Friday, August 15, 2014

Discussing Helmets and Concussions

Over the past few months, I've written several articles on concussions including their impact in the NHLin soccer, along with specific case studiesdiscussing current research and new methods, and how head injuries should be managed

A topic I'd like to discuss has come up in the media a lot over the past few weeks; new helmets that are meant to stop or limit concussions and claiming to do so. 


There is general agreement among the medical community that concussion incidence can be reduced through rule changes in play, changes in concussion protocol and procedures, and teaching proper hitting and tackling techniques. However, there remains debate as to whether the design of helmets can also help reduce the incidence of concussions. 


This is an issue that Deadspin covered very well when the NFL announced a $60 million partnership with GE and Under Armour to "tackle concussion-safety science," of which $10 million would be dedicated to developing "improved helmet technology." When you consider the NFL only spent $60 million (or 0.6% of the NFL's annual revenue) over a 5-year partnership, it's extremely disappointing, especially when 1/6 of the money will go to something [helmets] that may not help reduce concussions at all. It comes into question how much the NFL really cares about the long-term safety and health of it's current players. 


The issue regarding helmets arose again (and was once again covered by Deadspin well) when researchers at Virginia Tech released that they would be looking to rate and design new hockey helmets to reduce concussion risk


To understand why improving helmets wouldn't help reduce concussion risk, it's important to understand the mechanism behind the injury:


UNDERSTANDING CONCUSSIONS - HOW ARE THEY CAUSED?


Also know as a mild traumatic brain injury (mTBI), the concussion is the most common type of traumatic brain injury. Concussion experts have been working together to develop consensus-based principles to establish a consensus definition of what occurs during a mTBI, what a diagnosis entails, and encourage correct return to play (RTP) decisions. The Concussion in Sport Group defined a concussion as:

Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include:  
  1. Concussion may be caused either by a direct blow to the head, face, beck or elsewhere on the body with an "impulsive" force transmitted to the head.
  2. Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously. However, in some cases, symptoms and signs may evolve over a number of minutes to hours.
  3. Concussion may result in neuropathological changes but the acute clinical symptoms  largely reflect a functional disturbance rather than a structural injury and, as such, no abnormality is seen on standard structural neuroimaging studies.
  4. Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. However, it is important to note that in some cases symptoms may be prolonged.  
In essence, the panel wanted to define concussion as an injury to the brain which creates a temporary loss in normal functioning. This injury is created by a force and may result in a variety of physical, cognitive and emotional symptoms which differ on a case-by-case basis.  

Something I'd like to highlight in this definition (which was put together at the 4th International Conference on Concussion in Sport and included 39 concussion experts) is that concussion isn't just a basic injury, it's a process. This is extremely important especially when recognizing that the onset of symptoms may occurs up to 24 hours after the original hit or injury and they may progress over time. Additionally, the panel agrees that contact with other parts of the body may result in a concussion, you do not need to be hit directly on the head. 


This is something that was highlighted by neurologists and concussion experts at Weill Cornell Medical College as well. In an article following the World Cup, Dr. Barry Kosofsky, a pediatric neurologist and concussion expert described the injury process with a nice metaphor: 

"The brain can be thought of as resembling a piece of broccoli, with the stalk (brain stem) at the base and the flower (cortex) on top. When someone experiences rotational torque resulting from a concussion, it is similar to stretching the part of the broccoli where the stalk meets the flower. The stalk is held in place but the brain is free to move, due to acceleration or de-acceleration. Concussions are not just due to direct hits, but also the stretching of these fibers due to torque."
The article continues with:
While impact and torque cause the initial injury, the physical symptoms of a concussion occur from the resulting neurometabolic cascade in the brain. This cascade causes cellular damage that inhibits neurons' ability to communicate with each other. The result is often impaired cognitive function and the mental fog experienced by athletes after a head injury. 
PREVENTING CONCUSSIONS - WHAT'S THE DEAL WITH HELMETS?

Helmets are designed to prevent and reduce skull fractures. Their basic design is one that is meant to lessen the blow by spreading the force of impact over a greater surface area. Helmets are designed to attenuate high-impact linear acceleration forces (front-to-back) but do not consider rotational acceleration, despite the strong evidence linking it to injury. 

Is it possible to design a helmet that could limit this? No, probably not. Your brain floats in the skull and is cushioned by a thin layer of cerebrospinal fluid. When the brain accelerations or deaccelerates due to a force (be it a hit to the head or neck) the brain can come crashing into the skull or suffer rotational damage. How could an outer shell limit this? The key in preventing concussions is not how hard the head is struck, but how the brain moves inside the skull due to impact. 

As the present moment, a concussion is a clinical diagnosis based largely on the observed injury mechanism and symptoms. While this is mostly due to the debated nature of the onset of injury, most of the public believe a concussion will only occur after a huge hit. In reality, it's important that team trainers, coaches and physicians be vigilant of players receiving a large amount of smaller hits or getting into contact and receiving multiple hits in a short period of time. A recent study evaluated the relationship between the force of impact and clinical outcome, finding that magnitude of impact did not correlate with clinical injury (Guskiewicz et al.). The study showed that despite the fact that the impact magnitude of the hits sustained by concussed athletes ranged from 60.5 to 168.7 g, no significant relationships between those impacts and symptom severity/neurocognitive functioning were found. Also, several players sustained hits at that impact threshold and were not diagnosed with concussions. 

