A Dictionary of Neurological Signs.Pdf

Total Page:16

File Type:pdf, Size:1020Kb

A Dictionary of Neurological Signs.Pdf A DICTIONARY OF NEUROLOGICAL SIGNS THIRD EDITION A DICTIONARY OF NEUROLOGICAL SIGNS THIRD EDITION A.J. LARNER MA, MD, MRCP (UK), DHMSA Consultant Neurologist Walton Centre for Neurology and Neurosurgery, Liverpool Honorary Lecturer in Neuroscience, University of Liverpool Society of Apothecaries’ Honorary Lecturer in the History of Medicine, University of Liverpool Liverpool, U.K. 123 Andrew J. Larner MA MD MRCP (UK) DHMSA Walton Centre for Neurology & Neurosurgery Lower Lane L9 7LJ Liverpool, UK ISBN 978-1-4419-7094-7 e-ISBN 978-1-4419-7095-4 DOI 10.1007/978-1-4419-7095-4 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2010937226 © Springer Science+Business Media, LLC 2001, 2006, 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) To Sue Nil satis nisi optimum CECILY: ...Dr Chasuble is a most learned man. He has never written a single book, so you can imagine how much he knows. Oscar Wilde The importance of being earnest: 1899, Act III The tendency to appear exact by disregarding the complexity of the factors is the old failing in our medical history. J. Curnow Cited in: Critchley M, Critchley EA. John Hughlings Jackson. Father of English Neurology. New York: Oxford University Press, 1998: 106 FOREWORD TO THE FIRST EDITION Neurology has always been a discipline in which careful physical examination is paramount. The rich vocabulary of neurology replete with eponyms attests to this historically. The decline in the importance of the examination has long been predicted with the advent of more detailed neuroimaging. However, neuroimag- ing has often provided a surfeit of information from which salient features have to be identified, dependent upon the neurological examination. A dictionary of neurological signs has a secure future. A dictionary should be informative but unless it is unwieldy, it cannot be compre- hensive, nor is that claimed here. Andrew Larner has decided sensibly to include key features of the history as well as the examination. There is no doubt that some features of the history can strike one with the force of a physical sign. There are entries for ‘palinopsia’ and ‘environmental tilt’ both of which can only be elicited from the history and yet which have considerable significance. There is also an entry for the ‘head turning sign’ observed during the history taking itself as well as the majority of entries relating to details of the physical examination. This book is directed to students and will be valuable to medical students, trainee neurologists, and professions allied to medicine. Neurologists often speak in shorthand and so entries such as ‘absence’ and ‘freezing’ are sensible and helpful. For the more mature student, there are the less usual as well as common eponyms to entice one to read further than the entry which took you first to the dictionary. Martin N. Rossor Professor of Clinical Neurology National Hospital for Neurology and Neurosurgery Queen Square London - ix - PREFACE TO THIRD EDITION To paraphrase John Hughlings Jackson (1835–1911), clinical phenomena are experiments on the nervous system made by disease. Neurological signs might therefore be (loosely) characterized as the ‘dependent variables’ of the experi- ments wrought by neurological disease. Observing or eliciting these signs may therefore give insight into neurological disease processes. (Details of neurolog- ical disorders mentioned in passing in this book may be found elsewhere, in a companion volume.1) However, as mentioned in the preface to the first edition of this book,2 the accuracy and precision of most neurological signs remain to be defined at the level of traditional probabilistic parameters (specificity, sensitivity, positive and negative predictive values, likelihood ratios, etc.), perhaps because this undertaking is a less alluring prospect for research than, say, neuroimaging and neurogenetics. Thankfully, the clinical examination still has some supporters (not merely apologists), and neurological signs feature prominently amongst the core competencies.3 Clinicians, as opposed to academics, may be ideally placed to undertake the aforementioned studies in the context of their day-to-day clinical practice. A.J. Larner REFERENCES 1. Larner AJ, Coles AJ, Scolding NJ, Barker RA. The A-Z of neurological practice. A guide to clinical neurology (2nd edition). London: Springer, in press. 