DOCSLIB.ORG

Traumaticinjuryto Peripheral Nerves

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Traumaticinjuryto Peripheral Nerves Jpn J Rehabil Med 2005; 42: 89-98 2004年／第 41回 日本リハビリテーション医学会 学術集会／東京 Invited Lecture Traumatic Injury to Peripheral Nerves Lawrence R Robinson, MD isolated nervous system injury, but may also Epidemiology of Peripheral Nerve often accompany CNS trauma, not only Trauma compounding the disability, but making recog- nition of the peripheral nerve lesion problem- Traumatic injury to peripheral nerves results atic. Of patients with peripheral nerve injuries, in considerable disability across the world. In about 60% have a traumatic brain injury. peacetime, peripheral nerve injuries commonly Conversely, of those with traumatic brain result from trauma due to motor vehicle acci- injury admitted to rehabilitation units,10-34% dents, and less commonly from penetrating have associated peripheral nerve injuries. trauma, falls and industrial accidents. Out of It is often easy to miss peripheral nerve injuries all patients admitted to Level I trauma centers, in the setting of CNS trauma. Since the neuro- it is estimated that roughly 2-3% have periph- logic history and examination is limited, early eral nerve injuries. If plexus and root hints to a superimposed peripheral nerve lesion injuries are also included,the incidence is about might be only flaccidity,areflexia,and reduced 5%. movement of a limb. In the upper limb,the nerve most commonly Peripheral nerve injuries are of significant reported injured is the radial nerve,followed by import as they impede recovery of function and ulnar and median nerves. Lower limb return to work, and carry risk of secondary peripheral nerve injuries are less common,with disabilities from falls,fractures,or other secon- the sciatic most frequently injured,followed by dary injuries. An understanding of the classifi- peroneal and rarely tibial or femoral nerves. cation,pathophysiology and electrodiagnosis of Fractures of nearby bones are commonly as- these lesions is critical to the appropriate diag- sociated,such as humeral fractures with radial nosis, localization and management of periph- neuropathy. eral nerve trauma. In wartime,peripheral nerve trauma is much more common and much of our knowledge Classification of Nerve Injuries about peripheral nerve injury,repair and recov- ery comes from experience derived in World There are two predominant schemes that War I and II, and subsequent wars. have been proposed for classification of periph- Peripheral nerve injuries may be seen as an eral nerve traumatic injuries; that of Seddon Used by permission, copyright 2000AAEM. This manuscript is based on the monograph “Traumatic Injury to Peripheral Nerves”published by the AAEM in Muscle& Nerve 2000; 23: 863-873. The monograph can be purchased from AAEM at (507)-288-0100. Professor and Chair, Department of Rehabilitation Medicine, University of Washington, Seattle, WA 98195 リハビリテーション医学 VOL.42 NO.2 2005年 2月 Lawrence R ROBINSON Table 1 Classification systems for nerve injury Seddon Sunderland Pathology Prognosis Classification Classification Neurapraxia First Degree Myelin Injury or Ischemia Excellent recovery in weeks to months Axonotmesis Axons Disrupted Good to poor, depending upon integrity of Variable Stromal Disruption supporting structures and distance to muscle Second Degree Axons Disrupted Good, depending upon distance to muscle Endoneurial Tubes Intact Perineurium Intact Epineurium Intact Third Degree Axons Disrupted Poor Endoneurial Tubes Disrupted Axonal misdirection Perineurium Intact Surgery may be required Epineurium Intact Fourth Degree Axons Disrupted Poor Endoneurial Tubes Disrupted Axonal misdirection Perineurium Disrupted Surgery usually required Epineurium Intact Neurotmesis Fifth Degree Axon Disrupted No spontaneous recovery Endoneurial Tubes Disrupted Surgery required Perineurium Disrupted Prognosis after surgery guarded Epineurium Dis rupted Adapted from Dillingham. and that of Sunderland(Table 1). The for- scar tissue that axonal regrowth is impossible. mer is more commonly used in the literature. Examples are s harp injury, some traction Seddon has used the terms neurapraxia, axono t- injuries or injection of