Neurogenic Bowel Dysfunction in Patients with Multiple Sclerosis Open Access to Scientific and Medical Research DOI
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Detrusor Sphincter Dyssynergia: a Review of Physiology, Diagnosis, and Treatment Strategies
Review Article Detrusor sphincter dyssynergia: a review of physiology, diagnosis, and treatment strategies John T. Stoffel Department of Urology, University of Michigan, Ann Arbor, MI, USA Correspondence to: John T. Stoffel, MD. Department of Urology, University of Michigan, Ann Arbor, MI, USA. Email: [email protected]. Abstract: Detrusor sphincter dyssynergia (DSD) is the urodynamic description of bladder outlet obstruction from detrusor muscle contraction with concomitant involuntary urethral sphincter activation. DSD is associated with neurologic conditions such as spinal cord injury, multiple sclerosis, and spina bifida and some of these neurogenic bladder patients with DSD may be at risk for autonomic dysreflexia, recurrent urinary tract infections, or upper tract compromise if the condition is not followed and treated appropriately. It is diagnosed most commonly during the voiding phase of urodynamic studies using EMG recordings and voiding cystourethrograms, although urethral pressure monitoring could also potentially be used. DSD can be sub-classified as either continuous or intermittent, although adoption of this terminology is not widespread. There are few validated oral pharmacologic treatment options for this condition but transurethral botulinum toxin injection have shown temporary efficacy in reducing bladder outlet obstruction. Urinary sphincterotomy has also demonstrated reproducible long term benefits in several studies, but the morbidity associated with this procedure can be high. Keywords: Detrusor sphincter dyssynergia (DSD); neurogenic bladder; urodynamics; external urinary sphincter (EUS) Submitted Nov 30, 2015. Accepted for publication Jan 05, 2016. doi: 10.3978/j.issn.2223-4683.2016.01.08 View this article at: http://dx.doi.org/10.3978/j.issn.2223-4683.2016.01.08 Introduction Physiology The human bladder has two functions—to store and During storage of urine, afferent nerves carry information empty urine. -
Acute Cerebellar Ataxia Associated with Intermittent ECG Pattern Similar to Wellens Syndrome and Transient Prominent QRS Anterior Forces
Acute cerebellar ataxia associated with intermittent ECG pattern similar to Wellens syndrome and transient prominent QRS anterior forces Andrés Ricardo Pérez-Riera, MD, PhD. Post-Graduates Advisor at Design of Studies and Scientific Writing Laboratory in the ABC Faculty of Medicine - ABC Foundation - Santo André – São Paulo – Brazil Raimundo Barbosa-Barros, MD. Specialist in Cardiology by the Brazilian Society of Cardiology (SBC) Specialist in Intensive Care by the Sociedade Brasileira de Terapia Intensiva Chief of the Coronary Center of the Hospital de Messejana Dr. Carlos Alberto Studart Gomes. Fortaleza - Brazil Adrian Baranchuk, MD FACC FRCPC Associate Professor of Medicine and Physiology - Cardiac Electrophysiology and Pacing - Director, EP Training Program - Kingston General Hospital - FAPC 3, 76 Stuart Street K7L 2V7, Kingston ON Queen's University - Canada Male patient, 56 years old, white, uncontrolled hypertension, was admitted to our emergency department (ED) with reports of sudden dizziness, headache of abrupt onset, nausea, vomiting and weakness in the lower limbs. Physical examination drew attention to the presence of manifestations suggestive of cerebellar syndrome: impaired coordination in the trunk or arms and legs, inability to coordinate balance, gait, extremity, uncontrolled or repetitive eye movements, (nystagmus), dyssynergia, dysmetria, dysdiadochokinesia, dysarthria (cerebellar ataxia). Normal myocardial necrosis markers and normal electrolytes ECO 1: anteroseptal-apical akinesis; LVEF = 30% ECO 2 (third day): -
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. -
Autosomal Dominant Cerebellar Ataxia Type I: a Review of the Phenotypic and Genotypic Characteristics