2. Larner AJ. A dictionary of neurological signs. Clinical neurosemiology. Dordrecht: Kluwer, 2001: xii. 3. Verghese A, Horwitz RI. In praise of the physical examination. BMJ 2009; 339: b5448. - xi - ACKNOWLEDGEMENTS In preparing this third edition, particular thanks are due to friends and colleagues who have commented on the earlier editions, namely (in alphabetical order) Alasdair Coles, Anu Jacob, Alex Leff, Miratul Muqit, Parashkev Nachev, and Sivakumar Sathasivam. At Springer, I am grateful for support and encour- agement received from Paula Callaghan, Lindsey Reilly, Brian Belval, Brian O’Connor, Richard Lansing, and Manika Power. All errors and shortcomings whichremainareentirelymyownwork. - xiii - CONTENTS Foreword to the First Edition by Martin N. Rossor ix Preface to Third Edition xi Acknowledgements xiii A: Abadie’s Sign to Autotopagnosia 1 B: Babinski’s Sign to Butt-First Manoeuvre 55 C: Cacogeusia to Czarnecki’s Sign 71 D: Dalrymple’s Sign to Dystonia 101 E: Ear Click to Eyelid Apraxia 125 F: Face–hand Test to Funnel Vision 135 G: Gag Reflex to Gynaecomastia 155 H: Habit Spasm to Hypotropia 165 I: Ice Pack Test to Iridoplegia 193 J: Jacksonian March to Junctional Scotoma, Junctional Scotoma of Traquair 199 K: Kayser–Fleischer Rings to Kyphoscoliosis 203 L: Lagophthalmos to Luria Test 207 M: Macrographia to Myotonia 215 N: Narcolepsy, Narcoleptic Syndrome to Nystagmus 237 - xv - O: Obscurations to Overflow 247 P: Pagophagia to Pyramidal Signs, Pyramidal Weakness 259 Q: Quadrantanopia to Quadrupedalism 303 R: Rabbit Syndrome to Ross’s Syndrome 305 S: Saccades to Synkinesia, Synkinesis 319 T: ‘Table Top’ Sign to Two-Point Discrimination 343 U: Uhthoff’s Phenomenon to Utilization Behaviour 355 V: Valsalva Manoeuvre to Vulpian’s Sign 359 W: Waddling Gait to Wry Neck 369 X: Xanthopsia to Xerophthalmia, Xerostomia 377 Y: Yawning to Yo-Yo-Ing 379 Z: Zeitraffer Phenomenon to Zoom Effect 381 - xvi - A Abadie’s Sign Abadie’s sign is the absence or diminution of pain sensation when exerting deep pressure on the Achilles tendon by squeezing. This is a frequent finding in the tabes dorsalis variant of neurosyphilis, i.e. with dorsal column disease. Cross Reference Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the super- ficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdominal wall, from the flank to the midline, parallel to the line of the dermatomal strips, in upper (supraum- bilical), middle (umbilical), and lower (infraumbilical) areas. The manoeuvre is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. Superficial abdominal reflexes are lost in a number of circumstances: • Normal ageing; • Obesity; • Following abdominal surgery; • Following multiple pregnancies; • In acute abdominal disorders (Rosenbach’s sign). However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage (upper motor neurone lesions) above T6. Lesions at or below T10 lead to selective loss of the lower reflexes with the upper and middle reflexes intact, in which case Beevor’s sign may also be present. All abdominal reflexes are preserved with lesions below T12. Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the progressive lateral sclerosis variant of motor neurone disease from multiple sclerosis. However, no prospective study of abdominal reflexes in multiple sclerosis has been reported. Reference Dick JPR. The deep tendon and the abdominal reflexes. Journal of Neurology, Neurosurgery and Psychiatry 2003; 74: 150–153. Cross References Beevor’s sign; Upper motor neurone (UMN) syndrome A.J. Larner, A Dictionary of Neurological Signs, 1 DOI 10.1007/978-1-4419-7095-4_1, C Springer Science+Business Media, LLC 2011 A Abducens (VI) Nerve Palsy Abducens (VI) Nerve Palsy Abducens (VI) nerve palsy causes a selective weakness of the lateral rectus mus- cle resulting in impaired abduction of the eye, manifest clinically as diplopia on lateral gaze, or on shifting gaze from a near to a distant object. Abducens (VI) nerve palsy may be due to: • Microinfarction in the nerve, due to hypertension, diabetes mellitus; • Raised intracranial pressure: a ‘false-localizing sign’, possibly caused by stretching of the nerve in its long intracranial course over the ridge of the petrous temporal bone; • Nuclear pontine lesions: congenital, e.g.
