Reverse Engineering Your Neurology Exam

Total Page:16

File Type:pdf, Size:1020Kb

Reverse Engineering Your Neurology Exam Reverse Engineering your Neurology Exam Alex Gillingham & Alex Reynolds Lead Physician Associates National Hospital of Neurology & Neurosurgery FPA CPD Conference October 2019 Objectives • Key history aspects • Simple neuro-anatomy • Localisation • Approach to exam • Case examples Why We Do What We Do History = When & What Exam = Where & Why Why We Do What We Do History is KEY focuses exam For each section: Think Why? What does it mean? Exam: • Refine localisation and differential • Looks for additional signs -> change diagnosis Speed of symptoms Tempo pathology •Instantaneous epilepsy (electrical) or vascular •Seconds – hours Ischemia (evolving stroke) or infection •Hours – days inflammatory, or infection •Weeks – months autoimmune, neoplastic, infection (TB) Exam Section Location • Mental status supratentorial, cerebral hemispheres • Cranial Nerves brainstem & posterior fossa • Coordination Cerebellum • Sensory Spinal thalamic tracts • Motor corticospinal tract & LMN • Gait coordination various areas SUPRATENTORIAL INFRATENTORIAL TRACTS SPINAL CORD PERIPHERAL NERVE Tracts, lots and LOTS of Tracts • About 150+ different tracts identified so far • Each tract transmits signals from one part of the nervous system to another • Most well known are: Corticospinal, corticobular and spinal thalamic What are tracts? • Tracts themselves are specific UMN bundles with a specific origin and ending within the central nervous system. • Still confused??? Imagine a power station (the Brain) The power station needs to supply electricity to a house (the limb) To send electricity, the power station uses electric pylons to transmit signals to the house (neural-tracts) The house uses the electricity as a light switch (Bicep), kettle (tricep), phone charger (brachio- radialis) etc. • This is an example of the corticospinal tract. Cortex Spinal tract LMN or peripheral nerves Case: ‘Facial Weakness’ • Fast onset • Differential diagnosis? • Stroke/CVA, Bells palsy – Rarely – Ramsay hunt syndrome, brain stem tumours. Case: ‘Facial Weakness’ Key areas for exam? •CN exam – Specifically which CN nerves? •Motor •Sensation Location Location LOCATION! • There are 3 key areas where a stroke can occur for isolated facial weakness. – Motor cortex – Brain stem – Peripheral nerves • Have you ever asked the question: • How do you get facial weakness in an MCA stroke? Cortico - bulbar tract • Facial motor innervation is via the cortico- bulbar tract • Nerve bundles which relay cortex signals to the brain stem. • The cortico-bulbar tract innervates the NUCELUS of CN 7 But what about forehead sparing? Bells Palsy But…… • Isolated facial weaknesses rarely happens. • What if a patient comes to you with facial weakness, with arm weakness (1/5) and leg weakness (3/5)? Case - Arm and leg weakness • Its all about your history and examination! Strength scale Out of 5 0 = no movement 1 = muscle flicker 2 = movement without gravity 3= movement against gravity, with no resistance 4= Movement against gravity with mild resistance 5 = full power Strength - exam pearls • Test each side individually COMPARE AND CONTRAST EACH SIDE • Ask patient to do movement against gravity 1st power at least = 3 • Only need maximal strength for 1 second – If ?pain limitation – prompt 1,2,3 GO! Case - Arm and leg weakness Corticospinal tract • Information for motor function travels down the corticospinal tract. • Contralateral nerve innervation happens because the tract crosses over the decussation in the medulla oblongata. General principles of weakness in CVA • If ARM weakness is GREATER than LEG weakness – MORE LIKELY