Radiculopathy and Motor Neuron Disorders
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Peroneal Neuropathy Misdiagnosed As L5 Radiculopathy: a Case Report Michael D Reife1,2* and Christopher M Coulis3,4,5
Reife and Coulis Chiropractic & Manual Therapies 2013, 21:12 http://www.chiromt.com/content/21/1/12 CHIROPRACTIC & MANUAL THERAPIES CASE REPORT Open Access Peroneal neuropathy misdiagnosed as L5 radiculopathy: a case report Michael D Reife1,2* and Christopher M Coulis3,4,5 Abstract Objective: The purpose of this case report is to describe a patient who presented with a case of peroneal neuropathy that was originally diagnosed and treated as a L5 radiculopathy. Clinical features: A 53-year old female registered nurse presented to a private chiropractic practice with complaints of left lateral leg pain. Three months earlier she underwent elective left L5 decompression surgery without relief of symptoms. Intervention and outcome: Lumbar spine MRI seven months prior to lumbar decompression surgery revealed left neural foraminal stenosis at L5-S1. The patient symptoms resolved after she stopped crossing her legs. Conclusion: This report discusses a case of undiagnosed peroneal neuropathy that underwent lumbar decompression surgery for a L5 radiculopathy. This case study demonstrates the importance of a thorough clinical examination and decision making that ensures proper patient diagnosis and management. Keywords: Peroneal neuropathy, Lumbar radiculopathy, Chiropractic Background Case presentation The most common entrapment neuropathy in the lo- The patient is a 53-year-old registered nurse who was wer extremity is common peroneal mononeuropathy, ac- referred to the author’s office in August 2003 by her pri- counting for approximately 15% of all mononeuropathies mary care physician with a chief complaint of left leg in adults [1]. Most injuries occur at the fibular head and pain. Her symptoms began in October 2002 after she fell can be the result of many factors including chronic low off an ambulance landing on her left hip. -
Brachial-Plexopathy.Pdf
Brachial Plexopathy, an overview Learning Objectives: The brachial plexus is the network of nerves that originate from cervical and upper thoracic nerve roots and eventually terminate as the named nerves that innervate the muscles and skin of the arm. Brachial plexopathies are not common in most practices, but a detailed knowledge of this plexus is important for distinguishing between brachial plexopathies, radiculopathies and mononeuropathies. It is impossible to write a paper on brachial plexopathies without addressing cervical radiculopathies and root avulsions as well. In this paper will review brachial plexus anatomy, clinical features of brachial plexopathies, differential diagnosis, specific nerve conduction techniques, appropriate protocols and case studies. The reader will gain insight to this uncommon nerve problem as well as the importance of the nerve conduction studies used to confirm the diagnosis of plexopathies. Anatomy of the Brachial Plexus: To assess the brachial plexus by localizing the lesion at the correct level, as well as the severity of the injury requires knowledge of the anatomy. An injury involves any condition that impairs the function of the brachial plexus. The plexus is derived of five roots, three trunks, two divisions, three cords, and five branches/nerves. Spinal roots join to form the spinal nerve. There are dorsal and ventral roots that emerge and carry motor and sensory fibers. Motor (efferent) carries messages from the brain and spinal cord to the peripheral nerves. This Dorsal Root Sensory (afferent) carries messages from the peripheral to the Ganglion is why spinal cord or both. A small ganglion containing cell bodies of sensory NCS’s sensory fibers lies on each posterior root. -
Level Diagnosis of Cervical Compressive Myelopathy: Signs, Symptoms, and Lesions Levels
