The Usefulness of Proximal Radial Motor Conduction in Acute Compressive Radial Neuropathy
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An Improved Technique for Radial Nerve Conduction Studies
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.30.4.332 on 1 August 1967. Downloaded from J. Neurol. Neurosurg. Psychiat., 1967, 30, 332 An improved technique for radial nerve conduction studies ALLAN W. DOWNIE1 AND THOMAS R. SCOTT From the Division of Neurology, Department of Medicine, School of Medicine, University ofNorth Carolina, Chapel Hill, North Carolina, U.S.A. A technique for recording evoked sensory potentials MATERIALS AND METHOD from the radial nerve has already been reported by us (Downie and Scott, 1964). This technique, The apparatus used was a TECA two-channel electro- myograph. The recording electrodes consisted of a pair although reliable, is time consuming and occasion- of chlorided silver discs 1 cm. in diameter, mounted ally difficult and the amplitude of potentials may be 2 5 cm. apart on a plastic base. The active recording as low as 1 to 2 microvolts. The purpose of this electrode was placed over the largest palpable branch communication is to describe a simpler technique by of the radial nerve as it crossed the tendon of the extensor which potentials of greater amplitude can be pollicis longus. The distal recording electrode was placed obtained. In addition, the segment of nerve tested is over the first dorsal interosseous muscle but not neces- Protected by copyright. one which can be readily identified and biopsied if sarily over the nerve, of which the position in this area so desired without causing unpleasant or disturbing cannot be precisely determined (Fig. 1). An experiment sensory loss to the subject. made to assess the importance of the position of this electrode showed no significant difference in latency to The location of a nerve which is to be tested is peak when it was placed in turn on three points along usually determined by stimulating its motor fibres a line between the tendons of the extensor pollicis and finding the stimulus site from which maximal longus and extensor indicis provided the interelectrode muscle contraction is obtained. -
A Guide to Transthyretin Amyloidosis
A Guide to Transthyretin Amyloidosis Authored by Teresa Coelho, Bo-Goran Ericzon, Rodney Falk, Donna Grogan, Shu-ichi Ikeda, Mathew Maurer, Violaine Plante-Bordeneuve, Ole Suhr, Pedro Trigo 2016 Edition Edited by Merrill Benson, Mathew Maurer What is amyloidosis? Amyloidosis is a systemic disorder characterized by extra cellular deposition of a protein-derived material, known as amyloid, in multiple organs. Amyloidosis occurs when native or mutant poly- peptides misfold and aggregate as fibrils. The amyloid deposits cause local damage to the cells around which they are deposited leading to a variety of clinical symptoms. There are at least 23 different proteins associated with the amyloidoses. The most well-known type of amyloidosis is associated with a hematological disorder, in which amyloid fibrils are derived from monoclonal immunoglobulin light-chains (AL amyloidosis). This is associated with a clonal plasma cell disorder, closely related to and not uncommonly co-existing with multiple myeloma. Chronic inflammatory conditions such as rheumatoid arthritis or chronic infections such as bronchiectasis are associated with chronically elevated levels of the inflammatory protein, serum amyloid A, which may misfold and cause AA amyloidosis. The hereditary forms of amyloidosis are autosomal dominant diseases characterized by deposition of variant proteins, in dis- tinctive tissues. The most common hereditary form is transthyretin amyloidosis (ATTR) caused by the misfolding of protein monomers derived from the tetrameric protein transthyretin (TTR). Mutations in the gene for TTR frequently re- sult in instability of TTR and subsequent fibril formation. Closely related is wild-type TTR in which the native TTR protein, particu- larly in the elderly, can destabilize and re-aggregate causing non- familial cases of TTR amyloidosis. -
Expert Consensus Recommendations to Improve Diagnosis of ATTR Amyloidosis with Polyneuropathy