noxious drugs. Progno- mesis, and neurotmesis to describe peripheral sis for spontaneous recovery is extremely poor nerve injuries.Neurapraxia is a comparative- without surgical intervention. Sunderland ly mild injury with motor and sensory loss but uses a more subdivided scheme to describe no evidence of Wallerian degeneration. The peripheral nerve injuries, with five groups nerve distally conducts normally. Focal instead of three. demyelination and/or ischemia are thought to be the etiologies of the conduction block. Electrodiagnosis: Timing of Changes and Recovery may occur within hours,days,weeks, Determining Degree of Injury or up to a few months. Axonotmesis is common- ly seen in crush injuries. The axons and their 1. The Compound Motor Action Potential myelin sheaths are broken,yet the surrounding Neurapraxia: In purely neurapraxic lesions, stroma (i.e.the endoneurium,perineurium,and the compound muscle action potential(CMAP) epineurium) remains partially or fully intact. will change immediately after injury,assuming Wallerian degeneration occurs, but subsequent one can stimulate both above and below the site axonal regrowth may proceed along the intact of the lesion (Fig.1). When recording from endoneurial tubes. Recovery ultimately distal muscles and stimulating distal to the site depends upon the degree of internal disorgani- of the lesion, the CMAP should always be zation in the nerve as well as the distance to the normal since no axonal loss and no Wallerian end organ. Sunderland’s classification (below) degeneration has occurred. Moving stimulation further divides this category. Neurotmesis proximal to the lesion will produce a smaller or describes a nerve that has been either complete- absent CMAP, as conduction in some or all ly severed or is so markedly disorganized by fibers is blocked. It should be remembered that Jpn J Rehabil Med VOL.42 NO.2 2005 Traumatic Injury to Peripheral Nerves Fig.1 Diagrammatic representation of changes in Fig.2 Diagrammatic representation of changes in the compound muscle action potential the compound muscle action potential (CMAP) after axonotmesis and neurot- (CMAP)after neurapraxia. mesis. amplitudes normally fall with increasing dis- tance between stimulation and recording ; “few days”thereafter, the CMAP and motor hence there is some debate about how much of conduction studies look the same as those seen a drop in amplitude is sufficient to demonstrate in a neurapraxic lesion. Nerve segments distal conduction block. Amplitude drops exceeding to the lesion remain excitable and demonstrate 20% over a 25cm distance or less are clearly normal conduction while proximal stimulation abnormal; smaller changes over smaller dis- results in an absent or small response from tances are likely also suggestive of an abnor- distal muscles . Early on,this picture looks the mality. In addition to conduction block,partial same as conduction block and can be confused lesions also often demonstrate concomitant with neurapraxia. Hence neurapraxia and slowing across the lesion. This slowing may be axontomeis can not be distinguished until due to either loss of faster conducting fibers or sufficient time for Wallerian degeneration in all demyelination of surviving fibers. All these motor fibers has occurred, typically about 9 changes in the CMAP will generally persist days post injury(Fig.2). until recovery takes place,typically by no more As Wallerian degeneration occurs,the ampli- than a few months post injury. Most important- tude of the CMAP elicited with distal stimula- ly, the distal CMAP will never drop in ampli- tion will fall. This starts at about day3and is tude in purely neurapraxic injuries, since no complete by about day 9. Neuromuscular axon loss or Wallerian degeneration occurs and junction transmission fails before nerve ex- the distal nerve segment remains normally citability.Thus in complete axonotmesis at excitable. day 9, one has a very different picture from Axonotmesis and Neurotmesis : Electro- neurapraxia. There are absent responses both diagnostically, complete axonotmesis (equiva- above and below the lesion. Partial axon loss lent to Sunderland grades 2,3and 4)and com- lesions will produce small amplitude motor plete neurotmesis look the same, since the responses, with the amplitude of the CMAP difference between these types of lesions is in roughly proportional to the number of surviving the integrity of the supporting structures,which axons. One can compare side-to-side CMAP have no electrophysiologic function. Thus amplitudes to estimate the degree of axon loss, these lesions can be grouped together as though inherent side to side variability of up to axonotmesis for the purpose of this discussion. 