Elmer Press Original Article J Neurol Res • 2013;3(5):135-141 Level Diagnosis of Cervical Compressive Myelopathy: Signs, Symptoms, and Lesions Levels Naoki Kasahata ficult to accurately localize the lesion before radiographic Abstract diagnosis. However, neurological level diagnosis of spinal cord is important for accurate lesion-specific level diagnosis, Background: To elucidate signs and symptoms corresponding to patients’ treatment, avoiding diagnostic error, differential di- each vertebral level for level-specific diagnoses. agnosis, and especially for accurate level diagnosis of other nonsurgical myelopathies. Moreover, level diagnosis should Methods: We studied 106 patients with cervical compressive my- be considered from multiple viewpoints. Therefore, we in- elopathy. Patients who showed a single compressive site on mag- tend to make level diagnosis of myelopathy more accurate. netic resonance imaging (MRI) were selected, and signs, symp- Previously, lesion-specific level diagnoses by determin- toms, and the levels of the MRI lesions were studied. ing a sensory disturbance area or location of numbness in Results: Five of 12 patients (41.7%) with C4-5 intervertebral level the hands had the highest accuracy [1, 2]. Previous stud- lesions showed decreased or absent biceps and brachioradialis re- ies reported that C3-4 intervertebral level lesions showed flexes, while 4 of these patients (33.3%) showed generalized hyper- increased or decreased biceps reflexes, deltoid weakness, reflexia. In comparison, 5 of 24 patients (20.8%) with C5-6 inter- and sensory disturbance of arms or forearms [1, 3, 4], while vertebral level lesions showed decreased or absent triceps reflexes; C4-5 intervertebral level lesions showed decreased biceps however, 9 of these patients (37.5%) showed decreased or absent reflexes, biceps weakness, and sensory disturbance of hands biceps and brachioradialis reflexes. -
Neuropathy, Radiculopathy & Myelopathy
Neuropathy, Radiculopathy & Myelopathy Jean D. Francois, MD Neurology & Neurophysiology Purpose and Objectives PURPOSE Avoid Confusing Certain Key Neurologic Concepts OBJECTIVES • Objective 1: Define & Identify certain types of Neuropathies • Objective 2: Define & Identify Radiculopathy & its causes • Objective 3: Define & Identify Myelopathy FINANCIAL NONE DISCLOSURE Basics What is Neuropathy? • The term 'neuropathy' is used to describe a problem with the nerves, usually the 'peripheral nerves' as opposed to the 'central nervous system' (the brain and spinal cord). It refers to Peripheral neuropathy • It covers a wide area and many nerves, but the problem it causes depends on the type of nerves that are affected: • Sensory nerves (the nerves that control sensation>skin) causing cause tingling, pain, numbness, or weakness in the feet and hands • Motor nerves (the nerves that allow power and movement>muscles) causing weakness in the feet and hands • Autonomic nerves (the nerves that control the systems of the body eg gut, bladder>internal organs) causing changes in the heart rate and blood pressure or sweating • It May produce Numbness, tingling,(loss of sensation) along with weakness. It can also cause pain. • It can affect a single nerve (mononeuropathy) or multiple nerves (polyneuropathy) Neuropathy • Symptoms usually start in the longest nerves in the body: Feet & later on the hands (“Stocking-glove” pattern) • Symptoms usually spread slowly and evenly up the legs and arms. Other body parts may also be affected. • Peripheral Neuropathy can affect people of any age. But mostly people over age 55 • CAUSES: Neuropathy has a variety of forms and causes. (an injury systemic illness, an infection, an inherited disorder) some of the causes are still unknown. -
Surgery for Lumbar Radiculopathy/ Sciatica Final Evidence Report
