DOCSLIB.ORG

Catatonic Syndrome As the Presentation of Encephalitis In

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Catatonic Syndrome As the Presentation of Encephalitis In Case report BMJ Case Rep: first published as 10.1136/bcr-2020-240550 on 4 June 2021. Downloaded from Catatonic syndrome as the presentation of encephalitis in association with COVID-19 Damaris Vazquez- Guevara,1 Sandra Badial- Ochoa,1 Karen M Caceres- Rajo,2 Ildefonso Rodriguez- Leyva 1,3 1Neurology, Hospital Central Dr SUMMARY noticed that the patient had apathy, slow Ignacio Morones Prieto, San Luis COVID-19 has shown different neurological thinking and decreased mobility. On presenta- Potosi, Mexico 2 manifestations even sometimes there are the initial or tion to the emergency department, her heart rate Internal Medicine, Facultad the main presentation. was 110 beats per minute. Neurological exam- de Medicina, Universidad The following case report is about a middle-aged ination revealed stupor, muteness, fixed gaze, Autonoma de San Luis Potosi, San Luis Potosi, Mexico woman who, over 3 days, developed fever, clinical negativism, stiffness in the left hemibody, gegen- 3Facultad de Medicina, neurological alterations (stupor, muteness, fixed gaze and halten sign on the right side of the body, global Universidad Autonoma de San catatonia), cerebrospinal fluid (16 lymphocytes) and an hyperreflexia and no neck stiffness. The Bush- Luis Potosi, San Luis Potosi, electroencephalogram (EEG) (4–6 Hz generalised activity) Francis Catatonia rating scale was 19 points. Mexico with characteristics of encephalitis. A serum IgG, IgM, The approach was based on catatonic syndrome nasopharyngeal swab PCR for SARS-CoV -2. The patient (video 1). Initially, a CT scan of the head was Correspondence to responded positively to support measures, symptomatic requested without alterations. An electroenceph- Dr Ildefonso Rodriguez-Leyv a; and corticosteroid treatment. At discharge, the patient alogram (EEG) showed generalised slow activity ilrole@ yahoo. com. mx was independent and improved considerably. (figure 1). Even during the EEG, the patient had We report the presence of catatonia as a possible and Accepted 29 April 2021 motor stereotypes that did not correlate with atypical manifestation of encephalitis in association with brain activity. Initial blood test reported a white COVID-19. cell count of 9.5×109 (reference range 4–11), C reactive protein of 5.7 mg/L. Serum electrolytes, creatine phosphokinase, the liver and renal BACKGROUND functions were normal, and thiamine levels were Much of the focus regarding the COVID-19 unremarkable. Lumbar puncture revealed an pandemic was initially centred on cardiovas- opening pressure of 17cm H2O. The white blood cular, pulmonary and haematologic complica- cell count in the cerebrospinal fluid (CSF) was 16 mm3 (100% lymphocytes). Treatment with tions. However, the prevalence of neurological http://casereports.bmj.com/ symptoms in these patients has become more acyclovir for the probable viral encephalitis and evident.1 One of these conditions is catatonia, a diazepam infusion for the catatonic syndrome described in 1874 by Karl Kahlbaum as a very was started. diverse psychomotor syndrome with a clinical On day 2 of admission, she had a cough, a picture ranging from mutism, catalepsy agita- fever of 102.92°F (39.4°C), and 88% oxygen tion to echolalia, echopraxia and stereotypes.2 saturation on pulse oximetry. On examination, The most common aetiology of catatonia is a chest auscultation was normal. CT of the chest psychiatric illness, and there were reports of showed basal bilateral pulmonary infiltrate. A other general medical conditions. The frequency serum IgG, IgM and a nasopharyngeal swab PCR of catatonia due to general medical conditions test for the SARS- CoV-2 was performed. on October 1, 2021 by guest. Protected copyright. represents 20%–39% of aetiology in catatonia CSF cytology was normal. The direct Gram syndrome.3 The most common neurological stain of the CSF and CSF culture was negative, aetiologies were metabolic encephalopathy, and PCR was negative for herpes virus (HSV) autoimmune, paraneoplastic and infectious type 1 and 2. MRI of the brain showed no encephalitis.4 abnormalities. The mechanism used by a virus to cause neuro- The approach was then focused on autoim- logical damage is an immune dysregulation asso- mune aetiology, and she