While cricket is an unlikely source of concussion, the fierce contagion of media coverage surrounding Rugby and Gaelic Football has led to difficulties in deciphering real from perceived risk. The surge in public interest has forced this young science to mature quickly. The principles of managing head injury have not changed, but there is now a greater awareness that concussion is a traumatic brain injury (TBI).

Concussion is a poorly understood, historical term, used to describe a low velocity injury causing brain “shaking.” This results in a nebulous cluster of non-specific symptoms. The most recent attempt to redefine the term was in 2012 (Zurich). The key features of concussion involve the transmission of an impulsive force to the head, the rapid onset of transient, spontaneously resolving neurological impairment, and clinical symptoms that may or may not involve loss of consciousness¹.

Intrinsic to this definition is the viewpoint that concussion is a reversible syndrome caused by a functional, rather than a structural disturbance. On the surface, the absence of associated structural changes on conventional neuroimaging studies would seem to support this. However, as early as 1974, Ommaya et al. recognized that biomechanical sheer forces in concussion caused disruption of the mesencephalon, representing a diffuse TBI².

Not all of the symptoms associated with concussion are as temporary as physicians have traditionally come to believe. These are sometimes lumped together into a “post-concussion syndrome”, including: headache, disturbances to cognition, emotion, behaviour, and sleep patterns^3. These may persist for weeks to months after the original injury. A growing body of studies have examined the association between repeated concussion and long term risks of depression and suicide⁴. Premature return to play after concussion is also associated with higher risk of time loss injuries⁵. It also exposes the player to Second Impact Syndrome (SIS).

We need little reminder of the case of Benjamin Robinson in 2011 who tragically died from SIS. In SIS, an individual sustains a second impact before the first has resolved, followed by a rapid neurological deterioration with the development of significant cerebral oedema⁶. Although our understanding of this phenomenon is limited, the idea of preventing additional injury in brain trauma is not a novel concept.

Repeated concussion is associated with long term structural changes in the brain. Pathological studies of NFL players’ brains have shown neurodegenerative changes with neurofibrillary tangles and tau-positive neuritic threads, which has come to be known as chronic traumatic encephalopathy (CTE)⁷. This is well established in the literature and Ireland is no stranger to it. When Kenny Nuzum, the former prop from Landsdowne rugby club died in 2014, the Dublin City Coroner attributed his death to CTE, sustained from repeated head collisions, making it a landmark case.

More research is needed to correlate the symptoms to the pathological findings. Tau protein is not specific to head trauma.  It can be seen in neurodegenerative conditions, drug abuse and aging without neurological deficits. At present, the distribution of tau deposition is what differentiates CTE from other tauopathies⁸. It is unclear whether these pathological changes represent an inevitable, progressive neurodegenerative condition from playing contact sport.

In the midst of these fears and potential risks, how do we ensure player safety?

The goal of pitchside assessment should be focused on identifying individuals who have had a concussion and promptly removing them from play. These include symptoms such as loss of consciousness, seizures, balance disturbances, confusion, disorientation, behavioural changes, as well as any focal neurological signs. Different screening methods, such as the IRB’s Head Injury Assessment (HIA) tool or the Sport Concussion Assessment Tool (SCAT3), can assist in the decision-making process in situations where the symptoms seem unclear, but any clinical suspicion of concussion should be followed up with a removal from play and concussion management.

Once a player has been removed from play, the cornerstone of management is physical and cognitive rest until the acute symptoms resolve, and then a graded program of exertion prior to medical clearance and return to play¹.  However, the duration of time and type of rest required to prevent the occurrence of long term sequelae is neither understood nor well documented. Leddy et al. recently suggested that absolute rest beyond the first few days after concussion may be detrimental to recovery. Instead, they advocate that sub-symptom threshold exercise improves activity tolerance and is an appropriate treatment option for this patient population⁹.

In order to help assess the severity of a concussion, there has been a push to identify biomarkers and develop blood tests mild traumatic brain injury. A recent prospective study showed that blood levels of GFAP and ubiquitin C-terminal hydrolase L1 (UCH-L1) correlated with moderate TBI as well as radiological findings on CT brain. The markers are first detectible within 1 hour, reach their peak over 20 hours, and decline over 72 hours¹⁰. However, more sensitive assays will be needed if this is to play a role in assessing mild TBI.

It is essential that sports physicians keep up to date with new developments in concussion management. Figures which will be released in the coming weeks by World Rugby show the number of “head injuries” in the RWC 2015 increased significantly compared to the 2011 tournament. By contrast, the incidence of other injuries remained unchanged. This was also seen in the recently published English Professional Rugby Surveillance Project. Results from this study show the overall likelihood of a player sustaining a match or training injury remained stable last season and within the expected range of variation seen since the project began in 2002. We would contend that the spike in “concussion” rates is related to successful educational/awareness programmes and not a reflection of a physical change in the sport.

