Concussion

Overview of a concussion

If you are a fan of sports, medicine, or movies, there’s a good chance you’ve seen the movie Concussion with Will Smith. The movie sheds light on the recent and ongoing battle of player safety and long-term brain health between the NFL and concussion researchers. Will Smith, portraying Dr. Bennett Omalu, uses a woodpecker as a famous example to describe the kinematics within the skull during a concussion.

Woodpeckers, who are designed to bang their heads against a solid surface repeatedly, can run their tongues into their skull and wrap them around their brains. A woodpecker’s brain also occupies most of the skull’s space. These two attributes limit the amount that the brain can move within the skull while pecking.¹ On top of this, a woodpecker’s skull has denser bone in the back, which directs much of the force away from the brain. In turn, a woodpecker can routinely handle 1500 g of force.¹

Humans, on the other hand, have brains that essentially float within the skull in a fluid called cerebrospinal fluid (like shaking a pickle in a jar). This is not a good design to withstand repeated blows to the head. Therefore, mechanical forces are transmitted through the skull and brain during contact. In comparison to Mr. Woodpecker, the acceleration force needed to produce a concussion, by one study, was only 56.1 g.²

Mechanical forces with a concussion

A concussion, despite being called a concussion, is classified as a mild Traumatic Brain Injury or mTBI.³ An mTBI is separated from a more severe injury by several factors. One distinct factor is a lack of physical damage to the brain itself in the form of a brain bleed or an object breaking the skull and piercing the brain. The damage to the brain during a concussion is microscopic.³ 

Therefore, common medical imaging such as an MRI would be negative with a concussion. The damage to the brain is caused purely by the force transmitted through the skull during contact with the head. Two broad categories of force cause a traumatic brain injury – contact force and inertial force.⁴

Contact forces

Contact forces occur when the head is struck by an object (think Angels’ Matt Shoemaker taking a 105-mph line drive off the head) and typically create localized brain damage beneath the contact area. With more significant contact force, the brain can physically shake within the skull. A coup injury occurs when a moving object contacts a stationary head creating a bruise on the brain at the contact site. A contrecoup injury often occurs when a moving head contacts a stationary object, forcing the floating human brain to accelerate-then-decelerate within the skull. This causes the brain to crash into the skull on the opposite side of the contact, bruising the opposite side of the brain.⁵ These bruises (or cerebral contusions) often lead to brain bleeds and are visible on imaging. Due to this, contact forces often create moderate or severe brain injuries (Shoemaker had emergency brain surgery that day).⁴

Inertial forces

Inertial forces, on the other hand, are the acceleration forces transmitted to the brain at the moment of impact and can occur as linear or rotational acceleration.⁴ The brain is one of the softest biological tissues in our body; therefore, it is highly susceptible to rotational acceleration and shearing.⁴ This acceleration creates widespread damage within the brain tissue, shearing and stretching neurons.^3,4 This shearing and neuronal damage sparks the true culprit behind concussions: the biochemical cascade.³

Biochemical Changes

As stated before, damage to the brain during a concussion is microscopic; however, it changes how brain cells function. This is due to chemical imbalances throughout the brain.³ When neuronal disruption occurs during injury, the affected neurons depolarize (or activate). When cells depolarize they release energy in the form of ions. This mass depolarization throughout the brain creates a large ionic imbalance between cells. (Imagine someone bumping into you while seasoning your favorite slice of pizza with red pepper flakes, and you accidentally dump the whole jar on your pizza. The pizza to pepper flake ratio is unacceptable.)

In order to attempt to restore stability, ionic “pumps” that live on nearby neurons begin to exchange ions (you try to pick off the pepper flakes one by one). These ion pumps also require energy to fire; however, this is widespread throughout the brain (your pizza is covered) which creates the age old dilemma of supply and demand (your arm gets tired). This results in neuronal “depression,” which spreads throughout the brain as neurons cannot function properly (your pizza is too spicy, sorry).³

Due to the acceleration force, axons (which are the routes by which neurons communicate) are also stretched and sheared which decreases their ability to send and receive signals. On top of all this, blood flow to the brain is reduced after a concussion and there is an increasing level of inflammation due to all the damaged neurons.² This ionic imbalance can last 7-10 days,³ which is why the general consensus is that most concussion symptoms resolve in 10-14 days.