Surgery for Lumbar Radiculopathy/ Sciatica Final evidence report April 13, 2018 Health Technology Assessment Program (HTA) Washington State Health Care Authority PO Box 42712 Olympia, WA 98504-2712 (360) 725-5126 www.hca.wa.gov/hta [email protected] Prepared by: RTI International–University of North Carolina Evidence-based Practice Center Research Triangle Park, NC 27709 www.rti.org This evidence report is based on research conducted by the RTI-UNC Evidence-based Practice Center through a contract between RTI International and the State of Washington Health Care Authority (HCA). The findings and conclusions in this document are those of the authors, who are responsible for its contents. The findings and conclusions do not represent the views of the Washington HCA and no statement in this report should be construed as an official position of Washington HCA. The information in this report is intended to help the State of Washington’s independent Health Technology Clinical Committee make well-informed coverage determinations. This report is not intended to be a substitute for the application of clinical judgment. Anyone who makes decisions concerning the provision of clinical care should consider this report in the same way as any medical reference and in conjunction with all other pertinent information (i.e., in the context of available resources and circumstances presented by individual patients). This document is in the public domain and may be used and reprinted without permission except those copyrighted materials that are clearly noted in the document. Further reproduction of those copyrighted materials is prohibited without the specific permission of copyright holders. -
International Standards for Neurological Classification of Spinal Cord Injury (Revised 2011)
International standards for neurological classification of spinal cord injury (Revised 2011) Steven C. Kirshblum1,2, Stephen P. Burns3, Fin Biering-Sorensen4, William Donovan5, Daniel E. Graves6, Amitabh Jha7, Mark Johansen7, Linda Jones8, Andrei Krassioukov9, M.J. Mulcahey10, Mary Schmidt-Read11, William Waring12 The authors are the members of the International Standards Committee of ASIA. 1UMDNJ/New Jersey Medical School, 2Kessler Institute for Rehabilitation, 3University of Washington School of Medicine, Seattle, Washington, 4Clinic for Spinal Cord Injuries, Rigshospitalet, and Faculty of Health Sciences, University of Copenhagen, Denmark, 5University of Texas, Houston, Texas, 6University of Kentucky, 7Craig Hospital, Englewood, CO, 8Geron Corporation, Menlo Park, CA, USA, 9International Collaboration on Repair Discoveries, Vancouver, British Columbia, Canada, 10Shriners Hospital for Children, 11Magee Rehabilitation Hospital, Philadelphia, PA, 12Medical College of Wisconsin, Milwaukee, Wisconsin Introduction above which they exit (i.e. C1 exits above the C1 vertebra, This article represents the content of the booklet, just below the skull and C6 nerve roots pass between the International Standards for Neurological Classification C5 and C6 vertebrae) whereas C8 exists between the C7 of Spinal Cord Injury, revised 2011, published by the and T1 vertebra; as there is no C8 vertebra. The C1 American Spinal Injury Association (ASIA). For further nerve root does not have a sensory component that is explanation of the clarifications and changes in this tested on the International Standards Examination. revision, see the accompanying article (Kirshblum S., The thoracic spine has 12 distinct nerve roots and the et al. J Spinal Cord Med. 2011:DOI 10.1179/ lumbar spine consists of 5 distinct nerve roots that are 107902611X13186000420242 each named accordingly as they exit below the level of the The spinal cord is the major conduit through which respective vertebrae. -
Patient Information
PATIENT INFORMATION Cervical Radiculopathy A MaineHealth Member What is a Cervical Radiculopathy? Cervical radiculopathy (ra·dic·u·lop·a·thy) is when a nerve in your neck gets irritated. It can cause pain numbness, tingling, or weakness. Neck pain does not mean you have a pinched nerve, although it may be present. What causes cervical radiculopathy? Factors that cause cervical radiculopathy include: ■■ Bulging or herniated discs ■■ Bone spurs These are all common and result from normal wear and tear. A nerve may be irritated by a particular activity (reaching, lifting), a trauma (such as a car accident or fall), or no clear cause at all, other than normal life activity. Smoking does increase the wear and tear so it is important to quit smoking. What is a herniated disc? Your discs act like cushions between the bones in the neck. When the outer coating of the disc (the