Neurological Symptoms in Pharmagotherapy of Psychoses

Faurbye, Arild; Rasch, P. J.; Petersen, P; Brandborg, G.; Pakkenberg, H.

doi:10.1111/j.1600-0447.1964.tb05731.x

Cited by 252 publications

(61 citation statements)

References 16 publications

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“…gestörte Bewegung bedeutet. Spätdyskinesien wurden ursprünglich von Sigwald et al als "dyskinesie facio-bucco-linguo-masticatice" beschrieben [3], der Terminus "tardive dyskinesia" findet sich zum ersten Mal bei Faurbye et al [4].…”

Section: Definitionunclassified

Antipsychotikainduzierte tardive Syndrome

Fleischhacker

Hofer

Jagsch³

et al. 2016

Neuropsychiatr

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Section: Definitionunclassified

Antipsychotikainduzierte tardive Syndrome

Fleischhacker

Hofer

Jagsch³

et al. 2016

Neuropsychiatr

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“…Dance-like, writhing movements of the truncal and appendicular muscles could also occur [4][5][6]. The term 'tardive dyskinesia' was coined by Faurbye et al [7] in 1964 in recognition of the delayed onset of these symptoms following long-term exposure to antipsychotic medications. The cumulative incidence of TD has been shown to be 5% after one year, 27% after 5 years, 43% after 10 years, and 52% after 15 years of typical antipsychotic exposure [8].…”

Section: Tardive Dyskinesia and Drd3 Polymorphism: 'Typical' And 'Atymentioning

confidence: 99%

Ethical and Policy Considerations in the Application of Pharmacogenomic Testing for Tardive Dyskinesia: Case Study of the Dopamine D3 Receptor

Shamy¹,

Zai²,

Basile³

et al. 2011

CPPM

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Tardive dyskinesia (TD) is a serious adverse effect often associated with the first generation antipsychotic medications used in the management of mental health disorders such as schizophrenia. Pharmacogenomics is the study of human genomic variation in relation to individual and population variability in medication response and side effects. Neuropsychiatry is one of the clinical domains in which pharmacogenomic approaches have been extensively studied. In the late 1990s, the Glycine9 (Gly9) allele of the Serine-9-Glycine (Ser9Gly) polymorphism in dopamine D3 receptor gene (DRD3) was found to be associated with both a liability to, and worsened severity of, TD in schizophrenic patients treated with typical antipsychotics. This initial discovery has been subsequently replicated and testing for the Ser9Gly polymorphism has now become commercially available. The question that currently presents itself is whether its use should be encouraged for patients who may be prescribed a typical or atypical antipsychotic medication. However, the translation of this new technology to clinical practice presents multiple social, ethical and policy challenges. Though pharmacogenomic testing holds much promise in this scenario, many important questions remain to be answered before its widespread use can be medically and ethically justified. This article highlights the key advances in our understanding of the role of human genetic variation in the D3 receptor in relation to TD. Then, issues of uncertainty, consent, confidentiality, and access are considered with respect to the use of DRD3 polymorphism testing in risk stratification for susceptibility to tardive dyskinesia. We propose three recommendations that may help bring this technology into the clinic: 1) prospective pharmacogenomic studies of DRD3 polymorphism and TD risk should be conducted; 2) the design of such studies should be influenced by scientists, ethicists and policy makers to protect potentially vulnerable patients; and 3) appropriate knowledge transfer to front-line health care workers must take place.

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“…The term tardive dyskinesia was coined in 1964 by Faurbye et al 3 in an article that described patients who had developed chronic involuntary movements several months after starting antipsychotic treatment. In the following decades, the link between antipsychotics and TD became widely accepted, with attempts to find effective treatments for TD beginning in the early 1970s.…”

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confidence: 99%

Revisiting the Abnormal Involuntary Movement Scale

Kane

Correll

Nierenberg

et al. 2018

J. Clin. Psychiatry

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Objective: To provide an historic overview of the Abnormal Involuntary Movement Scale (AIMS) in clinical trials of tardive dyskinesia (TD), with current recommendations for analyzing and interpreting AIMS data. Participants: Seven psychiatrists and 1 neurologist were selected by the workshop sponsor based on each individual's clinical expertise and research experience. Evidence: Using PubMed entries from January 1970 to August 2017, participants selected studies that used the AIMS to evaluate TD treatments. The selections were intended to be representative rather than prescriptive or exhaustive, and no specific recommendations for TD treatment are implied. Consensus Process: The Working Group met in October 2016 to discuss the AIMS as an assessment tool, outline the challenges of translating clinical trial results into everyday clinical practice, and propose different methods for reporting AIMS data in clinically relevant terms. Recommendations for selecting TD studies for review, analyzing and interpreting AIMS data, and synthesizing discussions among the participants were initiated during the onsite workshop and continued remotely throughout development of this report. Disagreements were resolved via group e-mails and teleconferences. Consensus was based on final approval of this report by all workshop participants. Conclusions: For both research and clinical practice, the AIMS is a valid measure for assessing TD and the effects of treatment, but alternative analyses of AIMS data (eg, effect size, minimal clinically important difference, response analyses, category shifts) may provide broader evidence of clinical effectiveness. No single analysis of AIMS data can be considered the standard of clinical efficacy; multiple analytic approaches are recommended. J Clin Psychiatry 2018;79(3) T ardive dyskinesia (TD) is a chronic disorder characterized by involuntary stereotyped, choreic, athetoid, and/or dystonic movements in 1 or more areas of the body, including the orofacial region (eg, tongue thrusting, lip smacking and/or pursing, grimacing), extremities (eg, stereotypic piano-playing movements, flexion/extension of the ankles or toes), and torso (eg, choreoathetoid movements, pelvic rocking).:1,2 This disorder can result from exposure to dopamine receptor blocking agents (DRBAs) such as antipsychotics and drugs used to treat gastrointestinal disorders (eg, metoclopramide). 2 Given the difficulty in treating TD, prevention, close monitoring, and earliest possible diagnosis are critical in optimizing patient outcomes.The term tardive dyskinesia was coined in 1964 by Faurbye et al 3 in an article that described patients who had developed chronic involuntary movements several months after starting antipsychotic treatment. In the following decades, the link between antipsychotics and TD became widely accepted, with attempts to find effective treatments for TD beginning in the early 1970s. 4 With development of the newer secondgeneration (atypical) antipsychotics, it was hoped that the risk for medication-in...

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Neurological Symptoms in Pharmagotherapy of Psychoses

Cited by 252 publications

References 16 publications

Antipsychotikainduzierte tardive Syndrome

Antipsychotikainduzierte tardive Syndrome

Ethical and Policy Considerations in the Application of Pharmacogenomic Testing for Tardive Dyskinesia: Case Study of the Dopamine D3 Receptor

Revisiting the Abnormal Involuntary Movement Scale

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