Journal of Neurology https://doi.org/10.1007/s00415-019-09688-0 REVIEW Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy David Adams1 · Yukio Ando2 · João Melo Beirão3 · Teresa Coelho4 · Morie A. Gertz5 · Julian D. Gillmore6 · Philip N. Hawkins6 · Isabelle Lousada7 · Ole B. Suhr8 · Giampaolo Merlini9,10 Received: 10 December 2019 / Revised: 20 December 2019 / Accepted: 23 December 2019 © The Author(s) 2020 Abstract Amyloid transthyretin (ATTR) amyloidosis with polyneuropathy (PN) is a progressive, debilitating, systemic disease wherein transthyretin protein misfolds to form amyloid, which is deposited in the endoneurium. ATTR amyloidosis with PN is the most serious hereditary polyneuropathy of adult onset. It arises from a hereditary mutation in the TTR gene and may involve the heart as well as other organs. It is critical to identify and diagnose the disease earlier because treatments are available to help slow the progression of neuropathy. Early diagnosis is complicated, however, because presentation may vary and family history is not always known. Symptoms may be mistakenly attributed to other diseases such as chronic infammatory demyelinating polyradiculoneuropathy (CIDP), idiopathic axonal polyneuropathy, lumbar spinal stenosis, and, more rarely, diabetic neuropathy and AL amyloidosis. In endemic countries (e.g., Portugal, Japan, Sweden, Brazil), ATTR amyloidosis with PN should be suspected in any patient who has length-dependent small-fber PN with autonomic dysfunction and a family history of ATTR amyloidosis, unexplained weight loss, heart rhythm disorders, vitreous opacities, or renal abnormali- ties. In nonendemic countries, the disease may present as idiopathic rapidly progressive sensory motor axonal neuropathy or atypical CIDP with any of the above symptoms or with bilateral carpal tunnel syndrome, gait disorders, or cardiac hypertro- phy. -
Practical Neurology: Peripheral Neuropathy for the Internist
Practical Neurology: Polyneuropathy for the Non-Neurologist Steven A. Day, MD Providence Neurological Specialties Definitions Foundational Principle: With neurological problems think of LOCALIZATION before SYNDROME Definitions • Neuronopathy – Motor neuronopathy – Sensory neuronopathy • Radiculopathy • Plexopathy • Neuropathy – Mononeuropathy – Polyneuropathy The Netter Collection of Medical Illustrations, Volume 1, Nervous System, 2002 “ROOTS” C4 TRUNKS C5 Dorsal scapular n. C6 TRUNKS C7 Suprascapular n. T1 DIVISIONS Musculocut- aneous n. CCF CORDS 2002 Long thoracic n. TERMINAL NERVES CCF ©2002 Axillary n. Radial n. Median n. Ulnar n. Definitions ‘Neuropathy’ is a diagnosis which specifies the location of pathology, not a symptom Definitions • Axonal = axon loss pathology • Demyelinating = myelin loss pathology Topical Diagnosis in Neurology, 3rd ed. 1998 Topical Diagnosis in Neurology, 3rd ed. 1998 Duss’ Topical Diagnosis in Neurology, 4th ed. 2005 Polyneuropathy Polyneuropathy: Typical Presentation • Insidious onset • Distal (toes, pads of feet) • Gradual progression • Complaints are primarily sensory Polyneuropathy: Key Exam Features • Sensory – Distal gradient of sensory loss • Pin prick or cold • Monofilament • Cotton wisp • Vibration at toes and ankles • Proprioception: toe movements Polyneuropathy: Key Exam Features • Motor – Is there intrinsic foot or hand muscle atrophy? – Weakness pattern • Distal • Proximal and distal • Asymmetric – Able to stand/elevate on toes and heels? Polyneuropathy: Key Exam Features • Reflexes – Distal -
Anatomical, Clinical, and Electrodiagnostic Features of Radial Neuropathies
Anatomical, Clinical, and Electrodiagnostic Features of Radial Neuropathies a, b Leo H. Wang, MD, PhD *, Michael D. Weiss, MD KEYWORDS Radial Posterior interosseous Neuropathy Electrodiagnostic study KEY POINTS The radial nerve subserves the extensor compartment of the arm. Radial nerve lesions are common because of the length and winding course of the nerve. The radial nerve is in direct contact with bone at the midpoint and distal third of the humerus, and therefore most vulnerable to compression or contusion from fractures. Electrodiagnostic studies are useful to localize and characterize the injury as axonal or demyelinating. Radial neuropathies at the midhumeral shaft tend to have good prognosis. INTRODUCTION The radial nerve is the principal nerve in the upper extremity that subserves the extensor compartments of the arm. It has a long and winding course rendering it vulnerable to injury. Radial neuropathies are commonly a consequence of acute trau- matic injury and only rarely caused by entrapment in the absence of such an injury. This article reviews the anatomy of the radial nerve, common sites of injury and their presentation, and the electrodiagnostic approach to localizing the lesion. ANATOMY OF THE RADIAL NERVE Course of the Radial Nerve The radial nerve subserves the extensors of the arms and fingers and the sensory nerves of the extensor surface of the arm.1–3 Because it serves the sensory and motor Disclosures: Dr Wang has no relevant disclosures. Dr Weiss is a consultant for CSL-Behring and a speaker for Grifols Inc. and Walgreens. He has research support from the Northeast ALS Consortium and ALS Therapy Alliance. -
