1. THE IMPORTANCE OF MILD TBI RECOGNITION AND MANAGEMENT OF SPORTS RELATED CONCUSSION AND THE MYSTERY OF CTE
Stephen E. Olvey, M.D.
Associate Professor of Clinical Neurology/Neurosurgery
Founding Fellow FIA Institute for Motor Sport Safety and Sustainability, Paris
Scientific Advisory Panel, NOCSAE
Chief Medical Officer U.S. Grand Prix, Austin

2. CONCUSSION or
MILD TBI

3. WHY THIS IS A HOT TOPIC?
There are > 1 million sports related mTBIs reported annually in the U.S alone. Millions more worldwide.
Sports concussion is unique in that it appears to be mild, but carries a high risk of recurrent concussion and possible subsequent chronic illness due to early return to competition and too many concussions, too close together.
Long term dysfunction may follow repeated clinical and sub-clinical concussions. Estimated that up to 20% of retired NFL players have early dementia.
>98% of sports related head injuries are concussions.
Misunderstanding of concussion still permeates the medical profession.

4. FOOTBALL AS A MAJOR ISSUE
An estimated 4.5 million children play football in organized games each year in the U.S.
In 2007, 920,000 athletes under age 18 were treated in ER,s and physician offices for football related injuries. Girl’s soccer, ice hockey are 2nd and 3rd.
47% had suffered at least one concussion and 35% had more than one. Actual numbers are likely much higher. One Canadian hockey study revealed 21.5/1000 exposures. – Echlin, Neurosurgery Focus, 2012
Post suicide18 yo found at autopsy to have changes compatible with chronic traumatic encephalopathy.

5. FOOTBALL CONTINUED
NEURODEGENERATIVE MORTALITY RATE IN PROFESSIONAL FOOTBALL PLAYERS IS 3 X THAT OF THE GENERAL POPULATION!
INCIDENCE OF ALZHEIMER’S AND ALS IS 4X THAT OF THE GENERAL POPULATION!
-Lehman et. al. Neurology, 2012

6. CLINICAL DILEMMA Growing health problem in all contact sports.
No proven acute treatment. Injury must run its course.
Severity of a concussion is not known until it has resolved. The final outcome may take years.
Uncertainty remains about when it is safe to return to competition.
Multiple criteria and guidelines exist; all based primarily on subjective, clinical factors and the duration of impairment. They do not, unfortunately correlate with outcome.
No one knows what officially constitutes a “concussion”.

7. OLD DEFINITION
“A reversible injury to the brain due to traumatic forces resulting in amnesia and/or loss of consciousness.”

8. NEW DEFINITION
“ A clinical syndrome of biomechanically induced alteration of brain function, typically affecting memory and disorientation, which may involve loss of consciousness.” - American Academy of Neurology, 2013

9. EXPANDED 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 is the rule.
May or may not have post concussion symptoms.
Repeated sub-clinical head accelerations will likely become part of the definition in the near future.
-4th International Conference on Concussion

10. CHRONIC TRAUMATIC ENCEPHALOPATHY
Known since 1928 as Dementia
Pugilistica. (Boxers almost exclusiviely)
Growing issue in contact sports as well as
military exposure to IED’s.
Major health, legal, financial, and moral issue.
Currently can only be diagnosed on post
mortem examination.
Majority opinion is that CTE can be
prevented with timely recognition and treatment
of concussions, and improved methods of
prevention.

11. CTE Currently, no large scale epidemiological studies have been done.
Problem is: Until recently, concussion was thought to be rather innocuous.
Multiple studies are now in progress.
Comprehensive review in Journal of Neuropathology, Exp. Neurology, 2010
citing, 118 references

12. CTE
Work utilizing survey research from the Center for the Study of Retired Athletes has shown that both mild cognitive impairment and depression are more common than expected in age-matched controls and that a higher incidence is associated with 3 or more concussions. -Bailes, et. al. J Neurosurg. 11/13

13. CTE CURRENTLY DEFINED
A degenerative brain disease associated with repeated brain trauma both clinical and sub-clinical in nature often beginning in early childhood.
Stepwise deterioration in memory, insight, judgment, development of movement disorders, and finally full blown dementia.
Presence of an abnormal protein called “tau” in the form of neurofibrillary and astrocytic tangles often perivascular in location. Decreased brain weight
Eventually leads to progressive cellular death.

