9781441967237.Pdf

Total Page:16

File Type:pdf, Size:1020Kb

9781441967237.Pdf The Neurologic Diagnosis wwwwwwwwww Jack N. Alpert The Neurologic Diagnosis A Practical Bedside Approach Jack N. Alpert, MD St. Luke’s Episcopal Hospital Department of Neurology University of Texas Medical School at Houston Houston, TX, USA [email protected] ISBN 978-1-4419-6723-7 e-ISBN 978-1-4419-6724-4 DOI 10.1007/978-1-4419-6724-4 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2011941214 © Springer Science+Business Media, LLC 2012 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 identifi ed 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) In Memory of Morris B. Bender, a superlative clinical neurologist of the twentieth century, who stimulated my lifelong interest in the manifestations, evaluation, and diagnosis of patients with neurologic diseases. His infl uence permeates this text. wwwwwwwwww Foreword Assessment of neurological complaints, a high percent of a family practitioner and internist’s practice, requires an accurate history and a careful neurological examination. As Dr. Alpert expertly discusses in detail, the history provides clues to the clinical diagnosis while the complementary neurological exami- nation localizes the lesion(s). Dr. Alpert is able to distil out from his over four decades of a busy practice and from his excellent teaching of medical stu- dents and neurological trainees a logical, readable, and provocative approach to each neurological complaint. In a chapter of 36 cases of “Diagnostic Dilemmas ,” one’s clinical acumen is challenged with practical questions and astute observations. By discussing neurological disorders in terms of ten “ Neuroanatomic Diagnoses ,” Dr. Alpert compartmentalizes neurological diseases into conve- nient and manageable discrete entities. By building upon the unique anatomy and physiology of each unit, greater logic is made in one’s deductive reason- ing for a diagnostic conclusion. Special emphasis is given to the “Six Major Decussations ” with clinical correlations, as with strokes, autonomic disor- ders, neuromuscular diseases and the poorly responsive patient. A separate chapter on “ Common Symptoms in the Neurology Clinic ” is a potpourri of frequently seen and rare cases which will challenge the beginner and the experienced practitioner of neurology. This textbook is highly recommended to the serious student of clinical neurosciences, be they medical students, trainees, or practitioners. Houston, TX, USA Frank M. Yatsu Chairman, Emeritus Department of Neurology University of Texas Medical School at Houston vii wwwwwwwwww Preface The purpose of this introductory text is to simplify the method of making a neurologic diagnosis. Medical students are often intimidated by a deluge of data and extensive differential diagnoses. They have no organizational struc- ture to follow. Diagnostic techniques of general medicine are not applicable. Neurology is a unique specialty since it requires the intermediary step of an anatomic diagnosis prior to proffering a differential diagnosis. Yet, the required knowledge of neuroanatomy need not be profound for the student who will specialize in any fi eld other than neurology and neurosurgery. This text is directed to medical students and residents who will all be regu- larly faced with numerous patients who have neurologic symptomatology. Typical one month rotations out of 4 years of medical school are clearly inad- equate training to make a cogent neurologic diagnosis, especially since subse- quent instruction is commonly provided by upper level residents who have the same background and numerous misconceptions. This is not a comprehensive text. The emphasis will be on establishing a neuroanatomic diagnosis before formulating a differential diagnosis. A thorough discussion of diseases will not be included. Treatment will seldom be discussed since it is likely to change radically over time. Redundancy of basic principles is purposeful. Repetition is the mother of learning or as William Gowers, an eminent neurologist of the early twentieth century, remarked, “A teacher who hesitates to repeat, shrinks from his most important duty, and a learner who dislikes hearing the same thing twice over lacks his most essential acquisition.” Houston, TX, USA Jack N. Alpert ix wwwwwwwwww Acknowledgments Without the encouragement, assistance, and patience of my wife, Ruth, this book would never have been realized. My children, Richard, Daniel, Ariela, Jessica and my sister Barbara supplied never-ending interest and support. After a desultory beginning, the urging of Jessica, in particular, prompted me to actively pursue publication. Dr. Srinivasa Kandula contributed crucial assistance in selecting, creating, and sketching many of the illustrations. His eager, enthusiastic collaboration was vital to the completion of this text. Mike de la Flor added his expertise to several illustrations. Drs. Ernesto Infante and Frank Yatsu provided me with sound and indis- pensable advice with their reviews of the entire manuscript. I am grateful for their hard work, assistance, and positive feedback. Donna J. Williams was my invaluable, conscientious transcriptionist. Her technical expertise was outstanding. Her willingness to work late at night, answer questions, and complete just another chapter revision was truly remarkable. Additional neurologists who added useful critiques, interest, and sugges- tions include Drs. Stanley Appel, Randolph Evans, James Grotta, Victor Rivera, and Loren Rolak. Dr. Irving Fishman assisted in reviewing the physi- ology of the genitourinary system. I am most appreciative of their help and encouragement. xi wwwwwwwwww Contents 1 Introduction .................................................................................. 