Why Electromyoneurography Instead Of
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Electrophysiological Changes in Patients with Impaired Glucose Tolerance
Turkish Journal of Endocrinology and Metabolism, (2000) 4 : 123-128 ORIGINAL ARTICLE Electrophysiological Changes in Patients with Impaired Glucose Tolerance Serdar Güler* Dilek Berker** Hüseyin Tu¤rul Atasoy*** Bekir Çak›r** Hilmi Uysal*** Yalç›n Aral* Ankara Education and Research Hospital, Departments, Ankara, Turkey * Endocrinology and Metabolism ** Internal Medicine *** Neurology The effect of impaired glucose tolerance on neuropathy is not well characterized. This study is performed to clarify the status of peripheral neuropathy in patients with impaired glucose tolerance with no symptoms of neuropathy. Twenty-two patients with impaired glucose tolerance with no signs of neuropathy, and 11 healthy controls are examined with electromyoneurography. We have found electrophysiological changes in 13 of 22 patients with IGT, and in only one case of the 11 subjects in the control group. Mean H reflex latencies of the right and left medial vastus muscles were significantly longer in the patient group than the control group (17.0±1.7 vs. 15.6±2.5 msec, p<0,02; and 17.1±1.8 vs. 15.7±2.4 msec; p<0,01, respectively). Our results indicate that electrophysiological changes of the peripheral nerves are very common in patients with impaired glucose tolerance. Early diagnosis and mana- gement of impaired glucose tolerance may be particularly important in order to prevent the development of chronic complications. Key words: Impaired glucose tolerance, polyneuropathy, electromyoneurography, electrophysiological studies, electrophysiological abnormalities Introduction Activation of polyol pathway, nonenzymatic gly- cosylation, epineural vascular atherosclerosis, endo- Diabetes Mellitus (DM) is one of the most fre- neurial microvascular disease, dysfunction of endo- quent causes of peripheral neuropathy (1). -
Neurological Complications of Cancer Immunotherapy
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2021 Neurological complications of cancer immunotherapy Roth, Patrick ; Winklhofer, Sebastian ; Müller, Antonia M S ; Dummer, Reinhard ; Mair, Maximilian J ; Gramatzki, Dorothee ; Le Rhun, Emilie ; Manz, Markus G ; Weller, Michael ; Preusser, Matthias Abstract: Immunotherapy has emerged as a powerful therapeutic approach in many areas of clinical on- cology and hematology. The approval of ipilimumab, a monoclonal antibody targeting the immune cell receptor CTLA-4, has marked the beginning of the era of immune checkpoint inhibitors. In the mean- time, numerous antibodies targeting the PD-1 pathway have expanded the class of clinically approved immune checkpoint inhibitors. Furthermore, novel antibodies directed against other immune checkpoints are currently in clinical evaluation. More recently, bispecific antibodies, which link T cells directly to tumor cells as well as adoptive T cell transfer with immune cells engineered to express a chimeric antigen receptor, have been approved in certain indications. Neurological complications associated with the use of these novel immunotherapeutic concepts have been recognized more and more frequently. Immune check- point inhibitors may cause various neurological deficits mainly by alterations of the peripheral nervous system’s integrity. These include radiculopathies, neuropathies, myopathies as well as myasthenic syn- dromes. Side effects involving the central nervous system are less frequent but may result in severe clinical symptoms and syndromes. The administration of chimeric antigen receptor (CAR) T cell is subject to rigorous patient selection and their use is frequently associated with neurological complications includ- ing encephalopathy and seizures, which require immediate action and appropriate therapeutic measures. -
The Role of Molecular Mimicry in the Etiology of Guillain Barré Syndrome