Bringing it back to helmets, once again, I'll refer to the Conference panel:
There is no good clinical evidence that currently available protective equipment will prevent concussion, although mouth-guards have a definite role in preventing dental and orofacial injury. Biomechanical studies have shown a reduction in impact forces to the brain with the use of head gear and helmets, but these findings have not been translated to show a reduction in concussion incidence. 
This is echoed in a 2013 report on youth sports-related concussion by the Institute of Medicine and National Research Council which stated "There is limited evidence that current helmet designs reduce the risk of sports-related concussion."

A study done by the Cleveland Clinic compared newer NFL "concussion reduction technology" helmets along with other NFL-approved helmets with vintage "leatherhead" helmets used in the 1940s. Researchers wanted to know how the newer helmets compared in impact testing (which they of course excelled) but also in rotational acceleration. The study found that "in many instances the head impact doses and head-injury risks while wearing vintage leatherheads were comparable to or better than htose while wearing widely used 21st-century helmets." None of the helmets were protecting what causes a concussion, the brain moving inside the skull. 

Micky Collins, director of the UPMC Sports Medicine Concussion Program, went on to comment that "there's no helmet out there that will ever prevent a concussion from happening. The main focus should be treating athletes as soon as the symptoms appear."

Even Dr. Henry Feur, member of the NFL's Head, Neck and Spine Committee echoed these statements saying “It’s always some new material. We’ve heard it for years. Reducing the G-forces in a collision may help with concussions, but it has yet to be proven. The problem is that the brain is encased in fluid, and in cases of rotational force, there is little you can do to stop the brain from crashing against the skull.” 

CONCLUSION

There's a multitude of studies published about concussions, helmets, mechanism of injury and rates of sports-related concussion. I won't list them all here as most of them all agree that incidence of concussion is similar regardless of the helmet brand or what the helmet is selling. 


Some studies may state that use of sport-specific helmets have been found to reduce head injuries such as concussions. However, these case studies have a hard time eliminating confounding factors such as: 

  • Risk-avoidant behavior leading to less injury rather than the helmet itself
  • Concussions that aren't diagnosed 
  • The use of protective equipment adversely affecting player behavior, encouraging risky hits.

The problem is, parents and players are eating up the marketing for these "Five-Star" and "Concussion-reducing technology" helmets. Sales for five-star football helmets which run upwards of $250 have soared in the last year, while older helmets have plunged. This is about money right now. 

The research being done at Virginia Tech and other institutions is not a bad thing. If they can somehow find a way to decrease rotational acceleration inside the skull via an outer-shell, it would be ground-breaking. It is, however, extremely unlikely. 

SOURCES

Bartsch A, Benzel E, Miele V and Prakash V. Impact test comparisons of 20th and 21st century American Football Helmets. J Neurosurg 116:222-233, 2012. Published online November 4, 2011; DOI:10.3171/2011.9.JNS111059.

McCrory P, et al. Br J Sports Med 2013;47:250-258.

McCrory P, et al. Br J Sports Med 2013;47:268-271.

Guskiewicz KM, Mihalik JP, Shankar V, et al. Measurement of head impacts in collegiate football players: relationship between head impact biomechanics and acute clinical outcome after concussion. Neurosurgery 2007;61:1244–52. 


Institute of Medicine and National Research Council. Sports-Related Concussions in Youth: Improving the Science, Changing the Culture. Washington, DC: The National Academies Press, 2014.

Monday, July 28, 2014

A Primer on Concussions in Soccer : The Negligence of FIFA Regarding Head Injuries

In this article I'll examine briefly what a concussion is, the prevalence of concussion in the sport of soccer, and also discuss three incidents of head injury that occurred during this past FIFA World Cup.

WHAT IS A CONCUSSION

Mild traumatic brain injury (mTBI), or concussion, is the most common type of traumatic brain injury/ While typically not too serious in most cases, concussion has a serious risk of short and long-term sequelae. At the 4th International Conference on Concussion in Sport (Zurich, November 2012), a panel discussion took place to obtain a consensus-based definition of a concussion. The Concussion in Sport Group (CISG) defined a concussion as follows:
Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include:
In essence, a concussion is a head injury with a temporary loss of brain function that may result in a variety of physical, cognitive, and emotional symptoms. Presently, concussion is a clinical diagnosis based largely on the observed injury mechanism (point of contact, force on head area, etc.), signs, and symptoms. The first step towards a diagnosis of a concussion is actual recognition of the injury.

The hallmark signs and symptoms of acute sports concussion include (but are not limited to):
  • Loss of consciousness (LOC) 
    • However, the majority of concussions in sports occur without a LOC
  • Problems with attentional mechanisms 
    • Manifested as (but not limited to): slowness to answer questions and follow directions, easily distracted, poor concentration, vacant stare/glassy eyed.
  • Memory disturbance
  • Balance disturbance 
These symptoms may be apparent immediately after the head injury or other signs and symptoms of a concussion may evolve and appear gradually over several minutes. Additionally, over the course of the first 24 hours following a concussion injury, other signs and symptoms may manifest. However, it's important to note that there is a large range of these symptoms and they often vary, not all of these symptoms are seen in every case of sports concussion. The most common symptoms reported in concussion literature include:
  • Somatic symptoms such as headache
  • Cognitive symptoms such as feeling like in a fog
  • Emotional symptoms such as lability
  • Physical symptoms such as LOC and amnesia
  • Behavior changes such as irritability
  • Cognitive impairment
  • Sleep disturbance (insomnia)
  • Dizziness and balance problems
  • Blurred vision
  • Fatigue
If any one or more of these symptoms is recognized, a concussion should be suspected and a management plan should be implemented.

