Acute Flaccid Paralysis Field Manual
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The Epidemiology of the Cerebral Palsies
Clinics in Developmental Medicine No. 87 The Epidemiology of the Cerebral Palsies Edited by FIONA STANLEY EVA ALBERMAN 1984 Spastics International Medical Publications OXFORD: Blackwell Scientific Publications Ltd. PHILADELPHIA: J. B. Lippincott Co. CHAPTER 11 Prenatal and Perinatal Risk Factors in a Survey of 681 Swedish Cases BENGT and GUDRUN HAGBERG I, that am curtail'd of this fair proportion, Cheated of feature by dissembling nature, , Deform'd, unfinish'd, sent before my time Into this breathing world, scarce half made up, And that so lamely and unfashionable That dogs bark at me, as I halt by them. Shakespeare, Richard III Introduction The aim of this chapter is to try and shed light on more specific aspects of the main groups of prenatal causes and risk factors for cerebral palsy, their mutual importance, and particularly their relationship to superimposed detrimental perinatal events. This survey is based on an investigation of 681 cases born in Sweden from 1959 to 1976. In our original retrospective analysis of causes of cerebral palsy (Hagberg et al. 1975a), it was found necessary to make certain generalisations about the aetiological groupings. Only the risk factor that was considered to be the predominating possible cause was used for classification. There is no doubt that this oversimplifies the issue as it neglects the complex network of different interacting detrimental risk factors that are present in the majority of cases, and in all probability underlie the development of brain lesions. Definitions For the purpose of the Swedish investigation, the following definition of cerebral palsy was used: a non-progressive 'disorder of movement and posture due to a defect or lesion of the immature brain' (Bax 1964). -
Acute Flaccid Paralysis Syndrome Associated with West Nile Virus Infection --- Mississippi and Louisiana, July--August 2002
Acute Flaccid Paralysis Syndrome Associated with West Nile Virus Infection --- Mississippi and Louisiana, July--August 2002 Weekly September 20, 2002 / 51(37);825-828 Acute Flaccid Paralysis Syndrome Associated with West Nile Virus Infection --- Mississippi and Louisiana, July--August 2002 West Nile virus (WNV) infection can cause severe, potentially fatal neurologic illnesses including encephalitis and meningitis (1,2). Acute WNV infection also has been associated with acute flaccid paralysis (AFP) attributed to a peripheral demyelinating process (Guillain-Barré Syndrome [GBS]) (3), or to an anterior myelitis (4). However, the exact etiology of AFP has not been assessed thoroughly with electrophysiologic, laboratory, and neuroimaging data. This report describes six cases of WNV-associated AFP in which clinical and electrophysiologic findings suggest a pathologic process involving anterior horn cells and motor axons similar to that seen in acute poliomyelitis. Clinicians should evaluate patients with AFP for evidence of WNV infection and conduct tests to differentiate GBS from other causes of AFP. Case Reports Case 1. In July 2002, a previously healthy man aged 56 years from Mississippi was admitted to a local hospital with a 3-day history of fever, chills, vomiting, confusion, and acute painless weakness of the arms and legs. On physical examination, he had tremor and areflexic weakness in both arms and asymmetric weakness in the legs with hypoactive reflexes; sensation was intact. Laboratory abnormalities included a mildly elevated protein in the cerebrospinal fluid (CSF) (Table). An evolving stroke was diagnosed, and the patient was treated with anticoagulant therapy; subsequently, the illness was attributed to GBS, and intravenous immune globulin (IVIG) therapy was initiated. -
Cerebral Palsy the ABC's of CP