14. Middle aged, NFL player post suicide
73 yo champion
boxer
No CTE

15. BOSTON UNIVERSITY STUDY
68 CASES OF CTE STUDIED EXTENSIVELY
AGES: 17 – 98
50 FOOTBALL PLAYERS 33 IN NFL, 9 COLLEGE, 6 HS, 4 NHL, 8 BOXERS, 6 VETERANS OF IRAQ, AFGANISTAN
ASSOCIATION FOUND WITH ALZHEIMERS AND ALS. 4X THAT OF THE GENERAL POPULATION.
Ann McKee, Director CSTE
(Center for the study of traumatic encephalopathy)

16. FAMILY INTERVIEWS
STAGE 1: Persistent headaches and inability to concentrate.
STAGE 2: Depression, explosive behavior, and short term memory impairment.
STAGE 3: Executive function, judgment, multitasking, worsening cognitive issues.
STAGE 4: End stage dementia
(89% of subjects followed this pattern)

17. NOT JUST A BUMP ON THE HEAD
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 auto-regulation in the area of the brain affected.
Concomitant decrease in regional cerebral blood
flow with a resultant energy crisis…

18. INJURY AFTERMATH
Brain is vulnerable to further injury during this period due primarily to altered cerebral glucose metabolism. (20 minutes to several days?)
The hyperglycolysis that results, depletes cellular ATP resulting in an energy crisis. Decreased blood flow in the area limits the brain’s ability to supply enough glucose to satisfy the normal supply/demand relationship. Rise in lactate.
The result is seriously altered brain function.
If “too much” calcium influx, neuronal cell death may occur; seen in the most severe forms of concussion

19. POSSIBLE ROLE OF INFLAMASOMES
Recently discovered intracellular protein bundles thought to be the precursor's to the inflammatory cascade – the “IL Gang”.
Unknown what triggers what inflamasome.
Thought to cause long term derangements in the brain due to an inflammatory reaction that occurs in stages and develops more extensively with repeated insults too close together. (Immunocytotoxicity, “primed glial cells”)
- Blaylock, Maroon, Surg, Neurology, Int. 2011

20. PATHOPHYSIOLOGY SUMMARIZED
There is a period of energy crisis and vulnerability during which secondary insults must be avoided (persistent “primed” glial cells) - return to play issues
Post- mild 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!

22. THERAPUTIC IMPLICATIONS

23. WHAT HAPPENS IF CONCUSSED ANIMAL IS CONFINED POST INJURY?
WHAT HAPPENS IF AN ANIMAL IS CONFINED POST INJURY?

25. BIOMECHANICS Translational (linear) Rotational (rare) Angular
(combined)

26. TWO TYPES OF ACCELERATION APPLICATION
Impulsive loading, now called non-contact loading (whiplash, shaking baby), and Impact loading (skull vs. a hard surface)
In general impact loading produces much higher forces than does impulsive loading.
Significant TBI can result from both!

27. NON-CONTACT (IMPULSIVE) LOADING
No direct impact to the head, head placed in motion by impact directed elsewhere, no skull deformation

28. Shaken Baby
Syndrome

29. PREVENTION
WHAT GOOD IS A HELMET
ANYWAY?

30. HELMETS HELMET PROTECTS WEARER FROM EXTERNAL IMPACTS.
HELMET LINER ABSORBS SOME OF AN INTERNAL IMPACT (BRAIN IMPACTING SKULL)
HELMET KEEPS YOUR HEAD WARMER
IT IS GENERALLY QUIETER INSIDE THE HELMET.
HELMET ITSELF CAN INFLICT INJURY!
THERE IS NO CONCUSSION PROOF HELMET!!

31. CURRENT TESTS ARE ONLY SOMEWHAT REFINED FROM THIS EARLY TEST METHOD

32. FOOTBALL HELMETS TODAY
BASED ON TESTS DESIGNED IN MID 60’S
MUST PROTECT FROM A FORCE THAT WOULD CAUSE A LINEAR SKULL FRACTURE IN A CADAVER HEAD.
ANGULAR ACCELERATION NOT CONSIDERED.
MINIMAL REFINEMENTS SINCE THE 70’S
WEIGHT GIVEN LITTLE CONSIDERATION.
COME IN SIZES SMALL, MEDIUM, LARGE

33. Wt = >5.5 lbs.
Cost =
Comfort/fit pads
Inner liner
Shell

34. MOTOR SPORTS HELMETS TODAY
WEIGHT GIVEN GREAT CONSIDERATION .
MULTIPLE LAYERS AND SPECIAL WEAVES TO CREATE GREATER IMPACT PROTECTION.
VISOR PROTECTION (F-18 WINDSHIELD)
CUSTOM FITTED TO INDIVIDUAL DRIVER

35. Wt = 2.2 lbs.
Cost =

36. CONSIDERATIONS
AT LEAST % OF CONCUSSIONS DO NOT INVOLVE IMPACT AT ALL. NEAR 50% IN RACING
ANGULAR ACCELERATION INCREASES GEOMETRICALLY AS WEIGHT OF A HELMET INCREASES.
FOOTBALL HELMET MUST TOLERATE REPEATED HITS.
RACING HELMET DESIGNED TO WITHSTAND THE “BIG ONE”
LINERS THEREFORE HAVE DIFFERENT REQUIRMENTS.
BRAIN DOES IMPACT INSIDE OF SKULL – SOME AREAS NOT SO FRIENDLY.
SIGNIFICANT SHEARING INJURY OCCURS WITH ANGULAR ACCELERATION FROM BOTH IMPACT AND NON-IMPACT TRAUMA.