was treated empirically ciated with a failure in motor connectivity; this with a bolus of methylprednisolone 1 g per day suggests dysfunction of the movement circuit for 5 days. (thalamus, cerebellum, pontine nuclei, the corti- On day 3 of admission, she presented with © BMJ Publishing Group cocortical pathways, the supplementary motor orofacial dyskinesias, upper limb stereotypies Limited 2021. No commercial area, among others), with a cytokine- related and waxy postures. A thyroid nodule was re-use . See rights and injury, damage to specific receptors, inflamma- detected with standard thyroid tests, antiper- permissions. Published by BMJ. 5 tion and secondary hypoxia along nerve fibres. oxidase antibodies, and antithyroglobulin anti- To cite: Vazquez- Guevara D, bodies were negative. The histological report of Badial- Ochoa S, Caceres- Rajo KM, et al. BMJ CASE PRESENTATION the thyroid nodule was lymphoid hyperplasia. Case Rep 2021;14:e240550. A- 43- year old woman was brought to the emer- Serum IgG and IgM and PCR were positive doi:10.1136/bcr-2020- gency department suffering from stupor, silence for SARS-CoV -2; the patient presented mild 240550 and staring. Three days prior, her husband typical respiratory symptoms. The catatonic Vazquez- Guevara D, et al. BMJ Case Rep 2021;14:e240550. doi:10.1136/bcr-2020-240550 1 Case report BMJ Case Rep: first published as 10.1136/bcr-2020-240550 on 4 June 2021. Downloaded from nodule was identified, and a biopsy was performed, which led to a high suspicion of Hashimoto’s encephalitis.9 However, there was normal thyroid function, a pathology report of the thyroid nodule showed lymphoid hyperplasia, and negative antiperoxidase and antithyroglobulin antibodies were found. The patient presented mild respiratory symptoms, and CT showed basal bilateral pulmonary infiltrate. Serum IgG, IgM and PCR were positive for SARS-CoV -2. CSF was not tested for SARS- CoV-2 because many reports did it and concluded the lack of PCR to detect SARS-CoV -2 on CSF.10 We could not rule out other possibilities due to the family’s economic limitations and our institution, such as other autoimmune limbic encephalitides (Anti- NMDA (N- methyl- D- aspartate) receptor, anti-LGI1 (Leucine-rich glioma-inactivated 1) and Anti- CASPR2 (Contactin Associated Protein 2).11 The encephalitis was classified as possibly viral and associated with a pulmonary process caused by COVID-19 and a rare manifestation of a catatonic syndrome. TREATMENT The initial treatment was for the catatonic syndrome with low doses of infusion diazepam with no good response. Initially, with probable viral encephalitis, the patient was under treatment with acyclovir only 2 days; it was discon- tinued after negative CSF PCR for HSV. The respiratory symptoms were treated with supplemental oxygen therapy. Apart from acyclovir, no specific treatment was given for encephalitis due to a lack of diagnostic certainty. The patient was treated with an intravenous bolus of methylpredniso- lone for 5 days, and then she received oral prednisone. OUTCOME AND FOLLOW-UP There was a remarkable improvement when finished with the boluses of steroids. The patient awoke with significant http://casereports.bmj.com/ cognitive decline characterised by the disorientation of time and a deficit of the working, short and semantic memory with 17 on the Montreal Cognitive Assessment in Spanish (MoCA- S) test. She also presented rest tremor on the right hand and hypokinesia, with hypokinesia on the left hemi- body and rest tremor on the right hand. Uncited Video 1 In this short movie, it is possible to observe the At discharge from the hospital, the patient could walk and catatonic activity in the patient perform daily living activities such as bathing, eating and dressing. on October 1, 2021 by guest. Protected copyright. syndrome was related to encephalitis in association with DISCUSSION COVID-19. The COVID-19 pandemic infection is caused by the SARS- CoV-2. The primary manifestation is a respiratory DIFFERENTIAL DIAGNOSIS syndrome, where the symptoms are fever, dry cough, fatigue, Initially, our differential diagnosis included psychiatric cata- dyspnoea, chest pain, fatigue and myalgia.10 There are many tonic syndrome (schizophrenia or bipolar syndrome) or neurological manifestations in the central nervous system and organic brain disorders causes.6 The approach of the cata- peripheral nervous system; these