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Mild TBI in Contact Sports: are they really mild?

Mild TBI in Contact Sports: are they really mild?

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  • As a physician, I recently reviewed the State of the Art Medical Care for TBI…I see no appreciable advances since my training in 1986! If we can’t treat TBI…we MUST prevent it!


  • 1. Mild Traumatic Brain Injury in Contact Sports: Are They Really Mild?
    Julian E. Bailes, M.D.
    Professor and Chairman
    Department of Neurosurgery
    West Virginia University School of Medicine
  • 2. Disclosure
    Research Funded by and J. Bailes consultant for Martek Biosciences, Inc.
    Research Funded by BHR Pharma, Inc.
  • 3.
  • 4. Roethlisberger’s Injury Highlights Nerve Center for Head Trauma
    Published: January 1, 2009
  • 5. “The football fields of our nation have been a vast proving ground or laboratory for the study of tragic neurological sequelae of head and neck trauma in man” Richard Schneider 1967
  • 6. What is a Concussion?
    Temporary disruption of normal brain function
    Also called Mild Traumatic Brain Injury (MTBI)
    Caused by a blow or motion to the head
    Results in brain movement inside skull
    From collisions, falls, striking objects/ground
    90% occur without losing consciousness
    Continuing to play results in vulnerability to more injury, chronic disability or even death
    Brain scans usually normal
  • 7. Cellular Injury from MTBI
    Neuronal membrane disruption opens voltage-dependent K+ channels
    Widespread release of glutamate
    Thru NMDA receptors, increase occurs in intracellular Ca++
    Mitochondrial injury leads to impaired respiration, reactive O2 species,
    Oxid cellular injury, ATP failure,
    abnormal glucose metabolism
    Caspase-mediated apoptosis
  • 8. Ultrastructural injury
    Neurofilaments and microtubules provide framework for axonal transport
    Anterograde/retrograde movement of membrane materials to/from somata
    Molecular motors kinesins/dyneins
    Both mechanical damage & delayed/progressive ultrastructural injury from proteolysis by intracellular calpains
    Axonal transport is interrupted
  • 9.
  • 10. Mechanoporation
    Straight line forces do not cause MTBI
    Head motion, more than head contact causes MTBI
    Rotational, angular forces cause tension force vectors which affect the neuron
    A traumatic membrane defect occurs
    The brain attempts to “self-seal” these porations
  • 11.
  • 12. Acceleration-Deceleration Injury: Brain movement within skull
    Rotation: Never prevented, perhaps increased, by helmets
  • 13. KE=1/2M XV2
    HIC= V1-V2/HD
  • 14. Cumulative Effects in Collegiate Athletes
    3 concussions: 3X’s risk of future events
    1 in 15: 2nd concussion same season (usually within 7-10 days)
    Each concussion takes longer to recover
    Based on symptom duration, 69% moderate & 15% severe
  • 15. Center for the Study of Retired AthletesKevin Guskiewicz, PhDJulian E. Bailes, MDUniversity of North Carolina at Chapel HillWest Virginia University School of MedicineNational Football League Players’ Association
  • 16. Life After Football:
    Health of NFL Retirees
    Funded by:
    NFL Players Association
    Office of the Vice-Chancellor for Research, UNC-CH
    Department of Exercise & Sport Science, UNC-CH
    Injury Prevention Research Center, UNC-CH
  • 17.
  • 18.
  • 19.
  • 20. Dementia Risk Seen in Players in N.F.L. Study
  • 21. Retire: Are Some Players Vulnerable to Dementia?
  • 22. Chronic Traumatic Encephalopathy
  • 24.
  • 25.
  • 26.
  • 27.
  • 28.
  • 29. Concussion: Is There Any Hope for Prevention?
  • 30. Fluid Percussion Model
    application of a fluid pressure pulse to the intact dura through a craniotomy
    replicates clinical contusion without skull fracture
    petechial hemorrhage in the brain parenchyma, axonal damage, subarachnoid hemorrhage, tissue tears followed by focal necrosis and cell loss, and characteristic vascular damage at the gray/white interface defined as “gliding contusion”