I'd like to focus on amnesia because it will come into play later. Amnesia is a common physical symptom associated with mTBI. Amnesia almost always involves loss of memory for the traumatic event but frequently includes loss of recall for events immediately before (retrograde amnesia) and after (anterograde amnesia) the traumatic event.

Since concussions are often hard to recognize and to diagnose, the Zurich Consensus on Concussion in Sport proposed diagnostic criteria for sideline evaluation. An athlete shows any of the following, they need to be removed from play and assessed.
  • Initial obvious physical signs consistent with concussion (LOC, balance problems)
  • Teammates, trainers, coaches observe cognitive or behavior changes in functioning consistent with concussion symptoms reported
  • Any concussion symptoms reported by the athlete injured
  • Abnormal neurocognitive or balance examination
Following a removal from play:
  • Physician evaluated the player using standard emergency management principles, most notably to exclude  severe head trauma or cervical spine injury
  • Once first aid issues are addressed, assessment of the concussive injury should be made using the SCAT3 or other sideline assessment tools (NHL uses ImPACT concussion testing, read here: http://www.impacttest.com/about/)
  • The player should not be left alone following the injury and serial monitoring for deterioration is essential over the initial few hours following injury
  • A player with diagnosed concussion should not be allowed to return to play on the same day. 
    • It has been unanimously agreed that an athlete should not return to play on the same day of the injury. Studies have shown that athletes allowed back into play following a concussion may demonstrate neuropsychological deficits post injury. 
CONCUSSION MANAGEMENT AND RECOVERY

The graduated return to play protocol following a concussion is a stepwise process and is outline below: 

In this stepwise progression, an athlete only proceeds to the next level if they are asymptomatic at the current level. Each step should take at least 24 hours, making the minimum amount of time to proceed through the full rehabilitation protocol one full week. Athletes should never return to play on the same day as an injury.

CONCUSSIONS IN THE SPORT OF SOCCER

Most people associate concussions with violent/physical sports, specifically American football, hockey and boxing. Of all sports played in the United States, football is the sport associated with the greatest number of traumatic brain injuries, but it also has the largest number of participants.

In the US, soccer is a sport growing in popularity. Between 1982 ad 2008, approximately 7.2 million men and 5.2 million women played soccer at the high school level and an additional 430,000 men and 322,000 women at the college level (Cantu and Mueller).

Recently, a study (Rosenthal et al) was published which analyzed data from High School Reporting Information Online (HS RIO), a national high school sports injury surveillance system. In this system, high schools across the nation with at least 1 certified athletic trainer were invited to participate. The trainers would log into the system and report injuries and athlete-exposures (AE) which was defined as 1 athlete participating in 1 competition or practice. The study used a sample of 100 schools for participation in the concussion rate study and focused on 9 sports: baseball, boys and girls basketball, football, boys and girls soccer, wrestling, softball and girls volleyball. These sports were chosen because data was available from 2005-2006 through 2011-2012.

The study reported the following rates:

"The HS RIO data showed a significant increase in overall concussion rate in the 7-year period of the study. The rates significantly increased in 5 of the 9 sports studied and showed increasing trends in the others. As can be seen from our results, the majority of the rate increase for all sports was observed after the 2008-2009 academic year."
The graphs from the study shown below show total concussion rates for girls and boys sports from 2005-2006 through 2001-2012:


As you can see, the rate of concussions has increased in both boys and girls soccer. However, girls sustain a higher rate of concussions.


Another study (Gessel et al) also used the HSRIO data to survey the injury and drive targeted injury-prevention projects.  The researchers determined that the risk factors for concussion in soccer differed significantly by sex. Concussions in soccer players most frequently occur as a result of head to head collisions in the act of heading the ball; 40.5% of the time in males and 36.7% in females. Girls soccer players sustain a greater proportion of concussions related to contact to the ground (22% compared to 6%) and contact with the ball (18.3% compared to 8.2%). Another risk factor for concussions in soccer is playing the position of keeper, with 21.7% of injuries to goalkeepers being concussions, compared with 11.1% of injuries to other positions.


Up to 50% of players admit to bending the truth about their symptoms to get back into action more quickly. It's imperative to teach them that a brain injury is not like any others, it could be irreversible. You can cause serious damage by not being honest about your symptoms and condition and by returning to play with a brain injury.

There are three incidents that occurred to three separate players and national teams during the FIFA World Cup that I'd like to discuss.

Thursday, July 3, 2014

Progress and Significance of Current Concussion Research - Developing a Blood Biomarker for Brain Injury

If you read my post on Concussions in the NHL, you'll know that a concussion is considered to be among the most complex injuries to diagnose in sports medicine. A concussion is a clinical diagnosis based largely on the observed injury mechanism (point of contact, force on head area, etc.), signs, and symptoms. Due to the fact that there is no true [perfect] diagnostic test for a concussion, physicians must rely on patient-reported symptoms and neurological testing to make a diagnosis. Additionally, unlike other neurological injuries, most concussions cannot be identified by advanced neuroimaging techniques such as CT scans or MRIs.