Macedonian pharmaceutical bulletin, 56 (1,2) 3 - 12 (2010) ISSN 1409 - 8695 UDC: 616.833-022 : 579.835.12.083.3 Review The role of molecular mimicry in the etiology of Guillain Barré Syndrome Aleksandra Grozdanova1*, Slobodan Apostolski2, Ljubica Suturkova1 1 Institute for Pharmaceutical chemistry, Faculty of Pharmacy, “St Cyril and Methodius” University, Skopje 2 Outpatient Neurological Clinic, Belgrade, Serbia Received: May 2011; Accepted: June 2011 Abstract Molecular mimicry between host tissue structures and microbial components has been proposed as the pathogenic mechanism for trig- gering of autoimmune diseases by preceding infection. Recent studies stated that molecular mimicry as the causative mechanism remains unproven for most of the human diseases. Still, in the case of the peripheral neuropathy Guillain-Barré syndrome (GBS) this hypothesis is supported by abundant experimental evidence. GBS is the most frequent cause of acute neuromuscular paralysis and in some cases occurs after infection with Campylobacter jejuni (C. jejuni). Epidemiological studies, showed that more than one third of GBS patients had ante- cedent C. jejuni infection and that only specific C. jejuni serotypes are associated with development of GBS. The molecular mimicry be- tween the human gangliosides and the core oligosaccharides of bacterial lipopolysaccharides (LPSs) presumably results in production of antiganglioside cross-reactive antibodies which are likely to be a contributory factor in the induction and pathogenesis of GBS. Antigan- glioside antibodies were found in the sera from patients with GBS and by sensitization of rabbits with gangliosides and C. jejuni LPSs an- imal disease models of GBS were established. GBS as prototype of post-infection immune-mediated disease probably will provide the first verification that an autoimmune disease can be triggered by molecular mimicry. -
Electromyography and Nerve Conduction Studies in Patients With
ogy & N ol eu ur e ro N p h f y o s l Ziegler MS, J Neurol Neurophysiol 2014, 5:3 i o a l n o r g u y o DOI: 10.4172/2155-9562.1000203 J Journal of Neurology & Neurophysiology ISSN: 2155-9562 Research Article Open Access Electromyography and Nerve Conduction Studies in Patients with Lumbar Spinal Stenosis: Is Neurophysiological Examination an Important Tool? Marcus Sofia Ziegler1, Renata Siciliani Scalco2, Erasmo de Abreu Zardo1, Jefferson Becker2 and Irenio Gomes2* 1Department of Orthopaedics & Spine Surgery, Hospital São Lucas Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil 2Department of Neurology, Hospital São Lucas Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil *Corresponding author: Irenio Gomes, Hospital Sao Lucas, and Avenida Ipiranga 6690 - 3 ºandar - IGG Porto Alegre - RS – Brasil, CEP 90610-000, Tel: +55 (51) 3336.8153 / 3320.3000; E-mail: [email protected] Received Date: Jan 21, 2014 Accepted Date: Apr 25, 2014 Published Date: Apr 30, 2014 Copyright: © 2014 Ziegler MS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Background: There is no single test that defines properly lumbar spinal stenosis (LSS) diagnosis, and diagnosis of the syndrome continues to rely on clinical judgment. LSS symptoms may be broad and may be seen in multiple disorders in elderly. Hypothesis: To identify the role of electromyography and nerve-conduction studies on LSS diagnosis. -
MSM 300 11 05 11.Pdf
DIVISION OF HEALTH CARE FINANCING AND POLICY MEDICAID SERVICES MANUAL TABLE OF CONTENTS RADIOLOGY SERVICES 300 INTRODUCTION ...........................................................................................................................1 301 REGULATORY AUTHORITY ......................................................................................................1 302 DEFINITIONS .................................................................................................................................1 303 MEDICAID POLICY ......................................................................................................................1 303.1 RADIOLOGICAL STUDIES ..........................................................................................................1 303.1A COVERAGE AND LIMITATIONS ...............................................................................................1 303.1B PROVIDER RESPONSIBILITY.....................................................................................................2 303.1C RECIPIENT RESPONSIBILITY ....................................................................................................3 303.1D AUTHORIZATION PROCESS ......................................................................................................3 303.2 SCREENING MAMMOGRAPHY .................................................................................................3 303.2A COVERAGE AND LIMITATIONS ...............................................................................................3 -