Cerebral Palsy The ABC’s of CP Toni Benton, M.D. Continuum of Care Project UNM HSC School of Medicine April 20, 2006 Cerebral Palsy Outline I. Definition II. Incidence, Epidemiology and Distribution III. Etiology IV. Types V. Medical Management VI. Psychosocial Issues VII. Aging Cerebral Palsy-Definition Cerebral palsy is a symptom complex, (not a disease) that has multiple etiologies. CP is a disorder of tone, posture or movement due to a lesion in the developing brain. Lesion results in paralysis, weakness, incoordination or abnormal movement Not contagious, no cure. It is static, but it symptoms may change with maturation Cerebral Palsy Brain damage Occurs during developmental period Motor dysfunction Not Curable Non-progressive (static) Any regression or deterioration of motor or intellectual skills should prompt a search for a degenerative disease Therapy can help improve function Cerebral Palsy There are 2 major types of CP, depending on location of lesions: Pyramidal (Spastic) Extrapyramidal There is overlap of both symptoms and anatomic lesions. The pyramidal system carries the signal for muscle contraction. The extrapyramidal system provides regulatory influences on that contraction. Cerebral Palsy Types of brain damage Bleeding Brain malformation Trauma to brain Lack of oxygen Infection Toxins Unknown Epidemiology The overall prevalence of cerebral palsy ranges from 1.5 to 2.5 per 1000 live births. The overall prevalence of CP has remained stable since the 1960’s. Speculations that the increased survival of the VLBW preemies would cause a rise in the prevalence of CP have proven wrong. Likewise the expected decrease in CP as a result of C-section and fetal monitoring has not happened. -
ICD9 & ICD10 Neuromuscular Codes
ICD-9-CM and ICD-10-CM NEUROMUSCULAR DIAGNOSIS CODES ICD-9-CM ICD-10-CM Focal Neuropathy Mononeuropathy G56.00 Carpal tunnel syndrome, unspecified Carpal tunnel syndrome 354.00 G56.00 upper limb Other lesions of median nerve, Other median nerve lesion 354.10 G56.10 unspecified upper limb Lesion of ulnar nerve, unspecified Lesion of ulnar nerve 354.20 G56.20 upper limb Lesion of radial nerve, unspecified Lesion of radial nerve 354.30 G56.30 upper limb Lesion of sciatic nerve, unspecified Sciatic nerve lesion (Piriformis syndrome) 355.00 G57.00 lower limb Meralgia paresthetica, unspecified Meralgia paresthetica 355.10 G57.10 lower limb Lesion of lateral popiteal nerve, Peroneal nerve (lesion of lateral popiteal nerve) 355.30 G57.30 unspecified lower limb Tarsal tunnel syndrome, unspecified Tarsal tunnel syndrome 355.50 G57.50 lower limb Plexus Brachial plexus lesion 353.00 Brachial plexus disorders G54.0 Brachial neuralgia (or radiculitis NOS) 723.40 Radiculopathy, cervical region M54.12 Radiculopathy, cervicothoracic region M54.13 Thoracic outlet syndrome (Thoracic root Thoracic root disorders, not elsewhere 353.00 G54.3 lesions, not elsewhere classified) classified Lumbosacral plexus lesion 353.10 Lumbosacral plexus disorders G54.1 Neuralgic amyotrophy 353.50 Neuralgic amyotrophy G54.5 Root Cervical radiculopathy (Intervertebral disc Cervical disc disorder with myelopathy, 722.71 M50.00 disorder with myelopathy, cervical region) unspecified cervical region Lumbosacral root lesions (Degeneration of Other intervertebral disc degeneration, -
Miller Fisher Syndrome, Facial Diplegia and Multiple Cranial Nerve Palsies Ashfaq Shuaib and Werner J
LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES Variants of Guillain-Barre Syndrome: Miller Fisher Syndrome, Facial Diplegia and Multiple Cranial Nerve Palsies Ashfaq Shuaib and Werner J. Becker ABSTRACT: We report the experience at a large teaching hospital over a 10 year period with Miller Fisher Syndrome, facial diplegia, and multiple cranial nerve palsies. In these patients, absence of drowsiness on examination, normal cranial CT scans, albumino-cytological dissociation on CSF examination and slowing of nerve conduction, all suggest that a peripheral nerve dysfunction is the underlying mechanism. Pertinent literature is reviewed, in an attempt to separate these probable variants of