AN MCA STROKE • If LEG weakness is greater than ARM weakness – More likely ACA STROKE BUT….. • Why do we do sensory exams???? • The central gyrus: – Motor- PRE-central (more forward) – Sensory- POST-central Sensory exam • Sensory exam is divided into 5 separate segments: • Light touch • Sharp dull • Vibration • Proprioception • Temperature Lets say… • Our patient has facial weakness + arm weakness with reduced light touch in their arm. Somatosensory tracts • A two stage tract • These tracts usually go via the THALAMUS • Motor tracts are usually 1 single tract which terminate in the cortex. Why is this important? • Location • Location • LOCATION! Sensory exam 2 main sensory • 5 key areas: tracts: • Light touch • Spinothalamic • Sharp dull • Dorsal column • Proprioception Supratentoral • Temperature • Vibration • Thalamus • Cortex Spinothalamic: Pain and Light touch Dorsal column: Proprioception and vibration and temperature (Some light touch goes via dorsal column!!!!) Always use sharp dull when assessing the spinothalamic tract Spino-thalamic • 3 key areas for a CNS lesion: • Thalamus • Spinal cord • Cortex Sensory exam • The sensory exam examines different areas of the SPINAL CORD and to an extent the thalamus + cortex. • VERY important in spinal cord injury patients, as it affects management and rehabilitation potential • ASIA scores- • Single biggest indicator for spinal cord injury is weakness and reduced/absent sensory examinations • You can then locate the level of the injury at level of the dermatome. So…. Lets say… • Facial weakness + arm weakness with reduced sharp dull in their arm. • Where are the possible lesion locations? • If the patient had reduced vibration and proprioception. • Which part of the spine are you examining for? • Where could the lesions be? Almost there… • Our patient has facial weakness, arm weakness and reduced light touch in their arm • Where are the possible locations for their lesion? • If our patient has facial weakness, arm weakness and a NORMAL sensation exam • Where are the possible locations for their lesion? Finally… Leg weakness with abnormal vibration? Case: ‘Clumsy walking’ D/Dx •Neuro –cerebellar disease – sensory issues –Vestibular •Neurosurgical – stroke – hydrocephalus Case: ‘Clumsy walking’ Key areas for exam? •Gait – normal & tandem •Coordination •Proprioception (eye movements) Exam: Gait High stepping gait Exam: Gait Gait Disturbance – helps localise the problem •Sensory/ Proprioception – ‘high stepping’ – AND Joint-position, vibration reduced •Vestibular – veers to affected side • AND Nystagmus Exam: Gait Wide-based gait Tandem walk elicits earlier signs of ataxia Note truncal ataxia Exam: Gait • Bradykinesia Parkinsonism • Shuffling • Stooped • Reduced arm swing Exam: Gait Gait Disturbance – helps localise the problem •Cerebellar – broad-based, irregular – AND Incoordination, rebound •Basal Ganglia (parkinsonism) – shuffling, festination, stooped, no arm-swing – AND bradykinesia, resting tremor, rigidity What to examine Next? Exam: Coordination – Rapid-alternating movements • rate, amplitude, rhythm, force • Dysdiadochokinesia – clumsy, irregular – Upper Limb: Finger-nose • Intention tremor • Dysmetria – past-pointing – Lower Limb: Heel – Shin • Ataxia – Rebound/ Overshoot Cerebellum Controls… •INTEGRATES sensory & Motor subsystems VESTIBULAR SYSTEM LIMB & POSTURAL MUSCLES PROPRIOCEPTIVE (spinocerebellar) CEREBELLUM MOTOR PLAN THALAMUS (Cerebral Motor Cortex) Exam Pearls: Coordination Clear instructions & Demo Dysmetria - Past-pointing/ overshoot – requires extension away from the body Dysdiadochokinesia– listen to ask much as you hear it! – Irregular rhythm Lack of smooth movements Sign Cerebellar location Truncal