30-50% limits the accuracy of the estimate. Immediately after axonotmesis and for a Using the CMAP amplitude to estimate the リハビリテーション医学 VOL.42 NO.2 2005年 2月 Lawrence R ROBINSON 2. Compound or Sensory Nerve Action Potentials Neurapraxia: The sensory nerve action potential (SNAP)and compound nerve action potential(CNAP)will show changes similar to the CMAP after focal nerve injury. In the setting of neurapraxia,there is a focal conduc- tion block at the site of the lesion,with preser- ved distal amplitude. However,the criteria for establishing conduction block in sensory nerve Fig.3 Diagrammatic representation of changes in fibers are substantially different than that for the compound muscle action potential the CMAP. When recording nerve action (CMAP)after
Load more

Recommended publications
  • Respiratory Management in the Patient with Spinal Cord Injury
    Hindawi Publishing Corporation BioMed Research International Volume 2013, Article ID 168757, 12 pages http://dx.doi.org/10.1155/2013/168757 Review Article Respiratory Management in the Patient with Spinal Cord Injury Rita Galeiras Vázquez,1 Pedro Rascado Sedes,2 Mónica Mourelo Fariña,1 Antonio Montoto Marqués,3,4 and M. Elena Ferreiro Velasco3 1 Critical Care Unit, Complexo Hospitalario Universitario A Coruna,˜ CP. 15006, A Coruna,˜ Spain 2 Critical Care Unit, Complexo Hospitalario Universitario de Santiago de Compostela, CP. 15702, Santiago de Compostela, Spain 3 Spinal Cord Injury Unit, Complexo Hospitalario Universitario A Coruna,˜ CP. 15006, A Coruna,˜ Spain 4 Department of Medicine, University of A Coruna,˜ CP. 15006, A Coruna,˜ Spain Correspondence should be addressed to Rita Galeiras Vazquez;´ [email protected] Received 30 April 2013; Revised 11 July 2013; Accepted 30 July 2013 Academic Editor: Boris Jung Copyright © 2013 Rita Galeiras Vazquez´ et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Spinal cord injuries (SCIs) often lead to impairment of the respiratory system and, consequently, restrictive respiratory changes. Paresis or paralysis of the respiratory muscles can lead to respiratory insufficiency, which is dependent on the level and completeness of the injury. Respiratory complications include hypoventilation, a reduction in surfactant production, mucus plugging, atelectasis, and pneumonia. Vital capacity (VC) is an indicator of overall pulmonary function; patients with severely impaired VC may require assisted ventilation. It is best to proceed with intubation under controlled circumstances rather than waiting until the condition becomes an emergency.
    [Show full text]
  • Nerve Injury Classifications – Seddon's and Sunderland's
    The Pain Source Makes Learning About Pain, Painless http://thepainsource.com Nerve Injury Classifications – Seddon’s and Sunderland’s Author : admin By Chris Faubel, MD -- Understanding nerve injury classification is essential for prognostic value clinically. Some basic anatomy, along with the two classification systems, and their corresponding EMG findings need to be learned and remembered. Two classification systems exist (and are frequently tested in various exams): 1. Seddon's classification (neuropraxia, axonotmesis, neurotmesis) 2. Sunderland's classification (types 1-5) To understand the systems, you must first review some basic nerve anatomy. There are three connective tissue layers in the CNS and PNS. 1. epineurium 2. perineurium 3. endoneurium Individual nerve fibers (single axons) are covered with varying amounts of myelin and then covered by endoneurium. These individually wrapped nerve fibers are then grouped into bundles of fibers called fascicles, which are covered by perineurium. Finally, groups of fascicles are bundled together to form the peripheral nerve (such as the median nerve), which is covered by epineurium. Seddon's classification: Neuropraxia 1 / 3 The Pain Source Makes Learning About Pain, Painless http://thepainsource.com Physical Medicine & Rehabilitation Board Review - Sara Cuccurullo, MD refers to local myelin injury with the axon still intact and functional motor > sensory fibers affected considered a temporary paralysis of the nerve fiber least severe injury usually from crush injury or ischemia Electrodiagnostic
