Living with a Spinal Cord Injury
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A Sign It's Time for BOTOX®
When OAB* due to MS† makes matters worse… A sign it’s time for BOTOX® Ask your patients if they still have leakage or can’t tolerate their current OAB medication *Overactive bladder. †Multiple sclerosis. Indication Detrusor Overactivity Associated With a Neurologic Condition BOTOX® for injection is indicated for the treatment of urinary incontinence due to detrusor overactivity associated with a neurologic condition (eg, SCI, MS) in adults who have an inadequate response to or are intolerant of an anticholinergic medication. IMPORTANT SAFETY INFORMATION, INCLUDING BOXED WARNING WARNING: DISTANT SPREAD OF TOXIN EFFECT Postmarketing reports indicate that the effects of BOTOX® and all botulinum toxin products may spread from the area of injection to produce symptoms consistent with botulinum toxin effects. These may include asthenia, generalized muscle weakness, diplopia, ptosis, dysphagia, dysphonia, dysarthria, urinary incontinence, and breathing difficulties. These symptoms have been reported hours to weeks after injection. Swallowing and breathing difficulties can be life threatening, and there have been reports of death. The risk of symptoms is probably greatest in children treated for spasticity, but symptoms can also occur in adults treated for spasticity and other conditions, particularly in those patients who have an underlying condition that would predispose them to these symptoms. In unapproved uses and in approved indications, cases of spread of effect have been reported at doses comparable to those used to treat Cervical Dystonia -
Autonomic Dysreflexia – a Medical Emergency a Guide for Patients
Autonomic Dysreflexia – A Medical Emergency A guide for patients Only applicable to T6 level and above Key Points • Autonomic Dysreflexia (AD) is a medical emergency that occurs due to a rapid rise in blood pressure in response to a harmful or painful stimulus below the level of your Spinal Cord Injury (SCI) • It occurs in people with SCI at T6 and above but has in rare occasions been reported in individuals with SCI as low as T8 • If left untreated your blood pressure can rise to dangerous levels, risking stroke, cardiac problems, seizures, even death • Typically there is a pounding headache as your blood pressure rises. Other symptoms can include redness and sweating above the level of your SCI, slow heart rate, goosebumps, nausea, nasal congestion, blurred vision, shortness of breath and anxiety • Some or all of the symptoms may be present • AD can be triggered by any continuous painful or irritating stimulus below the level of your lesion. The most common causes are related to the bladder or bowel • Relieving the cause of the AD will resolve your AD episode • If the cause cannot be found or treated, medication is required to lower your blood pressure which may require a visit to your nearest emergency department • All people with SCI at T6 and above should carry their Autonomic Dysreflexia Medical Emergency Card at all times • The best treatment for AD is prevention • People at risk of AD often carry an ‘AD Kit’ with them – items useful to resolve AD such as catheters and prescribed medication 1 What is Autonomic Dysreflexia? Autonomic Dysreflexia (AD) is a medical emergency. -
Treatment of Autonomic Dysreflexia for Adults & Adolescents with Spinal
Treatment of Autonomic Dysreflexia for Adults & Adolescents with Spinal Cord Injuries Authors: Dr James Middleton, Director, State Spinal Cord Injury Service, NSW Agency for Clinical Innovation. Dr Kumaran Ramakrishnan, Honorary Fellow, Rehabilitation Studies Unit, Sydney Medical School Northern, The University of Sydney, and Consultant Rehabilitation Physician & Senior Lecturer, Department of Rehabilitation Medicine, University Malaya. Dr Ian Cameron, Head of the Rehabilitation Studies Unit, Sydney Medical School Northern, The University of Sydney. Reviewed and updated in 2013 by the authors. AGENCY FOR CLINICAL INNOVATION Level 4, Sage Building 67 Albert Avenue Chatswood NSW 2067 PO Box 699 Chatswood NSW 2057 T +61 2 9464 4666 | F +61 2 9464 4728 E [email protected] | www.aci.health.nsw.gov.au Produced by the NSW State Spinal Cord Injury