manifestations are considered tonic syndrome was for organic brain disorders. direct effects of the nervous system’s virus, para-infectious or On the day of admission, a CT of the head was performed post- infectious immune- mediated disease.12 The neurolog- to search for lesions such as brain haemorrhages and ical manifestations in the current COVID-19 pandemic are bi-frontal masses; however, it was unremarkable. Status olfactory and taste disorders, dizziness, altered mental status, epilepticus was suspected, so a trial with benzodiazepines seizure, acute cerebrovascular disease, neuralgia, ataxia, was initially performed without clinical improvement. Guillain-Barre syndrome and encephalitis.13 There are few An EEG was conducted during which stereotypes were case reports about encephalitis, where the main neurological presented, which did not correlate with the brain activity clinical presentation
Load more

Recommended publications
  • Neuropsychological Aspects of Frontal Lobe Epilepsy
    Neuropsychological aspects of frontal lobe epilepsy. Dominic Upton, Doctor of Philosophy. Institute of Neurology. University of London. LONDON, WON 36G ROCKEFELLER MEOICAL LIBRARY INSTITUTE OF NEUROLOGY THE NATIONAL HOSPITAL QUEEN SQUARE, LONDON, WCIN 33G CLASS ACCN No. d a t e W c ProQuest Number: 10017771 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a complete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest. ProQuest 10017771 Published by ProQuest LLC(2016). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States Code. Microform Edition © ProQuest LLC. ProQuest LLC 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106-1346 Abstract. This study sought to increase our understanding of the neuropsychological consequences of frontal lobe epilepsy and surgery for this condition. In so doing, some suggestions were made on the role of the frontal lobes, and ways of assessing possible dysfunction in this area. The performance of a large group of subjects with clearly defined frontal lobe epilepsy (n=74), was examined on a comprehensive battery of neuropsychological measures. The performance of this group was compared to a control group of subjects with clearly defined temporal lobe epilepsy (n=57). There were few consistent group differences in test performance. Neither were there any strong relationships between test scores and epilepsy related variables.
    [Show full text]
  • Co-Morbidities and Dementia
    VOLUME 21 ISSUE 1 SPRING- SUMMER 2011 Published by the National Association of Professional Geriatric Care of Managers 3275 West Ina Road Suite 130 Tucson, Arizona Geriatric Care Management 85741 520.881.8008 / phone 520.325.7925 / fax www.caremanager.org Co-Morbidities and Dementia Guest Editor’s Message .............................................................................2 By Karen Knutson, MSN, MBA Dementia, Diabetes, Hypertension, and Alcohol Abuse: A Case Study of Medical Co-morbidities ....................................................3 By Karen Knutson, MSN, MBA Alzheimer’s Disease Co-morbidities ............................................................7 By M. Reza Bolouri, M.D. Frontal Lobe Disorders and Dementia.........................................................9 By Patricia Gross, Ph.D., ABPP-CN A Different Dementia: Different Challenges ...............................................13 By Sharon Mayfield, BSN of Geriatric Care Management Spring/Summer 2011 Guest Editor’s Message Coordinating the Complex Care of Clients with Dementia and Co-Morbidities By Karen Knutson, MSN, MBA, RN Care managers play a pivotal role in in psychiatric classification, co- options available for our clients? coordinating the care of their clients. morbidity does not necessarily imply Selected articles have been chosen As people live longer, the complexity the presence of multiple diseases, to provide more understanding of of life will continue and the increasing but rather an inability of a single the co-morbidities associated with prevalence of chronic disease will diagnosis to account for all of the dementia. Hopefully you will find pose many challenges for coordinating individual’s symptoms. new insights and approaches to such complex care. While the experts hash out integrate into your practice. In health care, co-morbidity is definitions of co-morbidity there The first article which I authored, defined in two different ways.
