Concomitant Treatment of Neuroleptic Malignant Syndrome and Psychosis

Goldwasser, Harry D.; Hooper, James F.; Spears, Nicki M.

doi:10.1192/bjp.154.1.102

Cited by 24 publications

(4 citation statements)

References 9 publications

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“…This could account for the observation that serum CPK levels during NMS are positively correlated with 24-h urinary catecholamine metabolite excretion levels (77). The appearance of elevated muscle enzyme levels before clinical signs of autonomic instability indicates that hypermetabolism may precede the full syndrome (85). Hypermetabolism related to hyperthyroidism, in the absence of central dopamine blockade, can produce a syndrome similar to NMS (86).…”

Section: Pathophysiologymentioning

confidence: 99%

Neuroleptic malignant syndrome: risk factors, pathophysiology, and treatment

Ananth

Aduri

Parameswaran

et al. 2004

Acta Neuropsychiatr.

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Neuroleptic malignant syndrome (NMS) is associated with the administration of antipsychotic agents and other drugs such as l-dopa, antidepressants, and antihistaminic agents. Unexpected changes in mental status, new-onset catatonia, episodic tachycardia, tachypnea, hypertension, dysarthria, dysphagia, diaphoresis, sialorrhea, incontinence, low-grade temperature elevations, and rigidity should arouse suspicion. Several lines of evidence provide support for the involvement of dopamine. Most of the drugs implicated in NMS are D2 dopamine receptor antagonists. Central noradrenergic activity is also possibly related to the disorder, as sympathetic hyperactivity is associated with the active phase of NMS. Currently, the definitive role of GABA deficiency in NMS is yet to be established. Differential diagnosis should include malignant hyperthermia, lethal catatonia, lithium toxicity, serotonin syndrome, and heat stroke. A high degree of suspicion and the discontinuation of antipsychotic agents even if the diagnosis is not established are essential for the safety of the patient. Treatment of NMS should be individualized and be based empirically on the character, duration, and severity of the clinical signs and symptoms noted. The initial step in the treatment of NMS is the removal of the offending agent. Full-blown NMS is a serious condition and requires immediate supportive, nutritive, and electrolyte therapies. The administration of drugs that can improve NMS, such as IV dantrolene and/or oral bromocriptine, may also be taken into consideration, based on the severity and nature of the NMS.

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Section: Pathophysiologymentioning

confidence: 99%

Neuroleptic malignant syndrome: risk factors, pathophysiology, and treatment

Ananth

Aduri

Parameswaran

et al. 2004

Acta Neuropsychiatr.

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“…At that time he was receiving regular sulpiride and carbamaze pine, and an occasional dose of haloperidol. All three drugs have been implicated in NMS (Addonizio et a!, 1986;Goldwasser et a!, 1989;Peet & Collier, 1990). However, Shalev & Munitz (1986) felt that 90% of NMS cases arose within 10 days of starting the offending drug.…”

Section: Discussionmentioning

confidence: 99%

Neuroleptic Malignant Syndrome in a Case of Acute Post-traumatic Psychosis

Watts

1991

Br J Psychiatry

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“…Levenson (1985) proposed elevation of CK as one of three major criteria for the diagnosis of NMS; pyrexia and muscular rigidity comprising the other two criteria. Addonozio et al (1986) included elevation of CK as one of nine criteria, while Goldwasser et al (1989) supported the idea that elevation of CK is a major sign of NMS and proposed that CK levels be used to monitor the condition. Others have warned against the over-interpretation of CK values.…”

Section: Introductionmentioning

confidence: 99%

The role of creatine kinase in the diagnosis of Neuroleptic Malignant Syndrome

O’Dwyer

Sheppard

1993

Psychol. Med.

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SynopsisElevation of serum creatine kinase (CK) concentrations occurs almost invariably in neuroleptic malignant syndrome (NMS). However, the role of CK levels in the diagnosis of the syndrome remains controversial. This study measured CK levels in patients who became pyrexial while on psychotropic medication and thereby mimicked some of the features of NMS. In all of these cases a diagnosis of infectious illness was made and patients responded to appropriate antibiotic therapy without alteration in psychotropic medication. Two other groups were studied for comparison – patients on psychotropics who were apyrexial and patients who became pyrexial but were not on psychotropics. Significant, unexpected elevations of CK were documented in 70% of those patients who became pyrexial while on psychotropics – in three cases elevation of concentrations to more than 1000 IU/1 (ten times reference value) were found. Thirty per cent of patients who became pyrexial but were not on psychotropics also developed elevation of CK but this was of a much smaller magnitude (lt; 200 IU/1 in five out of six cases). The results of the study suggest that elevation of CK is a non-specific finding, particularly in patients who become pyrexial on psychotropics. Use of CK as a diagnostic criterion may lead to overdiagnosis of NMS.

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Concomitant Treatment of Neuroleptic Malignant Syndrome and Psychosis

Cited by 24 publications

References 9 publications

Neuroleptic malignant syndrome: risk factors, pathophysiology, and treatment

Neuroleptic malignant syndrome: risk factors, pathophysiology, and treatment

Neuroleptic Malignant Syndrome in a Case of Acute Post-traumatic Psychosis

The role of creatine kinase in the diagnosis of Neuroleptic Malignant Syndrome

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