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Neuroleptic Malignant Syndrome (neuroleptic + malignant_syndrome)
Selected AbstractsOlanzapine associated weight gain, Hyperglycemia and Neuroleptic Malignant Syndrome: case reportINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 4 2002Rhonda Malyuk Abstract We describe here a case of olanzapine associated weight gain, hyperglycemia and neuroleptic malignant syndrome in a 64 year-old woman with a significant medical history. Eighteen weeks after initiating olanzapine, Mrs X lost glycemic control, exhibited signs and symptoms consistent with neuroleptic malignant syndrome and gained 8.9 kg. We suggest that utilization of olanzapine in the less medically stable geriatric patient be implemented with vigilant monitoring for such complications mentioned above. Copyright © 2002 John Wiley & Sons, Ltd. [source] Neuroleptic malignant syndrome during olanzapine and levomepromazine treatmentACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2000K. Järventausta Objective: To date only five reports of neuroleptic malignant syndrome (NMS) related to olanzapine exist. The first case report was published in November 1998. Method: We report the case of a 78-year-old woman suffering from chronic schizophrenia who developed a NMS while being treated with olanzapine and levomepromazine. Before this her medication had been unchanged for more than 2 years. Results: When treated with olanzapine and levomepromazine, the patient had a fulminant NMS which was complicated with pneumonia. When the neuroleptic drug treatment was discontinued, the patient recovered. However, when this combination was restarted later due to severe agitation and hallucinations, the symptoms of NMS reappeared. Conclusion: This case report shows that the neuroleptic malignant syndrome can occur during olanzapine treatment as well as during treatment with conventional neuroleptics. This syndrome may develop even after a long and stable neuroleptic treatment. [source] Neurological complications of psychiatric drugs: clinical features and management,HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue S1 2008Peter M. Haddad Abstract This paper reviews the main neurological complications of psychiatric drugs, in particular antipsychotics and antidepressants. Extrapyramidal syndromes include acute dystonia, parkinsonism, akathisia, tardive dyskinesia and tardive dystonia. Extrapyramidal symptoms (EPS) are less frequent with atypical than with conventional antipsychotics but remain common in clinical practice partly due to lack of screening by health professionals. Neuroleptic malignant syndrome (NMS) consists of severe muscle rigidity, pyrexia, change in conscious level and autonomic disturbance but partial forms also occur. NMS is particularly associated with the initiation and rapid increase in dose of high-potency antipsychotics but it has been reported with all the atypical antipsychotics and rarely with other drugs including antidepressants. Serotonin toxicity comprises altered mental state (agitation, excitement, confusion), neuromuscular hyperactivity (tremor, clonus, myoclonus, hyper-reflexia) and autonomic hyperactivity and occurs on a spectrum. Severe cases, termed serotonin syndrome, usually follow the co-prescription of drugs that increase serotonergic transmission by different pathways, for example a monoamine oxidase inhibitor (MAOI) and a selective serotonin reuptake inhibitor (SSRI). Most antipsychotics and antidepressants lower the seizure threshold and can cause seizures; the risk is greater with clozapine than with other atypical antipsychotics and greater with tricyclic antidepressants (TCAs) than with SSRIs. In randomised controlled trials in elderly patients with dementia atypical antipsychotics are associated with a higher risk of stroke and death than placebo. Cohort studies suggest that conventional drugs carry at least the same risk. Cessation of treatment with antipsychotics and antidepressants can lead to a wide range of discontinuation symptoms which include movement disorders and other neurological symptoms. Clinicians need to be familiar with strategies to reduce the risk of these adverse events and to manage them when they arise. Their occurrence needs to be balanced against the benefits of psychiatric drugs in terms of efficacy and improved quality of life in a range of disorders. Copyright © 2007 John Wiley & Sons, Ltd. [source] Neuroleptic malignant syndrome with severe liver failureACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2003S. H. Urving A schizophrenic patient on long-time neuroleptic medication was admitted with ileus. Secondarily, a high fever, rigidity, mental confusion, tachycardia and hypotension developed. After bromocriptine was given, the temperature dropped by 2°C and the patient improved markedly. A diagnosis of neuroleptic malignant syndrome was made. Five years later she was re-admitted with similar symptoms and also severe liver failure. Meanwhile the discontinued neuroleptic medication had been reinstituted. Again bromocriptine reduced the temperature of approximately 2°C, and was paralleled by a normalization of liver function. To our knowledge this is the second report on severe liver failure in conjunction with neuroleptic malignant syndrome. The efficacy of bromocriptine in the treatment of this syndrome is underlined. [source] Neuroleptic malignant syndrome and its controversies,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 5 2010Branimir Margeti Abstract Purpose Neuroleptic malignant syndrome (NMS) is a rare and life