Letters to the Editor

Total Page:16

File Type:pdf, Size:1020Kb

Letters to the Editor Letters to the Editor Letters to the Editor © Copyright 2001 Physicians Postgraduate Press, Inc. Cost Savings With namic effects in patients who are already receiving other sedat- Intramuscular Anticholinergics ing agents and/or in the elderly, who may be more sensitive to these side effects. This intervention is easily implemented, does Sir: With the advent of atypical antipsychotics, novel anti- not appear to compromise patient care, and results in modest cost savings. convulsant agents, and selective serotonin reuptake inhibitors, the pharmacotherapy of psychiatric disorders has changed tre- mendously in the last decade. Although these newer medica- REFERENCES tions are generally better tolerated, and, in some cases, lessen associated costs of more frequent hospitalizations, they have 1. Bult J, Schiff G, Wisniewski M. Sertraline tablet splitting program. greatly impacted hospital pharmacy budgets. With few of these Hosp Pharm 1999;34:996–999 newer medications available generically, there is little opportu- 2. Holloman L, Marder S. Management of acute extrapyramidal effects induced by antipsychotic drugs. Am J Health Syst Pharm nity to decrease medication costs except Onein interventions personal such copy as may be printed 1 1997;54:2461–2477 tablet splitting. 3. Stanilla J, Simpson G. Treatment of extrapyramidal side effects. In: In an effort to reduce costs at our institution, we recently Schatzberg AF, Nemeroff CB, eds. Textbook of Psychopharmacology. identified high-use, high-cost items. As a result, one initiative 2nd ed. Washington, DC: American Psychiatric Press; 1998:349–369 we undertook was a policy of substituting generic parenteral 4. Tonda ME, Guthrie SK. Treatment of acute neuroleptic-induced diphenhydramine, 25 mg, for parenteral benztropine, 1 mg, movement disorders. Pharmacotherapy 1994;14:543–560 for the treatment and/or prophylaxis of antipsychotic-induced extrapyramidal symptoms (EPS). Significantly, parenteral John S. Markowitz, Pharm.D. benztropine is unavailable generically, but was the medication Stephen McLeod-Bryant, M.D. of choice at our institution for acute EPS or prophylaxis. Fur- Cherry Wyant Jackson, Pharm.D. ther, cost differences between the 2 products were substantial Medical University of South Carolina at $7.30 per single-use 2-mL glass ampul of benztropine Charleston, South Carolina (1 mg/mL) versus $0.40 per 2-mL multiuse vial of diphenhydra- mine (50 mg/mL). Although we could locate no controlled clini- cal efficacy trials of benztropine versus diphenhydramine for EPS, the use of both agents is widely accepted in the treatment Problems With Ensuring a Double Blind of acute dystonic reactions and pseudoparkinsonism.2–4 Diphen- hydramine is generally regarded as the more sedating agent as a Sir: We read with interest the article by Zanardi et al.1 evalu- result of its antihistamine effects, but this may be beneficial in ating the effectiveness of venlafaxine versus fluvoxamine in the some patients.3 Further, some patients may respond more rap- treatment of delusional depression. Delusional depression, as idly to diphenhydramine.4 the authors point out, is a difficult condition to treat with the The project was implemented via a joint memorandum to all limited treatment options available to clinicians. New treatment medical staff from the medical director and clinical coordinator trials such as that reported in this study are always welcome. We for pharmacy services at the institution that outlined the project have, however, 2 concerns about the design used by the authors and potential savings. The medical staff was encouraged to vol- that may have compromised the integrity of the blind in their untarily comply with the effort. study. Compliance with the project was excellent and almost im- Firstly, as the authors indicate, venlafaxine and fluvoxamine mediate. No adverse events or efficacy problems were reported work on different neurotransmitters. Consequently, the 2 drugs during the year that intramuscular diphenhydramine was used. have different side effect profiles, namely, sustained hyperten- Our hospital saved approximately $9000 in drug costs the first sion, dizziness, delayed ejaculation, and somnolence are more year, or $6.90 per dose, with the change to diphenhydramine. common with venlafaxine2 and gastrointestinal symptoms, mal- This savings is expected to continue on an annual basis. aise, sedation, tremor, and exacerbation of anxiety features are Our clinical findings are limited since we did not perform a associated with fluvoxamine.3 The authors report that the side rigorous assessment of individual differences in observed or effects were rated by “trained psychiatrists” using the Dosage perceived EPS in patients treated with one agent versus