Service. SHPN: (ACI) 140038 ISBN: 978-1-74187-972-8 Further copies of this publication can be obtained from the Agency for Clinical Innovation website at: www.aci.health.nsw.gov.au Disclaimer: Content within this publication was accurate at the time of publication. This work is copyright. It may be reproduced in whole or part for study or training purposes subject to the inclusion of an acknowledgment of the source. It may not be reproduced for commercial usage or sale. Reproduction for purposes other than those indicated above, requires written permission from the Agency for Clinical Innovation. © Agency for Clinical Innovation 2014 Published: February 2014 HS13-136 ACKNOWLEDGEMENTS This document was originally published as a fact sheet for the Rural Spinal Cord Injury Project (RSCIP), a pilot healthcare program for people with a spinal cord injury (SCI) conducted within New South Wales involving the collaboration of Prince Henry & Prince of Wales Hospitals, Royal North Shore Hospital, Royal Rehabilitation Centre Sydney, Spinal Cord Injuries Australia and the Paraplegic & Quadriplegic Association of NSW. -
Spinal Injury
SPINAL INJURY Presented by:- Bhagawati Ray DEFINITION Spinal cord injury (SCI) is damage to the spinal cord that results in a loss of function such as mobility or feeling. TYPES OF SPINAL CORD INJURY Complete Spinal Cord Injuries Complete paraplegia is described as permanent loss of motor and nerve function at T1 level or below, resulting in loss of sensation and movement in the legs, bowel, bladder, and sexual region. Arms and hands retain normal function. INCOMPLETE SPINAL CORD INJURIES Anterior cord syndrome Anterior cord syndrome, due to damage to the front portion of the spinal cord or reduction in the blood supply from the anterior spinal artery, can be caused by fractures or dislocations of vertebrae or herniated disks. CENTRAL CORD SYNDROME Central cord syndrome, almost always resulting from damage to the cervical spinal cord, is characterized by weakness in the arms with relative sparing of the legs, and spared sensation in regions served by the sacral segments. POSTERIOR CORD SYNDROME Posterior cord syndrome, in which just the dorsal columns of the spinal cord are affected, is usually seen in cases of chronic myelopathy but can also occur with infarction of the posterior spinal artery. BROWN-SEQUARD SYNDROME Brown-Sequard syndrome occurs when the spinal cord is injured on one side much more than the other. It is rare for the spinal cord to be truly hemisected (severed on one side), but partial lesions due to penetrating wounds (such as gunshot or knife wounds) or fractured vertebrae or tumors are common. CAUDA EQUINASYNDROME Cauda equina syndrome (CES) is a condition that occurs when the bundle of nerves below the end of the spinal cord known as the cauda equina is damaged. -
Wallerian Degeneration and Inflammation in Rat Peripheral Nerve Detected by in Vivo MR Imaging
741 Wallerian Degeneration and Inflammation in Rat Peripheral Nerve Detected by in Vivo MR Imaging DavidS. Titelbaum 1 To investigate the role of MR imaging in wallerian degeneration, a series of animal Joel L. Frazier 2 models of increasingly complex peripheral nerve injury were studied by in vivo MR. Robert I. Grossman 1 Proximal tibial nerves in brown Norway rats were either crushed, transected (neurotomy), Peter M. Joseph 1 or transected and grafted with Lewis rat (allograft) or brown Norway (isograft) donor Leonard T. Yu 2 nerves. The nerves distal to the site of injury were imaged at intervals of 0-54 days after surgery. Subsequent histologic analysis was obtained and correlated with MR Eleanor A. Kassab 1 3 findings. Crush injury, neurotomy, and nerve grafting all resulted in high signal intensity William F. Hickey along the course of the nerve observed on long TR/TE sequences, corresponding to 2 Don LaRossa edema and myelin breakdown from wallerian degeneration. The abnormal signal inten 4 Mark J. Brown sity resolved by 30 days after crush injury and by 45-54 days after neurotomy, when the active changes of wallerian degeneration had subsided. These changes were not seen in sham-operated rats. Our findings suggest that MR is capable of identifying traumatic neuropathy in a peripheral nerve undergoing active wallerian degeneration. The severity of injury may be reflected by the corresponding duration of signal abnormality. With the present methods, MR did not distinguish inflammatory from simple posttraumatic neuropathy. Wallerian degeneration is the axonal degeneration and loss of myelin that occurs when an axon is separated from its cell body. -