ataxia – Midline Ataxia Cerebellar MIDLINE Exam Tests: • Truncal stability • Walking/ Gait • Tandem gait Sign Cerebellar location Appendicular ataxia – extremities control Cerebellar Hemispheres Exam Tests: • Rapid alternating movements • Finger-to-nose • Toe-to-finger • Heel-to-shin • Rebound • Speech - dysarthria Rombergs NOT a specific cerebellar test! Localisation UMN Brain Brain stem or cord - Cerebral cortex - Brainstem - White matter- tracts (spinal cord) LMN Brain stem or cord Skeletal muscles - Motor cranial nerves - Anterior horn (Spinal cord) - Neuronal Axons - NMJ Signs Localisation LMN UMN • Wasting • No wasting • Weakness • Increased tone • Fasciculation (spasticity) • Reduced tone • Hyper-reflexia • Reduced reflexes • Upward plantars BUT WHY??? Lower Motor Neuron • ‘Final common LMN • Wasting pathway’ lost • Weakness • Immediate innervation • Fasciculation • Reduced/ loss of tone to muscle lost • Reduced/ loss of reflexes • Muscle is de-nervated • LOSS of innervation Upper Motor Neuron • Unregulated innervation • No inhibitory effect from the UMN • Constant “firing” developing into spasticity • INCREASE in all areas • Isolated weakness – anywhere in cortex to spinal cord • Global weakness + facial weakness – Cortex and/or brainstem • Global sensory with global weakness- Cortical or spinal if there is a level. • Complete loss of proprioception with preserved motor function –Dorsal column lesion Take away points 1. Always compare and contrast by isolating muscle groups 2. Think about where in the CNS you want to examine 3. Take your time getting a great history 4. Watch your patient walk in and shake their hand! Resources www.neuroexam.com Uni of Utah NeuroLogical Cases Uni of Toronto Neurological Exam ANY QUESTIONS?.
Recommended publications
  • New Observations Letters Familial Spinocerebellar Ataxia Type 2 Parkinsonism Presenting As Intractable Oromandibular Dystonia
    Freely available online New Observations Letters Familial Spinocerebellar Ataxia Type 2 Parkinsonism Presenting as Intractable Oromandibular Dystonia 1,2 2,3 1,3* Kyung Ah Woo , Jee-Young Lee & Beomseok Jeon 1 Department of Neurology, Seoul National University Hospital, Seoul, KR, 2 Department of Neurology, Seoul National University Boramae Hospital, Seoul, KR, 3 Seoul National University College of Medicine, Seoul, KR Keywords: Dystonia, spinocerebellar ataxia type 2, Parkinson’s disease Citation: Woo KA, Lee JY, Jeon B. Familial spinocerebellar ataxia type 2 parkinsonism presenting as intractable oromandibular dystonia. Tremor Other Hyperkinet Mov. 2019; 9. doi: 10.7916/D8087PB6 * To whom correspondence should be addressed. E-mail: [email protected] Editor: Elan D. Louis, Yale University, USA Received: October 20, 2018 Accepted: December 10, 2018 Published: February 21, 2019 Copyright: ’ 2019 Woo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution–Noncommercial–No Derivatives License, which permits the user to copy, distribute, and transmit the work provided that the original authors and source are credited; that no commercial use is made of the work; and that the work is not altered or transformed. Funding: None. Financial Disclosures: None. Conflicts of Interest: The authors report no conflict of interest. Ethics Statement: This study was reviewed by the authors’ institutional ethics committee and was considered exempted from further review. We have previously described a Korean family afflicted with reflex, mildly stooped posture, and parkinsonian gait. There was spinocerebellar ataxia type 2 (SCA2) parkinsonism in which genetic no sign of lower motor lesion, including weakness, muscle atrophy, analysis revealed CAG expansion of 40 repeats in the ATXN2 gene.1 or fasciculation.