In this post I'll highlight some current research on concussion.

WHAT WE KNOW

Concussion is still an injury that is largely debated. Most debate surrounds the long-term effects of the injury. What isn't debated is that a player suffering from a concussion should never return to play (RTP) the same day as the injury and should take a minimum of a few days off to recover and rest. Concussion in athletes practicing contact sports is a growing problem worldwide and new research has highlighted some important facts about the injury:

  • The underlying pathophysiology of a concussion is an acute disturbance of neuronal function combined with damage to neuronal and glial (neuronal support) cells. This acute disturbance may eventually present chronic consequences (Blennow et al.). 
  • Most concussions resolve after 7 days or within a couple weeks; however studies have revealed that 10-15% of concussions remain symptomatic more than a year after the injury. The chronic and sometimes even progressive symptoms of concussion have been linked to repeated injury occurring before the brain has properly recovered (Baugh et al.).
  • Cerebrospinal fluid (CSF) can show biochemical changes in the central nervous system (CNS). CSF biomarkers such as total tau (T-tau) and neurofilament light (NFL), show elevated levels of axonal damage after acute damage to the brain (Hesse et al. and Nylen et al.) 
    • The levels of these biomarkers correlate with the severity of the brain damage and eventually return to normal after a period of rest (Zetterberg et al. Neselius et al.).
    • CSF is obtained via a lumbar puncture, a sometimes painful procedure that is invasive and not optimal for routine testing.
A simple biomarker for concussion which can be used routinely and accurately as a diagnostic tool would be extremely useful for team physicians. This test could not only help diagnose a concussion, but also be useful in follow-up for concussed athletes and aid RTP decisions.

A recent study published in the JAMA Neurology Journal had the objective of "determining if sports-related concussion is associated with elevated levels of blood biochemical markers of injury..." The researchers collaborated with the Swedish Hockey League to conduct the research. 

THE STUDY

DESIGN
In the study Blood Biomarkers for Brain Injury in Concussed Professional Ice Hockey Players, Dr. Pashtun Shahim et al. researched an objective biomarker to help in clinical decisions regarding concussion. The study examined three biomarkers to determine their significance: 
  • Neuron-specific enolase (NSE) - a biomarker for neuronal injury (elevated levels found in boxers that had been repeatedly hit in the head (Zetterberg et al).
  • S-100B - a glial cell biomarker named S-100 calcium-binding protein B, elevated levels found in boxers who took head shots compared with boxers who only took body shots (Graham et al.).
  • Plasma T-tau - elevated levels found in Olympic boxers, which then normalized after rest (Neselius et al.).
The research was approved by the Swedish Ice Hockey Association and ran through the University of Gothenburg. With player's consents, team physicians of all 12 teams in the Swedish Hockey League would collect pre-season data, asking all players to take the Standardized Assessment of Concussion. Two of the consenting teams, Frölunda and Lülea, collected baseline blood samples from all their players prior to the start of the season. 

The study asked physicians to document signs and symptoms of concussion as well as any other examination findings when making their diagnosis. For players who suffered a concussion during the season, blood samples were collected at 1, 12, 36, 48, and 144 hours post-injury (or when the player returned to full-contact). 

RESULTS
Of the 288 players in the SHL, 35 had a sports-related concussion for the duration of the study. 28 of these players' samples were used in data analysis, as the remaining 7 players either withdrew consent or had an uncertain diagnosis. Of these 28 concussions,
  • Three (10.7%) suffered a loss of consciousness (LOC)
  • 25 (89%) experienced symptoms such as headaches, confusion, dizziness, or nausea. 
  • 15 (53.5%) had symptoms lasting longer than 6 days.
T-tau levels were significantly higher in post-concussion samples compared with the pre-season samples. Unfortunately, the S-100B and NSE post-concussion samples were not significantly different from the pre-season samples. However, the samples collected immediately after injury (1 hour) showed elevated levels of both T-tau and S-100B when compared with the pre-season samples. The levels of these two biomarkers peaked at this timepoint (1 hour post-concussion). The levels of T-tau 144 hours after injury remained significantly elevated when compared to baseline samples; however, this did not occur in S-100B and NSE samples.

Assessing the severity of a concussion is important in the management of the injury and determination of when to RTP. The level of T-tau was not significantly different post-concussion for different grades of concussion; however, players whose concussions had symptoms for > 10 days or experienced a LOC had some higher levels. The levels of S-100B 1 hour post-concussion were significantly higher in players that experienced a LOC and those players that had symptoms for > 10 days when compared to players whose symptoms resolved in 6 days.


CONCLUSION
The T-tau biomarker displayed a significant diagnostic accuracy level, where T-tau concentrations at 1 hour post-concussion could accurately predict the number of days it took for concussion symptoms to resolve and the players to experience a safe RTP. Plasma T-tau, while highly specific to the Central Nervous System (CNS), is a promising biomarker which can be used in the diagnosis of a concussion and RTP decisions.

The NHL and NHLPA should consider participating in more studies with researchers. The wealth of information that could be learned from just basic investigation on a few blood samples is highly valuable and could not only aid current players experiencing concussion but also help determine the NHL's future plan for limiting injury.