annulus) weakens or is injured, it may no longer be able to protect the soft spongy material (the nucleus) in the middle of the disc. At first the disc may bulge, eventually the nucleus can break through the annulus. This is called a herniated disc. What is a bone spur? Bone spurs are caused by pressure and extra stress on the bones of the spine (or vertebrae). The body responds to this constant stress by adding extra bone, which results in a bone spur. Bone spurs can pinch or put pressure on a nerve. Maine Medical Center Neuroscience Institute Page 1 of 4 Cervical Radiculopathy What are the common signs and symptoms of cervical radiculopathy? ■■ Pain in neck, shoulder blades, shoulder, and/or arms ■■ Tingling or numbness in arms ■■ Weakness in arm muscles Limited functional ability for tasks as reaching, lifting and gripping, or prolonged head postures as in reading What is the treatment for cervical radiculopathy? Most spine problems heal over time without surgery within 6 to 12 weeks. -
Reflex Testing in the Laboratory
Reflex Testing in The Laboratory Introductory Background Reflex testing is another way of obtaining information about a patient by health care personnel. Many of us are acquainted with some reflexes by virtue of having physical exams, e.g., patellar reflex (knee jerk), biceps, triceps, corneal and Achilles’ tendon reflex. This section deals with, essentially, circuitry of a biological nature. In order to understand this circuitry, it's important to have a fundamental grasp of the "parts" that make up this circuitry. The graphic, below, provides us with an introduction to this concept: A sensory (or afferent; AH fair unt) neuron picks up input (#1, above) and sends it to the spinal cord (#3, above). The portion of a neuron that brings the signal to the cell body is called the dendrite; the portion that sends the signal away from the cell body is called an axon (#5, above). When axons and dendrites from other cells have to communicate, they do so through a microscopic space called a synapse. In some instances, input has to be sent to the brain for interpretation. In others, it's interpreted right in the spinal cord and signals are sent out (motor or efferent; EE fair unt) to the effector organ. In simple stretch reflexes, only two neurons are involved: sensory and motor, graphic, above. In this figure, a stretch reflex is illustrated. The way it works is in this manner: 1) a tendon is stimulated (in this illustration by a reflex hammer), 2) the spindle (blue coil in the diagram) detects this stimulus and sends the input to the cord, 3) the information crosses one synapse (mono-synaptic) to a motor neuron that sends output to the spindle (green coil in diagram) and the muscle contracts. -
Electrodiagnosis of Brachial Plexopathies and Proximal Upper Extremity Neuropathies
Electrodiagnosis of Brachial Plexopathies and Proximal Upper Extremity Neuropathies Zachary Simmons, MD* KEYWORDS Brachial plexus Brachial plexopathy Axillary nerve Musculocutaneous nerve Suprascapular nerve Nerve conduction studies Electromyography KEY POINTS The brachial plexus provides all motor and sensory innervation of the upper extremity. The plexus is usually derived from the C5 through T1 anterior primary rami, which divide in various ways to form the upper, middle, and lower trunks; the lateral, posterior, and medial cords; and multiple terminal branches. Traction is the most common cause of brachial plexopathy, although compression, lacer- ations, ischemia, neoplasms, radiation, thoracic outlet syndrome, and neuralgic amyotro- phy may all produce brachial plexus lesions. Upper extremity mononeuropathies affecting the musculocutaneous, axillary, and supra- scapular motor nerves and the medial and lateral antebrachial cutaneous sensory nerves often occur in the context of more widespread brachial plexus damage, often from trauma or neuralgic amyotrophy but may occur in isolation. Extensive electrodiagnostic testing often is needed to properly localize lesions of the brachial plexus, frequently requiring testing of sensory nerves, which are not commonly used in the assessment of