1 2 The Ten Neuroanatomic Diagnoses ............................................ 3 Common Neurologic Signs: Localizing Value .............................. 4 Central Nervous System Disease (CNS), Peripheral Nervous System (PNS), and Muscle Disease (M) ............................................................ 4 Cerebral .......................................................................................... 4 Extrapyramidal ............................................................................... 7 Brainstem/Cerebellum ................................................................... 8 Spinal Cord Lesions (Myelopathies) ............................................. 11 Radiculopathy ................................................................................ 14 Plexopathy ...................................................................................... 16 Neuropathy ..................................................................................... 17 Neuromuscular Junction ................................................................ 19 Myopathy ....................................................................................... 20 Meningeal Disease ......................................................................... 21 Synopsis ......................................................................................... 23 Multiple Choice Questions ............................................................ 24 Answers .......................................................................................... 25 Bibliography .................................................................................. 26 3 The Neurologic History Holds the Diagnostic Keys .................. 27 Neurologic Symptoms in Psychiatric Disease ............................... 33 Bibliography .................................................................................. 35 4 Neurologic Examination .............................................................. 37 Vital Signs ...................................................................................... 37 Mental Status Examination ............................................................ 38 Visual Observations ................................................................... 38 Auditory Observations ............................................................... 39 Aphasia ...................................................................................... 39 Agnosia ...................................................................................... 41 Apraxia ....................................................................................... 41 Cranial Nerve Examination ............................................................ 45 Olfactory Nerve
Recommended publications
  • Pupillary Disorders LAURA J
    13 Pupillary Disorders LAURA J. BALCER Pupillary disorders usually fall into one of three major cat- cortex generally do not affect pupillary size or reactivity. egories: (1) abnormally shaped pupils, (2) abnormal pupillary Efferent parasympathetic fibers, arising from the Edinger– reaction to light, or (3) unequally sized pupils (anisocoria). Westphal nucleus, exit the midbrain within the third nerve Occasionally pupillary abnormalities are isolated findings, (efferent arc). Within the subarachnoid portion of the third but in many cases they are manifestations of more serious nerve, pupillary fibers tend to run on the external surface, intracranial pathology. making them more vulnerable to compression or infiltration The pupillary examination is discussed in detail in and less susceptible to vascular insult. Within the anterior Chapter 2. Pupillary neuroanatomy and physiology are cavernous sinus, the third nerve divides into two portions. reviewed here, and then the various pupillary disorders, The pupillary fibers follow the inferior division into the orbit, grouped roughly into one of the three listed categories, are where they then synapse at the ciliary ganglion, which lies discussed. in the posterior part of the orbit between the optic nerve and lateral rectus muscle (Fig. 13.3). The ciliary ganglion issues postganglionic cholinergic short ciliary nerves, which Neuroanatomy and Physiology initially travel to the globe with the nerve to the inferior oblique muscle, then between the sclera and choroid, to The major functions of the pupil are to vary the quantity of innervate the ciliary body and iris sphincter muscle. Fibers light reaching the retina, to minimize the spherical aberra- to the ciliary body outnumber those to the iris sphincter tions of the peripheral cornea and lens, and to increase the muscle by 30 : 1.