Sources:


  1. Baugh CM, Stamm JM, Riley DO, et al. Chronic traumatic encephalopathy; neurodegeneration following repetitive concussive and subconcussive brain trauma. Brain imaging Behav. 2012;6(2): 244-254. 
  2. Blennow K, Hardy J, Zetterberg H. The neuropathology and neurobiology of traumatic brain injury. Neuron. 2012;6(5);886-899. 
  3. Hesse C, Rosengren L, Vanmechelen E, et al. Cerebrospinal fluid markers for Alzheimer's disease evaluated after acute ischemic stroke. J Alzheimers Dis. 2000;2(3-4): 199-206. 
  4. Nylen K, Csajbok LZ, Ost M, et al. CSF-neurofilament correlates with outcome after aneurysmal subarachnoid hemorrhage. Neurosci Lett. 2006; 404(1-2); 132-136. 
  5. Zetterberg H, Hietala MA, Jonsson M, et al. Neurochemical aftermath of amateur boxing. Arch Neurol. 2006;63(9): 1277-1280. 
  6. Neselius S, BRisby H, Theodorsson A, Blennow K, Zetterberg H, Marcusson K. CSF-biomarkers in Olympic boxing; diagnosis and effects of repetitive head trauma. PLoS One. 2012;7(4):e33606. 
  7. Zetterberg H, Tanriverdi F, Unluhizarci K, Selcuklu A, Kelestimur F, Blennow K. Sustained release of neuron-specific enolase to serum in amateur boxers. Brain Inj. 2009:23(9): 723-726. 
  8. Graham MR, Myers T, Evans P, et al. Direct hits to the head during amateur boxing is associated with a rise in serum biomarkers for brain injury. Int J Immunopathal Pharmacol. 2011;24(1): 119-125. 
  9. Neselius S, Zetterberg H, Blennow K, et al. Olympic boxing is associated with elevated levels of the neuronal protein tau in plasma. Brain Inj. 2013;27(4): 425-433.

Saturday, April 19, 2014

Reviewing the David Backes injury, diagnosing a concussion

WHAT IS A CONCUSSION? 

Also known as a mild traumatic brain injury, the concussion is the most common type of traumatic brain injury. At the 4th International Conference on Concussion in Sport (Zurich, November 2012), a panel discussion took place to obtain a consensus-based definition of a concussion. The Concussion in Sport Group (CISG) defined a concussion as follows:
Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include:
In essence, a concussion is a head injury with a temporary loss of brain function that may result in a variety of physical, cognitive, and emotional symptoms.

Right now, a concussion is a clinical diagnosis based largely on the observed injury mechanism (point of contact, force on head area, etc.), signs, and symptoms. The first step towards a diagnosis of a concussion is actual recognition of the injury.

The hallmark signs of acute sports concussion include:
  • Loss of consciousness (LOC)
  • Problems with attentional mechanisms
    • Manifested as (but not limited to): slowness to answer questions and follow directions, easily distracted, poor concentration, vacant stare/glassy eyed. 
  • Memory disturbance
  • Balance disturbance
Over the course of the first 24 hours following a concussion injury, other signs and symptoms may manifest. However, it's important to note that there is a large range of these symptoms and they often vary, not all of these symptoms are seen in every case of sports concussion. The most common symptoms reported in concussion literature include:
  • Somatic symptoms such as headache
  • Cognitive symptoms such as feeling like in a fog
  • Emotional symptoms such as lability
  • Physical symptoms such as LOC and amnesia
  • Behavior changes such as irritability
  • Cognitive impairment
  • Sleep disturbance (insomnia)
  • Dizziness and balance problems
  • Blurred vision
  • Fatigue
If any one or more of these symptoms is recognized, a concussion should be suspected and a management plan should be implemented.

Since concussions are often hard to recognize and to diagnose, the Zurich Consensus on Concussion in Sport proposed diagnostic criteria for sideline evaluation. An athlete shows any of the following, they need to be removed from play and assessed.
  • Initial obvious physical signs consistent with concussion (LOC, balance problems)
  • Teammates, trainers, coaches observe cognitive or behavior changes in functioning consistent with concussion symptoms reported
  • Any concussion symptoms reported by the athlete injured
  • Abnormal neurocognitive or balance examination
Following a removal from play:
  • Physician evaluated the player using standard emergency management principles, most notably to exclude  severe head trauma or cervical spine injury
  • Once first aid issues are addressed, assessment of the concussive injury should be made using the SCAT3 or other sideline assessment tools (NHL uses ImPACT concussion testing, read here: http://www.impacttest.com/about/)
  • The player should not be left alone following the injury and serial monitoring for deterioration is essential over the initial few hours following injury
  • A player with diagnosed concussion should not be allowed to return to play on the same day. 
    • It has been unanimously agreed that an athlete should not return to play on the same day of the injury. Studies have shown that athletes allowed back into play following a concussion may demonstrate neuropsychological deficits post injury. 
CONCUSSION MANAGEMENT AND RECOVERY

The graduated return to play protocol following a concussion is a stepwise process and is outline below: 

In this stepwise progression, an athlete only proceeds to the next level if they are asymptomatic at the current level. Each step should take at least 24 hours, making the minimum amount of time to proceed through the full rehabilitation protocol one full week. Athletes should never return to play on the same day as an injury.