Recommended publications
  • A Case with Dyskinesia Induced by Pramipexole, Pregabalin And
    DO I:10.4274/Tnd.63497 Case Report / Olgu Sunumu A Case with Dyskinesia Induced by Pramipexole, Pregabalin and Gabapentin After Cardiopulmonary Resuscitation Kardiyopulmoner Resusitasyon Sonrası Pramipeksol, Pregabalin ve Gabapentin Kullanımının Tetiklediği Diskinezi Olgusu Dürdane Aksoy, Betül Çevik, Volkan Solmaz, Semiha Gülsüm Kurt, Orhan Sümbül Gaziosmanpaşa University School of Medicine, Department of Neurology, Tokat, Turkey Sum mary Drug-induced dyskinesias can be seen occasionally in clinical practice. Here we present a 70-year-old patient who developed a noticeable dyskinesia after the use of pramipexole, gabapentin, pregabalin respectively for his restless leg syndrome. Prior to this condition, he was hospitalized in intensive care unit for the myocardial infarction that required cardiopulmonary resuscitation, and he was discharged with no neurological deficits. The case presented here is a good example indicating the importance of being vigilant for drug-induced dyskinesias after hypoxic-ischemic encephalopathy, even though everything else seems right. (Turkish Journal of Neurology 2013; 19:148-150) Key Words: Hypoxic-ischemic encephalopathy, dyskinesia, pramipexole, gabapentin, pregabalin Özet İlaç kullanımı sonrasında ortaya çıkan hareket bozuklukları klinik pratikte zaman zaman karşılaştığımız sorunlardır. Burada kardiyopulmoner resüsitasyon gerektiren bir miyokard enfarktüsünün ardından bir süre yoğun bakımda kalan, nörolojik defisiti kalmadan iyileşen ancak daha sonra huzursuz bacak sendromu tedavisi için başlanan pramipeksol,
    [Show full text]
  • Sciencedirect.Com Sciencedirect
    cortex 89 (2017) 135e155 Available online at www.sciencedirect.com ScienceDirect Journal homepage: www.elsevier.com/locate/cortex Research report Agnosic vision is like peripheral vision, which is limited by crowding Francesca Strappini a,b,c, Denis G. Pelli d, Enrico Di Pace a and * Marialuisa Martelli a,b, a Department of Psychology, University of Rome La Sapienza, Rome, Italy b Neuropsychology Research Centre, IRCCS Foundation Hospital Santa Lucia, Rome, Italy c Neurobiology Department, Weizmann Institute of Science, Rehovot, Israel d Department of Psychology and Center for Neural Science, New York University, New York, NY, USA article info abstract Article history: Visual agnosia is a neuropsychological impairment of visual object recognition despite Received 23 April 2014 near-normal acuity and visual fields. A century of research has provided only a rudimen- Reviewed 14 July 2014 tary account of the functional damage underlying this deficit. We find that the object- Revised 24 October 2014 recognition ability of agnosic patients viewing an object directly is like that of normally- Accepted 13 January 2017 sighted observers viewing it indirectly, with peripheral vision. Thus, agnosic vision is Action editor Jason Barton like peripheral vision. We obtained 14 visual-object-recognition tests that are commonly Published online 1 February 2017 used for diagnosis of visual agnosia. Our “standard” normal observer took these tests at various eccentricities in his periphery. Analyzing the published data of 32 apperceptive Keywords: agnosia patients and a group of 14 posterior cortical atrophy (PCA) patients on these tests, Visual agnosia we find that each patient's pattern of object recognition deficits is well characterized by one Crowding number, the equivalent eccentricity at which our standard observer's peripheral vision is like Object recognition the central vision of the agnosic patient.