Guillain-Barre' Syndrome from brainstem encephalitis, with which they may be confused. RESUME: Variantes du syndrome de Guillain-Barre: le syndrome de Miller-Fisher, la diplegie faciale et les paralysies multiples des nerfs craniens. Nous rapportons l'observation de patients atteints du syndrome de Miller-Fisher, de diplegie faciale et de paralysies multiples des nerfs craniens, ayant consulte dans un hopital d'enseignement sur une p6riode de dix ans. Chez ces patients, l'absence de somnolence a l'examen, un CT-scan cranien normal, une dissociation albumino-cytologique a l'examen du LCR et une conduction lente a l'etude de la conduction nerveuse, suggerent que la dysfonction au niveau du nerf p6ripherique en est le m6canisme sous-jacent. Nous revoyons la literature pertinente, en tentant de separer ces variantes probables du syndrome de Guillain-Barr6 de l'enc6phalite du tronc cerebral, entite avec laquelle elles peuvent etre confondues. Can. J. Neurol. Sci. 1987; 14:611-616 The syndrome of ataxia, areflexia and ophthalmoplegia (AAO), We report here our analysis of patients admitted over a ten initially described by Bogaert et al in 1938,' became widely year period with AAO, multiple cranial nerve dysfunction and recognized after Miller Fisher's classic description of three facial diplegia. -
Research Journal of Pharmaceutical, Biological and Chemical Sciences
ISSN: 0975-8585 Research Journal of Pharmaceutical, Biological and Chemical Sciences The Ability to Reduce the Severity of Motor Disorders in Children With Cerebral Palsy. Makhov AS, and Medvedev IN*. Russian State Social University, st. V. Pika, 4, Moscow, Russia, 129226 ABSTRACT Children's cerebral palsy remains a frequent pathology in children. The effectiveness of the schemes used for the rehabilitation of these children remains low. Purpose: to evaluate the effectiveness of the author's technique, including therapeutic gymnastics and technical means, in children 7-9 years old with infantile cerebral palsy. The study was performed on 35 children aged 7-9 years with infantile cerebral palsy: 17 of them made up a control group, 18 - experimental. In the children studied, spastic diplegia or spastic tetra paresis was noted. The children of the experimental group used the author's complex correction, which includes curative gymnastics, the use of strength training, orthoses and verticalizers. Children of the control group are prescribed a traditional correction of infantile cerebral palsy. All children are assessed dynamics of motor skills on the scale of Cheylie, goniometry of knee joints, spasticity of muscles, and strength of the quadriceps muscle of the thigh. The results are processed by Student's test. As a result of the lessons, all children have achieved a positive dynamics of the indicators taken into account. A more pronounced positive dynamics of the strength of the quadriceps muscle (by 19.2%), the level of the motor skill (from 9.3 to 27.8%) and spasticity of the limb (by 26.5%) was achieved in the children of the experimental group. -
Cerebral Palsy
Cerebral Palsy What is Cerebral Palsy? Doctors use the term cerebral palsy to refer to any one of a number of neurological disorders that appear in infancy or early childhood and permanently affect body movement and muscle coordination but are not progressive, in other words, they do not get worse over time. • Cerebral refers to the motor area of the brain’s outer layer (called the cerebral cortex), the part of the brain that directs muscle movement. • Palsy refers to the loss or impairment of motor function. Even though cerebral palsy affects muscle movement, it is not caused by problems in the muscles or nerves. It is caused by abnormalities inside the brain that disrupt the brain’s ability to control movement and posture. In some cases of cerebral palsy, the cerebral motor cortex has not developed normally during fetal growth. In others, the damage is a result of injury to the brain either before, during, or