DOCSLIB.ORG

Autonomic Hyperreflexia Associated with Recurrent Cardiac Arrest

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Autonomic Hyperreflexia Associated with Recurrent Cardiac Arrest Spinal Cord (1997) 35, 256 ± 257 1997 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/97 $12.00 Autonomic hyperre¯exia associated with recurrent cardiac arrest: Case Report SC Colachis, III1 and DM Clinchot2 1Associate Professor and 2Assistant Professor, Department of Physical Medicine and Rehabilitation1, Director, SCI Rehabilitation, The Ohio State University, College of Medicine, Columbus, Ohio, USA Autonomic hyperre¯exia is a condition which may occur in individuals with spinal cord injuries above the splanchnic sympathetic out¯ow. Noxious stimuli can produce profound alterations in sympathetic pilomotor, sudomotor, and vasomotor activity, as well as disturbances in cardiac rhythm. A case of autonomic hyperre¯exia in a patient with C6 tetraplegia with recurrent ventricular ®brillation and cardiac arrest illustrates the profound eects of massive paroxysmal sympathetic activity associated with this condition. Keywords: autonomic hyperre¯exia; spinal cord injury; ventricular ®brillation Introduction Autonomic hyperre¯exia is a condition of paroxysmal by excessive sweating and ¯ushing. Past episodes of re¯ex sympathetic activity which occurs in response to autonomic hyperre¯exia were generally attributed to noxious stimuli in patients with spinal cord injuries re¯ex voiding, position changes and the presence of above the major splanchnic sympathetic out¯ow.1±3 pressure sores. The heightened sympathetic activity during an episode The attendant had completed the patient's morning of autonomic hyperre¯exia accounts for several of the bowel program, hygiene and dressing activities, and clinical features commonly observed including sudo- started to exit the apartment when he heard gasping. motor and pilomotor phenomenon,1,4 ± 6 vasomotor He returned to ®nd him pulseless, apneic, and sequelae,1 ± 4,7 and alterations in cardiac inotropic and cyanotic. There was no prior evidence of airway chronotropic activity.1,2,4,6,7 diculty. He called the emergency medical personal Cardiac abnormalities described in association with and began basic cardiopulmonary resuscitation mea- episodes of autonomic hyperre¯exia include bradycar- sures. After electrocardiography was made available, dia1,4,6,7 and tachycardia,2,6,7 premature atrial and the emergency medical team found the patient to be in ventricular contractions,1,8 atrial ®brillation9,10 and ventricular ®brillation. He was successfully cardio- conduction block.8 Despite the occurrence of these verted to sinus rhythm, intubated, and emergently arrhythmias associated with autonomic hyperre¯exia, transferred to our acute medical center. they are seldom recognized as a cause of cardiac arrest Initial evaluation in the emergency department in individuals with traumatic spinal cord injury. revealed no obvious etiology (e.g. hypoxemia, hypo- The following case of autonomic hyperre¯exia volemia, or metabolic disturbances) for the cardiac with recurrent ventricular ®brillation and cardiac arrest. Toxicology studies were unremarkable. How- arrest illustrates the profound eects of massive ever, wide variability in blood pressure was recorded paroxysmal sympathetic activity associated with this with pressures ranging from 108/66 ± 170/76 mmHg. condition. Approximately 90 min after arrival, during close observation, his rhythm returned to ventricular Case report ®brillation and he again had a cardiac arrest necessitating resuscitation eorts including cardiover- A 28 year old male with C6 motor and sensory sion. He was successfully resuscitated and was complete tetraplegia (ASIA Impairment Scale `A') transferred to the medical intensive care unit. A from a motor vehicle accident in 1983 experienced an pulmonary angiogram was normal. episode of cardiac arrest on 3 July 1994. He had been The patient's initial hospital course was complicated experiencing recurrent symptoms of autonomic hyper- by wide variations in systolic and diastolic blood re¯exia since the prior evening. His care attendant pressure which improved over the next few days, and noted increased symptoms of autonomic hyperre¯exia an aspiration pneumonia which resolved with treat- that morning during personal care activities manifested ment. He slowly regained consciousness but was confused for several days. This was attributed to anoxic encephalopathy which subsequently resolved. Correspondence: Sam C Colachis, M.D. An initial echocardiogram on 4 July 1994 revealed an Automic hyperreflexia with recurrent cardiac arrest SC Colachis and DM Clinchot 257 ejection fraction of only 27% with apical akinesia. The We hypothesize that heightened sympathetic adre- etiology for this was felt to be cardiac shock. A repeat nergic activity that occurred during an episode of examination performed on 7 July 1994 showed an autonomic hyperre¯exia resulted in a cardiac arrhyth- ejection fraction of 55%. Cardiac catheterization on 8 mia leading to