DOCSLIB.ORG

Tardive Dyskinesia: Minimizing Risk and Improving Outcomes in Schizophrenia and Other Disorders

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Tardive Dyskinesia: Minimizing Risk and Improving Outcomes in Schizophrenia and Other Disorders DECISION MAKER FORUM IN MANAGED CARE DECEMBER 2007 FACULTY Leslie Citrome, MD, MPH Tardive Dyskinesia: Director, Clinical Research and Evaluation Facility Minimizing Risk and Nathan S. Kline Institute for Psychiatric Research Orangeburg, New York Improving Outcomes in Professor of Psychiatry New York University Schizophrenia and Robert Dufresne, PhD, PhD, BCPS, BCPP Other Disorders Professor of Pharmacy Leslie Citrome, MD, MPH; Robert Dufresne, PhD, PhD, BCPS, BCPP; University of Rhode Island College and Judy M. Dyrud of Pharmacy Kingston, Rhode Island THE USE OF ANTIPSYCHOTIC AGENTS FOR PSYCHIATRIC DISORDERS In the United States, antipsychotic drugs are the cornerstone of treatment for schizo- This supplement to The American phrenia,1 for which about 2 million patients are treated annually.2 In addition, antipsychot- Journal of Managed Care is sponsored ic agents are widely used in the treatment of schizoaffective disorders and mood disorders by Eli Lilly and Company. with psychotic features. They are also sometimes prescribed for diagnoses that do not include a psychotic component.3 According to the US Department of Health and Human DISCLOSURES Services, 11 million antipsychotic prescriptions were paid by Medicaid in 1998, 51% of The faculty report the following which were for atypical antipsychotics.4 commercial disclosures: Psychosis can have a devastating impact on economic prospects, socialization, and qual- Dr Citrome: ity of life. Unfortunately, long-term treatment with antipsychotics carries the risk of seri- Consultant: Avanir, Bristol-Myers ous adverse effects, including tardive dyskinesia, which can have a substantial negative life Squibb, Eli Lilly, GlaxoSmithKline, impact.5 Because for many patients antipsychotics are the only effective treatment, clinicians Janssen, Jazz, Pfizer, Vanda; who prescribe them must be educated about their risks and guard against serious long-term Grant/research support: AstraZeneca, effects. Adverse effect risk can vary with individual patient vulnerabilities, treatment dura- Barr, Bristol-Myers Squibb, tion, dosage, and drug class (conventional/first-generation antipsychotics [FGAs] or atypi- Eli Lilly, Janssen, Pfizer; cal/second-generation antipsychotics [SGAs]). In schizophrenia, treatment is commonly life- Honoraria: Abbott, AstraZeneca, long; therefore the best treatment uses the antipsychotic agent with the best long-term effi- 6 Avanir, Bristol-Myers Squibb, Eli cacy-to-risk ratio for the individual patient. Lilly, GlaxoSmithKline, Janssen, MOTORIC ADVERSE EFFECTS Jazz, Pfizer, Vanda; Acute motoric adverse effects can begin to appear within the first few hours of antipsychotic Speaker’s bureau: Abbott, treatment. All antipsychotics can cause potentially fatal neuroleptic malignant syndrome, char- AstraZeneca, Eli Lilly, Pfizer. acterized by diffuse muscular rigidity, tremors, fever, labile blood pressure, and cognitive and Dr Dufresne: autonomic disturbances.7 Extrapyramidal symptoms (EPS) may develop in 50% to 60% of Consultant: Bristol-Myers Squibb, patients treated with FGAs.8 Dystonias appear as disturbances of muscle tone, whereas dyski- 9 Eli Lilly, JNJ (Janssen); nesias are disturbances of movement. Honoraria: Bristol-Myers Squibb, Eli Lilly, JNJ; Speaker’s bureau: Acute dystonia, involuntary and sometimes painful muscle contractions in neck, face, 10 10 Bristol-Myers Squibb, Eli Lilly, JNJ. tongue, or back, can usually be relieved with anticholinergic agents. 10 PUBLISHING STAFF Akathisia (motor restlessness) frequently manifests as pacing or inability to sit still. Acute akathisia does not always respond to antiparkinsonian drugs.11,12 Drug-induced Contributing Editor akathisia can be mistaken for psychotic agitation, sometimes leading clinicians to increase William H. Doutré, PharmD the antipsychotic dose.13 However, akathisia is best treated by reducing the dose or switch- Managing Editor ing antipsychotics.10,12 Elizabeth Turrin Design Director Drug-induced parkinsonism (tremors, rigidity, shuffling gait, extremely slow movement Michael Molfetto or paralysis)10 can be alleviated with antiparkinsonian agents including anticholinergics.10 Involuntary orofacial movements that seemed associated with neuroleptic treatment were A Supplement to described as