    [Show full text]
  • Cramp Fasciculation Syndrome: a Peripheral Nerve Hyperexcitability Disorder Bhojo A
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by eCommons@AKU Pakistan Journal of Neurological Sciences (PJNS) Volume 9 | Issue 3 Article 7 7-2014 Cramp fasciculation syndrome: a peripheral nerve hyperexcitability disorder Bhojo A. Khealani Aga Khan University Hospital, Follow this and additional works at: http://ecommons.aku.edu/pjns Part of the Neurology Commons Recommended Citation Khealani, Bhojo A. (2014) "Cramp fasciculation syndrome: a peripheral nerve hyperexcitability disorder," Pakistan Journal of Neurological Sciences (PJNS): Vol. 9: Iss. 3, Article 7. Available at: http://ecommons.aku.edu/pjns/vol9/iss3/7 CASE REPORT CRAMP FASCICULATION SYNDROME: A PERIPHERAL NERVE HYPEREXCITABILITY DISORDER Bhojo A. Khealani Assistant professor, Neurology section, Aga khan University, Karachi Correspondence to: Bhojo A Khealani, Department of Medicine (Neurology), Aga Khan University, Karachi. Email: [email protected] Date of submission: June 28, 2014, Date of revision: August 5, 2014, Date of acceptance:September 1, 2014 ABSTRACT Cramp fasciculation syndrome is mildest among all the peripheral nerve hyperexcitability disorders, which typically presents with cramps, body ache and fasciculations. The diagnosis is based on clinical grounds supported by electrodi- agnostic study. We report a case of young male with two months’ history of body ache, rippling, movements over calves and other body parts, and occasional cramps. His metabolic workup was suggestive of impaired fasting glucose, radio- logic work up (chest X-ray and ultrasound abdomen) was normal, and electrodiagnostic study was significant for fascicu- lation and myokymic discharges. He was started on pregablin and analgesics. To the best of our knowledge this is report first of cramp fasciculation syndrome from Pakistan.
    [Show full text]
  • Cerebellar Ataxia with Neuropathy and Vestibular Areflexia Syndrome
    n e u r o l o g i a i n e u r o c h i r u r g i a p o l s k a 4 8 ( 2 0 1 4 ) 3 6 8 – 3 7 2 Available online at www.sciencedirect.com ScienceDirect journal homepage: http://www.elsevier.com/locate/pjnns Case report Cerebellar ataxia with neuropathy and vestibular areflexia syndrome (CANVAS) – A case report and review of literature a a b a, Monika Figura , Małgorzata Gaweł , Anna Kolasa , Piotr Janik * a Department of Neurology, Medical University of Warsaw, Warsaw, Poland b 2nd Department of Clinical Radiology, Medical University of Warsaw, Warsaw, Poland a r t i c l e i n f o a b s t r a c t Article history: CANVAS (cerebellar ataxia with neuropathy and vestibular areflexia syndrome) is a rare Received 19 March 2014 neurological syndrome of unknown etiology. The main clinical features include bilateral Accepted 27 August 2014 vestibulopathy, cerebellar ataxia and sensory neuropathy. An abnormal visually enhanced Available online 6 September 2014 vestibulo-ocular reflex is the hallmark of the disease. We present a case of 58-year-old male patient who has demonstrated gait disturbance, imbalance and paresthesia of feet for 2 fl Keywords: years. On examination ataxia of gait, diminished knee and ankle re exes, absence of plantar reflexes, fasciculations of thigh muscles, gaze-evoked downbeat nystagmus and abnormal Cerebellar ataxia with neuropathy visually enhanced vestibulo-ocular reflex were found. Brain magnetic resonance imaging and vestibular areflexia syndrome revealed cerebellar atrophy. Vestibular function testing showed severely reduced horizontal Cerebellar ataxia nystagmus in response to bithermal caloric stimulation.
