Chronic Traumatic Encephalopathy: the Dangers of Getting “Dinged” Shaheen E Lakhan1* and Annette Kirchgessner1,2
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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. -
Blunt and Blast Head Trauma: Different Entities
International Tinnitus Journal, Vol. 15, No. 2, 115–118 (2009) Blunt and Blast Head Trauma: Different Entities Michael E. Hoffer,1 Chadwick Donaldson,1 Kim R. Gottshall1, Carey Balaban,2 and Ben J. Balough1 1 Spatial Orientation Center, Department of Otolaryngology, Naval Medical Center San Diego, San Diego, California, and 2 Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA Abstract: Mild traumatic brain injury (mTBI) caused by blast-related and blunt head trauma is frequently encountered in clinical practice. Understanding the nuances between these two distinct types of injury leads to a more focused approach by clinicians to develop better treat- ment strategies for patients. In this study, we evaluated two separate cohorts of mTBI patients to ascertain whether any difference exists in vestibular-ocular reflex (VOR) testing (n ϭ 55 en- rolled patients: 34 blunt, 21 blast) and vestibular-spinal reflex (VSR) testing (n ϭ 72 enrolled patients: 33 blunt, 39 blast). The VOR group displayed a preponderance of patients with blunt mTBI, demonstrating normal to high-frequency phase lag on rotational chair testing, whereas patients experiencing mTBI from blast-related causes revealed a trend toward low-frequency phase lag on evaluation. The VSR cohort showed that patients with posttraumatic migraine- associated dizziness tended to test higher on posturography. However, an indepth look at the total patient population in this second cohort reveals that a higher percentage of blast-exposed patients exhibited a significantly increased latency on motor control testing as compared to pa- tients with blunt head injury ( p Ͻ .02). These experiments identify a distinct difference be- tween blunt-injury and blast-injury mTBI patients and provide evidence that treatment strategies should be individualized on the basis of each mechanism of injury. -
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). -
Isolated Severe Blunt Traumatic Brain Injury: Effect of Obesity on Outcomes
CLINICAL ARTICLE J Neurosurg 134:1667–1674, 2021 Isolated severe blunt traumatic brain injury: effect of obesity on outcomes Jennifer T. Cone, MD, MHS,1 Elizabeth R. Benjamin, MD, PhD,2 Daniel B. Alfson, MD,2 and Demetrios Demetriades, MD, PhD2 1Department of Surgery, Section of Trauma and Acute Care Surgery, University of Chicago, Illinois; and 2Department of Surgery, Division of Trauma, Emergency Surgery, and Surgical Critical Care, LAC+USC Medical Center, University of Southern California, Los Angeles, California OBJECTIVE Obesity has been widely reported to confer significant morbidity and mortality in both medical and surgical patients. However, contemporary data indicate that obesity may confer protection after both critical illness and certain types of major surgery. The authors hypothesized that this “obesity paradox” may apply to patients with isolated severe blunt traumatic brain injuries (TBIs). METHODS The Trauma Quality Improvement Program (TQIP) database was queried for patients with isolated severe blunt TBI (head Abbreviated Injury Scale [AIS] score 3–5, all other body areas AIS < 3). Patient data were divided based on WHO classification levels for BMI: underweight (< 18.5 kg/m2), normal weight (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), obesity class 1 (30.0–34.9 kg/m2), obesity class 2 (35.0–39.9 kg/m2), and obesity class 3 (≥ 40.0 kg/ m2). The role of BMI in patient outcomes was assessed using regression models. RESULTS In total, 103,280 patients were identified with isolated severe blunt TBI. Data were excluded for patients aged < 20 or > 89 years or with BMI < 10 or > 55 kg/m2 and for patients who were transferred from another treatment center or who showed no signs of life upon presentation, leaving data from 38,446 patients for analysis. -
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. -
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. -
Traumatic Brain Injury (TBI)
Traumatic Brain Injury (TBI) Carol A. Waldmann, MD raumatic brain injury (TBI), caused either by blunt force or acceleration/ deceleration forces, is common in the general population. Homeless persons Tare at particularly high risk of head trauma and adverse outcomes to TBI. Even mild traumatic brain injury can lead to persistent symptoms including cognitive, physical, and behavioral problems. It is important to understand brain injury in the homeless population so that appropriate referrals to specialists and supportive services can be made. Understanding the symptoms and syndromes caused by brain injury sheds light on some of the difficult behavior observed in some homeless persons. This understanding can help clinicians facilitate and guide the care of these individuals. Prevalence and Distribution recover fully, but up to 15% of patients diagnosed TBI and Mood Every year in the USA, approximately 1.5 with MTBI by a physician experience persistent Swings. million people sustain traumatic brain injury disabling problems. Up to 75% of brain injuries This man suffered (TBI), 230,000 people are hospitalized due to TBI are classified as MTBI. These injuries cost the US a gunshot wound and survive, over 50,000 people die from TBI, and almost $17 billion per year. The groups most at risk to the head and many subsequent more than 1 million people are treated in emergency for TBI are those aged 15-24 years and those aged traumatic brain rooms for TBI. In persons under the age of 45 years, 65 years and older. Men are twice as likely to sustain injuries while TBI is the leading cause of death. -
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 -
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. -
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. -
Reanimating Hand Function After Spinal Cord Injury Using Nerve
rehabilitation a r t i c l e Mary Galea, AM FAHMS, B App Sc (Physio), BA, PhD is a Professorial Fellow at the Department of Medicine, University of Melbourne. Reanimating hand She is a Physiotherapist and Neuroscientist whose research programme includes both laboratory-based and clinical function after spinal projects with the overall theme of understanding the control of voluntary movement by the brain, and factors that promote recovery cord injury using following nervous system injury. Aurora Messina, BSc (Hons), PhD is a Senior Research Fellow at nerve transfer surgery the Department of Medicine and the Peter Doherty Institute, University of Melbourne, Australia. She is a Key Take Home Messages Age at injury, and injuries caused by morphologist with an interest 2 in the fields of nerve injury • Loss of hand and arm function is a falls have increased over time. Over half and regeneration, and tissue devastating consequence of cervical of the injuries affect the cervical spinal engineering. spinal cord injury cord,1 leading to tetraplegia, that is, some • Surgical approaches to reconstruct degree of paralysis in all four limbs as Bridget Hill, MCSP, arm and hand function in people with well as the trunk. In tetraplegia, the Postgrad Dip (Musc), PhD tetraplegia include tendon transfer degree of impairment of the upper limb, is a Physiotherapist and Early and nerve transfer surgery including the hand, will vary depending Career Researcher having • Nerve transfer surgery can be used on the level and completeness of injury. been awarded her PhD in in combination with tendon transfer Loss of function is greater the higher 2017. -
Understanding Traumatic Brain Injury in Women
WORKSHOP SUMMARY UNDERSTANDING TRAUMATIC BRAIN INJURY IN WOMEN NIH Main Campus, December 18-19, 2017 Table of Contents Executive Summary ........................................................................................................................................ 1 Introduction ................................................................................................................................................... 3 Background .................................................................................................................................................... 3 Welcome ....................................................................................................................................................... 4 Keynote: Identifying Sex Differences in Research: What Are the Challenges? ................................................ 4 Session I: Sex Differences in TBI across the Lifespan ...................................................................................... 6 The Epidemiology of Sex Differences in the Incidence of TBI ........................................................................................ 6 Sex Differences in Pediatric Cases of TBI ....................................................................................................................... 6 Sex Differences in Older Adults following TBI ............................................................................................................... 7 Session II: TBI as a Consequence of Intimate Partner