamine theory of migraine pathogenesis, first proposed by F. Sicuteri in 1977, has attracted renewed interest after an increased frequency of the dopamine D2 receptor (DRD2) gene allele NcoI C was found in patients with migraine with aura. Therefore we reviewed the relevant literature. The most compelling argument favoring an interictal hypersensitivity of dopamine receptors in migraineurs stems from pharmacologic studies of the gastric and autonomic effects of dopaminergic agents such as apomorphine, but none of these studies was blinded and placebo-controlled. Various DRD2 antagonists abort migraine attacks after parenteral administration, while mere is circumstantial evidence that dopamine agonists may be useful for prophylaxis. Most drugs used in these trials, however, lack selectivity for dopamine receptors. Both in pharmacological and therapeutic studies most patients had migraine without aura. We conclude that data suggesting a primary role for the dopaminergic system in migraine pathogenesis are unconvincing. Based on well established interactions between central amines, a reduced release of serotonin between attacks could lower dopamine release which would lead to receptor hypersensitivity.


Cephalalgia ◽  
2007 ◽  
Vol 27 (11) ◽  
pp. 1308-1314 ◽  
Author(s):  
S Akerman ◽  
PJ Goadsby

In the last 30 years dopamine has been considered as playing a role in the pathogenesis of migraine. The literature indicates that migraineurs are hypersensitive to dopamine agonists with respect to some of the premonitory symptoms of migraine such as nausea and yawning. There are various nonspecific dopamine D2 receptor antagonists that show good clinical efficacy in migraine, and also a number of polymorphisms of dopaminergic genes related to migraine. Animal studies have also shown that dopamine receptors are present in the trigeminovascular system, the area believed to be involved in headache pain, and neuronal firing here is reduced by dopamine agonists. There appears to be little effect of dopamine on peripheral trigeminal afferents. We assess some of the limitations of the clinical studies with regard to the therapeutics, and those found in the studies that discovered differences in genetic polymorphisms in migraine, and consider the implications of this on a dopaminergic hypothesis of migraine.


ChemInform ◽  
2010 ◽  
Vol 23 (18) ◽  
pp. no-no
Author(s):  
J. C. JAEN ◽  
B. W. CAPRATHE ◽  
L. D. WISE ◽  
S. J. SMITH ◽  
T. A. PUGSLEY ◽  
...  

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