DOCSLIB.ORG

Review the Neuro-Ophthalmology of Head Trauma

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Review the Neuro-Ophthalmology of Head Trauma Review The neuro-ophthalmology of head trauma Rachel E Ventura, Laura J Balcer, Steven L Galetta Lancet Neurol 2014; 13: 1006–16 Traumatic brain injury (TBI) is a major cause of morbidity and mortality. Concussion, a form of mild TBI, might be Department of Neurology, associated with long-term neurological symptoms. The eff ects of TBI and concussion are not restricted to cognition New York University School of and balance. TBI can also aff ect multiple aspects of vision; mild TBI frequently leads to disruptions in visual Medicine, New York, NY, USA functioning, while moderate or severe TBI often causes structural lesions. In patients with mild TBI, there might be (R E Ventura MD, Prof L J Balcer MD, Prof abnormalities in saccades, pursuit, convergence, accommodation, and vestibulo-ocular refl ex. Moderate and severe S L Galetta MD) TBI might additionally lead to ocular motor palsies, optic neuropathies, and orbital pathologies. Vision-based testing Correspondence to: is vital in the management of all forms of TBI and provides a sensitive approach for sideline or post-injury concussion Dr Steven L Galetta, Department screening. One sideline test, the King-Devick test, uses rapid number naming and has been tested in multiple athlete of Neurology, New York cohorts. University School of Medicine, New York, NY 10016, USA [email protected] Introduction particular of eye movements, needs coordination of Traumatic brain injury (TBI) is increasingly recognised as refl exive and voluntary activity, including frontoparietal a major cause of morbidity and mortality worldwide, with circuits and subcortical nuclei;15 these pathways are estimates of its incidence ranging from 106 to 790 per vulnerable to injury in mild to severe TBI. 100 000 people per year.1,2 Because around half of the circuits in the brain are involved in vision, many aspects of Defi cits in visual function in mild TBI the visual system are vulnerable to moderate, severe, or Saccades, antisaccades, and cognitive function mild TBI.3 Not surprisingly, a wide range of visual Saccadic eye movements involve a wide variety of complaints might follow head trauma, including cognitive processes and fi ndings from several studies photophobia, double vision, blurred vision, loss of vision, have shown abnormalities in saccade generation after all and visual processing problems. The topic of sports forms of brain trauma. The generation of saccades concussion, a mild form of TBI, has received a lot of media involves weighing aspects of the stimulus as well as attention as a result of increased recognition of potential processes incorporating goals and intentions.16 long-term deleterious eff ects of repeated concussive Visuospatial information is relayed from the occipital events, such as depression, altered cognition, and lobe and then processed in the posterior parietal cortex. neurodegenerative diseases (eg, chronic traumatic Saccades can then be refl exively generated from the encephalopathy and Alzheimer’s disease).4,5 Improvement parietal eye fi eld or intentionally generated in the frontal of the ways in which we screen for concussion is eye fi eld.16,17 The dorsolateral prefrontal cortex plays a part imperative, particularly since objective fi ndings can be in inhibition of refl exive saccades, in prediction of when subtle and athletes often under-report their symptoms.6 anticipatory saccades are needed, and in short-term Examination of the integrity of the visual system helps to spatial memory18 (table 1, fi gure 1). One frequently used both screen and monitor the recovery of patients with TBI. test to assess executive function is the assessment of antisaccades. Antisaccades are examined by having the TBI and concussion patient try to look away from a stimulus; this action TBI can be classifi ed as mild, moderate, or severe. needs inhibition of refl exive saccades and generation of Concussion is the most common form of TBI in a subset voluntary saccades. Saccades can also be used to test for of patients classifi ed as having mild TBI7–9 (see panel 1 for memory (eg, with the memory-guided saccade test) or to defi nitions).The diff erences between combat-related and assess attention (eg, with the gap-saccade test; panel 2). civilian TBI have not fully been elucidated, although it In a study in patients with mild TBI within 10 days of should be noted that mechanisms of blast-related head their injury, antisaccades were assessed with video- injury are complex and might include other injuries oculography and found to be impaired, with prolonged related to burns, toxic inhalation, and radiation exposure. saccadic latencies, high directional errors, and poor Many clinical features of post-concussive syndrome spatial accuracy, although simple refl exive saccades were mirror those of frontal and temporal lobe syndromes, normal.19 These patients also had impairments in including problems with executive function and memory-guided saccades.19,20 This work was then diffi culties