Perioperative Upper Extremity Peripheral Nerve Injury and Patient Positioning: What Anesthesiologists Need to Know
Anaesthesia & Critical Care Medicine Journal ISSN: 2577-4301 Perioperative Upper Extremity Peripheral Nerve Injury and Patient Positioning: What Anesthesiologists Need to Know Kamel I* and Huck E Review Article Lewis Katz School of Medicine at Temple University, USA Volume 4 Issue 3 Received Date: June 20, 2019 *Corresponding author: Ihab Kamel, Lewis Katz School of Medicine at Temple Published Date: August 01, 2019 University, MEHP 3401 N. Broad street, 3rd floor outpatient building ( Zone-B), DOI: 10.23880/accmj-16000155 Philadelphia, United States, Tel: 2158066599; Email: [email protected] Abstract Peripheral nerve injury is a rare but significant perioperative complication. Despite a variety of investigations that include observational, experimental, human cadaveric and animal studies, we have an incomplete understanding of the etiology of PPNI and the means to prevent it. In this article we reviewed current knowledge pertinent to perioperative upper extremity peripheral nerve injury and optimal intraoperative patient positioning. Keywords: Nerve Fibers; Proprioception; Perineurium; Epineurium; Endoneurium; Neurapraxia; Ulnar Neuropathy Abbreviations: PPNI: Perioperative Peripheral Nerve 2018.The most common perioperative peripheral nerve Injury; MAP: Mean Arterial Pressure; ASA CCP: American injuries involve the upper extremity with ulnar Society of Anesthesiology Closed Claims Project; SSEP: neuropathy and brachial plexus injury being the most Somato Sensory Evoked Potentials frequent [3,4]. In this article we review upper extremity PPNI with regards to anatomy and physiology, Introduction mechanisms of injury, risk factors, and prevention of upper extremity PPNI. Perioperative peripheral nerve injury (PPNI) is a rare complication with a reported incidence of 0.03-0.1% [1,2]. Anatomy and Physiology of Peripheral PPNI is a significant source of patient disability and is the Nerves second most common cause of anesthesia malpractice claims [3,4]. -
069-Workshop-Food Allergy
WORKSHOP Practical Pointers For Your Practice Short Snappers in Neurology: Clinical Strategies and Problems Alan E. Goodridge , MD, FRCPC Presented at Memorial University’s Wednesday at Noon Ask the Consultant Seminar, January 17, 2007. Scenario 1 The approach to the neurological hen faced with a examination Wneurological The neurological exam can be daunting, but strate - problem, it is helpful, gies can be developed to target the key aspects of the during the history, to n neurological exam to answer the clinical questions make ©a judgment utio raised by the history. When faced with a neurologi - ht rib ig ist ad, cal problem, it is helpful, during the history, to mayke rregarding Dwhetwhnelor the p ial n do a judgment regarding whether the probleom is more rc rs ca use C proeblemuseis monoarl e likely likely to be of peripheral or central nervous system mm rised pers o utho y for (CNS) origin. r C ed. Ato bceopof peripheral or o hibit ingle When there are localizianglseymptomprs,osuch ats a s S use prin CNS origin. acute presentatiofnoofra hemirpisleegdia, the ceanntrdal origin t utho view of theNprooblem wUilnl abe obvioluasy. ,With clinical prob - This approach contrasts with problems that, disp lems where there are usually no localizing symp - based on the history, suggest a peripheral nervous toms, such as a headache or a seizure, the clinical system origin. For example, when the symptoms are exam is primarily directed towards the question of a localized to one limb ( i.e., with pain and numbness possible problem of central origin. in one arm). -
A Case of Bickerstaff S Brainstem Encephalitis in Childhood '