    [Show full text]
  • The Clinical Presentation of Psychotic Disorders Bob Boland MD Slide 1
    The Clinical Presentation of Psychotic Disorders Bob Boland MD Slide 1 Psychotic Disorders Slide 2 As with all the disorders, it is preferable to pick Archetype one “archetypal” disorder for the category of • Schizophrenia disorder, understand it well, and then know the others as they compare. For the psychotic disorders, the diagnosis we will concentrate on will be Schizophrenia. Slide 3 A good way to organize discussions of Phenomenology phenomenology is by using the same structure • The mental status exam as the mental status examination. – Appearance –Mood – Thought – Cognition – Judgment and Insight Clinical Presentation of Psychotic Disorders. Slide 4 Motor disturbances include disorders of Appearance mobility, activity and volition. Catatonic – Motor disturbances • Catatonia stupor is a state in which patients are •Stereotypy • Mannerisms immobile, mute, yet conscious. They exhibit – Behavioral problems •Hygiene waxy flexibility, or assumption of bizarre • Social functioning – “Soft signs” postures as most dramatic example. Catatonic excitement is uncontrolled and aimless motor activity. It is important to differentiate from substance-induced movement disorders, such as extrapyramidal symptoms and tardive dyskinesia. Slide 5 Disorders of behavior may involve Appearance deterioration of social functioning-- social • Behavioral Problems • Social functioning withdrawal, self neglect, neglect of • Other – Ex. Neuro soft signs environment (deterioration of housing, etc.), or socially inappropriate behaviors (talking to themselves in
    [Show full text]
  • THE CLINICAL ASSESSMENT of the PATIENT with EARLY DEMENTIA S Cooper, J D W Greene V15
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2005.081133 on 16 November 2005. Downloaded from THE CLINICAL ASSESSMENT OF THE PATIENT WITH EARLY DEMENTIA S Cooper, J D W Greene v15 J Neurol Neurosurg Psychiatry 2005;76(Suppl V):v15–v24. doi: 10.1136/jnnp.2005.081133 ementia is a clinical state characterised by a loss of function in at least two cognitive domains. When making a diagnosis of dementia, features to look for include memory Dimpairment and at least one of the following: aphasia, apraxia, agnosia and/or disturbances in executive functioning. To be significant the impairments should be severe enough to cause problems with social and occupational functioning and the decline must have occurred from a previously higher level. It is important to exclude delirium when considering such a diagnosis. When approaching the patient with a possible dementia, taking a careful history is paramount. Clues to the nature and aetiology of the disorder are often found following careful consultation with the patient and carer. A focused cognitive and physical examination is useful and the presence of specific features may aid in diagnosis. Certain investigations are mandatory and additional tests are recommended if the history and examination indicate particular aetiologies. It is useful when assessing a patient with cognitive impairment in the clinic to consider the following straightforward questions: c Is the patient demented? c If so, does the loss of function conform to a characteristic pattern? c Does the pattern of dementia conform to a particular pattern? c What is the likely disease process responsible for the dementia? An understanding of cognitive function and its anatomical correlates is necessary in order to ascertain which brain areas are affected.