Guidelines for Standardization of Bed Rest Studies in the Spaceflight Context
GUIDELINES FOR STANDARDIZATION OF BED REST STUDIES IN THE SPACEFLIGHT CONTEXT Editors: Patrik Sundblad, Oleg Orlov Contributing authors: Oliver Angerer, Irina Larina, Ronita Cromwell GUIDELINES FOR STANDARDIZATION OF BED REST STUDIES IN THE SPACEFLIGHT CONTEXT International Academy of Astronautics Notice: The cosmic study or position paper that is the subject of this report was approved by the Board of Trustees of the International Academy of Astronautics (IAA). Any opinions, findings, conclusions, or recommendations expressed in this report are those of the authors and do not necessarily reflect the views of the sponsoring or funding organizations. For more information about the International Academy of Astronautics, visit the IAA home page at www.iaaweb.org. Copyright 2014 by the International Academy of Astronautics. All rights reserved. The International Academy of Astronautics (IAA), a non-governmental organization recognized by the United Nations, was founded in 1960. The purposes of the IAA are to foster the development of astronautics for peaceful purposes, to recognize individuals who have distinguished themselves in areas related to astronautics, and to provide a program through which the membership can contribute to international endeavors and cooperation in the advancement of aerospace activities. © International Academy of Astronautics (IAA) June 2014 Study Group report on: Guidelines for Standardization of Bed Rest Studies in the Spaceflight Context Printing of this Study was sponsored by: State Scientific Center of Russian Federation – Institute of Biomedical Problems of the Russian Academy of Sciences (IBMP) 76-A, Khoroshevskoyeshosse, 123007, Moscow, Russia e-mail: [email protected] International Academy of Astronautics 6 rue Galilée, BP 1268-16, 75766 Paris Cedex 16, France Cover Illustration source: NASA Guidelines for Standardization of Bed Rest Studies in the Spaceflight Context Guidelines for Standardization of Bed Rest Table of Content 1. -
Robert Jenkinson, MD
8/26/14 LIFE-THREATENING, INTRAOPERATIVE HEMODYNAMIC INSTABILITY IN A QUADRAPLEGIC Robert H. Jenkinson, M.D. Department of Anesthesiology University of Wisconsin Madison, WI Background o 57 year old quadraplegic male, remote C4-C5 spinal injury presenting for cystoscopy. n PMHx: Autonomic dysreflexia, OSA, neurogenic bowel/bladder. n Allergies: Sulfa drugs o Prior history of systolic blood pressure (SBP) near or above 200 mmHg while under GA for cystoscopy on multiple occasions. n Required nitroglycerine infusions. n Stable blood pressure with spinal anesthesia on one prior occasion. Case Description o L4-L5 spinal performed in OR n Intravenous midazolam (2mg) & fentanyl (50 mcg) n Intrathecal hyperbaric bupivacaine (12.5 mg) n Intravenous cefazolin (2g) o On return to supine position: n SBP rapidly decreased from baseline of 140 mmHg to 60 mmHg. n The patient became tachycardic. n Breathing pattern became shallow and bradypneic. n Level of responsiveness quickly decreased. 1 8/26/14 Case Description o Vasopressin and epinephrine boluses given. o Trachea intubated. Intra- arterial BP monitoring & central venous access established. § Vasopressin & epinephrine infusions started. o Diffuse blanching erythema noted. n No mucosal edema or wheezing. Case Description o Procedure cancelled. n Transported to medical ICU. n Weaned off vasopressors & extubated in 3 hours. n Serum tryptase 125 mcg/L (reference range 0.4 – 10.9). o Skin testing to bupivacaine: n No cutaneous, gastrointestinal, cardiovascular or respiratory symptoms. n No evidence of IgE-mediated hypersensitivity to bupivacaine. Discussion o Initial working diagnosis was a high or total spinal. o Tachycardia, skin changes and markedly elevated tryptase most consistent with anaphylactic reaction. -
Anatomy of the Spine