    [Show full text]
  • Taking the Mystery out of Abnormal Pupils
    Taking the mystery out of abnormal pupils No financial disclosures Course Title: Taking the mystery out [email protected] of abnormal pupils Lecturer: Brad Sutton, OD, FAAO Clinical Professor IU School of Optometry . •Review of Anatomy Iris anatomy Iris sphincter Iris dilator Parasympathetic pathway Sympathetic pathway Parasympathetic Pathway Parasympathetic Pathway Light stimulates the retina then impulse Four neuron arc travels with the ganglion cells through the Retina to the pretectal nucleus in the chiasm into the optic tracts. 80% go to the midbrain (1) LGN , 20% to the pretectal nuclei.They Pretectal nucleus to the EW nucleus (2) then hemidecussate and terminate at the EW nucleus EW nucleus to the ciliary ganglion (3) Ciliary ganglion to the iris sphincter with short ciliary nerves (4) 1 Points of Interest Sympathetic Pathway Within the second order neuron there are Three neuron arc 30 near response fibers for every light Posterior hypothalamus to ciliospinal response fiber. This allows for light - near center of Budge ( C8 - T2 ). (1) dissociation. Center of Budge to the superior cervical The third order neuron runs with cranial ganglion in the neck (2) nerve III from the brain stem to the ciliary Superior cervical ganglion to the dilator ganglion. Superficially located prior to the muscle (3) cavernous sinus. Points of Interest Second order neuron runs along the surface of the lung, can be affected by a Pancoast tumor Third order neuron runs with the carotid artery then with the ophthalmic division of cranial nerve V 2 APD Testing testing……………….AKA……… … APD / reverse APD Direct and consensual response Which is the abnormal pupil ? Very simple rule.
    [Show full text]
  • Complete and Incomplete Forms of the Benign Disorder Characterised By
    Br J Ophthalmol: first published as 10.1136/bjo.16.8.449 on 1 August 1932. Downloaded from THE BRITISH JOURNAL OF OPHTHALMOLOGY AUGUST, 1932 COMMUNICATIONS COMPLETE AND INCOMPLETE FORMS OF THE BENIGN DISORDER CHARACTERISED BY TONIC PUPILS AND ABSENT copyright. TENDON REFLEXES BY W. J. ADIE, M.D., F.R.C.P. PHYSICIAN, CHARING CROSS HOSPITAL AND ROYAL LONDON OPHTHALMIC HOSPITAL. OUT-PATIENT PHYSICIAN, THE NATIONAL HOSPITAL FOR NERVOUS DISEASES, QUEEN SQUARE http://bjo.bmj.com/ IN earlier papers on this subject it has been suggested that certain apparently dissimilar abnormal pupillary reactions formerly described as occurring in unrelated conditions are manifestations of the same disorder. The abnormal reactions are, on the one hand, the tonic pupillary reaction (syn. pupillotonia, myotonic reaction, tonic convergence reaction of pupils apparently inactive to light, on September 30, 2021 by guest. Protected Marcus's peculiar pupil phenomenon, non-luetic Argyll Robertson pupil, pseudo-Argyll Robertson pupil) and, on the other hand what may be called atypical phases of the tonic pupil. In the atypical phases tonic reactions are absent or difficult to detect and the state of the pupil in cases that present them is usually desig- nated by the term fixed pupil, ophthalmoplegia interna, iridoplegia or partial iridoplegia, of unknown origin. The disorder referred to, if the views expressed here are correct, may manifest itself in the following clinical forms: A. The complete form characterized by the presence in one or both eyes of the tonic convergence reaction in a pupil apparently Br J Ophthalmol: first published as 10.1136/bjo.16.8.449 on 1 August 1932.
    [Show full text]
  • GAZE and AUTONOMIC INNERVATION DISORDERS Eye64 (1)
    GAZE AND AUTONOMIC INNERVATION DISORDERS Eye64 (1) Gaze and Autonomic Innervation Disorders Last updated: May 9, 2019 PUPILLARY SYNDROMES ......................................................................................................................... 1 ANISOCORIA .......................................................................................................................................... 1 Benign / Non-neurologic Anisocoria ............................................................................................... 1 Ocular Parasympathetic Syndrome, Preganglionic .......................................................................... 1 Ocular Parasympathetic Syndrome, Postganglionic ........................................................................ 2 Horner Syndrome ............................................................................................................................. 2 Etiology of Horner syndrome ................................................................................................ 2 Localizing Tests .................................................................................................................... 2 Diagnosis ............................................................................................................................... 3 Flow diagram for workup of anisocoria ........................................................................................... 3 LIGHT-NEAR DISSOCIATION .................................................................................................................