the Records and Treatment Emergent Symptoms Scale (DOTES). other. Nonetheless, as a result of our experience and the known Some of the side effects outlined above were experienced by effectiveness of both agents, we believe clinicians can consider study participants, but the authors do not report the drugs with switching from intramuscular benztropine to diphenhydramine which they were associated. The blind of the study might have for the treatment or prophylaxis of antipsychotic-induced EPS. been broken because side effect profiles do provide significant However, since diphenhydramine may be more sedating than clues about the drug being tried.4 For instance, one could specu- benztropine, caution is advised to avoid additive pharmacody- late, even though the authors do not report, that the patient who J Clin Psychiatry 62:4, April 2001 295 Letters to the Editor dropped out of the study owing to a marked increase in blood Regarding the second and last concern that Drs. Kumar and pressure was likely to be on venlafaxine treatment. Two inter- Oakley-Browne had about the description of medication dispen- ventions have been reported to be helpful in this regard4: (1) one sation, we cannot help agreeing with them. In fact, being aware blinded psychiatrist monitors the therapeutic response and pos- of the importance of ensuring that the dispensation of medica- sible toxicity and another psychiatrist, who is not blinded, re- tions did not break the blind, we carefully followed these rules: ceives reports from the first psychiatrist and the laboratory and the external appearance of the capsules was identical for size, adjusts the dosage according to the study protocol; (2) the psy- consistency, and color; the number of capsules administered chiatrists are asked to guess what medication each patient is re- was the same in the 2 groups (1 capsule daily for the first 3 days ceiving. If the success rate of having a correct guess is higher and then 2 capsules daily for each patient); the time of adminis- than chance, then one could say that the blind is broken. tration for the 2 treatments during the day was the same (1 cap- Secondly, some important details about medication dispen- sule after dinner on the first 3 days with the addition of the sation are missing© Copyright that are important in 2001 ensuring a Physiciansdouble blind. second Postgraduate capsule after breakfast Press,from the fourth Inc. day on); and These include the number of tablets patients were having to medication dispensation was carried out by a member of the take, the external appearance of the tablets, and who dispensed nursing staff. Given these precautions, we feel confident in say- them to the patients.4 A conventional way to ensure blinding ing that our trial was not affected at all by such limitations. in studies in which patients have to take different numbers of In every randomized controlled study we carry out, we stick tablets owing to varying dose strengths is called the “double- to the suggestions so clearly outlined in the CONSORT state- placebo method.”4 Each group receives an identical number of ment.4 The problem arising from the full description of such tablets made by combining active medication and placebo. guidelines is the need of more space than is usually available in The findings of this pilot study should be interpreted in light scientific journals. of these factors, which could have been best outlined in the dis- cussion of the limitations of the study. REFERENCES REFERENCES 1. Zanardi R, Franchini L, Serretti A, et al. Venlafaxine versus fluvox- One personal copy may beamine printed in the treatment of delusional depression: a pilot double-blind 1. Zanardi R, Franchini L, Serretti A, et al. Venlafaxine versus fluvox- controlled study. J Clin Psychiatry 2000;61:26–29 amine in the treatment of delusional depression: a pilot double-blind 2. Markham Brown T, Stoudemire A. Psychiatric Side Effects of controlled study. J Clin Psychiatry 2000;61:26–29 Prescription and Over-the-Counter Medications. Washington, DC: 2. Mackay FR, Dunn NR, Martin RM, et al. Newer antidepressants: American Psychiatric Press; 1998 a comparison of tolerability in general practice. Br J Gen Pract 1999; 3. Medscape DrugInfo. Available at: http:// 49:892–896 www.promini.medscape.com/drugdb/search.asp. Accessed January 8, 3. Edwards JG, Anderson I. Systematic review and guide to selection of 2000 selective serotonin re-uptake inhibitors. Drugs 1999;57:507–533 4. CONSORT Group. Improving the quality of reporting of randomized 4. Spiker B. Guide to Clinical Trials. New York, NY: Raven Press; 1991 controlled trials: the CONSORT statement. JAMA 1996;276:637–639 Shailesh Kumar, M.R.C.Psych., M.Phil. Raffaella Zanardi, M.D. Lakeland Health Limited David Rossini, M.D. Rotorua, New
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]