    [Show full text]
  • Neutrophil-Lymphocyte Ratio in Catatonia
    Original article Neutrophil-lymphocyte ratio in catatonia SENGUL KOCAMER SAHIN1 https://orcid.org/0000-0002-5371-3907 CELAL YAşAMALI1 https://orcid.org/0000-0002-2813-2270 MUHAMMET BERKAY ÖZYÜREK2 https://orcid.org/0000-0002-7016-1411 GÜLÇIN ELBOğA1 https://orcid.org/0000-0003-3903-1835 ABDURRAHMAN ALTINDAğ1 https://orcid.org/0000-0001-5531-4419 AHMET ZIYA şAHIN3 https://orcid.org/0000-0001-5853-8709 1 Department of Psychiatry, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey. 2 Department of Psychiatry, Faculty of Medicine, Balıkesir University, Balıkesir, Turkey. 3 Department of Internal Medicine, Faculty of Medicine, Sanko University, Gaziantep, Turkey. Received: 05/18/2019 – Accepted: 01/14/2020 DOI: 10.1590/0101-60830000000232 Abstract Background: There is growing evidence of subclinical inflammation in mental disorders. Objective: The aim of this study was to investigate frequency of symptoms of catatonia and the newly diagnosed subclinical inflammatory markers which are neutrophil/lymphocyte (NLR), platelet/lymphocyte (PLR), monocyte/lymphocyte (MLR) ratios in catatonia patients due to mental disorders. Methods: Patients who were admitted to psychiatry clinic with the diagnosis of catatonia according to DSM 5 in the last two years and equal number of control group were included in this retrospective study. Univariate analysis of covariance controlled for possible confounders was used to compare NLR, PLR, MLR ratios between patients and the control group. Results: A total of 34 catatonia patients and 34 healthy controls were included in the study. Patients’ mean age was 30.88 + 13.4. NLR value was significantly higher in the patient group than control group. There was no significant difference between the patients and control group according to PLR, MLR values.Discussion: The presence of subclinical inflammation in catatonic syndrome due to mental disorders should be considered.
    [Show full text]
  • Dementia and Aphasia in Motor Neuron Disease: an Underrecognised Association?
    J Neurol Neurosurg Psychiatry 1998;65:881–889 881 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.6.881 on 1 December 1998. Downloaded from Dementia and aphasia in motor neuron disease: an underrecognised association? Wojtek P Rakowicz, John R Hodges Abstract predominantly sporadic, cases have subse- Objectives—To determine the prevalence quently been found in western countries.6–9 and nature of global cognitive dysfunction The most common pattern of cognitive and language deficits in an unselected decline in MND is a progressive dementia of population based cohort of patients with the frontal lobe type.10 It is unclear whether this motor neuron disease (MND). MND-frontal lobe dementia syndrome consti- Methods——A battery of neuropsycho- tutes the extreme end of a range of disease or logical and language tests was adminis- alternatively whether it represents a separate tered to patients presenting consecutively nosological entity. Whereas some early studies overa3yearperiodtoaregional neurol- which looked for intermediate degrees of ogy service with a new diagnosis of cognitive dysfunction in clinically non- sporadic motor neuron disease. demented patients with MND found no evidence of widespread impairment,11 others Results—The 18 patients could be divided reported poor performance in isolated tests of on the basis of their performance into 12 13 three groups: Three patients were de- memory or concentration. The emerging picture is of consistent abnormalities on tests of mented and had impaired language func- so-called “frontal executive” function, most tion (group 1); two non-demented patients notably decreased verbal fluency, aVecting a had an aphasic syndrome characterised large proportion of non-demented patients with Y by word finding di culties and anomia MND.