THE BACKES INJURY

St. Louis Blues captain David Backes left Game 2 today with 4:51 to play after a brutal check to the head by Chicago Blackhawks defenseman Brent Seabrook. Backes was behind the Blackhawks' net and overskated the puck, as he attempted to curl back towards the puck, Seabrook approached from the circles and leveled Backes with a check to the head.

Credit to @myregularface

The principal point of contact is Backes' head. Not only does Seabrook's shoulder hit Backes' head directly, but the back of his head hits the boards immediately after. Backes laid motionless on the ice following the hit, although he didn't lose consciousness, this isn't a good sign. When he tried to get up, Backes had balance issues and clearly looked dazed. As the Blues' athletic trainer held him back, Backes struggled to stay on his skates and needed help getting to the locker room. 

As bolded above, Backes clearly exhibits signs of a concussion with balance issues, a vacant stare and the inability to follow the athletic trainer's directions of staying out of the scrum following the hit. Backes left the game and didn't return for overtime which is the right move. Following a hit to the head, especially this severe, the player should never return to play the same day.

Backes will need a lot of rest. The Blues doctors will make a detailed management plan after an assessment today and tomorrow morning. Backes will want to play Monday night undoubtedly, but it probably isn't the best move following a hit like this. Concussions require a minimum of 6 days of recovery as detailed above, but this isn't often followed. Backes shouldn't be rushed back, especially considering the Blues are up 2-0 in the series. 

Tuesday, April 15, 2014

On-ice evaluation and management of head and neck injuries

In last night's final regular season game for the Vancouver Canucks, a scary incident occurred towards the end of the second period. While going to retrieve the puck in the defensive zone, Daniel Sedin skated towards the end boards and took a hit from behind from Calgary Flames forward Paul Byron, going head-first into the glass.

Sedin lay still on the ice for several minutes before the Canucks physician and medical staff were able to complete the thorough neurological protocol. Sedin was taken to Vancouver General Hospital in stable condition on a stretcher and underwent further evaluation. Byron was assessed a five-minute major for boarding and a game misconduct.

The video below recaps the whole situation, including Sedin being stretchered off the ice:


The good news is that Sedin was released from the hospital later that night. He acquired a CT scan and is apparently injury free. He recaps the situation here on Canucks clean-out day:


Following a head or neck injury like Sedin's last night, there is strict protocol medical staff must follow.  I'll try to detail that as much as possible.

Head and neck injuries are usually the result of either direct (hit to the head) or indirect contact (hit causing the head/neck to be injured, a la Sedin). Head and neck injuries are the most serious in all of sports, as consequences of neurological injuries have a potentially high incidence of morbidity and mortality. Studies have estimated that 70% of traumatic deaths and 20% of permanent disability in sports-related injuries are due to head and neck injuries (Van Camp et al, Mueller et al.).

Head and neck injuries require immediate assessment and action. The initial assessment of an injury is important, but challenging for physicians. If an injury is fatal, it causes immediate neurological consequences that are easy to identify (ex: Professor Sid Watkins account of Aryton Senna's death from the documentary Senna). The most challenging aspect of assessing a neurological injury is identifying athletes with a 'mild' injury without immediate symptoms. Often, it takes concussion symptoms up to 24 hours to manifest. When initially assessing the injury, the mechanism and amount of force are considered in the diagnosis.

There are five steps to managing a head or neck injury that occurs during play. Physicians will always err on the side of caution. They are:

  1. Preparation for any neurological injury (assembling paramedics, equipment, worst-case scenarios)
  2. Suspicion and recognition (no official diagnosis made, based on observation and patient reporting)
  3. Stabilization and safety (depending on severity, could mean securing the body on a stretcher or just moving to a better location off-ice in a safe manner).
  4. Immediate treatment and possible secondary treatment (CPR if necessary, etc.)
  5. Evaluation for return to play (long-term...players suffering a possible concussion should NOT return to play the same day)

A physician will start with a basic safety evaluation which includes the ABC (Airway, Breathing and Circulation) evaluation. If the athlete doesn't have the normal ABC's (not breathing, no pulse) CPR should be initiated immediately (this is what happened with Peverley a few months ago).

Additionally, if there is any suspicion of a head or neck injury, the athlete should immediately be assessed for level of consciousness. The most extensively used tool that provides a prognostic indicator for recovery is the Glascow Coma Scale:

A score of >11 is associated with a good prognosis for recovery, while <7 is quite serious with a less favorable prognosis. These 'scales' are debated among the neurological community, however. Is there such a thing as 'mild' head injury if it has lifelong effects?

After checking the ABCs, if an athlete is conscious and alert, the physician will caution them to remain still; they will also ask them what is wrong and if they feel any pain. If an athlete has any head, neck, or back pain, they should not be moved until the spine is stabilized. The player's helmet and padding should not be removed; removal can cause unwanted motion or worsening of the fracture which could result in permanent nerve damage/paralysis. Players should not be moved until trained paramedics are able to assist. If players are in the prone position, proper log rolling technique is used to move them into a supine position for better assessment.

A hard cervical collar and a spine board should always be used to prevent further injury until a cervical injury can definitely be excluded. As seen in the image below from last night, Sedin is completely immobilized. He is strapped securely to the spine board, is wearing a neck brace (after having his helmet carefully removed by a trainer), and his head is strapped down.