Anatomy and Symptoms

The widespread damage throughout the brain is why concussion symptoms are so variable. This initial chemical cascade takes place instantaneously. Rapid shearing to neurons and axons and spreading “depression” can cause a loss of consciousness (although loss of consciousness does not mean your concussion is worse). When this spreading depression reaches the brainstem, the brain’s ability to communicate with the body can be momentarily disrupted. The response to this is decorticate or decerebrate posturing: AKA the fencing position (think Jahvid Best’s injury at Cal in 2009).

The axonal damage also creates impaired concentration, memory, and reaction time after the injury.² The ionic imbalance post-injury can create migraines, light sensitivity, and noise sensitivity. The inflammation within the brain and brainstem disrupts the communication between groups of neurons, which can create dizziness, lightheadedness, or visual changes. Finally, the prolonged energy crisis creates an increased susceptibility to another concussion as the brain is less able to respond to trauma.² Subjecting neurons to repeated concussions or to repeated sub-concussive forces can alter cell proteins or cell organization altogether. This is what leads to long-term deficits, brain atrophy (a reduction in brain size), and what we have come to know as CTE (chronic traumatic encephalopathy).²

New research is emerging that concussions can create long-term deficits that increase a player’s risk for injury.^6-9 Due to the changes in cell function, individuals with a concussion history are at an increased risk of a subsequent concussion.⁶ On top of this, athletes are at a significantly increased risk of a significant lower extremity injury (i.e., ACL tear, high-ankle sprain) after a concussion.^6,7

The brain regulates and fine tunes movement in real-time by comparing what the body sees and feels to what the brain has ordered the body to actually do. To accomplish this, the brain must quickly process and respond to all this incoming information. When the communication between neurons is disrupted, this task cannot be executed as quickly or accurately. The functional result is muscular control and joint stability when an athlete attempts to make a quick plant, cut, or change direction. This is especially difficult for the brain when paired with multiple tasks (like catching a pass or reading a block). The end result is an increased risk of injury.⁸ These deficits can also last years after the injury.⁹

Concussion Rehabilitation, Recovery, and NFL Guidelines

Unaffiliated Neurotrauma Consultant

At each NFL game, an unaffiliated neurotrauma consultant (UNC) is approved by the NFL’s Chief Medical Officer and assigned to cover each club on the sideline.¹⁰ The UNC, alongside an athletic trainer “spotter” in the booth, observes each play and the sideline to determine if a player has any sign or symptom of a concussion or participated in a play that could result in a concussion. If so, that player is removed immediately from the field.

Concussion Diagnosis

A sideline examination must be performed in full, which includes a review of “No-Go Symptoms” (symptoms that, if present, immediately disqualifies a player from returning), a review of the play, a review of all concussion symptoms, a cervical spine (neck) assessment, and observation of the player’s speech, gait, and eye movements. The UNC or club medical personnel must perform the assessment. A formal Locker Room Comprehensive Concussion Assessment must also be performed, documented, and compared to baseline data. A concussion diagnosis is given by a UNC or club physician, and the information is then relayed to the NFL’s Chief Medical Officer and the NFLPA’s Medical Director. The “Madden Rule” then takes effect, where the player is removed from the field and continuously monitored in the locker room until the game’s conclusion. The player then enters the NFL’s return-to-participation protocol, and subsequent evaluations are performed regularly.¹⁰

Concussion Rehabilitation

Research supports that graded activity and specifically targeted exercise, not rest, can significantly reduce recovery time after a concussion.^11-13 All return-to-play protocols involve a step-wise progression back to activity that is guided and/or limited by symptoms. The NFL’s policy is five stages: Phase 1 – Symptom Limited Light Physical/Cognitive Activity (normal daily tasks, stretching, light cardio), Phase 2 – Aerobic Exercise (upright bike, treadmill, dynamic stretching), Phase 3 – Football Specific Exercise (exercise that mimics sport specific activities, weight lifting), Phase 4 – Non-Contact Training Drills, Phase 5 – Full Activity/Clearance.¹³