    [Show full text]
  • 2020 Measure Value Set Colorectal Cancer Screening
    PT ‐ 2020 Measure Value Set_Colorectal Cancer Screening Numerator Value Set Name Code Definition Code System FOBT Lab Test 82270 CPT FOBT Lab Test 82274 CPT Colorectal cancer screening; fecal occult blood test, immunoassay, 1‐3 FOBT Lab Test G0328 HCPCS simultaneous (G0328) FOBT Lab Test 12503‐9 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐4th specimen LOINC FOBT Lab Test 12504‐7 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐5th specimen LOINC FOBT Lab Test 14563‐1 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐1st specimen LOINC FOBT Lab Test 14564‐9 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐2nd specimen LOINC FOBT Lab Test 14565‐6 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐3rd specimen LOINC FOBT Lab Test 2335‐8 Hemoglobin.gastrointestinal [Presence] in Stool LOINC FOBT Lab Test 27396‐1 Hemoglobin.gastrointestinal [Mass/mass] in Stool LOINC FOBT Lab Test 27401‐9 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐6th specimen LOINC FOBT Lab Test 27925‐7 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐7th specimen LOINC FOBT Lab Test 27926‐5 Hemoglobin.gastrointestinal [Presence] in Stool ‐‐8th specimen LOINC FOBT Lab Test 29771‐3 Hemoglobin.gastrointestinal.lower [Presence] in Stool by Immunoassay LOINC Hemoglobin.gastrointestinal.lower [Presence] in Stool by Immunoassay FOBT Lab Test 56490‐6 LOINC ‐‐2nd specimen Hemoglobin.gastrointestinal.lower [Presence] in Stool by Immunoassay FOBT Lab Test 56491‐4 LOINC ‐‐3rd specimen Hemoglobin.gastrointestinal.lower [Presence] in Stool by Immunoassay FOBT Lab Test 57905‐2
    [Show full text]
  • Physical Therapy Practice
    Physical Therapy Practice THE MAGAZINE OF THE ORTHOPAEDIC SECTION, APTA VOL. 18, NO. 2 2006 ORTHOPAEDIC CARDON REHABILITATION PRODUCTS, INC.™ Wurlitzer Industrial Park, 908 Niagara Falls Blvd. North Tonawanda, NY 14120 Telephone: 1-800-944-7868 • Fax: 716-297-0411 E-mail: [email protected] THE ACCEPTED STANDARD OF PERFORMANCE The Cardon Mobilization Table . Going beyond the third dimension . Now available with the patented option which eliminates the use of flexion and rotation levers. This allows the therapist to perform advanced manual therapy techniques with complete confidence and comfort with an ergonomically friendly design. The unique design provides more efficient and smooth setup while providing superior patient comfort. The option enhances patient care by allowing unsurpassed opportunity for more preciseness of treatment and monitoring of segments and joints. he design and concepts make this “T the best mobilization table manufactured today.” Professor Freddy Kaltenborn Autho, Int’l Lecturer in Manual Therapy he various sections have minimum flex “T allowing very accurate application of specific manual therapy techniques.” Olaf Evjenth ES! I would like to preview the Author, Int’l Lecturer in Manual Therapy Y Cardon Mobilization Table. Please rush your 15 minute VHS video (for standard model): SEE FOR Name: Title: YOURSELF Clinic/Institution: THESE Address: OUTSTANDING City: State: Zip Code: Telephone: Signature: FEATURES: CARDON REHABILITATION PRODUCTS, INC.™ • Accurate localization of the vertebral segment Wurlitzer Industrial Park, 908 Niagara Falls Blvd. • Precision and versatility of technique North Tonawanda, NY 14120 • Absolute control of the mobilization forces Telephone: 1-800-944-7868 • Fax: 716-297-0411 • Excellent stability for manipulation. E-mail: [email protected] Orthopaedic Practice Vol.
