DRSteve OlveyFIA 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 UnitUniversity of Miami/Miller School of MedicineFellow FIA Institute for Motor Sports Safety

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

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.

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

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…

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

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

How much rest before how much activity?

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

BIOMECHANICS

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)

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.

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

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”

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.

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.

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)

WHY USE NEUROPSYCH TESTING

Athletes with a mild TBI will often deny symptoms

Athletes may lack awareness of symptoms

Testing provides unique informationTrusting an athlete’s self-assessment

is very dangerous!Eliminates bias, favoritism, and

revenge

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

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

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!!!

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.

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!!!!

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)

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

22

Effect of Transfer Function Correction: Case 1

-500

50100150200250300350400450

-0.001 0.000 0.001 0.002 0.003 0.004 0.005 0.006 0.007Re

sulta

nt (G

)Time (Sec)

Test 1_2Lf Ear Lf Ear 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.

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