threatening condition usually defined as a complication of treatment with antipsychotics characterized by severe rigidity, tremor, fever, altered mental status, autonomic dysfunction, and elevated serum creatine phosphokinase and white blood cell count. The literature on this topic is rather extensive, but many aspects related to the syndrome are thought to be controversial. The aim of this paper, written with the clinician in mind, is to summarize some of the most prominent controversies that may have importance in usual clinical practice. Methods The literature was searched for reviews, reports on the series of cases, individual case reports of NMS, and other clinically and theoretically important information. Results There are controversies associated with virtually all important aspects of NMS. At the moment, it is not clear if this drug reaction is idiosyncratic or not, what diagnostic criteria are the most appropriate for usual clinical practice, and it seems that the estimated incidence is not in accordance with the number of treated patients. There are rather different approaches to the pathophysiological mechanisms, differential diagnosis, and treatment. Conclusions Some of the controversies related to NMS have an influence on our understanding of the condition and may have importance in clinical practice. There is a need for further research that should elucidate these controversies. Copyright © 2010 John Wiley & Sons, Ltd. [source] CYP2D6 gene deletion allele in patients with neuroleptic malignant syndrome: Preliminary reportPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2005DAIJI KATO md Abstract, Neuroleptic malignant syndrome (NMS) is a potentially fatal adverse reaction to psychopharmacologic treatment. Reported herein are two NMS patients with schizophrenia who were found to possess a CYP2D6 gene deletion allele (CYP2D6*5). The deletion results in decreased CYP2D6 activity, possibly leading to drug accumulation. Both patients with NMS had been treated with neuroleptics, including CYP2D6 substrates. Polymerase chain reaction (PCR) followed by restriction fragment length polymorphism analyses and long PCR were performed to detect CYP2D6 genotype. One patient was found to possess *5/*10; the other had a *1/*5 genotype. The present preliminary report suggests that pharmacokinetic factors cannot be excluded and the CYP2D6 polymorphism is possibly associated with the etiology of NMS. [source] Neuroleptic malignant syndrome during olanzapine and levomepromazine treatmentACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2000K. Järventausta Objective: To date only five reports of neuroleptic malignant syndrome (NMS) related to olanzapine exist. The first case report was published in November 1998. Method: We report the case of a 78-year-old woman suffering from chronic schizophrenia who developed a NMS while being treated with olanzapine and levomepromazine. Before this her medication had been unchanged for more than 2 years. Results: When treated with olanzapine and levomepromazine, the patient had a fulminant NMS which was complicated with pneumonia. When the neuroleptic drug treatment was discontinued, the patient recovered. However, when this combination was restarted later due to severe agitation and hallucinations, the symptoms of NMS reappeared. Conclusion: This case report shows that the neuroleptic malignant syndrome can occur during olanzapine treatment as well as during treatment with conventional neuroleptics. This syndrome may develop even after a long and stable neuroleptic treatment. [source] Olanzapine associated weight gain, Hyperglycemia and Neuroleptic Malignant Syndrome: case reportINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 4 2002Rhonda Malyuk Abstract We describe here a case of olanzapine associated weight gain, hyperglycemia and neuroleptic malignant syndrome in a 64 year-old woman with a significant medical history. Eighteen weeks after initiating olanzapine, Mrs X lost glycemic control, exhibited signs and symptoms consistent with neuroleptic malignant syndrome and gained 8.9 kg. We suggest that utilization of olanzapine in the less medically stable geriatric patient be implemented with vigilant monitoring for such complications mentioned above. Copyright © 2002 John Wiley & Sons, Ltd. [source] Neuroleptic malignant syndrome with severe liver failureACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2003S. H. Urving A schizophrenic patient on long-time neuroleptic medication was admitted with ileus. Secondarily, a high fever, rigidity, mental confusion, tachycardia and hypotension developed. After bromocriptine was given, the temperature dropped by 2°C and the patient improved markedly. A diagnosis of neuroleptic malignant syndrome was made. Five years later she was re-admitted with similar symptoms and also severe liver failure. Meanwhile the discontinued neuroleptic medication had been reinstituted. Again bromocriptine reduced the temperature of approximately 2°C, and was paralleled by a normalization of liver function. To our knowledge this is the second report on severe liver failure in conjunction with neuroleptic malignant syndrome. The efficacy of bromocriptine in the treatment of this syndrome is underlined. [source] Contemporary encephalitis lethargica presenting with agitated catatonia, stereotypy, and dystonia-parkinsonismMOVEMENT DISORDERS, Issue 15 2007Russell C. Dale PhD Abstract Encephalitis lethargica (EL) syndrome was classically described by Von Economo and has somnolent-ophthalmoplegic, hyperkinetic, and amyostatic-akinetic forms. We