Obsessive Compulsive Disorders: an Information Guide
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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. -
This Paper Has Been Accepted for Publication and Is Forthcoming in History Of
This paper has been accepted for publication and is forthcoming in History of Psychiatry https://us.sagepub.com/en-us/nam/journal/history-psychiatry#description Understanding the DSM-5: Stasis and change Rachel Cooper Lancaster University Philosophy, Lancaster University, Lancaster, LA1 4YL Email: [email protected] Acknowledgements I am grateful to the American Psychiatric Association for granting me access to their archives. A version of this paper has been presented at a number of conferences (Mind, Value and Mental Health. International Conference in Philosophy and Psychiatry. Oxford, July 2015; DSM-5 and the Future of Psychiatric Diagnosis. Brocher Symposium. Geneva, July 2014; Symposium on DSM-5, Innovatie en Stagnatie; het geval DSM. Conference of the Dutch section on philosophy & psychiatry. Leiden, June 2013). I am grateful for the comments of those present at these talks. I am also grateful to Roger Blashfield who read a draft of this paper and made many helpful suggestions. Acknowledgement of funding Work for this paper was funded by British Academy Mid-Career Research Fellowship MD120060. 1 Understanding the DSM-5: Stasis and change Abstract: This paper aims to understand the DSM-5 through situating it within the context of the historical development of the DSM series. When one looks at the sets of diagnostic criteria, the DSM-5 is strikingly similar to the DSM-IV. I argue that at this level the DSM has become ‘locked-in’ and difficult to change. At the same time, at the structural, or conceptual, level there have been radical changes, for example, in the definition of ‘mental disorder’, the role of theory and of values, and in the abandonment of multiaxial approach to diagnosis. -
Special Education Eligibility Requirements
Portland Public Schools Special Education Procedures Manual Section 4 Special Education Eligibility Requirements I. General Information about Eligibility A. Disability Categories--The Oregon Administrative Rules (OARs) specify minimum eligibility criteria for eleven disabilities: autism, communication disorder, deafblindness, hearing impairment, specific learning disability, mental retardation, orthopedic impairment, other health impairment, serious emotional disturbance, traumatic brain injury, and vision impairment. For each disability, the OARs specify the definition of the disability, who may make the eligibility decision, what information must be considered, and what criteria must be met. B. Eligibility Determination-- Eligibility decisions Eligibility Codes List must be made by a special education team 10 Intellectual Disability with the membership of an IEP team. The 20 Hearing Impairment special education team must always include 40 Vision Impairment someone who is knowledgeable of and 43 Deafblindness experienced in the education of students with 50 Communication Disorder the suspected disability. The team must 60 Emotional Disturbance include the student’s regular teacher, or if the 70 Orthopedic Impairment student does not have a regular teacher, a 74 Traumatic Brain Injury regular classroom teacher qualified to teach a 80 Other Health Impairment student of his or her age. 82 Autism Spectrum Disorder 90 Specific Learning Disability C. Primary/Secondary Disabilities--A student must be evaluated in all areas related to the suspected disability, and the IEP must address all of the student’s special education needs. If the special education team determines that a student is eligible in more than one category, the team must decide which disability is the primary disability. The primary disability should be the one that most adversely affects educational performance. -
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. -
1 Serious Emotional Disturbance (SED) Expert Panel
Serious Emotional Disturbance (SED) Expert Panel Meetings Substance Abuse and Mental Health Services Administration (SAMHSA) Center for Behavioral Health Statistics and Quality (CBHSQ) September 8 and November 12, 2014 Summary of Panel Discussions and Recommendations In September and November of 2014, SAMHSA/CBHSQ convened two expert panels to discuss several issues that are relevant to generating national and State estimates of childhood serious emotional disturbance (SED). Childhood SED is defined as the presence of a diagnosable mental, behavioral, or emotional disorder that resulted in functional impairment which substantially interferes with or limits the child's role or functioning in family, school, or community activities (SAMHSA, 1993). The September and November 2014 panels brought together experts with critical knowledge