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download full presentation - Concussion: its recognition and ...

  1. 1. DR Steve Olvey FIA Institute Fellow - USA
  2. 2. CONCUSSION RECOGNITION AND MANAGEMENT FIA MEDICINE IN MOTOR SPORT SUMMIT 2010 Stephen E. Olvey, M.D. Associate Professor Clinical Neurology/Neurosurgery Director Neuroscience Intensive Care Unit University of Miami/Miller School of Medicine Fellow FIA Institute for Motor Sports Safety
  3. 3. WHY THIS IS A HOT TOPIC?  There are 250,000 - 300,000 sports related TBIs reported annually in the U.S alone. Thousands more worldwide.  Sports concussion is unique in that it is generally mild, but carries a high risk of recurrent concussion and subsequent illness due to early return to competition.  Long term dysfunction often follows repeated concussions. (Mohamed Ali, Steve Young, Troy Aikman, and more than a few racing drivers)  Annual cost in the United States exceeds 1 billion dollars.  >98% of sports related head injuries are concussions.  Misunderstanding of concussion still permeates the medical profession
  4. 4. CLINICAL DILEMMA  Major health problem  No proven acute treatment. Injury must run its course.  Severity of the concussion not known until it has resolved. The final outcome may take years.  Uncertainty about when it is safe to return to competition.  Multiple criteria and guidelines exist; but these are based primarily on subjective clinical factors and the duration of impairment, they do not, unfortunately correlate with outcome.
  6. 6. OLD DEFINITION “A reversible injury to the brain due to traumatic forces, resulting in amnesia and/or loss of consciousness.”
  7. 7. NEW DEFINITION  Don’t need to have been unconscious  Don’t need to have directly hit your head  Don’t need to have been amnesic  Must have some concussion related symptoms  Normal routine CT or MRI  May or may not have post concussion symptoms  Repeated sub-clinical head accelerations will likely become part of the definition in the near future.
  9. 9. METABOLIC ABNORMALITIES  Potassium, glutamate, and glucose are immediately released from affected brain cells…  Calcium enters these disturbed cells in exchange for the K+…  Neurotransmitter release occurs with loss of autoregulation in the area of the brain affected…  Concomitant decrease in regional cerebral blood flow with a resultant energy crisis…
  10. 10. INJURY AFTERMATH  Brain is vulnerable to further injury during this period due to altered cerebral glucose metabolism. (20 minutes to a few days?)  The hyperglycolysis that results, depletes cellular ATP resulting in an energy crisis as decreased blood flow limits body’s ability to supply enough glucose to satisfy the supply/demand relationship for brain function.  Results in seriously altered brain function  It has been shown that if there is too much calcium influx, actual cell death may occur; seen in the most severe forms of concussion
  11. 11. NOT JUST A BUMP ON THE HEAD SUMMARY: There is a Triphasic metabolic response in mild TBI: Hyperglycolysis (hours-days) Metabolic depression (days-weeks) Metabolic recovery (days-weeks-mos.) None of the above is directly related to the initial clinical presentation.
  14. 14. THERAPEUTIC DELIMMA  How much rest before how much activity?
  15. 15.  There is a period of energy crisis and vulnerability during which secondary insults must be avoided---return to play issues  Post-traumatic physiological brain abnormalities in humans can last days to months.  Clinical assessment is inadequate to quantify post traumatic dysfunction.  Excessive activation or forced disuse of injured brain can worsen the outcome---therapeutic implications  The developing brain is uniquely vulnerable to trauma.--- It is different in kids! PATHOPHYSIOLOGY SUMMARIZED
  17. 17. THE TWO TYPES OF ACCELERATION  Translational acceleration- Total applied force passes through the center of gravity of the head (walking into a flag pole, hitting steering wheel head on)  Angular acceleration- Force generates motion around an axis (Whiplash, or left hook in boxing)
  18. 18. TWO TYPES OF ACCELERATION APPLICATION  Impulsive loading (whiplash, shaking baby, most open wheel crashes) and Impact loading (skull vs. a rigid surface as happens in rally cars, stock cars)  Impact loading in general produces much higher forces than does impulsive loading. Mild TBI may result from both.
  19. 19. DIAGNOSIS Physical Signs of Mild TBI  Any loss of consciousness  Retrograde or anterograde amnesia  Seizure at time of impact (so-called impact seizure)  Vacant stare  Inability to focus, easily distracted  Slurred speech, slow to answer questions  Disoriented, unsteady gait  Memory deficits, personality change  Emotionally unstable, inappropriate behavior  Delayed verbal and motor responses
  20. 20. DIAGNOSIS, CONT. Symptomatology  Headache ( nearly always present)  Dizziness, vertigo  Lack of awareness  Nausea, vomiting  Loss of balance  Feeling dazed, “dinghy”  Ringing in the ears (tinnitus)  Blurred or double vision (diplopia)  “Just not feeling right”
  21. 21. BOTTOM LINE  Examiner must have high index of suspicion based on mechanism of injury, velocity, in- car damage, helmet damage, damage to surrounding area, etc.  Athletes themselves will under report symptoms and out right lie to stay in the event.