    [Show full text]
  • Peripheral Nerve Regeneration and Muscle Reinnervation
    International Journal of Molecular Sciences Review Peripheral Nerve Regeneration and Muscle Reinnervation Tessa Gordon Department of Surgery, University of Toronto, Division of Plastic Reconstructive Surgery, 06.9706 Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada; [email protected]; Tel.: +1-(416)-813-7654 (ext. 328443) or +1-647-678-1314; Fax: +1-(416)-813-6637 Received: 19 October 2020; Accepted: 10 November 2020; Published: 17 November 2020 Abstract: Injured peripheral nerves but not central nerves have the capacity to regenerate and reinnervate their target organs. After the two most severe peripheral nerve injuries of six types, crush and transection injuries, nerve fibers distal to the injury site undergo Wallerian degeneration. The denervated Schwann cells (SCs) proliferate, elongate and line the endoneurial tubes to guide and support regenerating axons. The axons emerge from the stump of the viable nerve attached to the neuronal soma. The SCs downregulate myelin-associated genes and concurrently, upregulate growth-associated genes that include neurotrophic factors as do the injured neurons. However, the gene expression is transient and progressively fails to support axon regeneration within the SC-containing endoneurial tubes. Moreover, despite some preference of regenerating motor and sensory axons to “find” their appropriate pathways, the axons fail to enter their original endoneurial tubes and to reinnervate original target organs, obstacles to functional recovery that confront nerve surgeons. Several surgical manipulations in clinical use, including nerve and tendon transfers, the potential for brief low-frequency electrical stimulation proximal to nerve repair, and local FK506 application to accelerate axon outgrowth, are encouraging as is the continuing research to elucidate the molecular basis of nerve regeneration.
    [Show full text]
  • Resident Manual of Trauma to the Face, Head, and Neck
    Resident Manual of Trauma to the Face, Head, and Neck First Edition ©2012 All materials in this eBook are copyrighted by the American Academy of Otolaryngology—Head and Neck Surgery Foundation, 1650 Diagonal Road, Alexandria, VA 22314-2857, and are strictly prohibited to be used for any purpose without prior express written authorizations from the American Academy of Otolaryngology— Head and Neck Surgery Foundation. All rights reserved. For more information, visit our website at www.entnet.org. eBook Format: First Edition 2012. ISBN: 978-0-615-64912-2 Preface The surgical care of trauma to the face, head, and neck that is an integral part of the modern practice of otolaryngology–head and neck surgery has its origins in the early formation of the specialty over 100 years ago. Initially a combined specialty of eye, ear, nose, and throat (EENT), these early practitioners began to understand the inter-rela- tions between neurological, osseous, and vascular pathology due to traumatic injuries. It also was very helpful to be able to treat eye as well as facial and neck trauma at that time. Over the past century technological advances have revolutionized the diagnosis and treatment of trauma to the face, head, and neck—angio- graphy, operating microscope, sophisticated bone drills, endoscopy, safer anesthesia, engineered instrumentation, and reconstructive materials, to name a few. As a resident physician in this specialty, you are aided in the care of trauma patients by these advances, for which we owe a great deal to our colleagues who have preceded us. Additionally, it has only been in the last 30–40 years that the separation of ophthal- mology and otolaryngology has become complete, although there remains a strong tradition of clinical collegiality.