    [Show full text]
  • Catatonia in Depression: Prevalence, Clinical J Neurol Neurosurg Psychiatry: First Published As 10.1136/Jnnp.60.3.326 on 1 March 1996
    32632ournal ofNeurology, Neurosurgery, and Psychiatry 1996;60:326-332 Catatonia in depression: prevalence, clinical J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.60.3.326 on 1 March 1996. Downloaded from correlates, and validation of a scale Sergio E Starkstein, Gustavo Petracca, Alejandra Teson, Eran Chemerinski, Marcelo Merello, Ricardo Migliorelli, Ramon Leiguarda Abstract mute and immobile, with staring expression, Objectives-To examine the clinical cor- gaze fixed into space, with an apparent com- relates of catatonia in depression, to vali- plete loss of will, no reaction to sensory stim- date a scale for catatonia, and to assess uli, sometimes with the symptom of waxy the validity of the DSM-IV criteria of the flexibility completely developed, as in catatonic features specifier for mood dis- catalepsy, sometimes of a mild degree, but orders. clearly recognisable," and labelled this state Methods-A series of 79 consecutive "vesania katatonica".2 Stressing that catatonia patients with depression and 41 patients was not related to "affective" melancholy with Parkinson's disease without depres- sensu strictu, Wernicke suggested the term sion were examined using the modified "motilitatpsychose", and suggested that this Rogers scale (MRS), the unified disorder may be the result of dysfunction of a Parkinson's disease rating scale "psychomotor path", producing either akine- (UPDRS), and the structured clinical sis, parakinesis, or hyperkinesis.3 Whereas interview for DSM-III-R (SCID). Kahlbaum and Wernicke placed catatonia Results-Sixteen of the 79 depressed within the range of the affective disorders, patients (20%) had catatonia. Depressed Kraepelin4 considered catatonia as a type of patients with catatonia had significantly schizophrenia, and this disorder aroused little higher scores on the MRS than non-cata- interest until recently.
    [Show full text]
  • The Harmony of Illusions the Harmony of Illusions
    THE HARMONY OF ILLUSIONS THE HARMONY OF ILLUSIONS I NVENTING POST-TRAUMATIC STRESS DISORDER Allan Young PRINCETON UNIVERSITY PRESS PRINCETON, NEW JERSEY Copyright 1995 by Princeton University Press Published by Princeton University Press, 41 William Street, Princeton, New Jersey 08540 In the United Kingdom: Princeton University Press, Chichester, West Sussex All Rights Reserved Library of Congress Cataloging-in-Publication Data Young, Allan, 1938– The harmony of illusions : inventing post-traumatic stress disorder / Allan Young. p. cm. Includes bibliographical references and index. ISBN 0-691-03352-8 (cloth : alk. paper) 1. Post-traumatic stress disorder—Philosophy. 2. Social epistemology. I. Title. RC552.P67Y68 1995 616.85′21—dc20 95-16254 This book has been composed in Times Roman Princeton University Press books are printed on acid-free paper and meet the guidelines for permanence and durability of the Committee on Production Guidelines for Book Longevity of the Council on Library Resources Printed in the United States of America by Princeton Academic Press 10987654321 For Roberta Contents Acknowledgments ix Introduction 3 PART I: THE ORIGINS OF TRAUMATIC MEMORY One Making Traumatic Memory 13 Two World War I 43 PART II: THE TRANSFORMATION OF TRAUMATIC MEMORY Three The DSM-III Revolution 89 Four The Architecture of Traumatic Time 118 PART III: POST-TRAUMATIC STRESS DISORDER IN PRACTICE Five The Technology of Diagnosis 145 Six Everyday Life in a Psychiatric Unit 176 Seven Talking about PTSD 224 Eight The Biology of Traumatic Memory 264 Conclusion 287 Notes 291 Works Cited 299 Index 321 Acknowledgments I OWE a debt to colleagues and friends in the Department of Social Studies of Medicine and the Department of Psychiatry at McGill University: I thank Don Bates, Alberto Cambrosio, Margaret Lock, Faith Wallis, George Weisz, and Laurence Kirmayer for their invaluable advice.