early as 1957 and, along with limb and trunk movements described later, were called tardive dyskinesia (TD) in 1964.13 As the name “tardive” implies, TD was considered to be a result of months or years of exposure to antipsychotic drugs.13 Early reports consis- tently emphasized its persistence long after discontinuation of neuroleptics.13 These criteria remain today. OL44132 TARDIVE DYSKINESIA: MINIMIZING RISK AND IMPROVING OUTCOMES IN SCHIZOPHRENIA AND OTHER DISORDERS Training in the assessment of TD abnormal gait.25 It may affect neck elderly. In the Hillside study 23% of has decreased since prescribing prac- muscles first and present as an a subgroup of patients older than 55 tices have come to favor SGAs.14 abnormal head position.9 Some years developed TD within 2.2 years.15 Because many clinicians lack training authors contend that tardive dysto- Another prospective study of elderly in movement disorders and many nia can be mistaken for TD, and that patients found incidence of 59.8% patients do not complain of dyskine- TD identified within a year of after 3 years with FGAs.15 sias, TD may be underdiagnosed.15 antipsychotic initiation is usually tar- Whereas acute dystonia, akathisia, dive dystonia.26 No treatment for and drug-induced parkinsonism may tardive dystonia has been proven The incidence of TD is be transient and reversible with treat- generally effective. Tetrabenazine, higher in the elderly. ment, TD can be persistent.16,17 anticholinergics, clozapine, clon- Persistence is usually defined as sus- azepam, or the combination of cloza- tained TD symptoms >3 months after pine plus clonazepam have been Incidence of TD is also higher in withdrawal of the offending neurolep- helpful in some cases.9,25-28 In 1 mood disorders, sometimes even higher tic,9,18 but in some studies it can mean recent case, antipsychotics were dis- than in schizophrenia.32,33 TD incidence >3 months whether or not antipsy- continued and schizophrenia and may increase in the future as the use of chotic treatment continues.19 In up to severe tardive dystonia were man- antipsychotics increases for affective 50% of affected patients, TD becomes aged successfully with mood stabiliz- disorders and other nonschizophrenic chronic and irreversible.20 ers and benzodiazepines alone.29 indications.15 Akathisia was also noted in several Incidence and prevalence studies of the first reports of TD.13 Unlike that include outpatients may not con- In up to 50% of affected acute akathisia, tardive akathisia can trol for nonadherence. Up to 50% of worsen when the antipsychotic dose is outpatients fail to adhere to medica- patients, TD becomes lowered and can present with emergent tion schedules.2,18 In the context of chronic and irreversible. TD.12 In a study of chronic schizophre- nonadherence, patients may be devel- nia, discontinuation of antipsychotics oping TD with less total exposure to resulted in akathisia and withdrawal antipsychotics than is reported. Some dyskinesias described in the TD in a third of patients.12 When Another way to look at TD is in risk 1960s-1970s first appeared after neu- antipsychotics were restarted, the pa- related to years of neuroleptic expo- roleptic cessation but disappeared sev- tients who had exhibited akathisia at sure. The risk of TD is approximately eral weeks later.10,13 These symptoms, withdrawal persisted in exhibiting TD 5% per year of FGA exposure up to called withdrawal dyskinesia, reflect for up to 6 weeks, suggesting a rela- about 40 years of age.34 After age 40 the action of neuroleptics to suppress tionship between TD and late-onset years, the risk increases.34 In elderly or mask dyskinesia.21,22 akathisia.12 Tardive akathisia may be a patients, the risk in the first year of When TD first appears during preliminary stage of TD in some FGA exposure may be as high as antipsychotic use, withdrawal may ini- patients receiving long-term antipsy- 25%.14 However, the risk per year of tially worsen involuntary move- chotic treatment.12 SGA exposure has not been firmly ments.21,23 Later (sometimes in 1-2 established. A recent systematic review months) TD can remit spontaneously. INCIDENCE AND of current literature suggests annual Thus, withdrawal of antipsychotics, PREVALENCE OF TD TD incidence of about 1% per year when possible, is a primary treatment In an analysis of studies totaling with SGAs versus 5% per year with for TD.23 Dyskinesia that first appears nearly 35000 patients treated with FGAs.35 on withdrawal may be masked again if antipsychotics, the