with attention, memory, and concentration,10 extended to patients who had post-concussive syndrome and frontal and temporal lobe damage has been shown in with symptoms 3–5 months after their injury in neuropathological11 and imaging12 studies. Investigators comparison with patients who had good recovery. Those of studies using diff usion tensor imaging (DTI) to assess with post-concussive syndrome did worse in microstructural white matter changes in mild TBI antisaccades, in memory-guided saccades, and in a self- identifi ed a high prevalence of injury in the frontal lobes, paced saccade test in which patients were instructed to corpus callosum, and corona radiata, and diff usely in look back and forth between two points as rapidly as deep white matter.13,14 The cognitive control of vision, in possible.21 Kraus and colleagues22 identifi ed similar 1006 www.thelancet.com/neurology Vol 13 October 2014 Review results in patients with chronic TBI of duration greater than 6 months, and showed that eye movements were Panel 1: Glossary of terms more sensitive than neuropsychological testing for Concussion persisting neurological abnormalities in these patients. A traumatically induced transient disruption of brain function;9 a subset of mild traumatic Drew and colleagues23 noted that patients with acute brain injury. mild TBI had defi cits in a gap saccade test, in which the patient fi xates on one target and then has to orientate to Mild traumatic brain injury a peripheral target after a variable amount of time. The Traumatic brain injury has been deemed mild when there is a normal CT, Glasgow coma patients with mild TBI had longer saccadic reaction scale score (GCS) of 13–15, loss of consciousness of less than 30 min, alteration of mental 8 times compared with healthy controls when the state of less than 24 h, and post-traumatic amnesia for less than 24 h. temporal gap between the initial target and the new Accommodation target was short but not when it was long, which is The process by which the eye changes the shape of the lens to maintain focus on an object consistent with abnormalities in disengagement of as its distance varies. attention. Patients with mild TBI with acute or chronic Accommodative amplitude symptoms, therefore, seem to have impairments in Reciprocal of the focal length in metres. It can be subjectively measured by correcting for executive function, attention, and memory that can be distance vision and then having the subject move a near reading card towards the eyes associated with impaired saccadic function.19–23 Defi cits until the text is no longer in focus, then measuring the reciprocal of the distance in in subcortical visual pathway function were also seen as metres. Alternatively, the card could be initially placed close to the eyes and then pulled manifested by slowed self-paced saccades.21 Patients who away until the patient sees it clearly. Typically, the 20/30 line on a near card is used. For have recovered well from their TBI and do not have instance, a patient who has blurry vision at 10 centimetres has 1/(0.10 metres) or ongoing symptoms do not seem to have continued 10 dioptres of accommodative amplitude. 21 saccadic dysfunction, although further studies are Convergence fusional amplitude necessary to characterise the exact evolution of these eye The amount of prism glass that can be placed in front of the eyes at a particular distance movement abnormalities. Tests of saccades recorded before double vision is seen. It can be measured with a base out prism (eg, with the with video oculography enable examiners to provide an thicker edge facing outwards so the light is bent towards the nose) over one eye when the objective correlate to concussive and post-concussive patient focuses on a target. symptoms. Defi cits in saccades can also be identifi ed with a Phoria cursory clinical examination, though detecting Misalignment of the eyes that occurs only some of the time, such as when one eye is abnormalities of individual eye movements at the covered and the synchronisation between eyes is broken. The presence of phoria can be bedside or on the sideline can be challenging and tested for with the cross-cover test, in which the subject focuses on an object while each requires clinical experience (fi gure 2). In one prospective eye is alternatively covered while the uncovered eye is observed for movement. study of patients with blast-induced mild TBI, six (30%) Convergence insuffi ciency often leads to near phorias because the eyes cannot move in of 20 patients had saccadic dysfunction versus none of 20 tandem to align on a target. 24 in the control group. Exotropia A type of eye misalignment in which one eye is manifestly deviated outward. It can be Smooth pursuit congenital or acquired, constant, or intermittent. Predictive visual tracking can be used to assess higher cognitive functioning, because it requires attention, Exophoria anticipation, working memory, as well as smooth, and at Eye misalignment in which the eyes are deviated outward from each other in the absence times saccadic eye movements to maintain gaze on a of binocular fusion.