    [Show full text]
  • Approach to a Case of Congenital Heart Disease
    BAI JERBAI WADIA HOSPITAL FOR CHILDREN PEDIATRIC CLINICS FOR POST GRADUATES PREFACE This book is a compilation of the discussions carried out at the course for post-graduates on ” Clinical Practical Pediatrics” at the Bai Jerbai Wadia Hospital for Children, Mumbai. It has been prepared by the teaching faculty of the course and will be a ready-reckoner for the exam-going participants. This manual covers the most commonly asked cases in Pediatric Practical examinations in our country and we hope that it will help the students in their practical examinations. An appropriately taken history, properly elicited clinical signs, logical diagnosis with the differential diagnosis and sound management principles definitely give the examiner the feeling that the candidate is fit to be a consultant of tomorrow. Wishing you all the very best for your forthcoming examinations. Dr.N.C.Joshi Dr.S.S.Prabhu Program Directors. FOREWARD I am very happy to say that the hospital has taken an initiative to organize this CME for the postgraduate students. The hospital is completing 75 years of its existence and has 2 done marvelous work in providing excellent sevices to the children belonging to the poor society of Mumbai and the country. The hospital gets cases referred from all over the country and I am proud to say that the referrals has stood the confidence imposed on the hospital and its faculty. We do get even the rarest of the rare cases which get diagnosed and treated. I am sure all of you will be immensely benefited by this programme. Wish you all the best in your examination and career.
    [Show full text]
  • Cognitive Emotional Sequelae Post Stroke
    11/26/2019 The Neuropsychology of Objectives 1. Identify various cognitive sequelae that may result from stroke Stroke: Cognitive & 2. Explain how stroke may impact emotional functioning, both acutely and long-term Emotional Sequelae COX HEALTH STROKE CONFERENCE BRITTANY ALLEN, PHD, ABPP, MBA 12/13/2019 Epidemiology of Stroke Stroke Statistics • > 795,000 people in the United States have a stroke • 5th leading cause of death for Americans • ~610,000 are first or new strokes • Risk of having a first stroke is nearly twice as high for blacks as whites • ~1/4 occur in people with a history of prior stroke • Blacks have the highest rate of death due to stroke • ~140,000 Americans die every year due to stroke • Death rates have declined for all races/ethnicities for decades except that Hispanics have seen • Approximately 87% of all strokes are ischemic an increase in death rates since 2013 • Costs the United States an estimated $34 billion annually • Risk for stroke increases with age, but 34% of people hospitalized for stroke were < 65 years of • Health care services age • Medicines to treat stroke • Women have a lower stroke risk until late in life when the association reverses • Missed days of work • Approximately 15% of strokes are heralded by a TIA • Leading cause of long-term disability • Reduces mobility in > 50% of stroke survivors > 65 years of age Source: Centers for Disease Control Stroke Death Rates Neuropsychological Assessment • Task Engagement • Memory • Language • Visuospatial Functioning • Attention/Concentration • Executive
    [Show full text]
  • Lack of Motivation: Akinetic Mutism After Subarachnoid Haemorrhage