    [Show full text]
  • Axonotmesis of the Sciatic Nerve
    Diagnostic and Interventional Imaging (2012) 93, 398—400 LETTER / Neurology Axonotmesis of the sciatic nerve a,∗ b c c M. Ohana , S. Quijano-Roy , F. Colas , C. Lebreton , c c C. Vallée , R.-Y. Carlier a Radiology Department, Nouvel Hôpital Civil, Strasbourg University Hospitals, 1, place de l’Hôpital, 67000 Strasbourg, France b Paediatrics Department, Raymond-Poincaré Hospital, 104, boulevard Raymond-Poincaré, 92380 Garches, France c Radiology Department, Raymond-Poincaré Hospital, 104, boulevard Raymond-Poincaré, 92380 Garches, France Case report KEYWORDS Peripheral nerve; We report the case of an eight-year old girl who was admitted for aftercare and rehabilita- MRI; tion one month after a serious head injury that required a four-day stay in intensive care. Axonotmesis Initial investigations did not show any evidence of post-traumatic injury. During her admission, she developed significant pain in the left buttock radiating to the lower limb associated with a sensorimotor deficit. These disabling pains persisted at rest. The clinical examination revealed that the patient had great difficulty walking, presenting a limp, a tender point on palpation of the left buttock radiating to the thigh and the leg along a posterolateral course, with hyperaesthesia in the whole area. Extension of the leg and both flexion and extension of the foot were impossible; hip flexion was normal. Hypoaesthesia was noted on the inside of the left leg and foot. The left patellar and Achilles reflexes were absent. Vital signs were normal. First-line magnetic resonance imaging (MRI) of the lumbar spine did not reveal any abnormalities. An MRI of the pelvis and lower limbs was then carried out and this highlighted involve- ment of the sciatic nerve along its whole extra-perineal course (Fig.
    [Show full text]
  • Respiratory Management in the Patient with Spinal Cord Injury
    Hindawi Publishing Corporation BioMed Research International Volume 2013, Article ID 168757, 12 pages http://dx.doi.org/10.1155/2013/168757 Review Article Respiratory Management in the Patient with Spinal Cord Injury Rita Galeiras Vázquez,1 Pedro Rascado Sedes,2 Mónica Mourelo Fariña,1 Antonio Montoto Marqués,3,4 and M. Elena Ferreiro Velasco3 1 Critical Care Unit, Complexo Hospitalario Universitario A Coruna,˜ CP. 15006, A Coruna,˜ Spain 2 Critical Care Unit, Complexo Hospitalario Universitario de Santiago de Compostela, CP. 15702, Santiago de Compostela, Spain 3 Spinal Cord Injury Unit, Complexo Hospitalario Universitario A Coruna,˜ CP. 15006, A Coruna,˜ Spain 4 Department of Medicine, University of A Coruna,˜ CP. 15006, A Coruna,˜ Spain Correspondence should be addressed to Rita Galeiras Vazquez;´ [email protected] Received 30 April 2013; Revised 11 July 2013; Accepted 30 July 2013 Academic Editor: Boris Jung Copyright © 2013 Rita Galeiras Vazquez´ et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Spinal cord injuries (SCIs) often lead to impairment of the respiratory system and, consequently, restrictive respiratory changes. Paresis or paralysis of the respiratory muscles can lead to respiratory insufficiency, which is dependent on the level and completeness of the injury. Respiratory complications include hypoventilation, a reduction in surfactant production, mucus plugging, atelectasis, and pneumonia. Vital capacity (VC) is an indicator of overall pulmonary function; patients with severely impaired VC may require assisted ventilation. It is best to proceed with intubation under controlled circumstances rather than waiting until the condition becomes an emergency.
    [Show full text]
  • Diagnosis of the of the Extremities
    Postgrad Med J: first published as 10.1136/pgmj.22.251.255 on 1 September 1946. Downloaded from DIAGNOSIS OF THE COMMON FORMS OF NERVE INJURY OF THE EXTREMITIES By COLIN EDWARDS, M.B., B.S., M.R.C.P., D.P.M. History-taking is the first step in diagnosis and panying diminution or loss of reflexes. In the it is useful to know how varied the causes of peri- absence of an external wound or contusion near the pheral nerve injuries can be. Otherwise the true nerve concerned these muscle changes may be the nature of a traumatic lesion sometimes may not only guide. be suspected. Look first at the most peripheral muscles and The commoner ones are the result of:- particularly those which move the hands and feet. (I) Cutting and laceration. If these are normal (indicating an intact nerve (2) Stretching, which may be sudden (e.g. supply) it is uncommon, although not impossible, stretching of the sciatic by jumping upon the for muscles to be involved whose supply leaves extended foot) causing fibre rupture and those same nerves at a more proximal level. And haemorrhage, or prolonged (e.g. lying with the proximal involvement with normal peripheral arm extended for hours above the head) muscles only occurs close to the actual spot where ischaemia. causing the nerve is injured. The state of innervation of Contusion. the muscles moving the hands and feet gives no (3) to that of the limb (4) Concussion (including that produced by a guide, however, girdle muscles,Protected by copyright. "near miss" when a missile passes through as they are supplied by comparatively short nerves neighbouring tissues without touching the nerve).