describe 2 recent cases of EL characterized by an acute encephalitis with mixed movement disorders (dystonia-Parkinsonism plus stereotypy) and psychiatric disorders (agitated catatonia, coprolalia, and echo phenomena). Both patients suffered concurrent hyperkinetic and Parkinsonian features resulting in therapeutic challenges. Bradykinetic features responded to dopamine replacement therapy and both patients also had adverse affects to dopamine antagonists (oculogyric crises plus neuroleptic malignant syndrome). Investigation was unremarkable other than the presence of CSF lymphocytosis and oligoclonal bands. Despite prolonged in-patient stays and intensive care management, both patients have made complete recoveries. We believe these cases support the hypothesis that this syndrome is an inflammatory encephalitis that specifically effects dopamine neurotransmission. © 2007 Movement Disorder Society [source] Epidemiology of tardive dyskinesia: Is risk declining with modern antipsychotics?MOVEMENT DISORDERS, Issue 5 2006Daniel Tarsy MD Abstract Second-generation antipsychotic drugs (APDs), including aripiprazole, clozapine, olanzapine, risperidone, quetiapine, and ziprasidone dominate outpatient and inpatient clinical practice, having largely displaced the older neuroleptics. Modern APDs have relatively low risk for acute extrapyramidal syndromes characteristic of older neuroleptics, particularly acute dystonia and Parkinsonism, with variable risks of akathisia and the rare neuroleptic malignant syndrome. Anticipated reduction in risk of tardive dyskinesia (TD) is less well documented. Nearly 50 years after initial reports on TD, it is appropriate to reexamine the epidemiology of this potentially severe late adverse effect of long-term APD treatment in light of current research and practice. We compared recent estimates of incidence and prevalence of TD identified with some modern APDs to the epidemiology of TD in the earlier neuroleptic era. Such comparisons are confounded by complex modern APD regimens, uncommon exposure limited to a single modern APD, effects of previous exposure to typical neuroleptics, and neurological assessments that are rarely prospective or systematic. Available evidence suggests that the risk of TD may be declining, but longitudinal studies of patients never treated with traditional neuroleptics and exposed to only a single modern APD are required to quantify TD risks with specific drugs. Long-term use of APDs should continue to be based on research-supported indications, with regular specific examination for emerging TD. © 2006 Movement Disorder Society [source] CYP2D6 gene deletion allele in patients with neuroleptic malignant syndrome: Preliminary reportPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2005DAIJI KATO md Abstract, Neuroleptic malignant syndrome (NMS) is a potentially fatal adverse reaction to psychopharmacologic treatment. Reported herein are two NMS patients with schizophrenia who were found to possess a CYP2D6 gene deletion allele (CYP2D6*5). The deletion results in decreased CYP2D6 activity, possibly leading to drug accumulation. Both patients with NMS had been treated with neuroleptics, including CYP2D6 substrates. Polymerase chain reaction (PCR) followed by restriction fragment length polymorphism analyses and long PCR were performed to detect CYP2D6 genotype. One patient was found to possess *5/*10; the other had a *1/*5 genotype. The present preliminary report suggests that pharmacokinetic factors cannot be excluded and the CYP2D6 polymorphism is possibly associated with the etiology of NMS. [source] Genotype A1/A2 associated with neuroleptic malignant syndromeBIPOLAR DISORDERS, Issue 4 2005M Del Tacca [source] Effects of chlorpromazine on excitation,contraction coupling events in fast-twitch skeletal muscle fibres of the ratBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2004R Wagner Single mechanically skinned fibres from the rat extensor digitorum longus muscle, which allow access to intracellular compartments, were used to examine the effects of 0.5,100 ,M chlorpromazine hydrochloride (CPZ) on the major steps of the excitation,contraction (E,C) coupling to elucidate the involvement of skeletal muscle in the neuroleptic malignant syndrome (NMS). At 1 ,M, CPZ caused a 20,30% increase in the force response induced by t-system depolarisation and a marked increase in the rate of caffeine-induced SR Ca2+ release. At [CPZ]2.5 ,M, there was an initial increase followed by a marked decrease of the t-system depolarisation-induced force responses, while the potentiating effect on the caffeine-induced SR Ca2+ release remained. These effects were reversible. CPZ had no effect on the maximum Ca2+ -activated force, but caused reversible, concentration-dependent increases in the Ca2+ sensitivity of the contractile apparatus at [CPZ] 10 ,M, with a 50% predicted shift of 0.11 pCa (,log [Ca2+]) units at 82.3 ,M CPZ. CPZ did not alter the rate of SR-Ca2+ loading at 1 and 10 ,M, but reversibly reduced it by ,40% at 100 ,M by reducing the SR Ca2+ pump. Nevertheless, the SR Ca2+ content was greater when fibres became unresponsive to t-system-induced depolarisation in the presence than in the absence of 100 ,M CPZ. The results show that CPZ has concentration-dependent stimulatory and inhibitory effects on various steps of the E,C coupling, which can explain the involvement of skeletal muscle in NMS and reconcile previous divergent data on CPZ effects on muscle. British Journal of Pharmacology (2004) 141, 624,633. doi:10.1038/sj.bjp.0705655 [source] | ||||||||||||||||||||||