  22. 22. MANAGEMENT  ANY Symptoms or Signs: NO RETURN TO ANY SPORTS ACTIVITY; whether competition, or training  Driver or athlete should be medically evaluated and monitored every 5 min. for symptom/sign resolution or deterioration for at least 1 hr.
  24. 24. STATE OF THE ART  Neuro-psyche testing: ImPACT: Immediate Post-Concussion Assessment and Cognitive Testing  One of several available: Now used in Indy Car, Formula 1, NASCAR, NFL, NHL, World Cup Soccer, USSA, FISA, and FIFA.  Most extensively tested (Initially over 18,000 subjects)
  25. 25. WHY USE NEUROPSYCH TESTING  Athletes with a mild TBI will often deny symptoms  Athletes may lack awareness of symptoms  Testing provides unique information  Trusting an athlete’s self-assessment is very dangerous!  Eliminates bias, favoritism, and revenge
  26. 26. ImPACT ADVANTAGES  Minimizes practice effects (can’t out smart the test)  Measures reaction time to 1/100 th Sec.  Can be administered in a group setting  Can be administered by a Nurse or Athletic Trainer, even a PhD or MD  Now available for I-PHONE and other wireless use  < 30 Minutes to administer  24/7 World wide reporting of the results
  27. 27. HOW TO USE ImPACT  Initial preseason baseline testing on all athletes (now enough tests so not absolutely necessary)  Administer test as soon as practical following incident (readings returned in matter of minutes)  Diagnosis confirmed if test determined to be abnormal (more than 2 SD from baseline)  Repeat test at 48 hrs. and again at 7 days and every 7 days until normal.  Provides a definitive guide for return to competition
  28. 28. EFFECT OF REPEATED MILD TBI ON THE ATHLETE  An athlete with more than three previous concussions is 9 x more likely to have associated amnesia either anterograde or retrograde as well as post concussion symptoms  Retrograde amnesia: 10 x more likely to have a poor outcome  Anterograde amnesia: 4.2 x more likely to have a poor outcome  L.O.C. not predictive of outcome!!!
  29. 29. WHEN DO WE NEED CT/MRI?  Suspicion of a structural lesion: focal neurological signs, evidence of significant impact i.e. helmet, cockpit damage in racing  Seizure activity > 1 minute  Prolonged disturbance of consciousness or worsening level of consciousness while under observation  Persistent clinical or cognitive symptoms, doesn’t improve gradually over period of 2 to 3 weeks.
  30. 30. RETURN TO COMPETITION  Level 1. No activity, complete rest; once asymptomatic proceed to level 2  Level 2. Light aerobic exercise such as walking or stationary cycling  Level 3: Sport-specific training (skating in hockey, running in soccer, simulator, go-kart, family car in racing)  Level 4: Return to sport with supervised private practice with attention to consistent, competitive times or abilities  Level 5: Return to competition under observation during practice then competition  Any re-occurrence of symptoms along the line, athlete should go back to previous level!!!!
  31. 31. WHAT WE STILL DON’T KNOW  How many mild TBI’s are too many?  When is the brain really back to normal?  Is there effective pharmacotherapy?  Why some athletes are “brain injury prone”? - The exact role of age/development (kids and women are more vulnerable) - The role of genetics, seems to run in families - The role of other conditions (migraine, ADD)
  32. 32. WHAT HAVE WE LEARNED  Mild TBI can have long term effects  Most but not all athletes recover quickly  Age may be important in recovery  Neuropsychological testing is a useful tool  Management should involve multiple components  Total inactivity is bad but, activity too soon is also bad
  33. 33. 22 Effect of Transfer Function Correction: Case 1 -50 0 50 100 150 200 250 300 350 400 450 -0.001 0.000 0.001 0.002 0.003 0.004 0.005 0.006 0.007Resultant(G) Time(Sec) Test1_2 LfEar LfEar Ref Computed Lf Ear Ref • CT scan of Specimen 1 (EShock1) showing position of each ear mounted sensor. • From C. Bass and R. Salzar, Final Report 2008.
  34. 34. PREVENTION Stay inside and don’t do anything or Wear an approved/well fitted helmet (FIA 8860) Head and Neck restraint SYSTEM in 4 wheel vehicles Newer devices available for motorcycles (Leatt) Something to “catch” the head. Pad everything with energy absorbing material
  35. 35. THE END