around the history of this federal SED definition as well as clinical and measurement expertise in childhood mental disorders and their associated functional impairments. The goals for the two expert panel meetings were to operationalize the definition of SED for the production of national and state prevalence estimates (Expert Panel 1, September 8, 2014) and discuss instrumentation and measurement issues for estimating national and state prevalence of SED (Expert Panel 2, November 12, 2014). This document provides an overarching summary of these two expert panel discussions and conclusions. More comprehensive summaries of both individual meetings’ discussions and recommendations are found in the appendices to this summary. Appendix A includes a summary of the September meeting and Appendix B includes a summary of the November meeting). The appendices of this document also contain additional information about child, adolescent, and young adult psychiatric diagnostic interviews, functional impairment measures, and shorter mental health measurement tools that may be necessary to predict SED in statistical models. -
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. -
Depression Treatment Guide DSM V Criteria for Major Depressive Disorders
MindsMatter Ohio Psychotropic Medication Quality Improvement Collaborative Depression Treatment Guide DSM V Criteria for Major Depressive Disorders A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure. Note: Do not include symptoms that are clearly attributable to another medical condition. 1) Depressed mood most of the day, nearly every day, as 5) Psychomotor agitation or retardation nearly every day indicated by either subjec tive report (e.g., feels sad, empty, (observable by others, not merely subjective feelings of hopeless) or observation made by others (e.g., appears restlessness or being slowed down). tearful). (Note: In children and adolescents, can be irritable 6) Fatigue or loss of energy nearly every day. mood.) 7) Feelings of worthlessness or excessive or inappropriate 2) Markedly diminished interest or pleasure in all, or almost all, guilt (which may be delu sional) nearly every day (not activities most of the day, nearly every day (as indicated by merely self-reproach or guilt about being sick). either subjective account or observation). 8) Diminished ability to think or concentrate, or 3) Significant weight loss when not dieting or weight gain indecisiveness, nearly every day (ei ther by subjective (e.g., a change of more than 5% of body weight in a account or as observed by others). month}, or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make expected 9) Recurrent thoughts of death (not just fear of dying), weight gain.) recurrent suicidal ideation with out a specific plan, or a suicide attempt or a specific plan for committing suicide. -
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. -
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. -
Superior Health Council DSM (5): the USE AND
Superior Health Council DSM (5): THE USE AND STATUS OF DIAGNOSIS AND CLASSIFICATION OF MENTAL HEALTH PROBLEMS JUNE 2019 SHC № 9360 COPYRIGHT Federal Public Service Health, Food Chain Safety and Environment Superior Health Council Place Victor Horta 40 bte 10 B-1060 Bruxelles Tel.: 02/524 97 97 E-mail: [email protected] All rights reserved. Please cite this document as follows: Superior Health Council. DSM (5): The use and status of diagnosis and classification of mental health problems. Brussels: SHC; 2019. Report 9360. Public advisory reports as well as booklets may be consulted in full on the Superior Health Council website: www.css-hgr.be This publication cannot be sold. ADVISORY REPORT OF THE SUPERIOR HEALTH COUNCIL no. 9360 DSM (5): The use and status of diagnosis and classification of mental health problems In this scientific advisory report, which offers guidance to public health policy-makers, the Superior Health Council of Belgium provides recommendations on use of classifications in mental health for professionals, policy makers and researchers. This version was validated by the Board on June - 20191 SUMMARY The SHC notes that the most commonly used tools for diagnosing mental health problems (the Diagnostic and Statistical Manual of Mental Disorders (DSM), or the International Classification of Diseases and Related Health Problems (ICD)) pose several problems and recommends that they be used with caution and that the DSM categories not be at the centre of care planning. From an epistemological point of view, classifications are based on the assumption that mental disorders occur naturally, and that their designations reflect objective distinctions between different problems, which is not the case. -
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 -
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.