6Th National Congress of Neuroscience Safranbolu/Karabuk-Turkey, April 09-13,2007
NEUROANATOMY www.neuroanatomy.org VOLUME 6 [2007] Supplement 1 6th National Congress of Neuroscience Safranbolu/Karabuk-Turkey, April 09-13,2007 ABSTRACT BOOK Scientific Committee Organizing Committee Prof. Dr. Turgay DALKARA Prof.Dr. Bektas ACIKGOZ – Chairman Prof. Dr. Lutfiye EROGLU Assoc.Prof.Dr. Emine YILMAZ SIPAHI – Secretary Prof. Dr. Yucel KANPOLAT Assoc.Prof.Dr. Murat KALAYCI Prof. Dr. Fatma KUTAY Assoc.Prof.Dr. Sebnem KARGI Prof. Dr. A.Emre OGE Asst.Prof.Dr. Seyit ANKARALI Prof. Dr. Filiz ONAT Asst.Prof.Dr. Levent ATIK Prof. Dr. Cigdem OZESMI Asst.Prof.Dr. Mustafa BASARAN Prof. Dr. Gonul PEKER Asst.Prof.Dr. Rengin KOSIF Prof. Dr. Sakire POGUN Asst.Prof.Dr. Numan KONUK Prof. Dr. Ismail Hakki ULUS Asst.Prof.Dr. Aysun EROGLU UNAL Prof. Dr. Pekcan UNGAN Assoc..Prof.Dr. Ahmet GURBUZ Assoc.Prof.Dr. Pinar YAMANTURK-CELIK Asst.Prof.Dr. Nuray TURKER Assoc.Prof.Dr. Lutfiye KANIT Lect. Adnan CETINKAYA Assoc.Prof.Dr. Yasemin GURSOY-OZDEMIR Lect. Halime KARAGOL Assoc.Prof.Dr. Turker SAHINER Lect. Saban ESEN Assoc.Prof.Dr. Emine YILMAZ SIPAHI Lect. Afitap AYGUN Assoc.Prof.Dr. Emel ULUPINAR Res.Asst. Fulden ISIKDEMIR Asst.Prof.Dr. Aysun EROGLU UNAL Murat SURUCU Asst.Prof.Dr. Seyit ANKARALI Gokhan SAGLAM The conference is organized under the auspices of TUBITAK, TUBAS, BAD, Kardemir AS and Zonguldak Karaelmas University. e-ISSN 1303-1775 • p-ISSN 1303-1783 Honorary Editor Technical Editor Tuncalp Ozgen, MD M. Mustafa Aldur, MD-PhD Managing Editors Editors Mustafa Aktekin, MD-PhD M. Dogan Aksit, DVM-PhD Alp Bayramoglu, MD-PhD Ruhgun Basar, DDS-PhD M. Deniz Demiryurek, MD-PhD www.neuroanatomy.org Associate Editors A. -
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European Review for Medical and Pharmacological Sciences 2020; 24: 8151-8159 Improvement of pure sensory mononeuritis multiplex and IgG1 deficiency with sitagliptin plus Vitamin D3 M. MAIA PINHEIRO1,2, F. MOURA MAIA PINHEIRO3, L.L. PIRES AMARAL RESENDE4, S. NOGUEIRA DINIZ2, A. FABBRI5, M. INFANTE5,6,7 1UNIVAG University Center, Várzea Grande, Mato Grosso, Brazil 2Postgraduation Program in Biotechnology and Health Innovation, Professional Master Degree in Pharmacy, Anhanguera University of São Paulo, Brazil 3Hospital de Base – FAMERP, São José do Rio Preto, Brazil 4Oncovida – Oncology and Immunology Clinic, Cuiabá, Brazil 5Endocrine Unit, CTO Hospital, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy 6Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Rome, Italy 7UniCamillus, Saint Camillus International University of Health Sciences, Rome, Italy Abstract. – INTRODUCTION: Mononeuritis CONCLUSIONS: To the best of our knowledge, multiplex (MM) is an unusual form of peripher- this is the first case showing a remarkable clin- al neuropathy involving at least two noncontig- ical improvement of MM and selective IgG1 de- uous peripheral nerve trunks. The pure sensory ficiency achieved through a combination thera- form of MM occurs rarely. Immunoglobulin (Ig)G py with sitagliptin and vitamin D3. subclass deficiency is a clinically and genetical- ly heterogeneous disorder. Up to 50% of adults Key Words: with selective subnormal IgG1 levels or selec- Mononeuritis multiplex, Mononeuropathy multi- tive IgG1 deficiency have a concomitant auto- plex, Selective IgG1 deficiency, DPP-4 inhibitors, Sita- immune disorder. Herein, we report the case of gliptin, Vitamin D, Vitamin D3, Cholecalciferol, Hypo- a patient with MM and selective IgG1 deficiency vitaminosis D. -
Icd-9-Cm (2010)