    [Show full text]
  • Facial Myokymia: a Clinicopathological Study
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.37.6.745 on 1 June 1974. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry, 1974, 37, 745-749 Facial myokymia: a clinicopathological study P. K. SETHI1, BERNARD H. SMITH, AND K. KALYANARAMAN From the Department of Neurology, Edward J. Meyer Memorial Hospital anid School of Medicine, State University of New York at Buffalo, N. Y., U.S.A. SYNOPSIS Clinicopathological correlations are presented in a case of facial myokymia with facial palsy. The causative lesions were considered to be metastatic tumours to the pons and it was con- cluded that both the facial palsy and the myokymia were due to interruption of supranuclear path- ways impinging on the facial nucleus. Oppenheim (1916) described a patient with con- CASE REPORT tinuous undulation and fasciculation in the right A 57 year old white man was admitted to hospital on facial muscles. The movements had started in the 30 December 1971, suffering from productive cough, infraorbital region and progressed to involve the haemoptysis, and weight loss of some months' dura- entire territory of the facial nerve. He called the tion. He had been a heavy smoker for many years. Protected by copyright. condition facial myokymia, commented on its There was no history of fever or of pains around the association with sustained facial contraction, face. and expressed the view that, like facial palsy, it He was oriented as to time, place, and person but might be an early sign of multiple sclerosis. Kino confused and lethargic and unable to describe his (1928) reported three patients with undulating symptoms well.
    [Show full text]
  • TWITCH, JERK Or SPASM Movement Disorders Seen in Family Practice
    TWITCH, JERK or SPASM Movement Disorders Seen in Family Practice J. Antonelle de Marcaida, M.D. Medical Director Chase Family Movement Disorders Center Hartford HealthCare Ayer Neuroscience Institute DEFINITION OF TERMS • Movement Disorders – neurological syndromes in which there is either an excess of movement or a paucity of voluntary and automatic movements, unrelated to weakness or spasticity • Hyperkinesias – excess of movements • Dyskinesias – unnatural movements • Abnormal Involuntary Movements – non-suppressible or only partially suppressible • Hypokinesia – decreased amplitude of movement • Bradykinesia – slowness of movement • Akinesia – loss of movement CLASSES OF MOVEMENTS • Automatic movements – learned motor behaviors performed without conscious effort, e.g. walking, speaking, swinging of arms while walking • Voluntary movements – intentional (planned or self-initiated) or externally triggered (in response to external stimulus, e.g. turn head toward loud noise, withdraw hand from hot stove) • Semi-voluntary/“unvoluntary” – induced by inner sensory stimulus (e.g. need to stretch body part or scratch an itch) or by an unwanted feeling or compulsion (e.g. compulsive touching, restless legs syndrome) • Involuntary movements – often non-suppressible (hemifacial spasms, myoclonus) or only partially suppressible (tremors, chorea, tics) HYPERKINESIAS: major categories • CHOREA • DYSTONIA • MYOCLONUS • TICS • TREMORS HYPERKINESIAS: subtypes Abdominal dyskinesias Jumpy stumps Akathisic movements Moving toes/fingers Asynergia/ataxia
    [Show full text]
  • Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo
    A.qxd 9/29/05 04:02 PM Page 1 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 References Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the superficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdomi- nal wall, from the flank to the midline, parallel to the line of the der- matomal strips, in upper (supraumbilical), middle (umbilical), and lower (infraumbilical) areas. The maneuver 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 circum- stances: normal old age obesity after abdominal surgery after 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 neu- rone 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 primary lateral sclerosis vari- ant of motor neurone disease from multiple sclerosis.