mean corrected antipsychotics are restarted. Then it is prevalence of TD was 18.5%.30 The CHARACTERISTICS AND important to avoid both FGAs, with incidence of TD in young adults is 4% PATHOPHYSIOLOGY OF TD their higher associated incidence of to 5% annually, but the risk increases TD is characterized by movements TD, and concomitant anticholinergic with age and duration of neuroleptic that are involuntary, repetitive, and medications for acute drug-induced treatment.31 purposeless.8 The movements may be movement disorders, with their poten- In the Hillside study, the first long- of 3 possible types: chorea (variable, tial to exacerbate TD.20,23 term prospective study of TD inci- rapid, jerky or fidgety), athetoses Dystonia that persisted 20 months dence,15
Load more

Recommended publications
  • Tardive Dyskinesia
    Tardive Dyskinesia Tardive Dyskinesia Checklist The checklist below can be used to help determine if you or someone you know may have signs associated with tardive dyskinesia and other movement disorders. Movement Description Observed? Rhythmic shaking of hands, jaw, head, or feet Yes Tremor A very rhythmic shaking at 3-6 beats per second usually indicates extrapyramidal symptoms or side effects (EPSE) of parkinsonism, even No if only visible in the tongue, jaw, hands, or legs. Sustained abnormal posture of neck or trunk Yes Dystonia Involuntary extension of the back or rotation of the neck over weeks or months is common in tardive dystonia. No Restless pacing, leg bouncing, or posture shifting Yes Akathisia Repetitive movements accompanied by a strong feeling of restlessness may indicate a medication side effect of akathisia. No Repeated stereotyped movements of the tongue, jaw, or lips Yes Examples include chewing movements, tongue darting, or lip pursing. TD is not rhythmic (i.e., not tremor). These mouth and tongue movements No are the most frequent signs of tardive dyskinesia. Tardive Writhing, twisting, dancing movements Yes Dyskinesia of fingers or toes Repetitive finger and toe movements are common in individuals with No tardive dyskinesia (and may appear to be similar to akathisia). Rocking, jerking, flexing, or thrusting of trunk or hips Yes Stereotyped movements of the trunk, hips, or pelvis may reflect tardive dyskinesia. No There are many kinds of abnormal movements in individuals receiving psychiatric medications and not all are because of drugs. If you answered “yes” to one or more of the items above, an evaluation by a psychiatrist or neurologist skilled in movement disorders may be warranted to determine the type of disorder and best treatment options.
    [Show full text]
  • Tourette's Syndrome
    Tourette’s Syndrome CHRISTOPHER KENNEY, MD; SHENG-HAN KUO, MD; and JOOHI JIMENEZ-SHAHED, MD Baylor College of Medicine, Houston, Texas Tourette’s syndrome is a movement disorder most commonly seen in school-age children. The incidence peaks around preadolescence with one half of cases resolving in early adult- hood. Tourette’s syndrome is the most common cause of tics, which are involuntary or semi- voluntary, sudden, brief, intermittent, repetitive movements (motor tics) or sounds (phonic tics). It is often associated with psychiatric comorbidities, mainly attention-deficit/hyperac- tivity disorder and obsessive-compulsive disorder. Given its diverse presentation, Tourette’s syndrome can mimic many hyperkinetic disorders, making the diagnosis challenging at times. The etiology of this syndrome is thought to be related to basal ganglia dysfunction. Treatment can be behavioral, pharmacologic, or surgical, and is dictated by the most incapacitating symp- toms. Alpha2-adrenergic agonists are the first line of pharmacologic therapy, but dopamine- receptor–blocking drugs are required for multiple, complex tics. Dopamine-receptor–blocking drugs are associated with potential side effects including sedation, weight gain, acute dystonic reactions, and tardive dyskinesia. Appropriate diagnosis and treatment can substantially improve quality of life and psychosocial functioning in affected children. (Am Fam Physician. 2008;77(5):651-658, 659-660. Copyright © 2008 American Academy of Family Physicians.) ▲ Patient information: n 1885, Georges Gilles de la Tourette normal context or in inappropriate situa- A handout on Tourette’s described the major clinical features tions, thus calling attention to the person syndrome, written by the authors of this article, is of the syndrome that now carries his because of their exaggerated, forceful, and provided on p.