It is important to note that a player progresses to each stage once they are able to participate in a stage without symptoms. This typically occurs on a day-to-day basis but is not dependent upon a 24-hour period. Also, a player is not able to progress to stage 5 until neurocognitive testing (working memory, divided attention, reaction time, concentration) are all back to normal baselines, which are taken before each season.

Phase	Example Activity	Goal
1 – Light Activity	Routine daily activities as tolerated. Can include static or dynamic stretching, and light aerobic exercise without symptom exacerbation.	Recovery
2 – Aerobic Exercise	10-20 minutes on a stationary bike or treadmill with light to moderate intensity, supervised by the team medical staff. Duration and intensity of the aerobic exercise can be gradually increased over time if no symptoms or signs return during or after the exercise.	Progressive cardiovascular tolerance to progress recovery and assess for recurrent symptoms.
3 – Sport-Related Exercise	Increased duration and intensity of aerobic. Introduction of anaerobic exercise (sprinting, jumping) and introduction of non-contact sport specific drills (cone drills). Introduction of strength training supervised by medical staff.	Progressed cardiovascular intensity, introduction of weights, and increased variability of movement to assess for recurrent symptoms.
4 – Non-Contact Team Drills	All non-contact drills for the duration of practice.	Acclimation to all football demands except contact. Addition of cognitive aspect of position. Assess for recurrent symptoms.
5 – Full Clearance	Return-to-participation	Assess for tolerance of all football duties including contact without symptoms.

Concussions and recovery trajectories can vary greatly from athlete to athlete. Patrick Mahomes flew through the NFL protocol after suffering a concussion against the Browns in the 2021 AFC Divisional Round, playing (and playing well) the following week in the AFC Championship. On the other hand, the average NFL player returns to play in 19 days (according to data from the 2012-2015 seasons). New research is demonstrating that younger athletes do not fully recover until 28 days. However, the NFL’s policy and active return-to-pay guidelines do expedite player recovery.

Concussion Risk Factors

Nonetheless, certain risk factors predispose individuals to a longer recovery.^14-15 Most notably for NFL players, a history of previous concussions can significantly increase recovery time. Not only this, but players with a concussion history are more susceptible to another concussion, and multiple concussions can lead to the development of prolonged symptoms. These symptoms can make return-to-play more difficult and make NFL medical personnel take a much more conservative approach when progressing a player through a protocol.

The New NFL Guardian Cap

To try and reduce the prevalence of concussions, as well as repetitive sub-concussion forces, the NFL has recently implemented the use of Guardian Caps throughout the league. The exterior helmet padding, or “Bobble Heads,” as JJ Watt calls them, has led to mixed reviews. Different research studies have been performed on their potential benefit, with some trials citing reduced concussion rates, but objective studies also have mixed results.

Some studies find that there is a significant reduction in acceleration force, but this is dependent upon the contact occurring at certain locations on the helmet and at a higher velocity, which is not predictable in-game.¹⁶  Some data suggests that the added weight of the cap increases the force to the head and neck in certain contact conditions,¹⁷ and there is worry that the increased weight will drive players to duck or lead with their head while tackling. It will be interesting to see how the Guardian Cap affects the overall rate of concussions or if the changes in force transmission can affect concussion recovery. However, the NFL is being proactive in player safety and brain health and has developed concrete and productive guidelines and protocols with what is available with current research.