ventricular ®brillation and cardiac July 1994 was normal with a 64% ejection fraction. arrest. The witnessed recurrent ventricular ®brillation On 11 July 1994, he underwent electrophysiological with successful cardiac resuscitation allowed a rare studies which revealed no inducible ventricular opportunity to observe this commonly fatal arrhyth- tachycardia, normal sinus node, and no accessory mia in the presence of autonomic hyperre¯exia. In an pathway. In view of the two prior documented unwitnessed setting, death would certainly have episodes of ventricular ®brillation and cardiac arrest, occurred. the patient opted for an implantable internal cardiac It is interesting to speculate as to what extent de®brillator which was surgically placed on 13 July autonomic hyperre¯exia accounts for the deaths in 1994. He was subsequently discharged home. persons with chronic spinal cord injuries at risk for Our patient is currently enrolled in continuing this condition. Cardiac disease now accounts for a college education. He has had no further episodes of signi®cant number of deaths in the spinal cord injury cardiac arrest and the implanted de®brillator has not population.12 Deaths from cardiac causes in this discharged. population occur at a younger age than has been seen in the general population.12 It is possible that as Discussion individuals with chronic spinal cord injury age, they become more susceptible to the cardiac eects of Autonomic hyperre¯exia is associated with profound heightened sympathetic adrenergic activity occurring alterations in vasomotor,1 ± 4,7 pilomotor4 and sudo- during episodes of autonomic hyperre¯exia. This could motor activity.1,4 ± 6 Heightened sympathetic activity account for some of the unexpected deaths attributable associated with hypertensive crisis during an episode to cardiac disease. have resulted in seizures,3,4,6 retinal4 and intracranial The current case of autonomic hyperre¯exia in a hemorrhages,3 cerebral vascular accidents,3,8 coma3,6 patient with C6 tetraplegia with recurrent ventricular and death.3,6 Resolution of this autonomic phenomen- ®brillation and cardiac arrest illustrates the profound on occurs with removal of the noxious stimulus eects of massive paroxysmal sympathetic activity precipitating the event. associated with this condition. Cardiac abnormalities observed during an episode of autonomic hyperre¯exia include inotropic and chronotropic changes. Palpitations, chest pain,1 dyspnea,6,11 congestive heart failure4 and pulmonary References edema11 have all been reported. Tachycardia2,6 and re¯ex bradycardia1,2,4,6 are most commonly observed 1 Guttmann L, Whitteridge D. Eects of bladder distension on autonomic mechanisms after spinal cord injuries. Brain 1947; 70: in this setting, and are attributed to heightened 361 ± 404. noradrenergic sympathetic activity and re¯ex vagal 2 Kewalramani LS. Autonomic dysre¯exia in traumatic myelo- responses, respectively. Electrocardiographic abnorm- pathy. AmJPhysMed1980; 59: 1±21. alities observed during an attack of autonomic 3 Kursh ED, Freehafer A, Persky L. Complications of autonomic hyperre¯exia include premature atrial and ventricular dysre¯exia. JUrol1977; 118: 70 ± 72. 1,8 1 4 Brown BT, Carrion HM, Politano VA. Guanethidine sulfate in contractions, sinus tachycardia and bradycardia, the prevention of autonomic hyperre¯exia. J Urol 1979; 122: 55 ± alterations in T-wave and U-wave amplitudes,1 atrial 57. ®brillation,9,10 bigeminy8 and conduction block.8 We 5 Head H, Riddoch G. The automatic bladder, excessive sweating are unaware of any reports of ventricular ®brillation in and some other re¯ex conditions, in gross injuries of the spinal cord. Brain 1917; 40: 188 ± 263. association with autonomic hyperre¯exia. 6 Lindan R, Joiner B, Freehafer AA, Hazel C. Incidence and In the present patient, symptoms of autonomic clinical features of autonomic dysre¯exia in patients with spinal hyperre¯exia preceded an initial event of ventricular cord injury. Paraplegia 1980; 18: 285 ± 292. ®brillation and cardiac arrest. During emergency 7 Wurster RD, Randall WC. Cardiovascular responses to bladder department evaluation, wide variations in blood distension in patients with spinal transection. AmJPhysiol1975; 228: 1288 ± 1292. pressure were recorded and preceded ventricular 8 Guttmann L, Frankel HL, Paeslack V. Cardiac irregularities ®brillation. These variations in blood pressure persisted during labor in paraplegic women. Paraplegia 1965; 3: 141 ± 151. throughout the initial hospitalization but subsequently 9 Forrest GP. Atrial ®brillation associated with autonomic returned to his baseline blood pressure. No
Load more

Recommended publications
  • 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
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Scienti®C Review Spastic Movement Disorder