    [Show full text]
  • Motor Neurone Disease
    Neurology Motor neurone disease Margaret Zoing Matthew Kiernan Caring for the patient in general practice Motor neurone disease (MND) is a progressive Background neurodegenerative disease. It is characterised by motor Motor neurone disease is a neurodegenerative disease that systems failure that results in the death of nerves responsible leads to progressive disability – and eventually death – for all voluntary movements, leading to limb paralysis, within 2–3 years. weakness of the muscles of speech and swallowing, and Objective ultimately respiratory failure. Typically MND strikes patients This article describes the role of the general practitioner in at the prime of adult life, usually in the fifth to sixth decades, caring for patients with motor neurone disease. and has a short trajectory from diagnosis with an average life Discussion expectancy of less than 3 years.1 Current estimates are that The diagnosis of motor neurone disease relies on the 1400 people are living with MND in Australia at any time, presence of upper and lower motor neurone features. There with 370 newly diagnosed patients each year.2 More than one is currently no pathognomic test for motor neurone disease Australian dies every day from this most pernicious disease. and it largely remains a diagnosis of exclusion following an accurate clinical history, combined with basic screening The cause of MND remains unknown but appears heterogeneous. blood investigations and structural imaging of the brain Environmental factors may trigger an underlying susceptibility – toxins, and spinal cord. Neuro-physiological studies may be useful chemicals, metals and trauma have all been proposed.1 Most cases as an ancillary diagnostic tool.
    [Show full text]
  • By : Ali Younes Ali Dr : Mehdi Delrobaei
    K.N.Toosi University of Technology By : Ali younes ali Dr : Mehdi Delrobaei Contents 1-Introduction and general description 2-Signs and symptoms 3-Risk factors 4-Causes 5-Ways of detection 6-Treatment 7-References 1-Introduction and General description Fasciculations (muscle twitch): is a small, local, involuntary muscle contraction and relaxation which may be visible under the skin Deeper areas can be detected by electromyography (EMG) testing, though they can happen in any skeletal muscle in the body Fasciculations can often by visualized and take the form of a muscle twitch or dimpling under the skin, but usually do not generate sufficient force to move a limb Fasciculations arise as a result of spontaneous depolarization of a lower motor neuron leading to the synchronous contraction of all the skeletal muscle fibers within a single motor unit Usually, intentional movement of the involved muscle causes fasciculations to cease immediately, but they may return once the muscle is at rest again. Fasciculations have a variety of causes, the majority of which are benign, but can also be due to disease of the motor neurons They are encountered by virtually all healthy people, though for most, it is quite infrequent In some cases, the presence of fasciculations can be annoying and interfere with quality of life If a neurological examination is otherwise normal and EMG testing does not indicate any additional pathology, a diagnosis of benign fasciculation syndrome is usually made 2-Signs and symptoms The main symptom of fasciculation is focal or widespread involuntary muscle activity (twitching), which can occur at random or specific times (or places).
    [Show full text]
  • Part Ii – Neurological Disorders
    Part ii – Neurological Disorders CHAPTER 14 MOVEMENT DISORDERS AND MOTOR NEURONE DISEASE Dr William P. Howlett 2012 Kilimanjaro Christian Medical Centre, Moshi, Kilimanjaro, Tanzania BRIC 2012 University of Bergen PO Box 7800 NO-5020 Bergen Norway NEUROLOGY IN AFRICA William Howlett Illustrations: Ellinor Moldeklev Hoff, Department of Photos and Drawings, UiB Cover: Tor Vegard Tobiassen Layout: Christian Bakke, Division of Communication, University of Bergen E JØM RKE IL T M 2 Printed by Bodoni, Bergen, Norway 4 9 1 9 6 Trykksak Copyright © 2012 William Howlett NEUROLOGY IN AFRICA is freely available to download at Bergen Open Research Archive (https://bora.uib.no) www.uib.no/cih/en/resources/neurology-in-africa ISBN 978-82-7453-085-0 Notice/Disclaimer This publication is intended to give accurate information with regard to the subject matter covered. However medical knowledge is constantly changing and information may alter. It is the responsibility of the practitioner to determine the best treatment for the patient and readers are therefore obliged to check and verify information contained within the book. This recommendation is most important with regard to drugs used, their dose, route and duration of administration, indications and contraindications and side effects. The author and the publisher waive any and all liability for damages, injury or death to persons or property incurred, directly or indirectly by this publication. CONTENTS MOVEMENT DISORDERS AND MOTOR NEURONE DISEASE 329 PARKINSON’S DISEASE (PD) � � � � � � � � � � �
    [Show full text]
  • Paraneoplastic Neurological and Muscular Syndromes
    Paraneoplastic neurological and muscular syndromes Short compendium Version 4.5, April 2016 By Finn E. Somnier, M.D., D.Sc. (Med.), copyright ® Department of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark 30/01/2016, Copyright, Finn E. Somnier, MD., D.S. (Med.) Table of contents PARANEOPLASTIC NEUROLOGICAL SYNDROMES .................................................... 4 DEFINITION, SPECIAL FEATURES, IMMUNE MECHANISMS ................................................................ 4 SHORT INTRODUCTION TO THE IMMUNE SYSTEM .................................................. 7 DIAGNOSTIC STRATEGY ..................................................................................................... 12 THERAPEUTIC CONSIDERATIONS .................................................................................. 18 SYNDROMES OF THE CENTRAL NERVOUS SYSTEM ................................................ 22 MORVAN’S FIBRILLARY CHOREA ................................................................................................ 22 PARANEOPLASTIC CEREBELLAR DEGENERATION (PCD) ...................................................... 24 Anti-Hu syndrome .................................................................................................................. 25 Anti-Yo syndrome ................................................................................................................... 26 Anti-CV2 / CRMP5 syndrome ............................................................................................
    [Show full text]
  • A Dictionary of Neurological Signs
    FM.qxd 9/28/05 11:10 PM Page i A DICTIONARY OF NEUROLOGICAL SIGNS SECOND EDITION FM.qxd 9/28/05 11:10 PM Page iii A DICTIONARY OF NEUROLOGICAL SIGNS SECOND 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. FM.qxd 9/28/05 11:10 PM Page iv A.J. Larner, MA, MD, MRCP(UK), DHMSA Walton Centre for Neurology and Neurosurgery Liverpool, UK Library of Congress Control Number: 2005927413 ISBN-10: 0-387-26214-8 ISBN-13: 978-0387-26214-7 Printed on acid-free paper. © 2006, 2001 Springer Science+Business Media, Inc. 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, Inc., 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 dis- similar 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 propri- etary 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 omis- sions that may be made.
    [Show full text]
  • Full Text (PDF)
    RESIDENT & FELLOW SECTION Clinical Reasoning: Section Editor An 82-year-old man with worsening gait John J. Millichap, MD Sheena Chew, MD SECTION 1 neck and left leg cramps. He denied bowel or bladder Ivana Vodopivec, MD, An 82-year-old man with hypothyroidism presented symptoms. PhD with difficulty walking. The patient was previously healthy, playing com- Aaron L. Berkowitz, MD, One year prior to presentation, he noticed that his petitive sports at the national level into his late 70s. PhD legs occasionally “froze” when initiating walking. His His only medication was levothyroxine. gait progressively worsened over the year. He devel- oped balance difficulty, tripping and falling twice Question for consideration: Correspondence to without loss of consciousness. In the 4 months prior Dr. Chew: to presentation, he started using a cane, a rolling 1. What examination findings would help to localize [email protected] walker, then a wheelchair. He reported occasional the etiology of his abnormal gait? GO TO SECTION 2 From the Department of Neurology, Brigham and Women’s Hospital (S.C., I.V., A.L.B.), and Department of Neurology, Massachusetts General Hospital (S.C.), Harvard Medical School, Boston. Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article. e246 © 2017 American Academy of Neurology ª 2017 American Academy of Neurology. Unauthorized reproduction of this article is prohibited. SECTION 2 arm dysdiadochokinesia and right leg dysmetria, but The neurologic basis of gait spans the entire neuraxis, no left-sided or truncal ataxia.
    [Show full text]