    Netherlands Journal of Critical Care Submitted October 2015; Accepted March 2016 CASE REPORT Lack of motivation: Akinetic mutism after subarachnoid haemorrhage M.W. Herklots1, A. Oldenbeuving2, G.N. Beute3, G. Roks1, G.G. Schoonman1 Departments of 1Neurology, 2Intensive Care Medicine and 3Neurosurgery, St. Elisabeth Hospital, Tilburg, the Netherlands Correspondence M.W. Herklots - [email protected] Keywords - akinetic mutism, abulia, subarachnoid haemorrhage, cingulate cortex Abstract Akinetic mutism is a rare neurological condition characterised by One of the major threats after an aneurysmal SAH is delayed the lack of verbal and motor output in the presence of preserved cerebral ischaemia, caused by cerebral vasospasm. Cerebral alertness. It has been described in a number of neurological infarction on CT scans is seen in about 25 to 35% of patients conditions including trauma, malignancy and cerebral ischaemia. surviving the initial haemorrhage, mostly between days 4 and We present three patients with ruptured aneurysms of the 10 after the SAH. In 77% of the patients the area of cerebral anterior circulation and akinetic mutism. After treatment of the infarction corresponded with the aneurysm location. Delayed aneurysm, the patients lay immobile, mute and were unresponsive cerebral ischaemia is associated with worse functional outcome to commands or questions. However, these patients were awake and higher mortality rate.[6] and their eyes followed the movements of persons around their bed. MRI showed bilateral ischaemia of the medial frontal Cases lobes. Our case series highlights the risk of akinetic mutism in Case 1: Anterior communicating artery aneurysm patients with ruptured aneurysms of the anterior circulation. It A 28-year-old woman with an unremarkable medical history is important to recognise akinetic mutism in a patient and not to presented with a Hunt and Hess grade 3 and Fisher grade mistake it for a minimal consciousness state.
    [Show full text]
  • Analyzing Cohesive Devices in the Students Narrative
    ANALYZING COHESIVE DEVICES IN THE STUDENTS NARRATIVE TEXT WRITTEN BASED ON FRONT OF THE CLASS MOVIE SCRIPT (A Descriptive Research at the Third Semester in Muhammadiyah University of Makassar ) A THESIS Submitted at the Fulfillment to Accomplish Sarjana Degree at Faculty of Teacher Training and Education Makassar Muhammadiyah University MARSELLA 10535661515 ENGLISH EDUCATION DEPARTMENT FACULTY OF TEACHER TRAINING AND EDUCATION MUHAMMADIYAH UNIVERSITY OF MAKASSAR 2020 Jalan Sultan Alauddin No. 259Makassar UNIVERSITAS MUHAMMADIYAH MAKASSAR Telp : 0411-860837/860132 (Fax) FAKULTAS KEGURUAN DAN ILMU PENDIDIKANEmail : [email protected] Web : www.fkp.unismuh.ac.id PRODI PENDIDIKAN BAHASA INGGRIS SURAT PERNYATAAN Saya yang bertandatangan di bawah ini: Nama : Marsella NIM : 10535 6615 15 Jurusan : Pendidikan Bahasa Inggris Judul Skripsi : Analyzing Cohesive Devices In The Students Narrative Text Written Based On Front Of The Class Movie Script Dengan ini menyatakan bahwa skripsi yang saya buat di depan Tim penguji adalah hasil karya saya sendiri bukan hasil ciptaan orang lain atau pun dibuatkan oleh siapa pun. Demikianlah pernyataan ini saya buat dengan sebenar-benarnya dan saya bersedia menerima sanksi apabila pernyataan ini tidak benar. Makassar, 2020 Yang Membuat Pernyataan Marsella Jalan Sultan Alauddin No. 259Makassar UNIVERSITAS MUHAMMADIYAH MAKASSAR Telp : 0411-860837/860132 (Fax) FAKULTAS KEGURUAN DAN ILMU PENDIDIKANEmail : [email protected] Web : www.fkp.unismuh.ac.id PRODI PENDIDIKAN BAHASA INGGRIS SURAT PERJANJIAN Saya yang bertandatangan di bawah ini: Nama : Marsella NIM : 10535 6615 15 Jurusan : Pendidikan Bahasa Inggris Fakultas : Keguruan dan Ilmu Pendidikan Dengan ini menyatakan perjanjian sebagai berikut: 1. Mulai dari penyusunan proposal sampai dengan selesainya skripsi saya, saya akan menyusun sendiri skripsi saya, tidak dibuatkan oleh siapa pun.