    Spinal Cord (2000) 38, 389 ± 393 ã 2000 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/00 $15.00 www.nature.com/sc Scienti®c Review Spastic movement disorder V Dietz*,1 1Paracare, Paraplegic Centre of the University Hospital Balgrist, ZuÈrich, Switzerland This review deals with the neuronal mechanisms underlying spastic movement disorder, assessed by electrophysiological means with the aim of ®rst, a better understanding of the underlying pathophysiology and second, the selection of an adequate treatment. For the patient usually one of the ®rst symptoms of a lesion within the central motor system represents the movement disorder, which is most characteristic during locomotion in patients with spasticity. The clinical examination reveals exaggerated tendon tap re¯exes and increased muscle tone typical of the spastic movement disorder. However, today we know that there exists only a weak relationship between the physical signs obtained during the clinical examination in a passive motor condition and the impaired neuronal mechanisms being in operation during an active movement. By the recording and analysis of electrophysiological and biomechanical parameters during a functional movement such as locomotion, the signi®cance of, for example, impaired re¯ex behaviour or pathophysiology of muscle tone and its contribution to the movement disorder can reliably be assessed. Consequently, an adequate treatment should not be restricted to the cosmetic therapy and correction of an isolated clinical parameter but should be based on the pathophysiology and signi®cance of the mechanisms underlying the disorder of functional movement which impairs the patient. Spinal Cord (2000) 38, 389 ± 393 Keywords: spinal cord injury; spasticity; electrophysiological recordings; treatment Introduction Movement disorders are prominent features of impaired strength of electromyographic (EMG) activation of function of the motor systems and are frequently best antagonistic leg muscles as well as intrinsic and passive re¯ected during gait.
    [Show full text]
  • 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.
    [Show full text]
  • Neuromuscular Disorders Neurology in Practice: Series Editors: Robert A
    Neuromuscular Disorders neurology in practice: series editors: robert a. gross, department of neurology, university of rochester medical center, rochester, ny, usa jonathan w. mink, department of neurology, university of rochester medical center,rochester, ny, usa Neuromuscular Disorders edited by Rabi N. Tawil, MD Professor of Neurology University of Rochester Medical Center Rochester, NY, USA Shannon Venance, MD, PhD, FRCPCP Associate Professor of Neurology The University of Western Ontario London, Ontario, Canada A John Wiley & Sons, Ltd., Publication This edition fi rst published 2011, ® 2011 by Blackwell Publishing Ltd Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing program has been merged with Wiley’s global Scientifi c, Technical and Medical business to form Wiley-Blackwell. Registered offi ce: John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK Editorial offi ces: 9600 Garsington Road, Oxford, OX4 2DQ, UK The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK 111 River Street, Hoboken, NJ 07030-5774, USA For details of our global editorial offi ces, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell The right of the author to be identifi ed as the author of this work has been asserted in accordance with the UK Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.
    [Show full text]
  • Non-Progressive Congenital Ataxia with Cerebellar Hypoplasia in Three Families
    248 Non-progressive congenital ataxia with cerebellar hypoplasia in three families . No 1.6 Z. YAPICI & M. ERAKSOY . .. I.Y.. \ .~ ---················ No of Neurology, of Child Neuro/ogy, Facu/ty of Turkey Abstract Non-progressive with cerebellar hypoplasia are a rarely seen heterogeneous group ofhereditary cerebellar ataxias. Three sib pairs from three different families with this entity have been reviewed, and differential diagnosis has been di sc ussed. in two of the families, the parents were consanguineous. Walking was delayed in ali the children. Truncal and extremiry were then noticed. Ataxia was severe in one child, moderate in two children, and mild in the remaining revealed horizontal, horizonto-rotatory and/or vertical variable degrees ofmental and pvramidal signs besides truncal and extremity ataxia. In ali the cases, cerebellar hemisphere and vermis were in MRI . During the follow-up period, a gradual clinical improvement was achieved in ali the Condusion: he cu nsidered as recessive in some of the non-progressive ataxic syndromes. are being due to the rarity oflarge pedigrees for genetic studies. Iffurther on and clini cal progression of childhood associated with cerebellar hypoplasia is be a cu mbined of metabolic screening, long-term follow-up and radiological analyses is essential. Key Words: Cerebella r hy poplasia, ataxic syndromes are common during Patients 1 and 2 (first family) childhood. Friedreich 's ataxia and ataxia-telangiectasia Two brothers aged 5 and 7 of unrelated parents arc two best-known examples of such rare syn- presented with a history of slurred speech and diffi- dromes characterized both by their progressive nature culty of gait.