    [Show full text]
  • Tourette-Like Syndrome Following Low Dose Short-Term Neuroleptic Treatment Samarthji Lai and Esam Alansari
    LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES Tourette-like Syndrome Following Low Dose Short-term Neuroleptic Treatment Samarthji Lai and Esam AlAnsari ABSTRACT: A Tourette-like syndrome (TLS) may occur after long-term neuroleptic treatment. A review of 11 cases reported in the literature is given. We describe the onset of a TLS in a 13-year old boy with childhood schizophrenia after short term, low-dose treatment with thioridazine. The syndrome resolved 5 months after neuroleptic withdrawal. Subsequent exposure to neuroleptics (mainly perphenazine) induced a recurrence of motor tics and involuntary vocalizations which resolved on drug discontinuation. Awareness that neuroleptics may induce a TLS may lead to prompt recognition and avoidance of labelling the manifestations as symptoms of the underlying psychosis or attention-seeking behaviour. RESUME: Une syndrome analogue a ce de Gilles de la Tourette suivant le traitement prolonge par des neuroleptiques Un syndrome analogue au syndrome de Gilles de la Tourette peut survenir a la suite d'un traitement prolong^ par les neuroleptiques. Nous faisons une revue de 11 cas rapportes dans la litterature et nous decrivons le cas d'un jeune garcon de 13 ans souffrant de schizophrenic de I'enfance ayant presente un tel syndrome apres un traitement a la thioridazine a faible dose sur une courte periode de temps. Le syndrome s'est dissipe, 5 mois apres le retrait du neuroleptique. L'exposition subsequente a des neuroleptiques (surtout a la perphenazine), provoqua une reapparition des tics moteurs et des vocalisations involontaires qui disparurent a I'arret de la the>apie. La connaissance du fait que les neuroleptiques peuvent induire un syndrome analogue au Gilles de la Tourette peut conduire a un diagnostic rapide et eviter que ces manifestations soient etiquettees comme des symptomes de la psychose sous-jacente ou comme un comportement visant a attirer l'attention.
    [Show full text]
  • Clinical Study Clinic-Based Retrospective Analysis of Psychopharmacology for Behavior in Fragile X Syndrome
    Hindawi Publishing Corporation International Journal of Pediatrics Volume 2012, Article ID 843016, 11 pages doi:10.1155/2012/843016 Clinical Study Clinic-Based Retrospective Analysis of Psychopharmacology for Behavior in Fragile X Syndrome Elizabeth Berry-Kravis,1, 2 Allison Sumis,1 Crystal Hervey,1 and Shaguna Mathur1 1 Department of Pediatrics, RUSH University Medical Center, Chicago, IL 60612, USA 2 Departments of Neurology and Biochemistry, RUSH University Medical Center, Chicago, IL 60612, USA Correspondence should be addressed to Elizabeth Berry-Kravis, elizabeth [email protected] Received 12 December 2011; Revised 10 April 2012; Accepted 16 April 2012 Academic Editor: Sheffali Gulati Copyright © 2012 Elizabeth Berry-Kravis et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Fragile X syndrome (FXS) is associated with behavior that limits functioning, including distractibility, hyperactivity, impulsivity, hyperarousal, anxiety, mood dysregulation, and aggression. Medication response and side effect data were reviewed retrospectively for 257 patients (age 14 ± 11 years, range 4–60 years, 203 M, 54 F) attending an FXS clinic. Treatment success rates were defined as the percentage of positive response in the form of documented clinical report of improvement in the behavior(s) being targeted over at least a 6-month period on the medication, without side effects requiring medication discontinuance, while failures were defined as discontinuance of medication due to lack of clinical effectiveness or side effects. Success rate for treatment of targeted behaviors with trials of individual medications was 55% for stimulants, 53% for antidepressants, 62% for alpha2-agonists, and 54% for antipsychotics.