    [Show full text]
  • Read the 2013 PSHA Journal
    1 PSHA JOURNAL ANNUAL PUBLICATION OF THE PENNSYLVANIA SPEECH-LANGUAGE-HEARING ASSOCIATION DECEMBER 2013 EDITION 2 JOURNAL IS AN ANNUAL PUBLICATION OF THE PENNSYLVANIA SPEECH-LANGUAGE-HEARING ASSOCIATION 700 McKnight Park Drive, Suite 708 Pittsburgh, PA 15237 412.366.9858 (Phone) 412.366.8804 (Fax) [email protected] THE PENNSYLVANIA SPEECH-LANGUAGE-HEARING ASSOCIATION (PSHA), FOUNDED IN 1960, IS A PROFESSIONAL ORGANIZATION OF SPEECH-LANGUAGE PATHOLOGISTS, AUDIOLOGISTS, AND TEACHERS OF THE HEARING-IMPAIRED. AS SUCH, PSHA: Serves as a liaison between the American Speech-Language-Hearing Association and its Pennsylvania members. Represents its’ members interests in legislative affairs. Recommends standards for training and practices. Provides information about effective services and programs and services in communication disorders and other related fields. Works to inform the public about the professions, careers, programs, and services in the field of communication disorders. Encourages basic scientific study of the process of individual human communication. Monitors state Licensure Board activities. 2013-2014 PSHA EXECUTIVE BOARD PRESIDENT: Kathleen Helfrich-Miller PRESIDENT-ELECT: Amy Goldman PAST PRESIDENT: Craig Coleman VICE-PRESIDENT – PROFESSIONAL PRACTICE (SPEECH-LANGUAGE PATHOLOGY): Susan Hough VICE-PRESIDENT – PROFESSIONAL PRACTICE (AUDIOLOGY/EDUCATION): Jennifer Rakers VICE-PRESIDENT – PROFESSIONAL PREPARATION/CONTINUING EDUCATION: Joan Luckhurst VICE-PRESIDENT – MEMBERSHIP/ETHICAL PRACTICES: Nancy Carlino VICE-PRESIDENT – PUBLIC INFORMATION/PROFESSIONAL COMMUNICATION: Eileen Cirelli VICE-PRESIDENT – CONVENTION PLANNING/PROGRAMMING: Mary Beth Mason-Baughman VICE-PRESIDENT – GOVERNMENTAL RELATIONS: Caterina Stalteri VICE-PRESIDENT – PUBLICATIONS/EDITOR: Cheryl Gunter SECRETARY: Emily Katzaman TREASURER: Hunter Manasco Ex Officio STUDENT REPRESENTATIVE: Kathryn Young BUSINESS MANAGER: Diane Yenerall ACCOUNT MANAGER: Amy Caye 3 JOURNAL EDITOR Cheryl D. Gunter, Ph.D.
    [Show full text]
  • Catatonia in DSM-5
    Schizophrenia Research 150 (2013) 26–30 Contents lists available at ScienceDirect Schizophrenia Research journal homepage: www.elsevier.com/locate/schres Review Catatonia in DSM-5 Rajiv Tandon a,⁎, Stephan Heckers b, Juan Bustillo c, Deanna M. Barch d,e, Wolfgang Gaebel f, Raquel E. Gur g,h, Dolores Malaspina i,j, Michael J. Owen k, Susan Schultz l, Ming Tsuang m,n,o, Jim van Os p,q, William Carpenter r,s a Department of Psychiatry, University of Florida Medical School, Gainesville, FL, USA b Department of Psychiatry, Vanderbilt University, Nashville, TN, USA c Department of Psychiatry, University of New Mexico, Albuquerque, NM, USA d Department of Psychology, Washington University, St. Louis, MO, USA e Department of Psychiatry and Radiology, Washington University, St. Louis, MO, USA f Department of Psychiatry, Duesseldorf, Germany g Department of Psychiatry, Perlman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA h Department of Neurology and Radiology, Perlman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA i Department of Psychiatry, New York University, New York, NY, USA j Creedmoor Psychiatric Center, New York State Office of Mental Health, USA k MRC Centre for Neuropsychiatric Genetics and Genomics and Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, Wales, United Kingdom l Department of Psychiatry, University of Iowa School of Medicine, Iowa City, IA, USA m Center for Behavioral Genomics, Department of Psychiatry and Institute of Genomic Medicine, University
    [Show full text]
  • Catatonia, NMS, and Serotonin Syndrome