Whaley et al. Orphanet Journal of Rare Diseases 2011, 6:33 http://www.ojrd.com/content/6/1/33 REVIEW Open Access Autosomal dominant cerebellar ataxia type I: A review of the phenotypic and genotypic characteristics Nathaniel Robb Whaley1,2, Shinsuke Fujioka2 and Zbigniew K Wszolek2* Abstract Type I autosomal dominant cerebellar ataxia (ADCA) is a type of spinocerebellar ataxia (SCA) characterized by ataxia with other neurological signs, including oculomotor disturbances, cognitive deficits, pyramidal and extrapyramidal dysfunction, bulbar, spinal and peripheral nervous system involvement. The global prevalence of this disease is not known. The most common type I ADCA is SCA3 followed by SCA2, SCA1, and SCA8, in descending order. Founder effects no doubt contribute to the variable prevalence between populations. Onset is usually in adulthood but cases of presentation in childhood have been reported. Clinical features vary depending on the SCA subtype but by definition include ataxia associated with other neurological manifestations. The clinical spectrum ranges from pure cerebellar signs to constellations including spinal cord and peripheral nerve disease, cognitive impairment, cerebellar or supranuclear ophthalmologic signs, psychiatric problems, and seizures. Cerebellar ataxia can affect virtually any body part causing movement abnormalities. Gait, truncal, and limb ataxia are often the most obvious cerebellar findings though nystagmus, saccadic abnormalities, and dysarthria are usually associated. To date, 21 subtypes have been identified: SCA1-SCA4, SCA8, SCA10, SCA12-SCA14, SCA15/16, SCA17-SCA23, SCA25, SCA27, SCA28 and dentatorubral pallidoluysian atrophy (DRPLA). Type I ADCA can be further divided based on the proposed pathogenetic mechanism into 3 subclasses: subclass 1 includes type I ADCA caused by CAG repeat expansions such as SCA1-SCA3, SCA17, and DRPLA, subclass 2 includes trinucleotide repeat expansions that fall outside of the protein-coding regions of the disease gene including SCA8, SCA10 and SCA12. -
Ramsay Hunt Syndrome - Type II
Case Report Ramsay hunt syndrome - Type II Ravneet Ravinder Verma1, Ravinder Verma2* 1Ex Senior Resident, 2Senior ENT Consultant Surgeon, 1All India Institute of Medical Sciences, Delhi, 2Verma Hospital and Research Centre, Gujral Nagar, Jalandhar, Punjab India *Corresponding Author: Ravinder Verma Email: [email protected] Abstract Ramsay Hunt syndrome is the second most common cause of facial palsy. At least three separate neurological syndromes carry the name of Ramsay Hunt syndrome (RHS), their only connection being that they were all first described by James Ramsay Hunt. Ramsay Hunt syndrome (RHS) type 1 is a rare and nebulous entity that has alternatively been called dyssynergia cerebellaris myoclonica, dyssynergia cerebellaris progressiva, dentatorubral degeneration, or Ramsay Hunt cerebellar syndrome. Ramsay Hunt syndrome (RHS) type 2 is a disorder that is caused by the reactivation of preexisting herpes zoster virus in a nerve cell bundle (the geniculate ganglion). Ramsay Hunt syndrome type III, a less commonly referenced condition, and a neuropathy of the deep palmar branch of the ulnar nerve. Ramsay Hunt Syndrome Type II (RHS) is a rare neurological disorder. This syndrome is caused by the varicella zoster virus (VZV), the same virus that causes chickenpox in children and shingles (herpes zoster) in adults. In cases of Ramsay- Hunt syndrome Type II, previously inactive varicella-zoster virus is reactivated and spreads to affect the facial nerves. The classic Ramsay Hunt syndrome, which always develops after a herpetic infection, also can be associated with vertigo, ipsilateral hearing loss, tinnitus, and facial paresis apart from otalgia. Magnetic resonance imaging (MRI) is a new and important tool for use in diagnosing and investigating diseases affecting the facial nerve. -
GASTROINTESTINAL MOTILITY DISORDERS, DIAGNOSIS and TREATMENT Policy Number: GAS014 Effective Date: February 1, 2019
UnitedHealthcare® Commercial Medical Policy GASTROINTESTINAL MOTILITY DISORDERS, DIAGNOSIS AND TREATMENT Policy Number: GAS014 Effective Date: February 1, 2019 Table of Contents Page COVERAGE RATIONALE ............................................. 1 CENTERS FOR MEDICARE AND MEDICAID SERVICES APPLICABLE CODES ................................................. 1 (CMS) .................................................................. 14 DESCRIPTION OF SERVICES ...................................... 2 REFERENCES ........................................................ 14 CLINICAL EVIDENCE ................................................ 4 POLICY HISTORY/REVISION INFORMATION ............... 17 U.S. FOOD AND DRUG ADMINISTRATION (FDA) ......... 13 INSTRUCTIONS FOR USE ........................................ 17 COVERAGE RATIONALE The following procedures are proven and medically necessary: Gastric electrical stimulation (GES) therapy for treating refractory diabetic gastroparesis that has failed other therapies, or chronic intractable (drug-refractory) nausea and vomiting secondary to gastroparesis of diabetic or idiopathic etiology Rectal manometry and rectal sensation, tone and compliance test Anorectal manometry Defecography for treating intractable constipation or constipation in members who have one or more of the following conditions that are suspected to be the cause of impaired defecation: o Pelvic floor dyssynergia (inappropriate contraction of the puborectalis muscle); or o Enterocele (e.g., after hysterectomy); or o Anterior rectocele -