    [Show full text]
  • Basilar Artery and Its Branches Called Pontine Arteries
    3 Farah Mohammad Ahmad Al-Tarefe Mohammad Al salem تذكر أ َّن : أولئك الذين بداخلهم شيء يفوق كل الظروف ، هم فقط من استطاعوا أ ّن يحققوا انجازاً رائعاً .... كن ذا همة Recommendation: Study this sheet after you finish the whole anatomy material . Dr.Alsalem started talking about the blood supply for brain and spinal cord which are mentioned in sheet#5 so that we didn't write them . 26:00-56:27/ Rec.Lab#3 Let start : Medulla oblengata : we will study the blood supply in two levels . A- Close medulla (central canal) : It is divided into four regions ; medial , anteromedial , posteriolateral and posterior region. Medially : anterior spinal artery. Anteromedial: vertebral artery posterolateral : posterior inferior cerebellar artery ( PICA). Posterior : posterior spinal artery which is a branch from PICA. B-Open medulla ( 4th ventricle ) : It is divided into four regions ; medial , anteromedial , posteriolateral region. Medially : anterior spinal artery. Anteromedial: vertebral artery posterolateral : posterior inferior cerebellar artery ( PICA). 1 | P a g e Lesions: 1- Medial medullary syndrome (Dejerine syndrome): It is caused by a lesion in anterior spinal artery which supplies the area close to the mid line. Symptoms: (keep your eyes on right pic). Contralateral hemiparesis= weakness: the pyramid will be affected . Contralateral loss of proprioception , fine touch and vibration (medial lemniscus). Deviation of the tongue to the ipsilateral side when it is protruded (hypoglossal root or nucleus injury). This syndrome is characterized by Alternating hemiplegia MRI from Open Medulla (notice the 4th ventricle) Note :The Alternating hemiplegia means ; 1- The upper and lower limbs are paralyzed in the contralateral side of lesion = upper motor neuron lesion .
    [Show full text]
  • Neurological Disorders in Liver Transplant Candidates: Pathophysiology ☆ and Clinical Assessment
    Transplantation Reviews 31 (2017) 193–206 Contents lists available at ScienceDirect Transplantation Reviews journal homepage: www.elsevier.com/locate/trre Neurological disorders in liver transplant candidates: Pathophysiology ☆ and clinical assessment Paolo Feltracco a,⁎, Annachiara Cagnin b, Cristiana Carollo a, Stefania Barbieri a, Carlo Ori a a Department of Medicine UO Anesthesia and Intensive Care, Padova University Hospital, Padova, Italy b Department of Neurosciences (DNS), University of Padova, Padova, Italy abstract Compromised liver function, as a consequence of acute liver insufficiency or severe chronic liver disease may be associated with various neurological syndromes, which involve both central and peripheral nervous system. Acute and severe hyperammoniemia inducing cellular metabolic alterations, prolonged state of “neuroinflamma- tion”, activation of brain microglia, accumulation of manganese and ammonia, and systemic inflammation are the main causative factors of brain damage in liver failure. The most widely recognized neurological complications of serious hepatocellular failure include hepatic encephalopathy, diffuse cerebral edema, Wilson disease, hepatic myelopathy, acquired hepatocerebral degeneration, cirrhosis-related Parkinsonism and osmotic demyelination syndrome. Neurological disorders affecting liver transplant candidates while in the waiting list may not only sig- nificantly influence preoperative morbidity and even mortality, but also represent important predictive factors for post-transplant neurological manifestations.