other types of lesions. INTRODUCTION Few anatomic structures are as daunting to medical students, residents, and prac- ticing physicians as the brachial plexus. Yet, detailed understanding of brachial plexus anatomy is central to electrodiagnosis because of the plexus’ role in supplying all motor and sensory innervation of the upper extremity and shoulder girdle. There also are several proximal upper extremity nerves, derived from the brachial plexus, Conflicts of Interest: None. Neuromuscular Program and ALS Center, Penn State Hershey Medical Center, Penn State College of Medicine, PA, USA * Department of Neurology, Penn State Hershey Medical Center, EC 037 30 Hope Drive, PO Box 859, Hershey, PA 17033. -
The Phenomenon of Multiple Stretch Reflexes
Henry Ford Hospital Medical Journal Volume 34 Number 1 Article 6 3-1986 The Phenomenon of Multiple Stretch Reflexes Robert D. Teasdall Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Teasdall, Robert D. (1986) "The Phenomenon of Multiple Stretch Reflexes," Henry Ford Hospital Medical Journal : Vol. 34 : No. 1 , 31-36. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol34/iss1/6 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. The Phenomenon of Multiple Stretch Reflexes Robert D. Teasdall, MD* Multiple stretch reflexes occur in muscles adjacent to or remote from the tap. The response may be ipsilateral or bilateral. These reflexes are encountered not only in normal subjects with brisk stretch reflexes but particularly in patients with lesions of the upper motor neuron. The concussion obtained by the blow is conducted along bone to muscle. Muscle spindles are stimulated, and in this manner independent stretch reflexes are produced in these muscles. This mechanism is responsible for the phenomenon of multiple stretch reflexes. The thorax and pelvis play important roles in the contralateral responses by transmitting these mechanical events across the midline. (Henry FordHosp Med J 1986;34:31-6) ontraction of muscles remote from the site of f)ercussion is Head and neck Cencountered in patients with brisk stretch reflexes. -
Fulminant Guillain–Barré Syndrome Post Hemorrhagic Stroke: Two Case Reports
Case Report Fulminant Guillain–Barré Syndrome Post Hemorrhagic Stroke: Two Case Reports Sameeh Abdulmana 1, Naif Al-Zahrani 1, Yahya Sharahely 2, Shahid Bashir 1 and Talal M. Al-Harbi 1,* 1 Neuroscience Centre, Neurology Department, King Fahad Specialist Hospital-Dammam, Dammam 31444, Saudi Arabia; [email protected] (S.A.); [email protected] (N.A.-Z.); [email protected] (S.B.) 2 Neurology Division, Medical Department, Dammam Medical Complex, Dammam 31444, Saudi Arabia; [email protected] * Correspondence: [email protected]; Tel.: +96-6138442222 (ext. 2270/2278); Fax: +96-6138150315 Abstract: Guillain–Barré syndrome (GBS) is an acute, immune-mediated inflammatory peripheral polyneuropathy characterized by ascending paralysis. Most GBS cases follow gastrointestinal or chest infections. Some patients have been reported either following or concomitant with head trauma, neurosurgical procedures, and rarely hemorrhagic stroke. The exact pathogenesis is not entirely understood. However, blood–brain barrier damage may play an essential role in triggering the autoimmune activation that leads to post-stroke GBS. Here, we present two cases of fulminant GBS following hemorrhagic stroke to remind clinicians to be aware of this rare treatable complication if a stroke patient develops unexplainable flaccid paralysis with or without respiratory distress. Keywords: Guillain–Barré syndrome; Guillain–Barré following stroke; intracranial hemorrhage; Citation: Abdulmana, S.; Al-Zahrani, hemorrhagic stroke complicated by radiculopathy N.; Sharahely, Y.; Bashir, S.; M. Al-Harbi, T. Fulminant Guillain–Barré Syndrome Post Hemorrhagic Stroke: Two Case Reports. Neurol. Int. 2021, 13, 190–194. 1. Introduction https://doi.org/10.3390/ Guillain, Barré, and Strohl first reported Guillain–Barré syndrome (GBS), or acute neurolint13020019 inflammatory demyelinating polyradiculoneuropathy, in 1916 [1]. -
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.