after birth. In either case, the damage is not repairable and the disabilities that result are permanent. Patients with cerebral palsy exhibit a wide variety of symptoms, including: • Lack of muscle coordination when performing voluntary movements (ataxia); • Stiff or tight muscles and exaggerated reflexes (spasticity); • Walking with one foot or leg dragging; • Walking on the toes, a crouched gait, or a “scissored” gait; • Variations in muscle tone, either too stiff or too floppy; • Excessive drooling or difficulties swallowing or speaking; • Shaking (tremor) or random involuntary movements; and • Difficulty with precise motions, such as writing or buttoning a shirt. The symptoms of cerebral palsy differ in type and severity from one person to the next, and may even change in an individual over time. -
A Immunosupressed Woman Presenting with Acute Flaccid
Journal of the Louisiana State Medical Society CLINICAL CASE OF THE MONTH An Immunosuppressed Woman Presenting with Acute Flaccid Paralysis and Progressive Respiratory Failure Rebeca Monreal, DO; Arturo Vega, MD; Francesco Simeone, MD; Lee Hamm, MD; Enrique Palacios, MD; Marlow Maylin, MD; and Fred A. Lopez, MD (Section Editor) A 68-year-old woman with membranous glomerulo- use. She lived with her husband on the Mississippi Gulf nephritis and hypertension presented in late August with Coast. Previously she was functional and independent with a tremor, weakness of the upper and lower extremities, all activities of daily living. headache and nausea. She had not been feeling well for the On physical examination her temperature was 98.6˚ F previous two weeks and also reported sore throat and nasal (though as high as 101.2˚ F); blood pressure 116/83 mmHg; congestion. Four days prior to admission her temperature pulse rate of 85 beats per minute; and a respiratory rate 12 was 100.8˚ F. Other symptoms included loose stools, head- breaths per minute. She appeared anxious, but was in no ache, fatigue, muscle weakness, dyspnea, dry heaves, and respiratory distress. She was able to follow commands and double vision. She initially saw her primary care physician. move all extremities, but had generalized muscle weakness Her serum creatinine at that time was 3.9 mg/dL (baseline (strength 3/5 throughout) and an intentional tremor of her 2.7) and her creatine phosphokinase (CPK) was 275 U/L. arms bilaterally. Ciprofloxacin by mouth was prescribed and oral hydration Vancomycin, ceftriaxone, and acyclovir were started recommended. -
Detection of Diphtheritic Polyneuropathy by Acute Flaccid Paralysis Surveillance, India Farrah J
SYNOPSIS Detection of Diphtheritic Polyneuropathy by Acute Flaccid Paralysis Surveillance, India Farrah J. Mateen,1 Sunil Bahl, Ajay Khera, and Roland W. Sutter Diphtheritic polyneuropathy is a vaccine-preventable tetanus-pertussis (DTP3) vaccine in 2011 (4). In 2004, illness caused by exotoxin-producing strains of Corynebac- the World Health Organization (WHO) reported 5,000 terium diphtheriae. We present a retrospective convenience deaths caused by diphtheria, all of which were in children case series of 15 children (6 girls) <15 years of age (mean <5 years of age (5). However, reporting of diphtheria is age 5.2 years, case-fatality rate 53%, and 1 additional case- variable, and some countries report cases inconsistently patient who was ventilator dependent at the time of last because of limited recognition among health care workers follow-up; median follow-up period 60 days) with signs and symptoms suggestive of diphtheritic polyneuropathy. All cas- and no dedicated surveillance systems (5). It is likely that es were identified through national acute flaccid paralysis many cases are not reported. surveillance, which was designed to detect poliomyelitis in Diphtheria is clinically considered to be a biphasic ill- India during 2002–2008. We also report data on detection of ness with initial symptoms of low-grade fever, sore throat, diphtheritic polyneuropathy compared with other causes of neck swelling, nasal twang, and usually ipsilateral palatal acute flaccid paralysis identified by this surveillance system. paralysis. The time between the first symptoms of diph- theria and the onset of polyneuropathy is deemed the la- tency period. Diphtheritic polyneuropathy occurs in ≈20% iphtheria is caused by toxin-producing strains of the of patients with diphtheria. -