    [Show full text]
  • Second Edition
    COVID-19 Evidence Update COVID-19 Update from SAHMRI, Health Translation SA and the Commission on Excellence and Innovation in Health Updated 4 May 2020 – 2nd Edition “What is the prevalence, positive predictive value, negative predictive value, sensitivity and specificity of anosmia in the diagnosis of COVID-19?” Executive Summary There is widespread reporting of a potential link between anosmia (loss of smell) and ageusia (loss of taste) and SARS-COV-2 infection, as an early sign and with sudden onset predominantly without nasal obstruction. There are calls for anosmia and ageusia to be recognised as symptoms for COVID-19. Since the 1st edition of this briefing (25 March 2020), there has been a significant expansion of literature on this topic, including 3 systematic reviews. Predictive value: The reported prevalence of anosmia/hyposmia and ageusia/hypogeusia in SARS-COV-2 positive patients are in the order of 36-68% and 33-71% respectively. There are reports of anosmia as the first symptom in some patients. Estimates from one study for hyposmia and hypogeusia: • Positive likelihood ratios: 4.5 and 5.8 • Sensitivity: 46% and 62% • Specificity: 90% and 89% The US Centres for Disease Control and Prevention (CDC) has added new loss or taste or smell to its list of recognised symptoms for SARS-COV-2 infection. To date, the World Health Organization has not. Conclusion: There is sufficient evidence to warrant adding loss of taste and smell to the list of symptoms for COVID-19 and promoting this information to the public. Context • Early detection of COVID-19 is key to the ongoing management of the pandemic.
    [Show full text]
  • Unifying the Motor & Non-Motor Features of Parkinson's Disease
    Unifying the Motor & Non-motor Features of Parkinson’s Disease Ali Shalash Professor of Neurology Chair of Ain Shams Movement Disorders Group Department of Neurology, Ain Shams Univeristy Cairo, Egypt AGENDA 1. Motor and non-motor Symptoms 2. Pathophysiology of Motor & NMS 3. Relation To Disease Course 4. NMS in motor subtypes 5. Motor & NMS fluctuation 6. Treatment of Motor & NMS: links Parkinson’s Disease • PD prevalence 1 % of populations older than 65 years (Abbas et al., 2018) • From 1990 to 2015, the number of with PD patients doubled to over 6 million, and double again to over 12 million by 2040 (Dorsey et al, 2018) • Aging populations, increasing longevity, decreasing smoking rates, and the by- products of industrialization MDS Clinical Diagnostic Criteria for PD Postuma et al 2015 MDS Clinical Diagnostic Criteria for PD Postuma et al 2015 Non-motor Symptoms of PD • Neuropsychiatric symptoms • Autonomic dysfunction • Depression up to 50-70 % • Drooling • Anxiety up to 60 % • Orthostatic hypotension 30–58% • Apathy 60 % • Urinary dysfunction • Psychosis up to 40% • Erectile dysfunction • Impulse control and related disorders • Gastrointestinal dysfunction 25–67% • Dementia, 24% to 40%. • Excessive sweating • Cognitive impairment 20-25% (other • Others than dementia mainly mild cognitive impairment) • Pain 30–85% • Fatigue 50% • Disorders of sleep and wakefulness • Olfactory dysfunction 90% • • Sleep fragmentation and insomnia Ophthalmologic dysfunction • Rapid eye movement sleep behavior disorder 65 % • Excessive daytime sleepiness Pathophysiology of Motor & NMS Neuropathology of PD: Motor Symptoms Two major pathologic processes: (a) premature selective loss of dopamine neurons: 30–70% cell loss ⇢ motor symptoms. (b) the accumulation of Lewy bodies, composed of α-synuclein Poewe, W.
