Concussion: its recognition and management

Report
DR
Steve Olvey
FIA Institute Fellow - USA
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
WHY THIS IS A HOT TOPIC?
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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
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.
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WHAT IS A CONCUSSION?
OLD DEFINITION
“A reversible injury to the brain due to
traumatic forces, resulting in amnesia
and/or loss of consciousness.”
NEW DEFINITION
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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.
PATHOPHYSIOLOGY
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…
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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
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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.
WHAT HAPPENS IF CONCUSSED ANIMAL IS CONFINED POST INJURY?
WHAT HAPPENS IF AN ANIMAL IS CONFINED POST INJURY?
THE DICOTOMY OF RETURN TO
COMPETITION
THERAPEUTIC DELIMMA
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How much rest before how much activity?
PATHOPHYSIOLOGY SUMMARIZED
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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!
BIOMECHANICS
THE TWO TYPES OF ACCELERATION
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Translational acceleration- Total applied force
passes through the center of gravity of the head
(walking into a flag pole, hitting steering wheel
head on)
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Angular acceleration- Force generates motion
around an axis (Whiplash, or left hook in
boxing)
TWO TYPES OF ACCELERATION
APPLICATION
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Impulsive loading (whiplash, shaking baby, most open wheel crashes) and Impact
loading (skull vs. a rigid surface as happens in rally cars, stock cars)
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Impact loading in general produces much higher forces than does impulsive loading.
Mild TBI may result from both.
DIAGNOSIS
Physical Signs of Mild TBI
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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
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”
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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.
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MANAGEMENT
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ANY Symptoms or Signs: NO RETURN TO
ANY SPORTS ACTIVITY; whether
competition, or training
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Driver or athlete should be medically
evaluated and monitored every 5 min. for
symptom/sign resolution or deterioration
for at least 1 hr.
WHEN IN DOUBT, SIT THEM
OUT!
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)
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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
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ImPACT ADVANTAGES
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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
HOW TO USE ImPACT
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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
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!!!
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WHEN DO WE NEED CT/MRI?
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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.
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!!!!
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WHAT WE STILL DON’T KNOW
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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)
WHAT HAVE WE LEARNED
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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
Effect of Transfer Function
Correction: Case 1
Test 1_2
Resultant (G)
Lf Ear
Lf Ear Ref
Computed Lf Ear Ref
450
400
350
300
250
200
150
100
50
0
-50
-0.001
0.000
0.001
0.002
0.003
0.004
0.005
0.006
0.007
Time (Sec)
• CT scan of Specimen 1
(EShock1) showing position of
each ear mounted sensor.
• From C. Bass and R. Salzar,
Final Report 2008.
22
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
THE END

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