Load more

Recommended publications
  • Binocular Vision Disorders  Prescribing Guidelines
    Prescribing for Preverbal Children Valerie M. Kattouf O.D. FAAO, FCOVD Illinois College of Optometry Associate Professor Prescribing for Preverbal Children Issues to consider: Age Visual Function Refractive Error Norms Amblyogenic Risk Factors Birth History Family History Developmental History Emmetropization A process presumed to be operative in producing a greater frequency of occurrence of emmetropia than would be expected in terms of chance distribution, as may be explained by postulating that a mechanism coordinates the formation and the development of the various components of the human eye which contribute to the total refractive power Emmetropization Passive process = nature and genetics 60% chance of myopia if 2 parents myopic (Ciuffrieda) Active process = mediated by blur and visual system compensates for blur Refractive Error Norms Highest rate of emmetropization – 1st 12-17 months Hyperopia Average refractive error in infants = +2 D > 1.50 diopters hyperopia at 5 years old – often remain hyperopic Refractive Error Norms Myopia 25% of infants are myopic Myopic Newborns (Scharf) @ 7 years 54% still myopic @ 7 years 46% emmetropic @ 7 years no hyperopia Refractive Error Norms Astigmatism Against the rule astigmatism more prevalent switches to with-the-rule with development At 3 1/2 years old astigmatism is at adult levels INFANT REFRACTION NORMS AGE SPHERE CYL 0-1mo -0.90+/-3.17 -2.02+/-1.43 2-3mo -0.47+/-2.28 -2.02+/-1.17 4-6mo -0.00+/-1.31 -2.20+/-1.15 6-9mo +0.50+/-0.99 -2.20+/-1.15 9-12mo +0.60+/-1.30 -1.64+/-0.62
    [Show full text]
  • Ophthalmological Findings in Children and Adolescents with Silver Russell
    Ophthalmological findings in children and adolescents with Silver Russell Syndrome Marita Andersson Gronlund, Jovanna Dahlgren, Eva Aring, Maria Kraemer, Ann Hellstrom To cite this version: Marita Andersson Gronlund, Jovanna Dahlgren, Eva Aring, Maria Kraemer, Ann Hellstrom. Oph- thalmological findings in children and adolescents with Silver Russell Syndrome. British Journal of Ophthalmology, BMJ Publishing Group, 2010, 95 (5), pp.637. 10.1136/bjo.2010.184457. hal- 00588358 HAL Id: hal-00588358 https://hal.archives-ouvertes.fr/hal-00588358 Submitted on 23 Apr 2011 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Ophthalmological findings in children and adolescents with Silver Russell Syndrome M Andersson Grönlund, MD, PhD1, J Dahlgren, MD, PhD2, E Aring, CO, PhD1, M Kraemer, MD1, A Hellström, MD, PhD1 1Institute of Neuroscience and Physiology/Ophthalmology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden. 2Institute for the Health of Women and Children, Gothenburg Paediatric Growth Research Centre (GP-GRC), The Sahlgrenska
    [Show full text]
  • 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.
    [Show full text]
  • 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).