37. NEUROPSYCHIATRIC TESTING FOR DIAGNOSIS
ImPACT: Immediate Post-Concussion Assessment and Cognitive Testing
Now used in NFL, Indy Car, Formula 1, NASCAR, NHL, World Cup Soccer, USSA, FISA, and FIFA.
Most extensively tested (Initially over 18,000 subjects)
Available worldwide in 17 languages 24/7

38. KING – DEVICK TEST Task of reading numbers in sequence.
Printed on 3 levels of cards.
Can be administered by anyone with simple training.
Quick and dirty assessment.

39. King-Devick vs. ImPACT (neither includes vestibular function/balance
< 2 minutes minutes
some learning no learning
(neither includes vestibular function/balance
important for return to competition)

40. THERE IS STILL NO AGREEMENT ON THE ROLE OF
COMPUTER OR PENCIL DERIVED NEURO-PSYCHE
TESTING.
HOWEVER; DUE TO THE LACK OF ANYTHING ELSE
NEARLY EVERY MAJOR SPORTING ATHORITY USES
IMPACT BASELINE TESTING AND SUBSEQUENTLY FOR
RETURN TO PLAY DETERMINATIONS. VESTIBULAR FUNCTION ALSO REQUIRES TESTING AND NORMALIZATION.

41. 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, sudden personality change
Emotionally instability, inappropriate behavior
Delayed verbal and motor responses

42. SYMPTAMATOLOGY Headache ( nearly always present > 90%)
Dizziness, vertigo
Lack of awareness
Nausea, vomiting
Loss of balance BESS; Balance Error Scoring System
Feeling dazed, “dinghy”
Ringing in the ears (tinnitus)
Blurred or double vision (diplopia)
Hyperacusis and/or photophobia
“Just not feeling right”

43. BOTTOM LINE
Examiner must have high index of suspicion based on mechanism of injury, helmet damage if any, damage to surrounding area, inside of vehicle, and behavior of the athlete.
Athletes themselves will under report symptoms and out right lie to stay in the event.
We must train coaches, trainers, other players, and families to recognize TBI

44. MANAGEMENT
ANY Symptoms or Signs: NO RETURN TO ANY SPORTS ACTIVITY; whether competition, or training – WHEN IN DOUBT, SIT THEM OUT!
Athlete should be medically evaluated and monitored every 5 min. for symptom/sign resolution or deterioration for at least 1 hr. then with another person to be aware of patient x 24 hours.

45. 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 – 3 – 9x greater risk for long term disability
Retrograde amnesia: 10 x more likely to have a poor outcome – chronic, long term symptoms
Anterograde amnesia: 4.2 x more likely to have a poor outcome – chronic symptoms
L.O.C. not predictive of outcome!!!

46. 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. Don’t improve gradually over period of 2 to 3 weeks.

47. RETURN TO COMPETITION
Level 1. No activity, complete rest until asymptomatic; once asymptomatic proceed to level 2
Level 2. Light aerobic exercise such as walking or stationary cycling with helmet on.
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 first, then competition.
Any re-occurrence of symptoms along the line, athlete must go back to the previous level!!!!

48. WHAT HAVE WE LEARNED Mild TBI can have long term catastrophic effects.
Most, but not all athletes recover quickly.
Age may be important in recovery. Old is bad.
Neuropsychological testing is a useful tool.
Management should involve multiple components.
Total inactivity is bad but, activity too soon is also bad.

49. WHAT WE STILL DON’T KNOW
How many mild TBI’s are too many?
How close together is too close?
When is the brain really back to normal?
Is there effective pharmacotherapy?
(Anti-inflamatories, neuro-protective agents)
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, APOE-
e4; all appear to be risk factors)

50. PREVENTION Stay inside and don’t do anything or
Wear an approved/well fitted helmet in contact
sports.
Head and Neck restraint SYSTEM in 4 wheel vehicles.
Newer devices now available for motorcycles.
Recognize concussion and get out of the game.
No return to activity until asymptomatic and NP test
is back to baseline.
Rule changes in football, hockey.

51. THANK YOU

52. WHAT WE ARE DOING AT THE “U”