Several challenges still remain in the amateur game. In professional rugby, an independent match day doctor assists team doctors. Amateur sport does not have this luxury. It is an ethical challenge for team doctors to objectively safeguard player welfare while preserving the players' autonomy and desire to play for the interests of the team.

To compound this, there appears to be a lack of understanding amongst some team doctors, in this country, regarding the guidelines for head injuries. This point was clearly highlighted in a recent Leinster schools senior cup game as well as an inter-county footballer inexplicably remained on the pitch after suffering a significant head injury. “If in doubt, sit them out.”

To this end, who ultimately has responsibility of ensuring that team physicians in both rugby and GAA are suitability qualified? The IRFU/GAA? Provincial/County boards? Individual clubs? Does the responsibility rest solely on the shoulders of the team physician? This question needs to be addressed in a timely manner. 

Player welfare contracts need to be in place before a team competes in a tournament. Sanctions should be placed if the team/physician do not adhere to the strict guidelines, similar to the Terms of Participation (ToP) set out by World Rugby. Independent specialists are also required, to externally review decisions with feedback to the individual player, their primary care physicians, and their club. The authors also suggest that referees are made aware of the concussion history of every player on the pitch prior to kickoff.

We are seeing more young men and women coming to our clinic after reported sporting head injuries. Awareness is improving, but it is up to the governing bodies and independent medics to provide expert advice in the recovery phase. Emotion and sensationalism need to be removed from this debate and evidence-based medicine implemented.

This manuscript reflect the views of the authors only and are not representative of the individual hospitals. The authors have no disclosures to make.

 

Correspondence:

Name: Mr. Philip O’Halloran

Email: [email protected]

 

References:

1. McCrory P, Meeuwisse WH, Aubry M, Cantu B, Dvorák J, Echemendia RJ, Engebretsen L, Johnston K, Kutcher JS, Raftery M, Sills A, Benson BW, Davis GA, Ellenbogen RG, Guskiewicz K, Herring SA, Iverson GL, Jordan BD, Kissick J, McCrea M, McIntosh AS, Maddocks D, Makdissi M, Purcell L, Putukian M, Schneider K, Tator CH, Turner M. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med. 2013 Apr;47:250-8.

2. Ommaya AK, Gennarelli TA. Cerebral concussion and traumatic unconsciousness. Correlation of experimental and clinical observations of blunt head injuries. 1974 Dec;97:633-54.

3.Ganti L, Khalid H, Patel PS, Daneshvar Y, Bodhit AN, Peters KR. Who gets post-concussion syndrome? An emergency department-based prospective analysis. Int J Emerg Med. 2014 Aug 20;7:31.

4. Fazel S, Wolf A, Pillas D, Lichtenstein P, Långström N. Suicide, fatal injuries, and other causes of premature mortality in patients with traumatic brain injury: a 41-year Swedish population study. JAMA Psychiatry. 2014 Mar;71:326-33.

5. Cross M, Kemp S, Smith A, Trewartha G, Stokes K. Professional Rugby Union players have a 60% greater risk of time loss injury after concussion: a 2-season prospective study of clinical outcomes. Br J Sports Med. 2015 Dec 1.

6. Hebert O, Schlueter K, Hornsby M, Van Gorder S, Snodgrass S, Cook C. The diagnostic credibility of second impact syndrome: A systematic literature review. J Sci Med Sport. 2016 Jan 6.

7. Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005 Jul;57:128-34

8. Cairns NJ, Dickson DW, Folkerth R, Keene CD, McKee A, Perl D, Thor Stein, Willie Stewart, Jean Paul Vonsattel: Report from the First NIH Consensus Conference to Define the Neuropathological Criteria for the Diagnosis of Chronic Traumatic Encephalopathy. NIH.gov.

9. Leddy J, Hinds A, Sirica D, Willer B. The Role of Controlled Exercise in Concussion Management. PM R. 2016 Mar;8:S91-S100.

10. Papa L, Brophy GM, Welch RD, Lewis LM, Braga CF, Tan CN, Ameli NJ, Lopez MA, Haeussler CA, Mendez Giordano DI, Silvestri S, Giordano P, Weber KD, Hill-Pryor C, Hack DC. Time Course and Diagnostic Accuracy of Glial and Neuronal Blood Biomarkers GFAP and UCH-L1 in a Large Cohort of Trauma Patients With and Without Mild Traumatic Brain Injury. JAMA Neurol. 2016 Mar 28.

P403