    Catatonia, NMS, and Serotonin Syndrome Christopher M. Celano, MD, FACLP Associate Director, Cardiac Psychiatry Research Program, Massachusetts General Hospital Assistant Professor of Psychiatry, Harvard Medical School October 22, 2020 www.mghcme.org Disclosure: Christopher Celano, MD Sunovion Company Pharmaceuticals Employment Management Independent Contractor Consulting Speaking & Teaching I Board, Panel or Committee Membership D – Relationship is considered directly relevant to the presentation I – Relationship is NOT considered directly relevant to the presentation www.mghcme.org Catatonia: How common is it? • 7.8-9.0% prevalence rate – Highest rates in non-psychiatric (i.e., medical) settings and in patients undergoing ECT. • 1.6-5.5% of all patients seen on psychiatry consultation service – Prevalence higher for older patients • Up to 46% of cases may have etiology that is not primarily psychiatric Grover 2015, Carroll 1994, Jaimes-Albornoz 2013, Fricchione 2008 www.mghcme.org When are you called? • Staff reports the patient is “Playing POSSUM” • Perseveration (speech or behavior) • Oppositionality to all requests • Speech that trails off or is whispereD • Slowed response to questions or commands • Undernourished (reports of decreased PO intake) • Motionless but awake www.mghcme.org Diagnosing Catatonia: DSM-5 DSM-5 requires 3 or more of the following: • Catalepsy • Posturing • Waxy flexibility • Mannerisms • Stupor • Stereotypies • Agitation • Grimacing • Mutism • Echolalia • Negativism • Echopraxia American Psychiatric Association 2013 www.mghcme.org Bush-Francis Rating Scale • Excitement • VerBigeration • Immobility/stupor • Rigidity • ComBativeness • Negativism • Autonomic Abnormality • Waxy flexiBility • Impulsivity • Withdrawal • Mutism • Automatic OBedience • Staring • Mitgehen • Posturing/catalepsy • Gegenhalten • Grimacing • AmBitendency • Echopraxia/echolalia • Grasp Reflex • Stereotypy • Perseveration • Mannerisms Bush 1996 www.mghcme.org Challenges with Diagnosis • Clarifying specific symptoms can be difficult – Rigidity vs.
    [Show full text]
  • Why Do Neurologists Miss Catatonia in Neurology Emergency? a Case
    Clinical Neurology and Neurosurgery 184 (2019) 105375 Contents lists available at ScienceDirect Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro Why do neurologists miss catatonia in neurology emergency? A case series T and brief literature review ⁎ Sucharita Ananda, Vimal Kumar Paliwala, , Laxmi S Singha, Ravi Uniyalb a Department of Neurology, SGPGIMS, Raebareli road, Lucknow, UP, India b Department of Neurology, King George Medical University, Lucknow, UP, India ARTICLE INFO ABSTRACT Keywords: Catatonia is a well-described clinical syndrome characterized by features that range from mutism, negativism Catatonia and stupor to agitation, mannerisms and stereotype. Causes of catatonia may range from organic brain disorders Extrapyramidal disorder to psychiatric conditions. Despite a characteristic syndrome, catatonia is grossly under diagnosed. The reason for Parkinsonism missed diagnosis of catatonia in neurology setting is not clear. Poor awareness is an unlikely cause because Major depression catatonia is taught among conditions with deregulated consciousness like vegetative state, locked-in state and Schizophrenia akinetic mutism. We determined the proportion of catatonia patients correctly identified by neurology residents in neurology emergency. We also looked at the alternate diagnosis they received to identify catatonia mimics. Twelve patients (age 22–55 years, 7 females) of catatonia were discharged from a single unit of neurology department from 2007 to 2017. In the emergency department,
    [Show full text]