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Michael Camilleri - One of the best experts on this subject based on the ideXlab platform.
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review article metoclopramide and Tardive Dyskinesia
Alimentary Pharmacology & Therapeutics, 2010Co-Authors: Archana Rao, Michael CamilleriAbstract:Summary Background Metoclopramide is a dopamine receptor antagonist which has been used for treatment of a variety of gastrointestinal symptoms over the last thirty years. In 2009, the FDA issued a black box warning regarding long-term or high-dose use of this medication because of the risk of developing Tardive Dyskinesia. Aims To review the mechanism of action and pharmacokinetic properties of metoclopramide, the risk of metoclopramide-induced Tardive Dyskinesia, potential mechanisms that may alter and to summarize the clinical context for appropriate use of the drug. Methods We conducted a PubMed search using the following key words and combined searches: metoclopramide, neuroleptics, Tardive Dyskinesia, incidence, prevalence, dopamine, receptors, pharmacokinetic, pharmacology, pharmacogenetics, DRD3 Ser9Gly polymorphism, cytochrome P450, p-glycoprotein, risk factors, gastroparesis, outcome, natural history. Results Available data show that risk of Tardive Dyskinesia from metoclopramide use is likely to be <1%, much less than the estimated 1–10% risk previously suggested in national guidelines. Tardive Dyskinesia may represent an idiosyncratic response to metoclopramide; pharmacogenetics affect pharmacokinetic and dopamine receptor pharmacodynamics in response to neuroleptic agents that cause similar neurological complications. Conclusion Community prevalence and pharmacogenetic mechanisms involved in metoclopramide-induced Tardive Dyskinesia require further study to define the benefit-risk ratio more clearly.
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Review article: metoclopramide and Tardive Dyskinesia.
Alimentary pharmacology & therapeutics, 2010Co-Authors: Archana Rao, Michael CamilleriAbstract:Summary Background Metoclopramide is a dopamine receptor antagonist which has been used for treatment of a variety of gastrointestinal symptoms over the last thirty years. In 2009, the FDA issued a black box warning regarding long-term or high-dose use of this medication because of the risk of developing Tardive Dyskinesia. Aims To review the mechanism of action and pharmacokinetic properties of metoclopramide, the risk of metoclopramide-induced Tardive Dyskinesia, potential mechanisms that may alter and to summarize the clinical context for appropriate use of the drug. Methods We conducted a PubMed search using the following key words and combined searches: metoclopramide, neuroleptics, Tardive Dyskinesia, incidence, prevalence, dopamine, receptors, pharmacokinetic, pharmacology, pharmacogenetics, DRD3 Ser9Gly polymorphism, cytochrome P450, p-glycoprotein, risk factors, gastroparesis, outcome, natural history. Results Available data show that risk of Tardive Dyskinesia from metoclopramide use is likely to be
John M. Kane - One of the best experts on this subject based on the ideXlab platform.
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Tardive Dyskinesia rates with atypical antipsychotics in adults prevalence and incidence
The Journal of Clinical Psychiatry, 2004Co-Authors: John M. KaneAbstract:Both conventional and atypical antipsychotics cause an up-regulation of dopamine-2 receptors and have been associated with Tardive Dyskinesia. Studies of adult and elderly subjects have shown a greater incidence of Tardive Dyskinesia among patients who were administered conventional antipsychotic drugs than those given atypical antipsychotic drugs. This article will review studies of the prevalence and incidence of Tardive Dyskinesia in patients taking antipsychotic agents.
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Tardive Dyskinesia and impaired glucose tolerance.
Human Psychopharmacology: Clinical and Experimental, 2002Co-Authors: Siow Ann Chong, Mythily, Alvin Lum, Chan Yiong Huak, John M. KaneAbstract:The authors examined the role of impaired glucose metabolism in the pathophysiology of Tardive Dyskinesia in schizophrenic patients with and without persistent TD. Glucose tolerance and insulin levels were determined in 86 patients with persistent Tardive Dyskinesia and in 108 patients without Tardive Dyskinesia. Dyskinesias were assessed by the abnormal involuntary movement scale (AIMS) and extrapyramidal symptoms by the Simpson—Angus rating scale (SARS). Fasting blood glucose levels were significantly lower while the first and second hour glucose levels did not reveal any differences in patients with Tardive Dyskinesia compared with those without Tardive Dyskinesia. Insulin levels did not differ in these two groups. Our cross-sectional epidemiological study does not suggest hyperglycemia to be a risk factor for Tardive Dyskinesia. However, prospective long-term studies with multiple assessment points are needed to clarify the role of glucose metabolism in the development of Tardive Dyskinesia. Copyright © 2002 John Wiley & Sons, Ltd.
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Does clozapine cause Tardive Dyskinesia
The Journal of clinical psychiatry, 1993Co-Authors: John M. Kane, Margaret G. Woerner, Simcha Pollack, Allan Z. Safferman, J.a. LiebermanAbstract:BACKGROUND The authors attempted to determine if chronic exposure to clozapine can cause Tardive Dyskinesia. METHOD Twenty-eight schizophrenic or schizoaffective patients with no prior history of definite Tardive Dyskinesia were treated with clozapine for at least 1 year, and their ongoing modified Simpson Dyskinesia Scale ratings were analyzed. These data were then compared with those of another group of similarly diagnosed patients who were treated with a conventional neuroleptic for at least 1 year. RESULTS Two patients in the clozapine-treated group (both of whom had ratings of questionable Tardive Dyskinesia at baseline) were later rated by the modified Simpson Dyskinesia Scale as having mild Tardive Dyskinesia on at least two consecutive ratings 3 months apart. Although there was uncertainty about whether clozapine definitely caused the Tardive Dyskinesia in those two patients, a survival analysis comparing the clozapine-treated group with the neuroleptic-treated group showed a lower risk of Tardive Dyskinesia developing in the clozapine-treated group. CONCLUSION This study was unable to definitively conclude whether clozapine causes Tardive Dyskinesia. However, if cases do develop, the risk of Tardive Dyskinesia is likely to be less with clozapine than with typical neuroleptics.