    [Show full text]
  • Neurological History and Physical Examination
    emedicine.medscape.com eMedicine Specialties > Clinical Procedures > none Neurological History and Physical Examination Kalarickal J Oommen, MD, FAAN, Professor and Crofoot Chair of Epilepsy, Department of Neurology, Chief, Section of Epilepsy, Texas Tech University Health Sciences Center; Medical Director, Texas Tech University Health Sciences Center (TTUHSC) Covenant Comprehensive Epilepsy Center Updated: Nov 25, 2009 Neurological History "From the brain and the brain only arise our pleasures, joys, laughter and jests, as well as our sorrows, pains, griefs, and tears.... These things we suffer all come from the brain, when it is not healthy, but becomes abnormally hot, cold, moist or dry." —Hippocrates The Sacred Disease, Section XVII Taking the patient's history is traditionally the first step in virtually every clinical encounter. A thorough neurologic history allows the clinician to define the patient's problem and, along with the result of physical examination, assists in formulating an etiologic and/or pathologic diagnosis in most cases.[1 ] Solid knowledge of the basic principles of the various disease processes is essential for obtaining a good history. As Goethe stated, "The eyes see what the mind knows." To this end, the reader is referred to the literature about the natural history of diseases. The purpose of this article is to highlight the process of the examination rather than to provide details about the clinical and pathologic features of specific diseases. The history of the presenting illness or chief complaint should
    [Show full text]
  • Movement Disorders and Gait Disturbances
    Movement disorders and gait disturbances Kovács Norbert PTE ÁOK Neurológiai Klinika Pécs 1 MD pathophysiology z Genetic mutation or environmental injury of basal ganglia functioning z Pallidum, thalamus, subthalamic nucleus, caudate nucleus, pedunculopintine nucleus 2 Vitek JL. Mov Disord 2002;17(Supp 3):S49-62 Phenomenology in MD Hyperkinetic Isokinetic Hypokinetic • Tremor (regular) • Ataxia • Rigidity • Chorea • Bradykinesia • Ballism • Hypokinesia • Dystonia • Athetosis • Myoclonus (jerky) • Tic (jerky) 3 Hyperkinetic movements 4 Tremor classification More or less regular, sinusoid movements Any body parts can be affected (e.g. limbs, neck, trunc, vocal cords) Classification: • Intensity (invisible, barely visible, moderate, severe) • Frequency (slow or fast) • Position – Rest tremor (e.g. Parkinsonism) – Postural tremor (e.g. hyperthyroidism) – Kinetic tremor (e.g. essential tremor) – Intention tremor (e.g. cerebellar tremor) 5 Rest tremor Cognition (e.g. counting), gait or talking about the disease 6 usually increases the amplitude Intention tremor The tremor amplitude is the highest at the target. Usually 7 caused by cerebellar problems. Postural –kinetic tremor 8 Postural –kinetic tremor 9 Essential tremor is the most frequent cause of kinetic tremor. Postural –kinetic tremor 10 Always examine water drinking, writing and tableware use -- QoL Deep brain stimulation for tremor 11 Chorea The word chorea denotes rapid irregular muscle jerks that occur involuntarily and unpredictably in different parts of the body. Most important cause is12 Parkinson’s disease Ballism Large involuntary movements involving the whole extremity. Usually accompanies the chorea. Vascular lesion e.g. in the area of subthalamic13 nucleus can produce Athetosis abnormal movements that are slow, sinuous, and writhing in character. 14 Dystonia • Not a disease, it is a syndrome • Involuntary phasic, movement and/or • Sustained, involuntary, abnormal muscle contractions.