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. -
The Ultimate Poker Face: a Case Report of Facial Diplegia, a Guillain-Barré Variant
CASE REPORT The Ultimate Poker Face: A Case Report of Facial Diplegia, a Guillain-Barré Variant Joshua Lowe, MD Brooke Army Medical Center, Department of Emergency Medicine, Fort Sam Houston, Texas James Pfaff, MD Section Editor: Christopher Sampson, MD Submission history: Submitted October 14, 2019; Revision received February 4, 2020; Accepted February 7, 2020 Electronically published April 23, 2020 Full text available through open access at http://escholarship.org/uc/uciem_cpcem DOI: 10.5811/cpcem.2020.2.45556 Introduction: Facial diplegia, a rare variant of Guillain-Barré syndrome (GBS), is a challenging diagnosis to make in the emergency department due to its resemblance to neurologic Lyme disease. Case report: We present a case of a 27-year-old previously healthy man who presented with bilateral facial paralysis. Discussion: Despite the variance in presentation, the recommended standard of practice for diagnostics (cerebrospinal fluid albumin-cytological dissociation) and disposition (admission for observation, intravenous immunoglobulin, and serial negative inspiratory force) of facial diplegia are the same as for other presentations of GBS. Conclusion: When presented with bilateral facial palsy emergency providers should consider autoimmune, infectious, idiopathic, metabolic, neoplastic, neurologic, and traumatic etiologies in addition to the much more common neurologic Lyme disease. [Clin Pract Cases Emerg Med. 2020;4(2):150–153.] Keywords: Facial Diplegia; Guillain-Barré variant. INTRODUCTION patient had recently traveled to San Antonio, Texas, for Facial diplegia is a rare variant of Guillain-Barré military exercises and received multiple vaccines five days syndrome (GBS) where patients present with bilateral facial prior to onset of symptoms. He began experiencing mild paralysis and paresthesia. -
Mechanisms of Injury in Dyskinetic Cerebral Palsy
Mechanisms of Injury in Dyskinetic Cerebral Palsy Alec Hoon, MD Associate Professor of Pediatrics Johns Hopkins University School of Medicine Director, Phelps Center for Cerebral Palsy Kennedy Krieger Institute Neurodevelopmental Evaluation Structure‐Function Genetic, Epigenetic, Clinical Phenotype Abnormalities Environmental Risk Factors CP Diagnosis Etiologic Diagnosis Child‐Family Rehabilitative Characteristics Management Medical Surgical Measurement CAM Cell‐Based therapy Techniques Outcome Key Concepts in Cerebral Palsy • Motor control‐ tone, posture, movement • 2‐3/1000 children • Risk factors include infection, inflammation, low birth weight, prematurity, genetic • Secondary to brain dysgenesis or injury • “Non‐progressive”‐ manifestations can change • Unilateral and bilateral phenotypes • A range of associated disorders • Etiology links to phenotype links to treatment 1 Cerebral Palsy‐ Clinical Phenotypes CEREBRAL PALSY Spastic Dyskinetic Ataxic Hypotonia Bilateral Unilateral Hypertonic Hyperkinetic Spastic Diplegia Hemiplegia Dystonic Rigid Dystonic Tetraplegia Quadriplegia Athetosis Chorea Hemiballismus Cascade of events in brain injury 1. Prenatal antecedents may be suspected‐(Freud) 2. Final common pathways often involve hypoxia‐ ischemia and infection‐inflammation 3. Injury may have a protracted time course 4. Injury may lead to myelin abnormalities, reduced plasticity and decreased cell number 5. Injury changes both developmental trajectory and may sensitive brain to later injury The Evolving Nature of Injury TIME