    [Show full text]
  • Current P SYCHIATRY
    CP_1006_Erickson.FinalREV3 9/21/06 8:59 AM Page 80 Current p SYCHIATRY Managing maladaptive behaviors in fragile X patients Psychotropics can improve hyperactivity, anxiety, and aggression Craig A. Erickson, MD Fellow, child and adolescent psychiatry ® Dowden Health Media Kimberly A. Stigler, MD Copyright Assistant professor For personalDavid use J. Posey, only MD Associate professor Christopher J. McDougle, MD Albert E. Sterne Professor and chairman Department of psychiatry Indiana University School of Medicine Christian Sarkine Autism Treatment Center James Whitcomb Riley Hospital for Children Indianapolis sychotropics1,2 are used to manage mal- P adaptive and interfering behaviors in 70% of patients with fragile X syndrome (FXS), the leading cause of hereditary mental retardation. Treatment tends to follow a developmental course: • In children, stimulants and alpha-2 agonists are used for attention-deficit/hyperactivity disorder (ADHD)-like symptoms. • In adolescents and adults, selective sero- tonin reuptake inhibitors (SSRIs) are used for anxiety/repetitive phenomena and second-generation antipsychotics (SGAs) for irritability. © images.com / Veer 80 VOL. 5, NO. 10 / OCTOBER 2006 For mass reproduction, content licensing and permissions contact Dowden Health Media. CP_1006_Erickson.FinalREV2 9/20/06 2:44 PM Page 81 Current p SYCHIATRY This course—which is often effective—is Box based primarily on anecdotal descriptions and on Fragile X syndrome’s genetic rationales borrowed from studies of ADHD, and behavioral features obsessive-compulsive disorder (OCD), and autis- tic disorder/related pervasive developmental dis- The term “fragile X” describes how the 3 orders (PDDs). Disease-modifying agents to tar- X chromosome of affected individuals get the underlying brain dysregulation inherent fractures in a folate-deprived medium.
    [Show full text]
  • Tardive Dyskinesia
    TARDIVE SYNDROMES PHENOMENOLOGY, PATHOPHYSIOLOGY, AND MANAGEMENT Cynthia Comella, MD, FAAN, FANA Professor of Neurological Sciences Rush University Medical Center Chicago, IL, USA Science never solves a problem without creating ten more George Bernard Shaw Objectives To describe the history of Tardive Dyskinesia To discuss epidemiology, risk factors and possible pathophysiologic mechanisms of tardive syndromes To demonstrate the varied phenomenology of TD To discuss treatment options for TD DOPAMINE RECEPTOR BLOCKING AGENTS (DRBA) AND TARDIVE DYSKINESIA Described in 1950’s within 5 yrs of development of chlorpromazine for psychosis Initial descriptions were drug induced parkinsonism Subsequently orobuccal-lingual movements persisting beyond medication discontinuation Continuous persistent movements in other regions subsequently described (limbs, face Term “tardive dyskinesia” in 1964 Frei K, Truong D, Fahn S, Jankovic J, Hauser R. J Neurol Sci 2018 Factor et al. Lancet Neurology 2019 DOPAMINE RECEPTOR BLOCKING AGENTS: ASSOCIATED MOVEMENT DISORDERS Acute disorders Acute dystonia Oculogyric crisis Sub-acute disorders Neuroleptic malignant syndrome Akathisia Parkinsonism Tardive disorders Stereotypy Chorea/athetosis Dystonia Akathisia (Tics, myoclonus, tremor) Dystonia Akathisia Neuroleptic Malignant Characteristic Tardive Dyskinesia Acute Tardive Acute Tardive Parkinsonism Syndrome Hours to Weeks to Days to Weeks to Days or weeks to Typical time to onseta Weeks to yearsb Hours to weeks days years months years years
    [Show full text]
  • Fragile X Syndrome
    European Journal of Human Genetics (2008) 16, 666–672 & 2008 Nature Publishing Group All rights reserved 1018-4813/08 $30.00 www.nature.com/ejhg PRACTICAL GENETICS In association with Fragile X syndrome Fragile X syndrome, an X-linked dominant disorder with reduced penetrance, is associated with intellectual and emotional disabilities ranging from learning problems to mental retardation, and mood instability to autism. It is most often caused by the transcriptional silencing of the FMR1 gene, due to an expansion of a CGG repeat found in the 50-untranslated region. The FMR1 gene product, FMRP, is a selective RNA-binding protein that negatively regulates local protein synthesis in neuronal dendrites. In its absence, the transcripts normally regulated by FMRP are over translated. The resulting over abundance of certain proteins results in reduced synaptic strength due to AMPA receptor trafficking abnormalities that lead, at least in part, to the fragile X phenotype. In brief Genetic testing for this repeat expansion is diagnostic for this syndrome, and testing is appropriate in all Fragile X syndrome is a common inherited form of children with developmental delay, mental retardation mental retardation that can be associated with features or autism. of autism. Fragile X syndrome is inherited from individuals, The physical features of fragile X syndrome are subtle usually females, who typically carry an unstable and may not be obvious. premutation allele of the CGG-repeat tract in The vast majority of cases of fragile X syndrome are FMR1. caused by the expansion to over 200 copies of a CGG Premutation carriers are themselves at risk of prema- repeat in the 50-untranslated region of FMR1 that shuts ture ovarian failure and the fragile X-associated tremor/ off transcription of the gene.