    [Show full text]
  • Síndrome De Tourette: Uma Análise Biográfica a Partir Do Filme “O Primeiro Da Classe”
    SÍNDROME DE TOURETTE: UMA ANÁLISE BIOGRÁFICA A PARTIR DO FILME “O PRIMEIRO DA CLASSE” Anne Caroline Silva Aires – Graduanda em Pedagogia José Batista de Farias Neto- Graduando em História Martha Valéria Silva Araújo– Graduanda em Pedagogia Adenize Queiroz de Farias- Orientadora Universidade Estadual da Paraíba (UEPB) [email protected] [email protected] [email protected] [email protected] Resumo A Síndrome de Tourette (ST) é uma síndrome neuropsiquiátrica que integra o espectro dos transtornos de tiques. Tiques são vocalizações ou movimentos involuntários, rápidos, não-rítmicos, repetitivos e estereotipados. Partindo deste pressuposto escolhemos o filme “O Primeiro da Classe”, para melhor entender e compreender como ocorre essa síndrome em Brad e como ele reagiu aos preconceitos encontrados na sociedade. Este artigo tem por objetivo analisar os fatores interligando os conteúdos pesquisados sobre a Tourette com os autores Loureiro (2012), Jankovic (2001) e Metz (2007) e com relação ao filme destacando os planos e sequência mais marcantes do mesmo. Nesta situação o filme supracitado traz uma história biográfica de Brad Cohen que desde os seus sete anos de idade sofre rejeições, tanto das instituições de ensino que estudou, quanto pelo seu pai. Na maior parte das vezes, o preconceito é resultado de falta de informação, desconhecimento, ignorância. De fato, algumas pessoas buscam algum tipo de segurança quando escolhem encapsular a diferença de alguém em algum tipo de rótulo. Essas rejeições se davam porque Brad fazer "barulhos", e as pessoas não entendiam, achava que era uma brincadeira de mau gosto e o desprezavam e o castigavam por isso. Brad nunca foi vítima da sua deficiência.
    [Show full text]
  • Dissociation Between Awareness and Spatial Coding: Evidence from Unilateral Neglect
    Dissociation between Awareness and Spatial Coding: Evidence from Unilateral Neglect Barbara Treccani1, Roberto Cubelli1, Roberta Sellaro1, Carlo Umiltà2, and Sergio Della Sala3 Downloaded from http://mitprc.silverchair.com/jocn/article-pdf/24/4/854/1777452/jocn_a_00185.pdf by MIT Libraries user on 17 May 2021 Abstract ■ Prevalent theories about consciousness propose a causal re- dissociate. A patient with left neglect, who was not aware of lation between lack of spatial coding and absence of conscious contralesional stimuli, was able to process their color and po- experience: The failure to code the position of an object is sition. However, in contrast to (ipsilesional) consciously per- assumed to prevent this object from entering consciousness. ceived stimuli, color and position of neglected stimuli were This is consistent with influential theories of unilateral neglect processed separately. We propose that individual object fea- following brain damage, according to which spatial coding of tures, including position, can be processed without attention neglected stimuli is defective, and this would keep their process- and consciousness and that conscious perception of an ob- ing at the nonconscious level. Contrary to this view, we report ject depends on the binding of its features into an integrated evidence showing that spatial coding and consciousness can percept. ■ INTRODUCTION the effects of processing of neglected stimuli on responses Awareness of a stimulus can be defined as the explicit to stimuli presented in the intact hemispace. Properties knowledge of its physical and semantic properties or sim- that can be processed implicitly include color and shape, ply of its existence. This knowledge can be demonstrated identity of alphanumerical symbols, and even the mean- by direct reports of the perception of the stimulus; for ing of words and pictures (Della Sala, van der Meulen, example, by naming it, categorizing it, or just by signaling Bestelmeyer, & Logie, 2010; Làdavas, Paladini, & Cubelli, its presence.
    [Show full text]