Unlike in Sedin's situation, if a cervical spine injury is excluded but there is still fear of a head injury, the player can be slowly assisted to a sitting position which could help decrease intracranial pressure. If the athlete is stable while sitting, they can be assisted to help stand and then escorted to the locker room for further evaluation. During this time, the physician should conduct a complete neurological exam and evaluation. If a head injury is suspected, the player should not return. If the athlete is in unstable condition or is at risk for a deterioration in condition, they should be transported to the hospital.


Sources:

Mueller FO, Cantu RC. Catastrophic injuries and fatalities in high school and college sports, fall
1982 – spring 1988. Med Sci Sports Exerc 1990;22(6):737 – 41.

G. Ghiselli et al. / Clin Sports Med 22 (2003) 445–465.

Van Camp SP, Bloor CM, Mueller FO, et al. Nontraumatic sports death in high school and
college athletes. Med Sci Sports Exerc 1995;27(5):641 – 7.

Sunday, April 13, 2014

Collection of posts at Sports Injury Alert

Lately I've been writing a few short-form articles for Sports Injury Alert's NHL Division when I have the spare time. They don't go as in-depth as some of my posts on my personal site as I aim for a quick analysis of an injury. You can find them here:

Sunday, March 16, 2014

An in-depth analysis of Rich Peverley's heart condition: What is atrial fibrillation and what does it mean for Peverley's hockey career?

Rich Peverley was a part of the huge Boston Bruins - Dallas Stars trade this past summer that sent Tyler Seguin to Dallas and Loui Eriksson and Reilly Smith to Boston (among other pieces). Peverley only missed one game last season and the Stars were happy to add the veteran to their otherwise young forward core.

DIAGNOSING ATRIAL FIBRILLATION 

As part of regular preseason testing, Peverley had an electrocardiogram (ECG/EKG), a simple test that records the heart's electrical activity. Unfortunately, Peverley's EKG was abnormal, showing that the player had atrial fibrillation (afib) - the most common cardiac arrhythmia (heart rhythm disorder/irregular heartbeat), present in about 5 million Americans.

EKG showing atrial fibrillation (top) compared with a normal sinus rhythm (bottom).
The bottom purple arrow shows a P wave (represent depolarization of the atria), which are absent in afib EKGs.
As described in the caption above, atrial fibrillation can be detected by certain abnormal characteristics on an EKG. One of the most common findings is the absence of P waves, which represent depolarization of the atria. Instead of a regular P wave, the EKG shows disorganized electrical activity before the Q wave and the large R waves. Another characteristic of afib is irregular R-R intervals, caused by an irregular conduction of impulses to the ventricles. The R-R interval on a EKG is shown below.


WHAT IS ATRIAL FIBRILLATION? 

To understand afib, you need to understand the heart's anatomy and electrical system. Your heart has four chambers - two atria (top) and two ventricles (bottom). The atria are small pumps that act as a primer, pushing blood into the ventricles which then pumps the blood out to the rest of the body. The electrical system is what causes the myocardium (muscle of the heart) to be stimulated and cause contraction in the chambers. 

The heart's electrical system controls the rate and rhythm of the heartbeat. With each heartbeat, an electrical signal spreads from the top of the heart in the atria to the bottom, causing the heart to contract and pump blood. In normal hearts, the electrical signal begins in the sinus node (or sinoatrial - SA node) which is located in the right atrium. The signal travels through the right and left atria, causing the atria to contract and pump blood into the ventricles, then moving to the atrioventricular (AV) node and slowing down slightly to allow the ventricles to fill up with blood. After the electrical signal leaves the AV node and travels down to the ventricles, causing them to contract and pump blood to the lungs and the rest of the body. This process is shown in the gifs below: 
A normal sinus rhythm
In atrial fibrillation, the electrical system is flawed. The signal doesn't begin in the SA node but rather at a different part of the atria or in several parts of the atria. The signals can clash and cause different impulses and don't travel normally, spreading throughout the atria in a rapid and disorganized manner. This causes the atria to fibrillate (quiver) and and the atria/ventricles to no longer beat in a coordinated way as the ventricles don't completely fill with blood.
Haywire electrical signals that occur during atrial fibrillation
As the electrical signal passes to the ventricles, they can beat too quickly (rapid ventricle response tachycardia) and the ventricle is pumping without completely filling with blood. With the heart beating so fast beyond normal range (tachycardia) and not pumping enough blood to the rest of the body, you become dizzy and nauseous. Eventually your blood pressure drops rapidly (hypotension) , your brain and muscles aren't receiving as much oxygen as they should, and you can pass out/collapse (syncope). 

Additionally, Afib increases the likelihood of a stroke because blood clots can form while swirling around the atria and not properly flowing through to the ventricles. 

TREATING ATRIAL FIBRILLATION 

Normally, afib resolves on it's own and the heart is able to reset and start pumping blood normally. Afib is fairly common and generally not life-threatening. The condition can be controlled with medications, starting with blood-thinners to prevent clots. It's highly unlikely Peverley was on an intense blood thinner such as warfarin but could have been taking low doses of aspirin. Doctors can also prescribe medications which can help control heart rate, such as beta blockers and calcium channel blockers. However, even with these medications, Peverley (as an NHL athlete) still faced huge risks due to the intense nature of the game which requires short bursts of activity.