    [Show full text]
  • Care of the Patient with Accommodative and Vergence Dysfunction
    OPTOMETRIC CLINICAL PRACTICE GUIDELINE Care of the Patient with Accommodative and Vergence Dysfunction OPTOMETRY: THE PRIMARY EYE CARE PROFESSION Doctors of optometry are independent primary health care providers who examine, diagnose, treat, and manage diseases and disorders of the visual system, the eye, and associated structures as well as diagnose related systemic conditions. Optometrists provide more than two-thirds of the primary eye care services in the United States. They are more widely distributed geographically than other eye care providers and are readily accessible for the delivery of eye and vision care services. There are approximately 36,000 full-time-equivalent doctors of optometry currently in practice in the United States. Optometrists practice in more than 6,500 communities across the United States, serving as the sole primary eye care providers in more than 3,500 communities. The mission of the profession of optometry is to fulfill the vision and eye care needs of the public through clinical care, research, and education, all of which enhance the quality of life. OPTOMETRIC CLINICAL PRACTICE GUIDELINE CARE OF THE PATIENT WITH ACCOMMODATIVE AND VERGENCE DYSFUNCTION Reference Guide for Clinicians Prepared by the American Optometric Association Consensus Panel on Care of the Patient with Accommodative and Vergence Dysfunction: Jeffrey S. Cooper, M.S., O.D., Principal Author Carole R. Burns, O.D. Susan A. Cotter, O.D. Kent M. Daum, O.D., Ph.D. John R. Griffin, M.S., O.D. Mitchell M. Scheiman, O.D. Revised by: Jeffrey S. Cooper, M.S., O.D. December 2010 Reviewed by the AOA Clinical Guidelines Coordinating Committee: David A.
    [Show full text]
  • Strabismus: a Decision Making Approach
    Strabismus A Decision Making Approach Gunter K. von Noorden, M.D. Eugene M. Helveston, M.D. Strabismus: A Decision Making Approach Gunter K. von Noorden, M.D. Emeritus Professor of Ophthalmology and Pediatrics Baylor College of Medicine Houston, Texas Eugene M. Helveston, M.D. Emeritus Professor of Ophthalmology Indiana University School of Medicine Indianapolis, Indiana Published originally in English under the title: Strabismus: A Decision Making Approach. By Gunter K. von Noorden and Eugene M. Helveston Published in 1994 by Mosby-Year Book, Inc., St. Louis, MO Copyright held by Gunter K. von Noorden and Eugene M. Helveston 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, without prior written permission from the authors. Copyright © 2010 Table of Contents Foreword Preface 1.01 Equipment for Examination of the Patient with Strabismus 1.02 History 1.03 Inspection of Patient 1.04 Sequence of Motility Examination 1.05 Does This Baby See? 1.06 Visual Acuity – Methods of Examination 1.07 Visual Acuity Testing in Infants 1.08 Primary versus Secondary Deviation 1.09 Evaluation of Monocular Movements – Ductions 1.10 Evaluation of Binocular Movements – Versions 1.11 Unilaterally Reduced Vision Associated with Orthotropia 1.12 Unilateral Decrease of Visual Acuity Associated with Heterotropia 1.13 Decentered Corneal Light Reflex 1.14 Strabismus – Generic Classification 1.15 Is Latent Strabismus
    [Show full text]
  • 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.
    [Show full text]
  • The Role of Vagal Nerve Root Injury on Respiration Disturbances In
    Original Investigation Original Received: 03.12.2013 / Accepted: 11.02.2014 DOI: 10.5137/1019-5149.JTN.9964-13.1 The Role of Vagal Nerve Root Injury on Respiration Disturbances in Subarachnoid Hemorrhage Subaraknoid Kanamada Solunum Bozuklukları Oluşmasında Vagal Sinir Kökü Hasarının Rolü Murteza CAKıR1, Canan AtALAY 2, Zeynep CAKıR3, Mucahit Emet3, Mehmet Dumlu AYDıN1, Nazan AYDıN4, Arif ONDER5, Muhammed CAlıK6 1Ataturk University, School of Medicine, Department of Neurosurgery, Erzurum, Turkey 2Ataturk University, School of Medicine, Department of Anesthesiology and Reanimation, Erzurum, Turkey 3Ataturk University, School of Medicine, Department of Emergency Medicine, Erzurum, Turkey 4Ataturk University, School of Medicine, Department of Psychiatry, Erzurum, Turkey 5Avrasya Hospital, Department of Neurosurgery, Istanbul, Turkey 6Ataturk University, School of Medicine, Department of Pathology, Erzurum, Turkey Corresponding Author: Murteza CAKır / E-mail: [email protected] ABSTRACT AIM: We examined whether there is a relationship between vagal nerve root injury and the severity of respiration disorders associated with subarachnoid hemorrhage (SAH). MaTERIAL and METHODS: This study was conducted on 20 rabbits. Experimental SAH was induced by injecting homologous blood into the cisterna magna. During the experiment, electrocardiography and respiratory rhythms were measured daily. After the experiment, any axonal injury or changes to the arterial nervorums of the vagal nerves were examined. All respiratory irregularities and vagal nerve degenerations were statistically analyzed. RESULTS: Normal respiration rate, as measured in the control group, was 30±6 bpm. In the SAH-induced group, respiration rates were initially 20±4 bpm, increasing to 40±9/min approximately ten hours later, with severe tachypneic and apneic variation. In histopathological examinations, axon density of vagal nerves was 28500±5500 in both control and sham animals, whereas axon density was 22250±3500 in survivors and 16450±2750 in dead SAH animals.