References

1. Gibson, LJ. Woodpecker pecking: how woodpeckers avoid brain injury. J of Zoo. 2006;270(3):462-465
2. Viono DC. Head Impact Biomechanics in Sport. In: Gilchrist, M.D. (eds) IUTAM Symposium on Impact Biomechanics: From Fundamental Insights to Applications. Solid Mechanics and Its Applications. 2005(124):121-130
3. Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014;75 Suppl 4(4):S24-S33.
4. Meaney DF, Smith DH. The biomechanics of concussion. Clin Sport Med. 2011;30(1):P19-31
5. Payne WN, Orlando J, Payne AN. Contrecoup brain injury. Statpearls. 2022. Last updated May, 22, 2022.
6. Reneker JC, Babl R, Flowers MM. History of concussion and risk of subsequent injury in athletes and service members: A systematic review and meta-analysis. Musculoskelet Sci Pract. 2019;42:173-185. doi:10.1016/j.msksp.2019.04.004
7. Lynall RC, Mauntel TC, Padua DA, Mihalik JP. Acute Lower Extremity Injury Rates Increase after Concussion in College Athletes. Med Sci Sports Exerc. 2015;47(12):2487-2492. doi:10.1249/MSS.0000000000000716
8. Lapointe AP, Nolasco LA, Sosnowski A, et al. Kinematic differences during a jump cut maneuver between individuals with and without a concussion history. Int J Psychophysiol. 2018;132(Pt A):93-98. doi:10.1016/j.ijpsycho.2017.08.003
9. Schmidt JD, Terry DP, Ko J, Newell KM, Miller LS. Balance Regularity Among Former High School Football Players With or Without a History of Concussion. J Athl Train. 2018;53(2):109-114. doi:10.4085/1062-6050-326-16
10. https://www.nfl.com/playerhealthandsafety/resources/fact-sheets/nfl-head-neck-and-spine-committee-s-concussion-diagnosis-and-management-protocolQuatman-Yates CC, Hunter-Giordano A, Shimamura KK, et al. Physical Therapy Evaluation and Treatment After Concussion/Mild Traumatic Brain Injury. J Orthop Sports Phys Ther. 2020;50(4):CPG1-CPG73. doi:10.2519/jospt.2020.0301
11. Quatman-Yates CC, Hunter-Giordano A, Shimamura KK, et al. Physical Therapy Evaluation and Treatment After Concussion/Mild Traumatic Brain Injury. J Orthop Sports Phys Ther. 2020;50(4):CPG1-CPG73. doi:10.2519/jospt.2020.0301
12. Leddy JJ, Master CL, Mannix R, et al. Early targeted heart rate aerobic exercise versus placebo stretching for sport-related concussion in adolescents: a randomised controlled trial. Lancet Child Adolesc Health. 2021;5(11):792-799. doi:10.1016/S2352-4642(21)00267-4
13. Buckley TA, Munkasy BA, Clouse BP. Acute Cognitive and Physical Rest May Not Improve Concussion Recovery Time. J Head Trauma Rehabil. 2016;31(4):233-241. doi:10.1097/HTR.0000000000000165
14. Kontos AP, Elbin RJ, Sufrinko A, Marchetti G, Holland CL, Collins MW. Recovery Following Sport-Related Concussion: Integrating Pre- and Postinjury Factors Into Multidisciplinary Care. J Head Trauma Rehabil. 2019;34(6):394-401. doi:10.1097/HTR.0000000000000536
15. Lau BC, Kontos AP, Collins MW, Mucha A, Lovell MR. Which on-field signs/symptoms predict protracted recovery from sport-related concussion among high school football players?. Am J Sports Med. 2011;39(11):2311-2318. doi:10.1177/0363546511410655
16. Breedlove KM, Breedlove E, Nauman E, Bowman TG, Lininger R. The Ability of an Aftermarket Helmet Add-On Device to Reduce Impact-Force Accelerations During Drop Tests. J Athl Train. 2017;52(9):802–808. doi: https://doi.org/10.4085/1062-6050-52.6.01
17. Bailey AM, Funk JR, Crandall JR, et al. Laboratory Evaluation of Shell Add-On Products for American Football Helmets for Professional Linemen. Ann Biomed Eng. 2021;49:2742-2759. doi: https://doi.org/10.1007/s10439-021-02842-8