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Directory of Open Access Journals Korean Journal of Pediatrics Vol. 53, No. 4, 2010 DOI : 10.3345/kjp.2010.53.4.607 Case report 1)jtj A case of Bickerstaff’s brainstem encephalitis in childhood Ji Youn Kim, M.D., Young Ok Kim, M.D., Young Jun Son, M.D. and Young Jong Woo, M.D. Department of Pediatrics, Chonnam National University Medical School, Gwangju, Korea = Abstract = Bickerstaff's brainstem encephalitis (BBE) is a rare disease diagnosed by specific clinical features such as 'progressive, relatively symmetric external ophthalmoplegia and ataxia by 4 weeks' and 'disturbance of consciousness or hyperreflexia' after the exclusion of other diseases involving the brain stem. Anti-ganglioside antibodies (GM, GD and GQ) in the serum or cerebrospinal fluid (CSF) are sometimes informative for the diagnosis of BBE because of the rarity of positive findings in other diagnositic methods: brain magnetic resonance imaging (MRI), routine CSF examination, motor nerve conduction study, and needle electromyography. We report a rare case of childhood BBE with elevated anti-GM1 antibodies in the serum, who had specific clinical symptoms such as a cranial polyneuropathy presenting as ophthalmoplegia, dysarthria, dysphagia, and facial weakness; progressive motor weakness; altered mental status; and ataxia. However, the brain MRI, routine CSF examination, nerve conduction studies, electromyography, somatosensory evoked potentials, and brainstem auditory evoked potentials were normal. BBE was suspected and the patient was successfully treated with intravenous immunoglobulins. (Korean J Pediatr 2010;53:607-611) Key Words : Encephalitis, Brain stem, Child bulins (IVIG) for the treatment of BBE suggests an auto- Introduction immune etiology5, 6). -
Peripheral Polyneuropathy in Patients Receiving Long-Term Statin Therapy
552 Turk Kardiyol Dern Ars 2019;47(7):552-553 doi: 10.5543/tkda.2019.52735 Invited Editorial / Davetli Editöryal Yorum Peripheral polyneuropathy in patients receiving long-term statin therapy Uzun dönem statin kullanan hastalarda periferik polinöropati gelişimi Öner Özdoğan, M.D. Department of Cardiology, Tepecik Training and Research Hospital, İzmir, Turkey Although drug-induced neuropathies (DIN) are not an enzyme which could Abbreviation: very common, they are one of the main reasons of pe- alter the neurons’ energy DIN Drug-induced neuropathies ripheral neuropathies.[1] DIN cause to sensory, motor, utilization.[6] On the con- ENMG Electroneuromyography and autonomic dysfunctions depending on the type of SAMs Statin-associated muscle trary; some animal stu- symptoms the peripheral nerve involvement. As significant re- dies have reported that covery could be observed after discontinuation of the statins provided a neuroprotective effect against pe- causal agent drug, early diagnosis is important. How- ripheral nerve injury.[7] In a recent Danish case-control ever, symptoms of DIN are usually seen after months study, use of statins in 370 cases, was not associated [2] or years of exposure. Therefore, defining the causal with an elevated risk of polyneuropathy. Similarly, no relationship between the drugs and long term side ef- association was observed between polyneuropathy fects like drug-induced peripheral neuropathies is not risk and long-term high-intensity statin.[8] easy always, and commonly missed. Electrodiagnos- tic tests are the most important methods to confirm In this issue of the Archives of Turkish Society tthe peripheral neuropathy.[3] We classify the type of of Cardiology, Ozdemir et al. -
Posterior Interosseous Neuropathy Supinator Syndrome Vs Fascicular Radial Neuropathy
Posterior interosseous neuropathy Supinator syndrome vs fascicular radial neuropathy Philipp Bäumer, MD ABSTRACT Henrich Kele, MD Objective: To investigate the spatial pattern of lesion dispersion in posterior interosseous neurop- Annie Xia, BSc athy syndrome (PINS) by high-resolution magnetic resonance neurography. Markus Weiler, MD Methods: This prospective study was approved by the local ethics committee and written Daniel Schwarz, MD informed consent was obtained from all patients. In 19 patients with PINS and 20 healthy con- Martin Bendszus, MD trols, a standardized magnetic resonance neurography protocol at 3-tesla was performed with Mirko Pham, MD coverage of the upper arm and elbow (T2-weighted fat-saturated: echo time/repetition time 52/7,020 milliseconds, in-plane resolution 0.27 3 0.27 mm2). Lesion