Afib can also be treated with a procedure known as a cardiac ablation. Peverley had an ablation earlier during the preseason, however, even following a successful ablation, almost a 1/3 of patients will have recurring symptoms. An ablation is a procedure where a catheter is threaded up into the heart through vessels in the leg and to the problem location of the heart.  Once the catheter is in place, electrodes on the end measure the electrical activity (detect an arrhythmia), detect the problem area, and they are then ablated either using radiofrequency pulses (which burn the area) or through cryoablation (freezes).

UPDATE: Peverley apparently did not undergo an ablation this past preseason. Peverley underwent a cardioversion procedure. There are two forms of cardioversion; synchronized electrical cardioversion and pharmacologic (chemical) cardioversion. Synchronized electrical cardioversion uses two electrode pads to deliver a therapeutic reversion shock that is timed at a certain point in the cardiac cycle (synchronization). This differs from defibrillation which is supposed to re-start the rhythm of the heart. Pharmacological cardioversion uses agents such as sodium channel blockers, beta blockers and calcium channel blockers to stabilize the heart (rhythm control).

WHAT HAPPENED ON MARCH 10TH? 

Not even halfway through the first period, Peverley finished a shift and collapsed suddenly on the Stars bench. In a chaotic scene, the Stars players were frantic to get the refs attention and stop the game. The trainers and medical staff immediately picked Peverley up and hustled him down the tunnel. Information was very limited and the press, announcers and fans were confused as to what just happened.
Amazing, no? The Stars then released this bit of information:
And everyone started worrying. Eventually, people connected the dots that Peverley had missed the preseason due to his afib, and even missed a game last week due to "feeling strange," a possible recurrence of his condition.

The following day, Dr. Gil Salazar (emergency physician) from UT Southwestern released a statement with the Stars explaining the situation and what the medical staff did with Peverley:
"We provided oxygen for him. We started an IV. We did chest compressions on him and defibrillated him, provided some electricity to bring a rhythm back to his heart, and that was successful with one attempt, which is very reassuring."
So, within a matter of minutes, Peverley got almost instantaneous CPR and a shock from an automated external defibrillator (AED). The fact that he needed to be shocked means his arrhythmia turns from a fib into vfib. It's excellent news that Peverley was conscious and talking after just one shock which probably re-started his normal heart rhythm.

Peverley will undergo a battery of tests including another EKG and probably an echocardiogram. It was revealed that Peverley now has a device that can detect his heart rhythm and deliver a shock if necessary.
This device is probably an implantable cadioverter defibrillator, which uses electrical pulses or shocks to help control life-threatening arrhythmias. The ICD has wires with electrodes that connect to the heart chambers and has the ability to detect an abnormal rhythm. ICDs aren't the same as pacemakers which can only give low-energy electrical pulses to correct certain irregular heartbeats. ICDs can give high-energy pulses which are needed to correct dangerous arrhythmias in the ventricles. The image below displays the difference:

UPDATE: Peverley hasn't had an ICD implanted yet, nor has he had an ablation. It's likely that the procedure he'll undergo in Cleveland will be an ablation or another cardioversion.It's unlikely Peverley will get an ICD since it would be nearly impossible to play in the future with one (getting hit would dislodge the leads). 

 Two days after the chaotic event, the Stars announced that Peverley is out for the season and will undergo a procedure on his heart and pursue other treatments.
It's probably best that Peverley isn't playing. He'll probably undergo an ablation. Another surgical option is the maze surgery, an open-heart surgery that is usually only done if absolutely necessary (such as for heart valve disease). During this procedure, the surgeon makes small cuts and burns in the atria to prevent the spread of disorganized electrical signals. Considering Peverley's condition (NHL athlete) it's very unlikely he'll undergo this procedure.

It's unclear what this means for the rest of his career. Everyone in the NHL wishes Pevs the best in this scary situation and we're glad he's doing well.

Saturday, March 15, 2014

Injury history of the deadline's traded players

A few huge moves were made at the NHL trade deadline. Below I'll list some of the major players traded their respective injury history so fans of the new player's team can understand what type of player they acquired and their accompanying injury history.

Monday, March 10, 2014

Quick Take: Dallas Stars Rich Peverley collapses on bench during 1st period, taken to hospital

Something went wrong during tonight's Columbus Blue Jackets @ Dallas Stars game as Stars players were frantic to get the referees attention and halt the game. After collapsing on the bench, Stars center Rich Peverley was rushed down the tunnel on a stretcher by the Dallas Stars trainers and medical staff. Peverley reportedly has an irregular heartbeat (arrhythmia) which could have contributed to his collapse. It is unclear at this time whether Peverley suffered a heart attack.

Sunday, March 9, 2014

Stars' Kari Lehtonen "not doing well" after last night's collision

After last night's Dallas Stars 4-3 win over the Minnesota Wild, Stars coach Lindy Ruff was upset about the hit that took his star goaltender out of the game at 6:37 of the third period. The Wild's Erik Haula came barreling over Lehtonen, causing the goaltender to lose his helmet and fall backwards, hitting the back of his head against the crossbar. Lehtonen immediately left the ice, looking very dazed as he was bleeding from his head.

Credit to u/crazy_canucklehead on r/hockey

In addition to stitches for the wound, it's probable Lehtonen suffered a concussion. Haula recieved 15 minutes in penalties, a major for charging and a 10 minute game misconduct.