    [Show full text]
  • Traumatic Injury to Peripheral Nerves
    AAEM MINIMONOGRAPH 28 ABSTRACT: This article reviews the epidemiology and classification of traumatic peripheral nerve injuries, the effects of these injuries on nerve and muscle, and how electrodiagnosis is used to help classify the injury. Mecha- nisms of recovery are also reviewed. Motor and sensory nerve conduction studies, needle electromyography, and other electrophysiological methods are particularly useful for localizing peripheral nerve injuries, detecting and quantifying the degree of axon loss, and contributing toward treatment de- cisions as well as prognostication. © 2000 American Association of Electrodiagnostic Medicine. Published by John Wiley & Sons, Inc. Muscle Nerve 23: 863–873, 2000 TRAUMATIC INJURY TO PERIPHERAL NERVES LAWRENCE R. ROBINSON, MD Department of Rehabilitation Medicine, University of Washington, Seattle, Washington 98195 USA EPIDEMIOLOGY OF PERIPHERAL NERVE TRAUMA company central nervous system trauma, not only Traumatic injury to peripheral nerves results in con- compounding the disability, but making recognition siderable disability across the world. In peacetime, of the peripheral nerve lesion problematic. Of pa- peripheral nerve injuries commonly result from tients with peripheral nerve injuries, about 60% have 30 trauma due to motor vehicle accidents and less com- a traumatic brain injury. Conversely, of those with monly from penetrating trauma, falls, and industrial traumatic brain injury admitted to rehabilitation accidents. Of all patients admitted to Level I trauma units, 10 to 34% have associated peripheral nerve 7,14,39 centers, it is estimated that roughly 2 to 3% have injuries. It is often easy to miss peripheral nerve peripheral nerve injuries.30,36 If plexus and root in- injuries in the setting of central nervous system juries are also included, the incidence is about 5%.30 trauma.
    [Show full text]
  • Pathophysiology of Peripheral Nerve Injury: a Brief Review
    Neurosurg Focus 16 (5):Article 1, 2004, Click here to return to Table of Contents Pathophysiology of peripheral nerve injury: a brief review MARK G. BURNETT, M.D., AND ERIC L. ZAGER, M.D. Department of Neurosurgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Clinicians caring for patients with brachial plexus and other nerve injuries must possess a clear understanding of the peripheral nervous system’s response to trauma. In this article, the authors briefly review peripheral nerve injury (PNI) types, discuss the common injury classification schemes, and describe the dynamic processes of degeneration and rein- nervation that characterize the PNI response. KEY WORDS • peripheral nerve • nerve injury • neurapraxia • axonotmesis • neurotmesis After a nerve is injured in the periphery, a complex and Lacerations such as those created by a knife blade are finely regulated sequence of events commences to remove another common PNI type, comprising 30% of serious in- the damaged tissue and begin the reparative process. Un- juries in some series.5 Whereas these can be complete like cellular repair in other areas of the body, the response transections, more often some nerve element of continuity of the peripheral nerve to injury does not involve mitosis remains. Because most research models involve a lacer- and cellular proliferation. Our understanding of the peri- ation-type injury mechanism because it is easily repro- pheral nerve regeneration process has increased signifi- duced, the details of nerve degeneration and regeneration cantly during the past several decades concurrent with discussed in this article are perhaps most representative of advances in cellular and molecular biology.