UW Health Guidelines for the Use of Botulinum Toxin
Botulinum Toxin – Adult/Pediatric – Ambulatory Clinical Practice Guideline Note: Active Table of Contents – Click to follow link EXECUTIVE SUMMARY ...................................................................................................................... 3 SCOPE ............................................................................................................................................... 4 METHODOLOGY ................................................................................................................................ 4 INTRODUCTION................................................................................................................................. 5 RECOMMENDATIONS ........................................................................................................................ 7 UW HEALTH IMPLEMENTATION ...................................................................................................... 12 REFERENCES .................................................................................................................................... 15 1 Copyright © 2017 University of Wisconsin Hospitals and Clinics Authority Contact: [email protected] Vermeulen, [email protected] Last Revised: 01/2017 Contact for Content: Name: Sara Shull, PharmD, MBA, BCPS Phone Number: 262-1817 Email: [email protected] Contact for Changes: Name: Philip Trapskin, PharmD, BCPS Phone Number: 265-0341 Email: [email protected] Guideline Author(s): Updated by Heather LaRue, PharmD, February -
Rehabilitation of Patients with Neurologic Tumors and Cancer-Related Central Nervous System Disabilities
3601_e22_p470-492 2/19/02 9:04 AM Page 470 22 Rehabilitation of Patients with Neurologic Tumors and Cancer-Related Central Nervous System Disabilities THERESA A. GILLIS, RAJESH YADAV, AND YING GUO Neurologic tumors may involve the brain or spinal cord compression can occur in 5% to 10% of can- cord and are either primary or metastatic. Patients cer cases (Barron et al., 1959). Immediate functional may become increasingly less independent as a re- consequences can include pain, sensory deficits, mo- sult of direct injury of neural structures responsible tor deficits, neurogenic bowel and bladder, and sex- for motor, sensory, cognitive, and speech functions. ual dysfunction. The indirect effects of chemotherapy and radiation Rehabilitation management of impairments and therapy (RT) add to the functional deficits patients disabilities is approached in the same manner as in experience. The number of patients involved is quite noncancerous neurologic diseases. However, the large. More than 15,000 new cases of primary brain pathology of the tumor and the anticipated course of tumor and 4000 new spinal tumors are diagnosed disease progression must be considered carefully every year (American Cancer Society, 1990). Ap- when developing rehabilitation goals as well as the proximately 2% of all cancer deaths are caused by time frame required to achieve these goals for an in- brain tumors, which account for roughly 11,000 dividual patient. The purpose of rehabilitation for deaths per year (American Cancer Society, 1990). cancer patients is similar to that for patients with Metastatic lesions from various sites account for 20% other diseases; emphasis is placed on restoring or to 40% of brain tumors (American Cancer Society, maximizing independence with activities of daily liv- 1990), occur in approximately 15% of cancer pa- ing (ADL), mobility, cognition, and communication. -
Clinical and Genetic Overview of Paroxysmal Movement Disorders and Episodic Ataxias
International Journal of Molecular Sciences Review Clinical and Genetic Overview of Paroxysmal Movement Disorders and Episodic Ataxias Giacomo Garone 1,2 , Alessandro Capuano 2 , Lorena Travaglini 3,4 , Federica Graziola 2,5 , Fabrizia Stregapede 4,6, Ginevra Zanni 3,4, Federico Vigevano 7, Enrico Bertini 3,4 and Francesco Nicita 3,4,* 1 University Hospital Pediatric Department, IRCCS Bambino Gesù Children’s Hospital, University of Rome Tor Vergata, 00165 Rome, Italy; [email protected] 2 Movement Disorders Clinic, Neurology Unit, Department of Neuroscience and Neurorehabilitation, IRCCS Bambino Gesù Children’s Hospital, 00146 Rome, Italy; [email protected] (A.C.); [email protected] (F.G.) 3 Unit of Neuromuscular and Neurodegenerative Diseases, Department of Neuroscience and Neurorehabilitation, IRCCS Bambino Gesù Children’s Hospital, 00146 Rome, Italy; [email