Ericka L. Breden - One of the best experts on this subject based on the ideXlab platform.
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Tetrabenazine for the Treatment of Tardive Dyskinesia
The Annals of pharmacotherapy, 2011Co-Authors: Jonathan G. Leung, Ericka L. BredenAbstract:Objective:To evaluate the safety and effectiveness of tetrabenazine for the treatment of Tardive Dyskinesia.Data Sources:Literature was accessed through MEDLINE (1966-September 2010) and The Cochrane Library using the terms tetrabenazine, Tardive Dyskinesia, and movement disorders. In addition, references from publications identified were reviewed.Study Selection and Data Extraction:All English-language articles identified from the data sources were reviewed.Data Synthesis:Options available for the management of Tardive Dyskinesia are limited. Tetrabenazine is a central monoamine-depleting agent approved by the Food and Drug Administration (or chorea associated with Huntington's disease. Three prospective studies of tetrabenazine in the treatment of Tardive Dyskinesia were identified, as well as 8 additional trials, 1 case series, and 8 case reports. Tetrabenazine may provide benefit in managing symptoms of Tardive Dyskinesia unresponsive to other treatment modalities. Treatment of Tardive Dyskinesia with...
Alexander B. Niculescu - One of the best experts on this subject based on the ideXlab platform.
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Oxidative Mechanisms and Tardive Dyskinesia
CNS Drugs, 2003Co-Authors: James B. Lohr, Ronald Kuczenski, Alexander B. NiculescuAbstract:Tardive Dyskinesia has been and continues to be a significant problem associated with long-term antipsychotic use, but its pathophysiology remains unclear. In the last 10 years, preclinical studies of the administration of antipsychotics to animals, as well as clinical studies of oxidative processes in patients given anti-psychotic medications, with and without Tardive Dyskinesia, have continued to support the possibility that neurotoxic free radical production may be an important consequence of antipsychotic treatment, and that such production may relate to the development of dyskinetic phenomena. In line with this hypothesis, evidence has accumulated for the efficacy of antioxidants, primarily vitamin E (α-tocopherol), in the treatment and prevention of Tardive Dyskinesia. Early studies suggested a modest effect of vitamin E treatment on existing Tardive Dyskinesia, but later studies did not demonstrate a significant effect. Because evidence has continued to accumulate for increased oxidative damage from antipsychotic medications, but less so for the effectiveness of vitamin E, especially in cases of long-standing Tardive Dyskinesia, alternative antioxidant approaches to the condition may be warranted. These approaches may include the use of antioxidants as a preventive measure for Tardive Dyskinesia or the use of other antioxidants or neuroprotective drugs, such as melatonin, for established Tardive Dyskinesia.
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Oxidative mechanisms and Tardive Dyskinesia.
CNS Drugs, 2003Co-Authors: James B. Lohr, Ronald Kuczenski, Alexander B. NiculescuAbstract:Tardive Dyskinesia has been and continues to be a significant problem associated with long-term antipsychotic use, but its pathophysiology remains unclear. In the last 10 years, preclinical studies of the administration of antipsychotics to animals, as well as clinical studies of oxidative processes in patients given antipsychotic medications, with and without Tardive Dyskinesia, have continued to support the possibility that neurotoxic free radical production may be an important consequence of antipsychotic treatment, and that such production may relate to the development of dyskinetic phenomena. In line with this hypothesis, evidence has accumulated for the efficacy of antioxidants, primarily vitamin E (alpha-tocopherol), in the treatment and prevention of Tardive Dyskinesia. Early studies suggested a modest effect of vitamin E treatment on existing Tardive Dyskinesia, but later studies did not demonstrate a significant effect. Because evidence has continued to accumulate for increased oxidative damage from antipsychotic medications, but less so for the effectiveness of vitamin E, especially in cases of long-standing Tardive Dyskinesia, alternative antioxidant approaches to the condition may be warranted. These approaches may include the use of antioxidants as a preventive measure for Tardive Dyskinesia or the use of other antioxidants or neuroprotective drugs, such as melatonin, for established Tardive Dyskinesia.
P S Gopinath - One of the best experts on this subject based on the ideXlab platform.
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Risperidone induced Tardive Dyskinesia - a case report.
Indian journal of psychiatry, 2002Co-Authors: O V Vasudevan, Denzil Pinto, P S GopinathAbstract:Risperidone is a serotonin - dopamine antagonist which has got less propensity to cause Tardive Dyskinesia than conventional antipsychotics. There have been few reports of Tardive Dyskinesia induced by risperidone. This is a report of a case of risperidone induced Tardive Dyskinesia. A 56 year old female with a 6 months history of paranoid schizophrenia, developed bucco-oro-masticatory abnormal involuntary movements after receiving risperidone 8 mg/day for about 1 year. She had some of the risk factors for the development of Tardive Dyskinesia like age, sex, anti-chotinergic drugs and earlier emergence of neuroleptic-induced parkinsonism. Clinicians must be aware of the possibility of the patients developing Tardive Dyskinesia when they are given the supposedly safe neuroleptic risperidone.