classification of the radial nerve trunk and its deep branch (which becomes the posterior interosseous nerve) was performed Correspondence to Dr. Bäumer: by visual rating and additional quantitative analysis of normalized T2 signal of radial nerve voxels. [email protected] Results: Of 19 patients with PINS, only 3 (16%) had a focal neuropathy at the entry of the radial nerve deep branch into the supinator muscle at elbow/forearm level. The other 16 (84%) had proximal radial nerve lesions at the upper arm level with a predominant lesion focus 8.3 6 4.6 cm proximal to the humeroradial joint. Most of these lesions (75%) followed a specific somato- topic pattern, involving only those fascicles that would form the posterior interosseous nerve more distally. Conclusions: PINS is not necessarily caused by focal compression at the supinator muscle but is instead frequently a consequence of partial fascicular lesions of the radial nerve trunk at the upper arm level. -
Musculoskeletal Disorders and Treatment
ISSN: 2572-3243 Terlemez et al. J Musculoskelet Disord Treat 2018, 4:045 DOI: 10.23937/2572-3243.1510045 Volume 4 | Issue 1 Journal of Open Access Musculoskeletal Disorders and Treatment ShorT CommEnTarY Diagnostic Ultrasound for Traumatic Radial Nerve Injury: A Visual Vignette Rana Terlemez*, Selda Çiftçi, Tülay Erçalık, Jülide Öncü, Figen Yilmaz and Banu Kuran Department of Physical Medicine and Rehabilitation, Şişli Hamidiye Etfal Training and Research Hospital, Turkey *Corresponding author: Rana Terlemez, MD, Department of Physical Medicine and Rehabilitation, Şişli Hamidiye Etfal Training and Research Hospital, Istanbul, Turkey, Tel: +90-5355544638, E-mail: Check for [email protected] updates A 35-year-old man had fallen down from the first lumbrical muscle grades were about 1/5. We also ob- floor and admitted emergency department with pain, served a sensory deficit in the radial nerve dermatome. swelling and deformity on the right elbow. The radio- In ultrasonographic examination, we observed thicken- graph showed fracture of the right supracondylar hu- ing in the nerve, increased hypoechogenicity and loss merus. After surgical exploration and internal fixations, of neuronal fascicle distinction at the distal part of the the patient referred to our clinic as elbow contracture elbow. No power Doppler signal was observed as a sign with traumatic median and ulnar nerve injury. The sur- of neovascularization (Figure 1). Electrodiagnostic stud- geon noted that radial nerve was seen as intact. In phys- ies also showed severe axonal injury to the radial nerve. ical examination strength of extensor carpi radialis, ex- Motor study of the radial nerve showed decrease in the tensor digitorum communis, extensor carpi ulnaris and compound muscle action potential (CMAP). -
Peripheral Nerve Disorders
CLINICAL GUIDELINES PND Imaging Policy Version 1.0 Effective February 14, 2020 eviCore healthcare Clinical Decision Support Tool Diagnostic Strategies: This tool addresses common symptoms and symptom complexes. Imaging requests for individuals with atypical symptoms or clinical presentations that are not specifically addressed will require physician review. Consultation with the referring physician, specialist and/or individual’s Primary Care Physician (PCP) may provide additional insight. CPT® (Current Procedural Terminology) is a registered trademark of the American Medical Association (AMA). CPT® five digit codes, nomenclature and other data are copyright 2017 American Medical Association. All Rights Reserved. No fee schedules, basic units, relative values or related listings are included in the CPT® book. AMA does not directly or indirectly practice medicine or dispense medical services. AMA assumes no liability for the data contained herein or not contained herein. © 2019 eviCore healthcare. All rights reserved. PND Imaging Guidelines V1.0 Peripheral Nerve Disorders (PND) Imaging Guidelines Abbreviations for Peripheral Nerve Disorders Imaging Guidelines 3 PN-1: General Guidelines 4 PN-2: Focal Neuropathy 5 PN-3: Polyneuropathy 7 PN-4: Brachial Plexus 8 PN-5: Lumbar and Lumbosacral Plexus 9 PN-6: Muscle Disorders 10 PN-7: Magnetic Resonance Neurography (MRN) 13 PN-8: Amyotrophic Lateral Sclerosis (ALS) 14 PN-9: Peripheral Nerve Sheath Tumors (PNST) 15 PN-10: Nuclear Imaging 16 ______________________________________________________________________________________________________