12 Anatomy of the Spine Overview The spine is made of 33 individual bones stacked one on top of the other. Ligaments and muscles connect the bones together and keep them aligned. The spinal column provides the main support for your body, allowing you to stand upright, bend, and twist. Protected deep inside the bones, the spinal cord connects your body to the brain, allowing movement of your arms and legs. Strong muscles and bones, flexible tendons and ligaments, and sensitive nerves contribute to a healthy spine. Keeping your spine healthy is vital if you want to live an active life without back pain. Spinal curves When viewed from the side, an adult spine has a natural S-shaped curve. The neck (cervical) and low back (lumbar) regions have a slight concave curve, and the thoracic and sacral regions have a gentle convex curve (Fig. 1). The curves work like a coiled spring to absorb shock, maintain balance, and allow range of motion throughout the spinal column. The muscles and correct posture maintain the natural spinal curves. Good posture involves training your body to stand, walk, sit, and lie so that the least amount of strain is placed on the spine during movement or weight-bearing activities. Excess body weight, weak muscles, and other forces can pull at the spine’s alignment: • An abnormal curve of the lumbar spine is lordosis, also called sway back. • An abnormal curve of the thoracic spine is Figure 1. (left) The spine has three natural curves that form kyphosis, also called hunchback. an S-shape; strong muscles keep our spine in alignment. -
Nerve Injury After Peripheral Nerve Block: Allbest Rights Practices Reserved
PRINTER-FRIENDLY VERSION AVAILABLE AT ANESTHESIOLOGYNEWS.COM Nerve Injury After Peripheral Nerve Block: AllBest rights Practices reserved. Reproduction and Medical-Legal in whole or in part without Protection permission isStrategies prohibited. Copyright © 2015 McMahon Publishing Group unless otherwise noted. DAVID HARDMAN, MD, MBA Professor of Anesthesiology Vice Chair for Professional Affairs Department of Anesthesiology University of North Carolina at Chapel Hill Chapel Hill, North Carolina Dr. Hardman reports no relevant financial conflicts of interest. he risk for permanent or severe nerve injury after peripheral nerve blocks (PNBs) is Textremely low, irrespective of its etiology (ie, related to anesthesia, surgery or the patient). The risk inherent in a procedure should always be explicitly discussed with the patient (sidebar, page 4). In fact, it may be better to define this phenomenon ultrasound-guided axillary blocks were used, demon- as postoperative neurologic symptoms (PONS) or peri- strated a very low nerve injury rate of 0.0037% at hos- operative nerve injuries (PNI) in order to help stan- pital discharge.1-7 dardize terminology. Permanent injury rates, as defined A 2009 prospective case series involving more than by a neurologic abnormality present at or beyond 12 7,000 PNBs, conducted in Australia and New Zealand, months after the procedure, have consistently ranged demonstrated that when a postoperative neurologic from 0.029% to 0.2%, although the results of a recent symptom was diagnosed, it was 9 times more likely to multicenter Web-based survey in France, in which be due to a non–anesthesia-related cause than a nerve ANESTHESIOLOGY NEWS • JULY 2015 1 block–related cause.6 On the other hand, it is well doc- PNI rate of 1.7% in patients who received a single-injec- umented in the orthopedic and anesthesia literature tion interscalene block (ISB). -
Is It Really Sciatica August, 2017
Is It Really Sciatica August, 2017 By Dr. Derek Conte One of the most common complaints we see from patients is that of sciatic pain. They will say, “I have sciatica!” And when I ask, “How do you know it is sciatica?” they will say that’s what their friend said, or that they went online and did a medical search, or my favorite: that their “regular” doctor told them. So, what is sciatica, what are its symptoms, and what exactly is the sciatic nerve? I’ll tell you that sciatica is one for the most misdiagnosed conditions we see. The sciatic nerve is the largest nerve in the body and is made up of five nerves which arise from the low back and sacrum. These nerves converge and travel beneath the buttocks and down the outside rear of the thigh to the back of the knee, where they divide. The tibial nerve goes straight down the back of the calf around the inside of the ankle and on to the underside of the foot. The two peroneal nerves cover the rest of the lower leg and top of the foot (see chart). Sciatica is the irritation of the sciatic nerve and can be caused in several ways. First, compression of the nerve must be present or there would be no pain. Beginning centrally and going out from the spinal cord the causes may be 1) Central canal stenosis which squeezes the entire cord and produces bilateral symptoms. 