ICD-9-CM (2010) PROCEDURE CODE LONG DESCRIPTION SHORT DESCRIPTION 0001 Therapeutic ultrasound of vessels of head and neck Ther ult head & neck ves 0002 Therapeutic ultrasound of heart Ther ultrasound of heart 0003 Therapeutic ultrasound of peripheral vascular vessels Ther ult peripheral ves 0009 Other therapeutic ultrasound Other therapeutic ultsnd 0010 Implantation of chemotherapeutic agent Implant chemothera agent 0011 Infusion of drotrecogin alfa (activated) Infus drotrecogin alfa 0012 Administration of inhaled nitric oxide Adm inhal nitric oxide 0013 Injection or infusion of nesiritide Inject/infus nesiritide 0014 Injection or infusion of oxazolidinone class of antibiotics Injection oxazolidinone 0015 High-dose infusion interleukin-2 [IL-2] High-dose infusion IL-2 0016 Pressurized treatment of venous bypass graft [conduit] with pharmaceutical substance Pressurized treat graft 0017 Infusion of vasopressor agent Infusion of vasopressor 0018 Infusion of immunosuppressive antibody therapy Infus immunosup antibody 0019 Disruption of blood brain barrier via infusion [BBBD] BBBD via infusion 0021 Intravascular imaging of extracranial cerebral vessels IVUS extracran cereb ves 0022 Intravascular imaging of intrathoracic vessels IVUS intrathoracic ves 0023 Intravascular imaging of peripheral vessels IVUS peripheral vessels 0024 Intravascular imaging of coronary vessels IVUS coronary vessels 0025 Intravascular imaging of renal vessels IVUS renal vessels 0028 Intravascular imaging, other specified vessel(s) Intravascul imaging NEC 0029 Intravascular -
The Hypotonic Infant: Clinical Approach
Journal of Pediatric Neurology 5 (2007) 181–187 181 IOS Press Review Article The hypotonic infant: Clinical approach Mohammed M.S. Jan∗ Department of Pediatrics, King Abdulaziz University Hospital, and Department of Neurosciences, King Faisal Specialist Hospital & RC, Jeddah, Saudi Arabia Received 27 November 2006 Revised 25 December 2006 Accepted 31 December 2006 Abstract. Hypotonia in infants can be a confusing clinical presentation leading to inaccurate evaluation and unnecessary investigations. Hypotonia can result from a variety of central or peripheral causes. Therefore, hypotonia is a phenotype of many clinical conditions with variable prognosis. It is important to recognize that hypotonia is not equivalent to weakness. Infants with central causes, such as Down syndrome, may have severe hypotonia with normal muscle strength. Peripheral hypotonia is frequently associated with weakness, which can be predominantly distal in neuropathies or predominantly proximal in myopathies. In general, central hypotonia is much more commonly encountered; however, the prognosis is worst for hypotonia secondary to neuromuscular pathology. The distinction between central and peripheral hypotonia is therefore critical for proper evaluation and management. Stepwise and accurate assessment is very important to reach the correct diagnosis promptly. In this review, I present a concise clinical approach for evaluating the hypotonic infant. Some practical tips and skills are discussed to improve the likelihood of obtaining an accurate diagnosis. Reaching a specific diagnosis is needed for providing appropriate therapy, prognosis, and counseling. Keywords: Infant, child, hypotonia, floppy, examination, approach 1. Introduction rological disorders one of the most difficult aspects of their clinical practice [6–8]. Hypotonia in infants Neurological disorders are common in Saudi Ara- and children can be a confusing clinical presentation, bia accounting for 25–30% of all consultations to pe- which often leads to inaccurate evaluation and unnec- diatrics [1]. -
Evaluating the Patient with Suspected Radiculopathy
EVALUATINGEVALUATING THETHE PATIENTPATIENT WITHWITH SUSPECTEDSUSPECTED RADICULOPATHYRADICULOPATHY Timothy R. Dillingham, M.D., M.S Professor and Chair, Department of Physical Medicine and Rehabilitation The Medical College of Wisconsin. RadiculopathiesRadiculopathies PathophysiologicalPathophysiological processesprocesses affectingaffecting thethe nervenerve rootsroots VeryVery commoncommon reasonreason forfor EDXEDX referralreferral CAUSESCAUSES OFOF RADICULOPATHYRADICULOPATHY HNPHNP RadiculiitisRadiculiitis SpinalSpinal StenosisStenosis SpondylolisthesisSpondylolisthesis InfectionInfection TumorTumor FacetFacet SynovialSynovial CystCyst Diseases:Diseases: Diabetes,Diabetes, AIDPAIDP MUSCULOSKELETALMUSCULOSKELETAL DISORDERSDISORDERS :: UPPERUPPER LIMBLIMB ShoulderShoulder BursitisBursitis LateralLateral EpicondylitisEpicondylitis DequervainsDequervains TriggerTrigger fingerfinger FibrositisFibrositis FibromyalgiaFibromyalgia // regionalregional painpain syndromesyndrome NEUROLOGICALNEUROLOGICAL CONDITIONSCONDITIONS MIMICKINGMIMICKING CERVICALCERVICAL RADICULOPATHYRADICULOPATHY Entrapment/CompressionEntrapment/Compression neuropathiesneuropathies –– Median,Median, Radial,Radial, andand UlnarUlnar BrachialBrachial NeuritisNeuritis MultifocalMultifocal MotorMotor NeuropathyNeuropathy NeedNeed ExtensiveExtensive EDXEDX studystudy toto R/OR/O otherother conditionsconditions MUSCULOSKELETALMUSCULOSKELETAL DISORDERSDISORDERS :: LOWERLOWER LIMBLIMB HipHip arthritisarthritis TrochantericTrochanteric BursitisBursitis IlliotibialIlliotibial BandBand -
ICD-9-CM Coordination and Maintenance Committee Meeting
ICD-9-CM Coordination and Maintenance Committee Meeting April 18-19, 2002 Diagnoses Welcome and announcements Donna Pickett, MPH, RHIA Co-chair, ICD-9-CM C&M Committee Neurologic conditions Laura Powers, M.D. American Academy of Neurology Muscle weakness ...................................................... pg.5 Memory loss ......................................................... pg.6 Encephalopathy ....................................................... pg.7 Myasthenia gravis in (acute) exacerbation .......................................... pg.8 Long-term antiplatelet/antithrombotic and anti-inflammatory use .......................... pg.9 History of Extracorporeal Membrane Oxygenation (ECMO) ........................... pg.10 Pediatric pre-birth visit for expectant mother ....................................... pg.11 Delayed separation of umbilical cord ............................................. pg.12 Vaccination for RSV ........................................................ pg.13 Bleeding esophageal ulcer ..................................................... pg.14 Encounter for lengthening of growth rod .......................................... pg.15 Decreased libido ........................................................... pg.16 Facial weakness ............................................................ pg.17 Asthma .................................................................. pg.18 Sickle cell disease ....................................................... pg.19-22 Encounter for insulin pump training and titration\Insulin -
BOOK of ABSTRACTS OXFORD ENCALS Meeting 2018
2018 MEETING 20-22 JUNE 2018 BOOK OF ABSTRACTS OXFORD ENCALS Meeting 2018 Acknowledgements ENCALS would like to thank the following sponsors for their generous support of this year’s meeting. Gold Sponsor Silver Sponsors Bronze Sponsors 2 ENCALS Meeting 2018 Poster Session 1: Wednesday 20th June, 18:00 - 19:30 Entrance Hall: A01 Hot-spot KIF5A mutations cause familial ALS David Brenner* (1), Rüstem Yilmaz (1), Kathrin Müller (1), Torsten Grehl (2), Susanne Petri (3), Thomas Meyer (4), Julian Grosskreutz (5), Patrick Weydt (1, 6), Wolfgang Ruf (1), Christoph Neuwirth (7), Markus Weber (7), Susana Pinto (8, 9), Kristl G. Claeys (10, 11, 12), Berthold Schrank (13), Berit Jordan (14), Antje Knehr (1), Kornelia Günther (1), Annemarie Hübers (1), Daniel Zeller (15), The German ALS network MND-NET, Christian Kubisch (16, 17), Sibylle Jablonka (18), Michael Sendtner (18), Thomas Klopstock (19), Mamede de Carvalho (8, 20), Anne Sperfeld (14), Guntram Borck (16), Alexander E. Volk (16, 17), Johannes Dorst (1), Joachim Weis (10), Markus Otto (1), Joachim Schuster (1), Kelly del Tredici (1), Heiko Braak (1), Karin M. Danzer (1), Axel Freischmidt (1), Thomas Meitinger (21), Tim M. Strom (21), Albert C. Ludolph (1), Peter M. Andersen (1, 9), and Jochen H. Weishaupt (1) Heterozygous missense mutations in the N-terminal motor or coiled-coil domains of the kinesin family member 5A (KIF5A) gene cause monogenic spastic paraplegia (HSP10) and Charcot-Marie-Tooth disease type 2 (CMT2). Moreover, heterozygous de novo frame-shift mutations in the C-terminal domain of KIF5A are associated with neonatal intractable myoclonus, a neurodevelopmental syndrome.