    [Show full text]
  • Medical Intervention in Fragile X Syndrome
    MEDICAL INTERVENTION IN FRAGILE X SYNDROME By Randi Hagerman, M.D. The M.I.N.D. Institute University of California, Davis Sacramento, CA 916-734-6348 Children and adults with fragile X syndrome often present to the physician with a variety of behavioral problems. These problems are typically seen in fragile X syndrome so they are presumed to be caused by a lack or a deficiency of normal FMR-1 protein (FMRP) production from the FMR1 gene which is dysfunctional in fragile X syndrome. FMRP is normally present in all neurons and its absence causes some changes in brain structure and function, and presumably changes in neurotransmitter systems that we can improve by the use of medication. Although there is presently no cure for fragile X syndrome, there are a variety of medications that can improve the behavior problems seen in fragile X syndrome. Not every fragile X child will have difficulty with the behaviors discussed below, and not every child will respond to each medication. When problems occur, a medication is usually prescribed on a trial basis and often two or more trials of medication are needed before finding one that works. Sometimes more than one medication is used to treat a combination of problems and sometimes medications are used together because of a synergistic effect. Side effects are discussed below and should be monitored carefully so that they do not become more problematic than the symptom, which is being treated. A close communication and follow up visits are needed with your doctor in order to adjust the medication level and monitor the side effects.
    [Show full text]
  • Movement Disorders Therapeutic Class Review (TCR)
    Movement Disorders Therapeutic Class Review (TCR) April 3, 2020 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, digital scanning, or via any information storage or retrieval system without the express written consent of Magellan Rx Management. All requests for permission should be mailed to: Magellan Rx Management Attention: Legal Department 6950 Columbia Gateway Drive Columbia, Maryland 21046 The materials contained herein represent the opinions of the collective authors and editors and should not be construed to be the official representation of any professional organization or group, any state Pharmacy and Therapeutics committee, any state Medicaid Agency, or any other clinical committee. This material is not intended to be relied upon as medical advice for specific medical cases and nothing contained herein should be relied upon by any patient, medical professional or layperson seeking information about a specific course of treatment for a specific medical condition. All readers of this material are responsible for independently obtaining medical advice and guidance from their own physician and/or other medical professional in regard to the best course of treatment for their specific medical condition. This publication, inclusive of all forms contained herein, is intended to be educational in nature and is intended to be used for informational purposes only. Send comments and suggestions to [email protected]. Movement
    [Show full text]
  • Persistent Akathisia Associated with Early Tardive Dyskinesia THOMAS R
    Postgrad Med J: first published as 10.1136/pgmj.60.703.359 on 1 May 1984. Downloaded from Postgraduate Medical Journal (May 1984) 60, 359-361 Persistent akathisia associated with early tardive dyskinesia THOMAS R. E. BARNES WALTER M. BRAUDE M.B., B.S., M.R.C.Psych. M.B., Ch.B., D.P.M., M.R.C.Psych. Psychiatric Research Unit, University of Cambridge Clinical School, Addenbrooke's Hospital, Trumpington Street, Cambridge CB2 2QE Summary admitted to hospital in July 1981 and diagnosed as Two psychiatric patients developed moderate or suffering from a schizophrenic illness. This was the severe oro-facial dyskinesia, and limb dyskinesia, at a first occasion that she had been prescribed antipsy- relatively young age and within a year of starting chotic medication, although there was evidence that antipsychotic drug-treatment. This early appearance psychotic symptoms, principally delusions, had been of tardive dyskinesia was preceded by akathisia that present for several years. She was treated initially had developed at the beginning of drug therapy and with oral chlorpromazine to a maximum dose of 500 persisted, despite the reduction of their drug doses to mg per day. Following a test dose of fluphenazine maintenance levels. The possibility that persistent decanoate (Modecate), 12-5 mg i.m., she was started akathisia may herald the early onset of tardive on regular injections of this depot drug, 37.5 mg i.m. dyskinesia, is discussed. every 3 weeks. Within a few days ofthe first injection she complained of an inability to keep her legs still copyright. KEY WORDS: schizophrenia, parkinsonism.