    [Show full text]
  • Mobile Gait Analysis: from Prototype Towards Clinical Grade Wearable
    FAU Studien aus der Informatik 6 Julius Hannink Mobile Gait Analysis: From Prototype towards Clinical Grade Wearable Julius Hannink Mobile Gait Analysis: From Prototype towards Clinical Grade Wearable FAU Studien aus der Informatik Band 6 Herausgeber der Reihe: Björn Eskofier, Richard Lenz, Andreas Maier, Michael Philippsen, Lutz Schröder, Wolfgang Schröder-Preikschat, Marc Stamminger, Rolf Wanka Julius Hannink Mobile Gait Analysis: From Prototype towards Clinical Grade Wearable Erlangen FAU University Press 2019 Bibliografische Information der Deutschen Nationalbibliothek: Die Deutsche Nationalbibliothek verzeichnet diese Publikation in der Deutschen Nationalbibliografie; detaillierte bibliografische Daten sind im Internet über http://dnb.d-nb.de abrufbar. Das Werk, einschließlich seiner Teile, ist urheberrechtlich geschützt. Die Rechte an allen Inhalten liegen bei ihren jeweiligen Autoren. Sie sind nutzbar unter der Creative Commons Lizenz BY-NC. Der vollständige Inhalt des Buchs ist als PDF über den OPUS Server der Friedrich-Alexander-Universität Erlangen-Nürnberg abrufbar: https://opus4.kobv.de/opus4-fau/home Bitte zitieren als Hannink, Julius. 2019. Mobile Gait Analysis: From Prototype towards Clinical Grade Wearable. FAU Studies FAU Studien aus der Informatik Band 6. Erlangen: FAU University Press. DOI: 10.25593/978-3-96147-173-7 Verlag und Auslieferung: FAU University Press, Universitätsstraße 4, 91054 Erlangen Druck: docupoint GmbH ISBN: 978-3-96147-172-0 (Druckausgabe) eISBN: 978-3-96147-173-7 (Online-Ausgabe) ISSN: 2509-9981 DOI: 10.25593/978-3-96147-173-7 Mobile Gait Analysis: From Prototype towards Clinical Grade Wearable Mobile Ganganalyse: Vom Prototyp in Richtung klinisch anwendbarer Systeme Der Technischen Fakultät der Friedrich-Alexander-Universität Erlangen-Nürnberg zur Erlangung des Doktorgrades Dr.-Ing.
    [Show full text]
  • Evaluating the Child with Unsteady Gait
    Review Article Evaluating the child with unsteady gait Mohammed M. Jan, MBChB, FRCP(C). ABSTRACT From the Department of Pediatrics, King Abdul-Aziz University Hospital, Jeddah, Kingdom of Saudi Arabia. Address correspondence and reprint request to: Prof. Mohammed M. S. Jan, Department of Pediatrics, King Abdul-Aziz University يعتبر خلل التوازن أثناء املشي من اﻷعراض الشائعة لدى اﻷطفال Hospital, PO Box 80215, Jeddah 21589, Kingdom of Saudi (Arabia. Tel. +996 (2) 6401000 Ext. 20208. Fax. +996 (2 بقسم الطوارئ واﻷعصاب. تتعدد أسباب خلل التوازن، ولكن E-mail: [email protected] .6403975 من أهم اولويات التقييم اﻷولى هو التأكد من عدم وجود التهاب أو ورم بالدماغ. التعرف علي املسببات احلميدة والغير عصبية ًأيضا eurological disorders are common in Saudi Arabia مهم لتفادى القيام بفحوصات متعددة دون احلاجة إليها أو تنومي Naccounting for up to 30% of all consultations to املريض باملستشفى. في هذه املقالة النقدية نقدم مراجعة حديثة pediatrics.1 Trauma, ingestion, and acute neurological عن تقييم الطفل املصاب بخلل التوازن مع مناقشة الفحوصات disorders are common, mainly as a result of improper الﻻزمة والعﻻج. قد يكون خلل التوازن ناجت عن مرض باملخيخ safety practices of many parents.2 Consanguineous أو مشكلة حسية، ًعلما بأن أمراض املخيخ قد تكون حادة، marriages also add to the problem, resulting in مزمنة، متدهورة، أو متقطعة. وتتعدد أسباب هذه املشكلة و increased prevalence of many inherited and genetic منها اﻹصابات، اﻻلتهابات، أمراض اﻻستقﻻب، العيوب اخللقية، neurological disorders.3,4 Unsteadiness and ataxia are واﻷورام. أما أسباب خلل التوازن الناجت عن مشاكل اﻹحساس relatively common neurological presentations of a فيكون بسبب تأثر في اﻷعصاب الطرفية أو احلبل الشوكي.