2) A subluxation (malposition of vertebrae) compresses nerves at the spine. 3) A bulging disc or osteophyte (bony spur) causing stenosis of intervertebral foramen, or a dramatic loss of disc height can also leave too little room for the nerves to exit the spine. -
A. PNS = Cranial and Spinal Nerves PNS Provides Connections Between
Anatomy Lecture Notes Chapter 14 A. PNS = cranial and spinal nerves PNS provides connections between body and CNS sensory vs motor visceral vs somatic PNS components: 1. sensory receptors - monitor changes in environment (stimuli) convert stimuli into signals sent viA sensory neurons to CNS 2. motor endings - control effectors a. somatic axon terminal of somatic motor neuron contains neurotransmitter (ACh) stored in vesicles motor end plate of skeletal muscle cell folded for large surface area; contains ACh receptors b. visceral visceral motor axon has varicosities containing vesicles of neurotransmitter membrane of effector cell contains receptors for the neurotransmitters 3. nerves and ganglia - connect CNS to receptors and motor endings Strong/Fall2008 page 1 Anatomy Lecture Notes Chapter 14 B. classification of receptors 1. by structure a. specialized dendritic endings of sensory neurons used for general senses free / unencapsulated example: root hair plexus (also called hair follicle receptor) encapsulated - dendrites enclosed in c.t. capsule that amplifies or filters stimuli example: Pacinian corpuscle b. receptor cells (specialized epithelial cells or neurons) that synapse with dendrites of afferent neurons \ used for special senses 2. by location of stimulus a. exteroceptor b. interoceptor c. proprioceptors are located in skeletal muscles, tendons, joints and ligaments they monitor the position and movement of the body muscle spindles Golgi tendon organs joint kinesthetic receptors 3. by type of stimulus detected a. mechanoreceptor -
Delayed Facial Palsy After Head Injury
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.40.4.342 on 1 April 1977. Downloaded from Journal ofNeurology, Neurosurgery, andPsychiatry, 1977, 40, 342-350 Delayed facial palsy after head injury K. PUVANENDRAN, M. VITHARANA, AND P. K. WONG From the University Department ofMedicine, and the Department ofOtorhinolaryngology, Singapore General Hospital, Singapore SUMMARY Where facial palsy follows head injury after many days, the mechanism is not clear, and there has been no detailed study on this condition. In this prospective study, an attempt is made to estimate this complication of head injury, and to study its pathogenesis, natural history, prognosis, and sequelae which differ markedly from Bell's palsy. It has a much worse prognosis and so surgical decompression should be considered early in this condition. The facial nerve is the motor cranial nerve which is studies, for prediction of prognosis at a time when most commonly affected in closed head injuries surgical intervention seems most advantageous. (Turner, 1943). In facial palsy which immediately follows a head injury, the mechanism is obvious, but Patients and methods Protected by copyright. it is not clear when the facial palsy follows the head injury after many days (Potter and Braakman, 1976). During the period May 1974-April 1975, there were Traumatic facial palsy has received much attention 6304 cases of head injury admitted to government but few authors distinguish between immediate and hospitals in Singapore. The chief criterion for delayed palsy. admission to hospital was the occurrence of traumatic Turner (1944) studied a selected group of war-time amnesia or unconsciousness, indicating concussion head injuries from a military hospital for head of the brain.