  • 31. Impact Acceleration Injury
    Weight drop onto steel helmet affixed to skull
    Produces reliable and reproducible injury
    High yield of traumatically injured axons in white matter tracts
  • 32. 32
    Confidential Information
    Increases Bcl2
    Sigma Receptor
    Possible Mechanisms of Action
    Reduce Apoptosis
    Decreases free radicals & lipid peroxidation
    Study funded by BHR Pharma, Inc
  • 33. Omega-3 Supplementation
    Recent evidence from animal studies suggests that supplementation with omega-3 fatty acids (particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)) improves functional outcomes following focal neural injury.
    Wu, A., Ying, Z. and Gomez-Pinilla F, “Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats,” J. Neurotrauma 21:10 1457-67 (2004).
  • 34. DHA facilitates brain function at optimal levels
    Neuronal networks
    PE, PS
    Connectivity, plasticity
    -neurite outgrowth
    -spine formation
    -light/dark adaptation
    Neuron processing ctr
    Psycho-motor function
    • vision, hearing, tactile
    • 39. info processing, focus
    • 40. info storage, recall, learning
    • 41. adaptation/problem solving
    • 42. coordination/language/communication
    = Cognition
  • 43. Immunohistochemistry
    Sham injured animals demonstrate paucity of APP positive axons with
    Retraction bulb morphology
  • 44. Immunohistochemistry
    Animals subjected to impact acceleration injury demonstrate APP positive axons with retraction bulb morphology at 30 days
  • 45. Immunohistochemistry
    Animals subjected to impact acceleration injury and supplemented with 10mg/kg/day DHA following impact injury demonstrate fewer APP positive axons with retraction bulb morphology at 30 days
  • 46. DHA Post-Injury Treatment
  • 47. AA/EPA Ratio
    % Change in AA/EPA ratio from baseline
  • 48. Caspase 3
    • p<0.05 high dose vs no treatment
  • Immunohistochemistry
    Likewise, animals subjected to impact acceleration injury and pre-supplemented with 40 mg/kg/day DHA demonstrate fewer APP positive axons with retraction bulb morphology at 30 days
  • 49. DHA Pre-Injury Treatment
  • 50. Morris Water Maze
    • p<0.05 high dose vs no treatment in both latency and error
  • 51.
  • 52.
  • 53.
  • 54.
  • 55.
  • 56. Are Helmets The Answer?
  • 57.
  • 58. X
    Abating Traumatic Brain Injury
    A SLOSH Approach
  • 59. SLOSH
    In fluid dynamics, the movement of a liquid or semi-solid inside another object
    First described by NASA, this sloshing effect can cause severe problems with vehicle stability/control due to a propensity to absorb external energy.
    In human anatomy terms, the vehicle or the container (skull) and its contents (brain) the semi-solid fluid-behaving matter
    Oscillation occurs only when the vehicle is partially filled
  • 60. What is the Teleological Function of the Omohyoid Muscle?
  • 61. Jugular Compression Device
    Non-compressible vertebrals
    The Quenckenstadt Maneuver
    has been safely used for nearly 100 years
  • 62. Brainstem APP Region of Interest
  • 63. RESULTS
  • 64. Concussion-Changes Coming
    Brain Injury Assoc: 3.8 million sports and recreation-related concussions in U.S. yearly
    More concussions or greater recognition?
    Baby boomers want to prevent chronic injuries
    Increased awareness and structured approach at every level
    Congressional hearings
    Recognition: younger brains still developing
    State legislation: OK, TX, WA, NM, VA, others-pending in 26 states
  • 65. Concussion Management
    Diagnosed concussion (certainly LOC) precludes RTP same day
    Player should be completely asymptomatic with normal neurological examination
    Neuropsychological testing
    Sometimes symptoms become more obvious later
    Treatment: physical and mental rest
    Rest period: 7-10 days, until no symptoms
    Avoidance of alcohol, caffeine, dehydration
    Omega-3 Fatty Acids-DHA
    Neck strengthening exercises