    [Show full text]
  • Traumatic Brain Injury Vision Rehabilitation Cases
    VISION REHABILITATION CASES CHUNG TO, OD CHRYSTYNA RAKOCZY, OD JAMES A HALEY VETERANS’ HOSPITAL T A M P A , F L CASE #1: PATIENT JS • 33 yo male active duty army soldier • 2012 – stateside fall accident during training • (-) no loss of consciousness • (+) altered consciousness x 24 hours • (+) post- traumatic amnesia x 24hrs CASE #1: PATIENT JS • Complaints since injury: • Intermittent, binocular, horizontal diplopia worse at near and when tired • Inability to read for longer than 10 min due to “eyes feeling tired“ • Chronic headaches with light sensitivity • Decreased memory • Dizziness CASE #1: PATIENT JS • Past Medical/Surgical History: • PRK OU x 2009 • C5-6 cervical fusion March 2013 • Medications: • ACETAMINOPHEN/OXYCODONE, ALBUTEROL, ALLOPURINOL, ATORVASTATIN, CETIRIZINE, DIAZEPAM, FISH OIL, FLUOXETINE, GABAPENTIN, HYDROCHLOROTHIAZIDE, LISINOPRIL, MINERALS/MULTIVITAMINS, MONTELUKAST SODIUM, NAPROXEN, OMEPRAZOLE , TESTOSTERONE CYPIONATE, ZOLPIDEM • Social History: • Married x 4yrs, 2 children • Denies tobacco/alcohol/illicit drug use • Family History: • Father: Diabetes: Glaucoma • Mother: Brain tumor glioblastoma CASE #1: PATIENT JS Sensory Examination Results Mental status Alert & orientated x 3 VA (distance, uncorrected) 20/15 OD, OS, OU VA (near, uncorrected) 20/20 OD, OS, OU Fixation Central, steady, accurate Color vision (Ishihara) 6/6 OD, OS Confrontation fields Full to finger counting OD, OS Stereopsis (uncorrected) Global: 200 sec of arc, Randot Local: 20 sec of arc, Wirt Worth 4 Dot Distance: ortho, no suppression Near:
    [Show full text]
  • Repairing Spinal Cord Nerves
    Repairing spinal cord nerves Ronald Schnaar The Johns Hopkins School of Medicine Traumatic spinal cord injury Edwin Smith Papyrus, Egypt, circa 1500 BC Earliest medical text on battlefield trauma, in which spinal cord injury was deemed: “An ailment not to be treated” Axon transection in traumatic nerve injury Modified from Brittis and Flanagan, Neuron (2001) 30, 11 Even after a microcrush injury, nerve axons fail to regenerate after injury optic nerve microcrush: Axon retraction Regeneration failure 24 h post-injury 2 wks post-injury 100100 µm µm Selles-Navarro, et al. (2001) Exp. Neurol. 167, 282-289 • The peripheral nervous system (PNS) is more permissive for axon regeneration than the central nervous system (CNS). • When PNS nerve sheath is grafted into a CNS injury, some CNS axons regenerate through the graft Adult Rat CNS axon regeneration David & Aguayo (1981) Science 214, 931-933 In vitro, superior cervical ganglion neurites extend on a surface coated without myelin (P) or on PNS myelin (PR), but not on a surface coated with CNS myelin (CR) Caroni & Schwab (1988) J Cell Biol 106, 1281-1288 Axon transection in traumatic nerve injury Modified from Brittis and Flanagan, Neuron (2001) 30, 11 Multiple axon regeneration inhibitors (ARI’s) accumulate at the site of a CNS injury • Myelin-associated glycoprotein (MAG) – on residual myelin • Nogo – on residual myelin • OMgp – on residual myelin • Chondroitin sulfate proteoglycan (CSPG) – on residual myelin and the astroglial scar Blocking one or more ARI may enhance axon regeneration after
    [Show full text]
  • Chronic Traumatic Encephalopathy: the Dangers of Getting “Dinged” Shaheen E Lakhan1* and Annette Kirchgessner1,2