    [Show full text]
  • Late-Onset Oro-Facial Dyskinesia in Spinocerebellar Ataxia Type 2: a Case Report Floriana Giardina1†, Giuseppe Lanza2,3*† , Francesco Calì3 and Raffaele Ferri3
    Giardina et al. BMC Neurology (2020) 20:156 https://doi.org/10.1186/s12883-020-01739-8 CASE REPORT Open Access Late-onset oro-facial dyskinesia in Spinocerebellar Ataxia type 2: a case report Floriana Giardina1†, Giuseppe Lanza2,3*† , Francesco Calì3 and Raffaele Ferri3 Abstract Background: Genetic familiar causes of oro-facial dyskinesia are usually restricted to Huntington’s disease, whereas other causes are often missed or underestimated. Here, we report the case of late-onset oro-facial dyskinesia in an elderly patient with a genetic diagnosis of Spinocerebellar Ataxia type 2 (SCA2). Case presentation: A 75-year-old man complained of progressive balance difficulty since the age of 60 years, associated with involuntary movements of the mouth and tongue over the last 3 months. No exposure to anti- dopaminergic agents, other neuroleptics, antidepressants, or other drugs was reported. Family history was positive for SCA2 (brother and the son of the brother). At rest, involuntary movements of the mouth and tongue were noted; they appeared partially suppressible and became more evident during stress and voluntary movements. Cognitive examination revealed frontal-executive dysfunction, memory impairment, and attention deficit. Brain magnetic resonance imaging (MRI) disclosed signs of posterior periventricular chronic cerebrovascular disease and a marked ponto-cerebellar atrophy, as confirmed by volumetric MRI analysis. A dopamine transporter imaging scan demonstrated a bilaterally reduced putamen and caudate nucleus uptake. Ataxin-2 (ATXN2) gene analysis revealed a 36 cytosine-adenine-guanine (CAG) repeat expansion, confirming the diagnosis of SCA2. Conclusions: SCA2 should be considered among the possible causes of adult-onset oro-facial dyskinesia, especially when the family history suggests an inherited cerebellar disorder.
    [Show full text]
  • What Is the Autonomic Nervous System?
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.suppl_3.iii31 on 21 August 2003. Downloaded from AUTONOMIC DISEASES: CLINICAL FEATURES AND LABORATORY EVALUATION *iii31 Christopher J Mathias J Neurol Neurosurg Psychiatry 2003;74(Suppl III):iii31–iii41 he autonomic nervous system has a craniosacral parasympathetic and a thoracolumbar sym- pathetic pathway (fig 1) and supplies every organ in the body. It influences localised organ Tfunction and also integrated processes that control vital functions such as arterial blood pres- sure and body temperature. There are specific neurotransmitters in each system that influence ganglionic and post-ganglionic function (fig 2). The symptoms and signs of autonomic disease cover a wide spectrum (table 1) that vary depending upon the aetiology (tables 2 and 3). In some they are localised (table 4). Autonomic dis- ease can result in underactivity or overactivity. Sympathetic adrenergic failure causes orthostatic (postural) hypotension and in the male ejaculatory failure, while sympathetic cholinergic failure results in anhidrosis; parasympathetic failure causes dilated pupils, a fixed heart rate, a sluggish urinary bladder, an atonic large bowel and, in the male, erectile failure. With autonomic hyperac- tivity, the reverse occurs. In some disorders, particularly in neurally mediated syncope, there may be a combination of effects, with bradycardia caused by parasympathetic activity and hypotension resulting from withdrawal of sympathetic activity. The history is of particular importance in the consideration and recognition of autonomic disease, and in separating dysfunction that may result from non-autonomic disorders. CLINICAL FEATURES c copyright. General aspects Autonomic disease may present at any age group; at birth in familial dysautonomia (Riley-Day syndrome), in teenage years in vasovagal syncope, and between the ages of 30–50 years in familial amyloid polyneuropathy (FAP).