    [Show full text]
  • Tardive Akathisia
    HEALTH & SAFETY: PSYCHIATRIC MEDICATIONS Tardive Akathisia FACT SHEET Tardive Akathisia BQIS Fact Sheets provide a general overview on topics important to supporting an individual’s health and safety and to improving their quality of life. This document provides general information on the topic and is not intended to replace team assessment, decision-making, or medical advice. This is the ninth of ten Fact Sheets regarding psychotropic medications. Intended Outcomes Individuals will understand the symptoms, common causes, and treatment of tardive akathisia. Definitions Akathisia: A movement disorder characterized by motor restlessness/a feeling of inner restlessness with a compelling need to be moving. Tardive akathisia: A severe prolonged form of akathisia which may persist after stopping the medica- tion causing the symptoms. Facts • Akathisia is: – the most common drug induced movement disorder. – a side effect of medication. – most often caused by antipsychotic medications that block dopamine. • Medications with akathisia as a potential side effect include: – Benzisothiazole (ziprasidone) – Benzisoxazole (iloperidone) – Butyrophenones (haloperidol, droperidol) – Calcium channel blockers (flunarizine, cinnarizine) – Dibenzazepine (loxapine, asenapine) – Dibenzodiazepine (clozapine, quetiapine) – Diphenylbutylpiperidine (pimozide) – Indolones (molindone) – Lithium – Phenothiazines (chlorpromazine, triflupromazine, thioridazine, mesoridazine, trifluoperazine, prochlorperazine, perphenazine, fluphenazine, perazine) Bureau of Quality Improvement
    [Show full text]
  • What Is Tardive Dyskinesia?
    What is Tardive Dyskinesia? 1919 University Avenue West, Suite 400, St. Paul, MN 55114 | Tel. 651-645-2948 or 888-NAMIHELPS | www.namihelps.org What is Tardive Dyskinesia? Tardive Dyskinesia (TD) is a side effect of taking antipsychotic medication. It’s a movement disorder that can appear months, years, even decades after starting to take antipsychotic medication. It’s estimated that 20-50% of people with depression, schizophrenia, bipolar disorder or schizoaffective disorder taking antipsychotics, particularly first generation, will develop TD. What are the symptoms? Signs and symptoms include: • repetitive jerking movements of the arms or legs • trunk and hip rocking, jerking or thrusting • rapid eye blinking • Tongue rolling, or darting in or out of the mouth • lip smacking. pursing or puckering, • jaw clenching or grimacing • twisting or rhythmic movement in the fingers or toes Who is at risk? We know that taking older “first generation” antipsychotics places someone at greater risk. Other risk factors include: • being a woman • being over age 55 • having diabetes • having a substance use disorder (including alcoholism) How can it be prevented? While TD can’t be prevented, it’s important to identify it early. It’s recommended that people be screened every six months or at least every year using what’s called “The Abnormal Involuntary Movement Scale”. Be sure to note which symptoms you are experiencing, when the symptoms began to appear, how frequent they are, and how they impact your daily routine. What are the treatments? If you or a loved one begins showing symptoms talk to your doctor right away – but do not abruptly stop taking the antipsychotic.
    [Show full text]