    Lakhan and Kirchgessner SpringerPlus 2012, 1:2 http://www.springerplus.com/content/1/1/2 a SpringerOpen Journal REVIEW Open Access Chronic traumatic encephalopathy: the dangers of getting “dinged” Shaheen E Lakhan1* and Annette Kirchgessner1,2 Abstract Chronic traumatic encephalopathy (CTE) is a form of neurodegeneration that results from repetitive brain trauma. Not surprisingly, CTE has been linked to participation in contact sports such as boxing, hockey and American football. In American football getting “dinged” equates to moments of dizziness, confusion, or grogginess that can follow a blow to the head. There are approximately 100,000 to 300,000 concussive episodes occurring in the game of American football alone each year. It is believed that repetitive brain trauma, with or possibly without symptomatic concussion, sets off a cascade of events that result in neurodegenerative changes highlighted by accumulations of hyperphosphorylated tau and neuronal TAR DNA-binding protein-43 (TDP-43). Symptoms of CTE may begin years or decades later and include a progressive decline of memory, as well as depression, poor impulse control, suicidal behavior, and, eventually, dementia similar to Alzheimer’s disease. In some individuals, CTE is also associated with motor neuron disease similar to amyotrophic lateral sclerosis. Given the millions of athletes participating in contact sports that involve repetitive brain trauma, CTE represents an important public health issue. In this review, we discuss recent advances in understanding the etiology of CTE. It is now known that those instances of mild concussion or “dings” that we may have previously not noticed could very well be causing progressive neurodegenerative damage to a player’s brain.
    [Show full text]
  • Chapter 18 CRANIAL NERVE INJURIES
    Cranial Nerve Injuries Chapter 18 CRANIAL NERVE INJURIES † ‡ SCOTT B. ROOFE, MD, FACS*; CAROLINE M. KOLB, MD ; AND JARED SEIBERT, MD INTRODUCTION CRANIAL NERVE V CRANIAL NERVE VII Evaluation Imaging Electrodiagnostic Testing Eye Care Nerve Exploration Nerve Repair Interposition Grafting Intratemporal Injuries Facial Nerve Decompression LOWER CRANIAL NERVES, IX THROUGH XII CRANIAL NERVE IX CRANIAL NERVE X CRANIAL NERVE XI CRANIAL NERVE XII SUMMARY CASE PRESENTATIONS Case Study 18-1 Case Study 18-2 *Colonel, Medical Corps, US Army; Program Director, Otolaryngology Residency, Tripler Army Medical Center, 1 Jarrett White Road, Honolulu, Hawaii 96859-5000; Assistant Professor of Surgery, Uniformed Services University of the Health Sciences †Major, Medical Corps, US Army; Staff Otolaryngologist, Fort Belvoir Community Hospital, 9300 Dewitt Loop, Fort Belvoir, Virginia 20112 ‡Captain, Medical Corps, US Army; Otolaryngology Resident, Tripler Army Medical Center, 1 Jarrett White Road, Honolulu, Hawaii 96859-5000 213 Otolaryngology/Head and Neck Combat Casualty Care INTRODUCTION Injuries to the head and neck rank as some of the cal to maximizing the outcomes for these patients. most common injuries suffered in the current combat The otolaryngologist clearly has a vital role in the environment. These injuries often lead to extensive management of nearly all cranial nerve injuries. bony and soft tissue disruption, which places the cra- However, in the combat environment, this specialty nial nerves at increased risk for damage. Functional generally focuses on deficits arising from cranial deficits of any of these nerves can be devastating to nerves VII and VIII as well as the lower cranial nerves, both appearance and function. Due to the complex IX through XII.
    [Show full text]