    [Show full text]
  • REVIEW Autonomic Assessment of Animals with Spinal Cord
    Spinal Cord (2009) 47, 2–35 & 2009 International Spinal Cord Society All rights reserved 1362-4393/09 $32.00 www.nature.com/sc REVIEW Autonomic assessment of animals with spinal cord injury: tools, techniques and translation JA Inskip1,2,4, LM Ramer1,2,4, MS Ramer1,2 and AV Krassioukov1,3 1International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada; 2Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada and 3Department of Medicine, Division of Physical Medicine and Rehabilitation, University of British Columbia, Vancouver, British Columbia, Canada Study design: Literature review. Objectives: To present a comprehensive overview of autonomic assessment in experimental spinal cord injury (SCI). Methods: A systematic literature review was conducted using PubMed to extract studies that incorporated functional motor, sensory or autonomic assessment after experimental SCI. Results: While the total number of studies assessing functional outcomes of experimental SCI increased dramatically over the past 27 years, studies with motor outcomes dramatically outnumber those with autonomic outcomes. Within the areas of autonomic dysfunction (cardiovascular, respiratory, gastrointestinal, lower urinary tract, sexual function and thermoregulation), not all aspects have been characterized to the same extent. Studies focusing on bladder and cardiovascular function greatly outnumber those on sexual function, gastrointestinal function and thermoregulation. This review addresses the disparity between well-established motor-sensory testing presently used in experimental animals and the lack of standardized autonomic testing following experimental SCI. Throughout the review, we provide information on the correlation between existing experimental and clinically used autonomic tests. Finally, the review contains a comprehensive set of tables and illustrations to guide the reader through the complexity of autonomic assessment and dysfunctions observed following SCI.
    [Show full text]
  • History-Of-Movement-Disorders.Pdf
    Comp. by: NJayamalathiProof0000876237 Date:20/11/08 Time:10:08:14 Stage:First Proof File Path://spiina1001z/Womat/Production/PRODENV/0000000001/0000011393/0000000016/ 0000876237.3D Proof by: QC by: ProjectAcronym:BS:FINGER Volume:02133 Handbook of Clinical Neurology, Vol. 95 (3rd series) History of Neurology S. Finger, F. Boller, K.L. Tyler, Editors # 2009 Elsevier B.V. All rights reserved Chapter 33 The history of movement disorders DOUGLAS J. LANSKA* Veterans Affairs Medical Center, Tomah, WI, USA, and University of Wisconsin School of Medicine and Public Health, Madison, WI, USA THE BASAL GANGLIA AND DISORDERS Eduard Hitzig (1838–1907) on the cerebral cortex of dogs OF MOVEMENT (Fritsch and Hitzig, 1870/1960), British physiologist Distinction between cortex, white matter, David Ferrier’s (1843–1928) stimulation and ablation and subcortical nuclei experiments on rabbits, cats, dogs and primates begun in 1873 (Ferrier, 1876), and Jackson’s careful clinical The distinction between cortex, white matter, and sub- and clinical-pathologic studies in people (late 1860s cortical nuclei was appreciated by Andreas Vesalius and early 1870s) that the role of the motor cortex was (1514–1564) and Francisco Piccolomini (1520–1604) in appreciated, so that by 1876 Jackson could consider the the 16th century (Vesalius, 1542; Piccolomini, 1630; “motor centers in Hitzig and Ferrier’s region ...higher Goetz et al., 2001a), and a century later British physician in degree of evolution that the corpus striatum” Thomas Willis (1621–1675) implicated the corpus
    [Show full text]
  • Cardiovascular Complications During the Acute Phase of Spinal Cord Injury
    Cardiovascular Complications during the Acute Phase of Spinal Cord Injury Mirkowski M Faltynek P Benton B McIntyre A Krassioukov A Teasell RW www.scireproject.com Version 7.0 Key Points Pseudoephedrine may be an effective adjuvant for the treatment of neurogenic shock during the acute phase post SCI; however, pseudoephedrine may require up to one month for effectiveness and may result in higher complication rates for older patients. The use of functional electrical stimulation in combination with tilt tables may be effective for the management of orthostatic hypotension during the acute and subacute phase post SCI. Tilt table verticalization may be effective for lowering heart rate in patients post SCI. Midodrine hydrochloride may be effective for the management of orthostatic hypotension during the acute phase post SCI. Methylprednisolone appear to not be effective for the management of heart rate variability post SCI. Hemodynamic support during the acute phase post SCI has been associated with improved neurological outcomes but no cause and effect relationship has been established. Oral albuterol appears to be effective for the management of bradycardia during the acute phase post SCI. Cardiac pacemaker implantation appears to be effective for the management of refractory bradycardia during the acute phase post SCI. Table of Contents 1.0 Executive Summary ................................................................................................................ 1 2.0 Methods ........................................................................................................................................
    [Show full text]