    [Show full text]
  • Gait Disorders
    What are the classical Gait Patterns for the Following Conditions? • Alzheimers Disease Gait Disorders • Hemiparetic Stroke • Parkinsons Disease T.Masud • Osteomalacia Nottingham University Hospitals NHS Trust • Lateral popliteal nerve palsy University of Nottingham University of Derby • Knee OA University of Southern Denmark • Vitamin B12 deficiency with dorsal column loss Statistical summaries of risk factors for falls From cohort studies- Perell 2001 RISK FACTOR Mean RR/OR Range Muscle weakness 4.4 (1.5-10.3) Falls history 3.0 (1.7-7.0) Gait deficit 2.9 (1.3-5.6) Balance deficit 2.9 (1.6-5.4) Use of assistive devices 2.6 (1.2-4.6) Visual deficit 2.5 (1.6-3.5) Arthritis 2.4 (1.9-2.7) Impaired ADLs 2.3 (1.5-3.1) Depression 2.2 (1.7-2.5) Cognitive impairment 1.8 (1.0-2.3) Age > 80 1.7 (1.1-2.5) Simple Model for Balance Balance Vision FALLS Vestibular Musculo- skeletal Proprioception Tactile sensation Activity & environmental hazards CNS Gait cycle [weight bearing] [progress] Running: stance 50% - swing 50%, then Asymmetry no double support period Stance phase Condition Disabled: increased bilateral stance phase Pain, weakness to increase double support period Impaired balance: vestibular, cerebellum dysfunction Clinical gait analysis Pattern Recognition of Gait Pattern recognition Hemiplegic Parkinsonian - Most quickly, recall from memory Apraxic Structured Approach Neuropathic - Hypothetico-deductive Ataxic - Basic gait knowledge / Anatomy Waddling Exhaustive strategy Spastic - Comprehensive and systematic evaluation Hyperkinetic Antalgic Gait Disorder in Older People High Level Gait Disorders by level of Sensorimotor Deficit Frontal Related • Apraxic •Cerebrovascular • Magnetic Low • Freezing High Middle •Dementia Level Level Level From- Alexander, Goldberg, Cleveland Clinic J Med 2005; 72: 592-600 High Level Gait Disorders High Level Gait Disorders Frontal Related Frontal Related •Cerebrovascular •Cerebrovascular •Dementia •Dementia •N.P.
    [Show full text]
  • Pupil and Accomodation Abnormalities
    PPUUPPIILL AANNDD AACCCCOOMMOODDAATTIIOONN AABBNNOORRMMAALLIITTIIEESS SympatheticSympathetic pathwaypathway ofof pupillarypupillary innervationinnervation PPuuppiillllaarryy lliigghhtt rreefflleexxeess ••PupilPupil diameterdiameter isis subjectsubject toto continuouscontinuous variationsvariations asas aa functionfunction ofof changeschanges inin luminanceluminance,, fixationfixation andand psychosensitivepsychosensitive stimulistimuli.. •• PupilsPupils mustmust bebe studiedstudied byby evaluatingevaluating theirtheir sizesize,, shapeshape,, symmetrysymmetry andand activityactivity ((dilationdilation andand constrictionconstriction).). •• ToTo evaluateevaluate sizesize andand symmetrysymmetry ofof pupilspupils,, patientspatients areare invitedinvited toto fixatefixate aa farawayfaraway objectobject,, whichwhich mustmust notnot bebe aa sourcesource ofof excessiveexcessive lightlight stimulationstimulation.. ••SSuubbsseeqquueennttllyy,, bbyy iilllluummiinnaattiinngg tthhee ppaattiieennttss’’ ffaaccee ffrroomm bbeellooww wwiitthh aa wweeaakk lliigghhtt ssoouurrccee,, bbootthh ppuuppiillss aarree ssiimmuullttaanneeoouussllyy oobbsseerrvveedd aanndd tthheeiirr ddiiaammeetteerrss aarree ddeetteerrmmiinneedd ((mmmm)).. •• IInn tthhee nnoorrmmaall ppooppuullaattiioonn,, ppuuppiill ddiiaammeetteerr tteennddss ttoo bbee ssmmaalllleerr iinn cchhiillddrreenn,, iinn tthhee eellddeerrllyy aanndd iinn ssuubbjjeeccttss wwiitthh ddaarrkk iirriiss.. •In general, anisocoria which changes with changes of luminance conditions must be considered pathologic,
    [Show full text]