    [Show full text]
  • Neurophysiology in Neurourology
    AANEM MONOGRAPH ABSTRACT: The bladder has only two essential functions. It stores and periodically empties liquid waste. Yet it is unique as a visceral organ, allowing integrated volitional and autonomous control of continence and voiding. Normal function tests the integrity of the nervous system at all levels, extending from the neuroepithelium of the bladder wall to the frontal cortex of the brain. Thus, dysfunction is common with impairment of either the central or peripheral nervous system. This monograph presents an overview of the neural control of the bladder as it is currently understood. A description of pertinent peripheral anatomy and neuroanatomy is provided, followed by an explanation of common neurophysiological tests of the lower urinary tract and associated structures, including both urodynamic and electrodiagnostic approaches. Clinical applications are included to illustrate the impact of nervous system dysfunction on the bladder and to provide indications for testing. Muscle Nerve 38: 815–836, 2008 NEUROPHYSIOLOGY IN NEUROUROLOGY MARGARET M. ROBERTS, MD, PhD AANEM, Illinois Urogynecology, LTD, Oak Lawn, Illinois, USA Accepted 29 January 2008 The bladder has two essential functions: the storage than 26 billion dollars.1,63,154 This is similar to the and periodic elimination of liquid waste. It has a prevalence of diabetes in the United States6,140 and capacity in the range of 400–500 ml1,2,44,56 in an the total cost of health care for the entire country of average adult but is typically emptied 5–7 times a Switzerland.86 Urinary retention, though less preva- day,3,24 often at much smaller volumes. With an av- lent in the general population, is a common condi- erage urine flow time of less than 30 s,91 the bladder tion in patients with neurologic disorders.
    [Show full text]
  • A Classification of Nerve Injuries by H
    BRITISH MEDICAL JOURNAL LONDON SATURDAY AUGUST 29 1942 A CLASSIFICATION OF NERVE INJURIES BY H. J. SEDDON, D.M., F.R.C.S. Nu,ffield Professor of Orthopaedic Surgery, University of Oxford In 1863, during the fiercest days of the American Civil War, In contemporary clinical practice there is no question what- Dr. W. A. Hammond, Surgeon-General to the Federal ever that in frequency and importance the first group of Armies, ordered the establishment of a unit for the observa- phenomena far outweigh the second, and it is with loss of tion and treatment of injuiries of the nervous system. A function alone that this classification is concerned. signal result of this instruction was the appearance in 1864 Although, as has been said, there is a fairly clear under- standing among clinicians and experimental workers about the of a little book by Weir Mitchell, Morehouse, and Keen, sequence of events following complete anatomical division of Gunshot Wounds and Other Injuries of Nerves. This a peripheral nerve, there is considerable confusion when we gave an account of the first organized study of nerve come to examine those numerous cases in which function is injuries, and in it we find not only the most perfect descrip- lost although anatomical continuity of the nerve is more or tion of causalgia, a condition that will always remain less preserved. No clear distinction has been drawn between associated with the name of Weir Mitchell, but descrip- those intraneural lesions that are followed by complete tions of nerve injuries as we see them to-day.
    [Show full text]
  • Traumatic Brachial Plexus Injury G
    TRAUMATIC BRACHIAL PLEXUS INJURY G. SHANKAR GANESH, DEMONSTRATOR, PHYSIOTHERAPY Mechanism of injury • High velocity injury - stretch injury • Low impact injury - stretch injury • Lacerations If the injury was sustained due to a high velocity accident e.g. a motorcycle RTA, then the likelihood of a more serious pathology is much greater than someone who has sustained an injury from a fall. Patients involved in high velocity accidents are also more likely to sustain other injuries e.g. Head injuries, spinal and upper limb fractures and vascular damage. Patients who have sustained a brachial plexus lesion will present with motor and sensory loss in all or part of the upper limb depending on the extent of the injury. Clinical factors indicating a relatively mild lesion: • Low impact • Incomplete lesion • No pain • Tinel’s sign • Absent Horner’s sign Clinical factors indicating a more serious lesion: • High impact injury • Complete lesion • Burning or shooting pains present since the time of injury 383 • Horner’s sign (ptosis or drooping of the eyelid with dilation of the pupil) Damage to the BP can also occur as the result of tumours or as a result of radiation treatment. Therapist guidelines for the management of patients with an acute brachial plexus injury (pre and post-surgery) Grades of injury The damage to the brachial plexus nerves can be classified into four different grades: 1. Pre-ganglionic tear.................Nerve root avulsion 2. Post-ganglionic tear...............Neurotmesis 3. Severe lesion in-continuity.....Axonotmesis 4. Mild lesion in-continuity........Neurapraxia The number and combination of nerves injured are very variable.
    [Show full text]