protected] (L.T.); [email protected] (G.Z.); [email protected] (E.B.) 4 Laboratory of Molecular Medicine, IRCCS Bambino Gesù Children’s Hospital, 00146 Rome, Italy; [email protected] 5 Department of Neuroscience, University of Rome Tor Vergata, 00133 Rome, Italy 6 Department of Sciences, University of Roma Tre, 00146 Rome, Italy 7 Neurology Unit, Department of Neuroscience and Neurorehabilitation, IRCCS Bambino Gesù Children’s Hospital, 00165 Rome, Italy; [email protected] * Correspondence: [email protected]; Tel.: +0039-06-68592105 Received: 30 April 2020; Accepted: 13 May 2020; Published: 20 May 2020 Abstract: Paroxysmal movement disorders (PMDs) are rare neurological diseases typically manifesting with intermittent attacks of abnormal involuntary movements. Two main categories of PMDs are recognized based on the phenomenology: Paroxysmal dyskinesias (PxDs) are characterized by transient episodes hyperkinetic movement disorders, while attacks of cerebellar dysfunction are the hallmark of episodic ataxias (EAs). -
Neurogenic Lower Urinary Tract Dysfunction
Guidelines on Neurogenic Lower Urinary Tract Dysfunction M.Stöhrer, D. Castro-Diaz, E. Chartier-Kastler, G. Del Popolo, G. Kramer, J. Pannek, P. Radziszewski, J-J. Wyndaele © European Association of Urology 2008 TABLE OF CONTENTS PAGE 1. AIM AND STATUS OF THESE GUIDELINES 4 1.1 Purpose 4 1.2 Standardization 4 1.3 References 4 2. BACKGROUND 4 2.1 Risk factors and epidemiology 4 2.1.1 Brain tumours 4 2.1.2 Dementia 4 2.1.3 Mental retardation 5 2.1.4 Cerebral palsy 2.1.5 Normal pressure hydrocephalus 5 2.1.6 Basal ganglia pathology (Parkinson’s disease, Huntington’s disease, 5 Shy-Drager syndrome, etc) 2.1.7 Cerebrovascular (CVA) pathology 5 2.1.8 Demyelinization 5 2.1.9 Spinal cord lesions 5 2.1.10 Disc disease 5 2.1.11 Spinal stenosis and spine surgery 5 2.1.12 Peripheral neuropathy 6 2.1.13 Other conditions (SLE) 6 2.1.14 HIV 6 2.1.15 Regional spinal anaesthesia 6 2.1.16 Iatrogenic 6 2.2 Standardization of terminology 6 2.2.1 Introduction 6 2.2.2 Definitions 7 2.3 Classification 9 2.3.1 Recommendation for clinical practice 10 2.4 Timing of diagnosis and treatment 10 2.5 References 10 3. DIAGNOSIS 19 3.1 Introduction 19 3.2 History 20 3.2.1 General history 20 3.2.2 Specific history 20 3.2.3 Guidelines for history taking 21 3.3 Physical examination 21 3.3.1 General physical examination 21 3.3.2 Neuro-urological examination 21 3.3.3 Laboratory tests 23 3.3.4 Guidelines for physical examination 23 3.4 Urodynamics 24 3.4.1 Introduction 24 3.4.2 Urodynamic tests 24 3.4.3 Specific uro-neurophysiological tests 25 3.4.4 Guidelines for urodynamics and uro-neurophysiology 25 3.5 Typical manifestations of NLUTD 25 3.6 References 26 4. -
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. -
Ataxias of Childhood
ATAXIAS OF CHILDHOOD Jayaprakash A. Gosalakkal, MD, FAAP BACKGROUND– This review examines the causes of ataxias in children. It is a relatively common manifestation of neurological diseases in children. The etiology of ataxia covers a broad range, from infections to rare hereditary metabolic diseases. A systematic approach is required to make the correct diagnosis. REVIEW SUMMARY– The more common causes of ataxias in children are discussed in detail. The importance of recognizing potentially reversible conditions such as vitamin E deficiency and Refsum’s disease is stressed. Recent advances in molecular genetics of some of the chronic ataxias are discussed. The importance of categorizing diseases based on the duration of symptoms and associated signs is discussed. Treatment options are mentioned. CONCLUSION– Ataxia is a common mode of presentation of cerebellar, posterior column, and vestibular disease in children. Awareness of the spectrum of disease entities that cause ataxia in childhood may lead to better diagnosis. KEY WORDS ataxia, cerebellar, childhood (THE NEUROLOGIST 7:300–306, 2001) The term ataxia refers to a special disorder of movement tected early in life in conditions such as Dejerine-Sottas resulting from lesions of the cerebellum or spinocerebellar disease by the ability to correct posture with eyes open but tracts. The disorders, which result in ataxia in children, are not with eyes closed. somewhat different from those in adults. Signs of ataxia in children may be detected as early as the first year of life. This ACUTE AND ACUTE EPISODIC ATAXIA is especially apparent when the child sits down and reaches for objects. Ataxias of childhood can be categorized initially Infectious and Postinfectious by ascertaining the following: 1) whether this is an acute, Acute cerebellar ataxia in children most often follows an acute recurrent, or chronic disorder; 2) if chronic, whether it infectious process.